https://proteopedia.org/api.php?action=feedcontributions&feedformat=atom&user=Kelly+DegnonProteopedia - User contributions [en]2026-09-16T21:27:49ZUser contributionsMediaWiki 1.43.8https://proteopedia.org/index.php?title=STK11&diff=2743680STK112017-04-27T00:50:55Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11 complexed with STRADA and MO25 (PDB code [[2wtk]])' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
'''Serine-threonine kinase 11''' (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity, and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STE20-related adaptor alpha (STRADA) and the mouse protein 25 (MO25). Both STRADA and MO25 allosterically promote the activation of STK11. In addition to activating STK11, MO25 stabilizes STK11 though interacting with the activation loop. The alpha helix is rotated into a closed conformation, conserving the salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene>. This is where the active conformation is formed <ref> PMID: 19892943 </ref>. STK11 facilitates cell cycle arrest through induction of a cyclin-dependent kinase inhibitor, p21WAF1, through a p53-dependent process to prevent cancer formation <ref name="loss"> PMID: 12861065</ref>. Cyclin-dependent kinase inhibitors like p21WAF1 function as a tumor suppressor gene that inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. The gene p21WAF1is also critical for regulating proper cell division. STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous expression of brg1 is able to induce cell cycle arrest thus resulting in a loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues <ref> PMID: 9428765 </ref>.<br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STRADA and MO25. STRADA, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRADA, and as a result enhances the kinase activity of STK11 <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine </ref>. STK11 has a <scene name='72/728131/Atp_binding_site/1'>ATP binding site</scene> located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an <scene name='72/728131/Active_site_1/1'>active site</scene> at Asp176, which serves as a proton acceptor <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref>.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). Individuals with this germline mutation are diagnosed with Peutz-Jeghers Syndrome (PJS), an autosomal dominant mutation caused by a disruption of the kinase domain. This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated with an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). <ref name="PJ"> PMID: 9425897</ref>, particularly p21WAF1 <ref name="loss" />. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase 2 to regulate apoptosis <ref> PMID: 25329316 </ref>. Therefore, a mutation in STK11 leads to CDKN1A malfunction resulting in uncontrolled growth. In addition to cancerous growth, PJS is also characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="PJ" />. <br />
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==Contributors==<br />
Kelly Degnon, Stephanie Thai, Momo Sullivan, Kristen Zielinski, Chelsea Amagoh<br />
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<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=User:Kelly_Degnon/Sandbox_1&diff=2743623User:Kelly Degnon/Sandbox 12017-04-26T00:49:28Z<p>Kelly Degnon: </p>
<hr />
<div>==Serine/Threonine-Protein Kinase STK11==<br />
<StructureSection load='Final.casp (2).pdb' size='340' side='right' caption='Structure of the STK11 Protein' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
To carry out enzymatic activities, STK11 forms a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances STRAD’s effect on STK11’s kinase activity. <br />
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<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
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[[Image:STK11.jpeg]]<br />
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== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
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<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
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This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
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<br />
==Contributors==<br />
Kelly Degnon, Stephanie Thai, Chelsea Amagoh, Momo Sullivan, Kristen Zielinski<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=STK11&diff=2588828STK112016-04-28T11:45:39Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11 complexed with STRADA and MO25' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase 11 (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity, and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STE20-related adaptor alpha (STRADA) and the mouse protein 25 (MO25). Both STRADA and MO25 allosterically promote the activation of STK11. In addition to activating STK11, MO25 stabilizes STK11 though interacting with the activation loop. The alpha helix is rotated into a closed conformation, conserving the salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene>. This is where the active conformation is formed <ref> PMID: 19892943 </ref>. STK11 facilitates cell cycle arrest through induction of a cyclin-dependent kinase inhibitor, p21WAF1, through a p53-dependent process to prevent cancer formation <ref name="loss"> PMID: 12861065</ref>. Cyclin-dependent kinase inhibitors like p21WAF1 function as a tumor suppressor gene that inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. The gene p21WAF1is also critical for regulating proper cell division. STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous expression of brg1 is able to induce cell cycle arrest thus resulting in a loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues <ref> PMID: 9428765 </ref>.<br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STRADA and MO25. STRADA, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRADA, and as a result enhances the kinase activity of STK11 <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine </ref>. STK11 has a <scene name='72/728131/Atp_binding_site/1'>ATP binding site</scene> located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an <scene name='72/728131/Active_site_1/1'>active site</scene> at Asp176, which serves as a proton acceptor <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref>.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). Individuals with this germline mutation are diagnosed with Peutz-Jeghers Syndrome (PJS), an autosomal dominant mutation caused by a disruption of the kinase domain. This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated with an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). <ref name="PJ"> PMID: 9425897</ref>, particularly p21WAF1 <ref name="loss" />. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase 2 to regulate apoptosis <ref> PMID: 25329316 </ref>. Therefore, a mutation in STK11 leads to CDKN1A malfunction resulting in uncontrolled growth. In addition to cancerous growth, PJS is also characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="PJ" />. <br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=STK11&diff=2588825STK112016-04-28T11:22:43Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11 complexed with STRADA and MO25' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase 11 (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity, and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STE20-related adaptor alpha (STRADA) and the mouse protein 25 (MO25). Both STRADA and MO25 allosterically promote the activation of STK11. In addition to activating STK11, MO25 stabilizes STK11 though interacting with the activation loop. The alpha helix is rotated into a closed conformation, conserving the salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene>. This is where the active conformation is formed <ref> PMID: 19892943 </ref>. STK11 facilitates cell cycle arrest through induction of a cyclin-dependent kinase inhibitor, p21WAF1, through a p53-dependent process to prevent cancer formation <ref name="loss"> PMID: 12861065</ref>. Cyclin-dependent kinase inhibitors like p21WAF1 function as a tumor suppressor gene that inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. The gene p21WAF1is also critical for regulating proper cell division. STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous expression of brg1 is able to induce cell cycle arrest thus resulting in a loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues <ref> PMID: 9428765 </ref>.<br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STRADA and MO25. STRADA, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11 <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine </ref>. STK11 has a <scene name='72/728131/Atp_binding_site/1'>ATP binding site</scene> located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an <scene name='72/728131/Active_site_1/1'>active site</scene> at Asp176, which serves as a proton acceptor <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref>.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). Individuals with this germline mutation are diagnosed with Peutz-Jeghers Syndrome (PJS), an autosomal dominant mutation caused by a disruption of the kinase domain. This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated with an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). <ref name="PJ"> PMID: 9425897</ref>, particularly p21WAF1 <ref name="loss" />. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase 2 to regulate apoptosis <ref> PMID: 25329316 </ref>. Therefore, a mutation in STK11 leads to CDKN1A malfunction resulting in uncontrolled growth. In addition to cancerous growth, PJS is also characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="PJ" />. <br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=STK11&diff=2588824STK112016-04-28T11:14:01Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11 complexed with STRADA and MO25' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase 11 (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity, and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STE20-related adaptor alpha (STRADA) and the mouse protein 25 (MO25). Both STRADA and MO25 allosterically promote the activation of STK11. In addition to activating STK11, MO25 stabilizes STK11 though interacting with the activation loop. The alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene>. This is where the active conformation is formed <ref> PMID: 19892943 </ref>. STK11 facilitates cell cycle arrest through induction of a cyclin-dependent kinase inhibitor, p21WAF1, through a p53-dependent process to prevent cancer formation <ref name="loss"> PMID: 12861065</ref>. Cyclin-dependent kinase inhibitors like p21WAF1 function as a tumor suppressor gene that inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. The gene p21WAF1is also critical for regulating proper cell division. STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous expression of brg1 is able to induce cell cycle arrest thus resulting in a loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues <ref> PMID: 9428765 </ref>.<br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STRADA and MO25. STRADA, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11 <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine </ref>. STK11 has a <scene name='72/728131/Atp_binding_site/1'>ATP binding site</scene> located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an <scene name='72/728131/Active_site_1/1'>active site</scene> at Asp176, which serves as a proton acceptor <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref>.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). Individuals with this germline mutation are diagnosed with Peutz-Jeghers Syndrome (PJS), an autosomal dominant mutation caused by a disruption of the kinase domain. This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated with an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). <ref name="PJ"> PMID: 9425897</ref>, particularly p21WAF1 <ref name="loss" />. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase 2 to regulate apoptosis <ref> PMID: 25329316 </ref>. Therefore, a mutation in STK11 leads to CDKN1A malfunction resulting in uncontrolled growth. In addition to cancerous growth, PJS is also characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="PJ" />. <br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=STK11&diff=2588823STK112016-04-28T11:11:44Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11 complexed with STRADA and MO25' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase 11 (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity, and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STE20-related adaptor alpha (STRADA) and the mouse protein 25 (MO25). Both STRADA and MO25 allosterically promote the activation of STK11. In addition to activating STK11, MO25 stabilizes STK11 though interacting with the activation loop. The alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene>. This is where the active conformation is formed <ref> PMID: 19892943 </ref>. STK11 facilitates cell cycle arrest through induction of a cyclin-dependent kinase inhibitor, p21WAF1, through a p53-dependent process to prevent cancer formation <ref name="loss"> PMID: 12861065</ref>. Cyclin-dependent kinase inhibitors like p21WAF1 function as a tumor suppressor gene that inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. The gene p21WAF1is also critical for regulating proper cell division. STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous expression of brg1 is able to induce cell cycle arrest thus resulting in a loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues <ref> PMID: 9428765 </ref>.<br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11 <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine </ref>. STK11 has a <scene name='72/728131/Atp_binding_site/1'>ATP binding site</scene> located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an <scene name='72/728131/Active_site_1/1'>active site</scene> at Asp176, which serves as a proton acceptor <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref>.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). Individuals with this germline mutation are diagnosed with Peutz-Jeghers Syndrome (PJS), an autosomal dominant mutation caused by a disruption of the kinase domain. This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated with an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). <ref name="PJ"> PMID: 9425897</ref>, particularly p21WAF1 <ref name="loss" />. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase 2 to regulate apoptosis <ref> PMID: 25329316 </ref>. Therefore, a mutation in STK11 leads to CDKN1A malfunction resulting in uncontrolled growth. In addition to cancerous growth, PJS is also characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="PJ" />. <br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=STK11&diff=2588822STK112016-04-28T11:10:36Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11 complexed with STRADA and MO25' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase 11 (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity, and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STE20-related adaptor alpha (STRADA) and the protein mouse protein 25 (MO25). Both STRADA and MO25 allosterically promote the activation of STK11. In addition to activating STK11, MO25 stabilizes STK11 though interacting with the activation loop. The alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene>. This is where the active conformation is formed <ref> PMID: 19892943 </ref>. STK11 facilitates cell cycle arrest through induction of a cyclin-dependent kinase inhibitor, p21WAF1, through a p53-dependent process to prevent cancer formation <ref name="loss"> PMID: 12861065</ref>. Cyclin-dependent kinase inhibitors like p21WAF1 function as a tumor suppressor gene that inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. The gene p21WAF1is also critical for regulating proper cell division. STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous expression of brg1 is able to induce cell cycle arrest thus resulting in a loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues <ref> PMID: 9428765 </ref>.<br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11 <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine </ref>. STK11 has a <scene name='72/728131/Atp_binding_site/1'>ATP binding site</scene> located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an <scene name='72/728131/Active_site_1/1'>active site</scene> at Asp176, which serves as a proton acceptor <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref>.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). Individuals with this germline mutation are diagnosed with Peutz-Jeghers Syndrome (PJS), an autosomal dominant mutation caused by a disruption of the kinase domain. This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated with an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). <ref name="PJ"> PMID: 9425897</ref>, particularly p21WAF1 <ref name="loss" />. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase 2 to regulate apoptosis <ref> PMID: 25329316 </ref>. Therefore, a mutation in STK11 leads to CDKN1A malfunction resulting in uncontrolled growth. In addition to cancerous growth, PJS is also characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="PJ" />. <br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=STK11&diff=2588791STK112016-04-28T04:17:00Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11 complexed with STRADA and MO25' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase 11 (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop. The STK11 alpha helix is rotated into a closed conformation, conserving the salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the active conformation is formed <ref> PMID: 19892943 </ref>. STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process <ref name="loss"> PMID: 12861065</ref>.<br />
P21 inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues <ref> PMID: 9428765 </ref>.<br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11 <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine </ref>. STK11 has a <scene name='72/728131/Atp_binding_site/1'>ATP binding site</scene> located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an <scene name='72/728131/Active_site_1/1'>active site</scene> at Asp176, which serves as a proton acceptor <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref>.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). Individuals with this germline mutation are diagnosed with Peutz-Jeghers Syndrome (PJS), an autosomal dominant mutation caused by a disruption of the kinase domain. This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated with an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). <ref name="PJ"> PMID: 9425897</ref>, particularly p21WAF1 <ref name="loss" />. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase 2 to regulate apoptosis <ref> PMID: 25329316 </ref>. Therefore, a mutation in STK11 leads to CDKN1A malfunction resulting in uncontrolled growth. In addition to cancerous growth, PJS is also characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="PJ" />. <br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=STK11&diff=2588788STK112016-04-28T03:54:03Z<p>Kelly Degnon: New page: <Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11 complexed with STRADA and MO25' scene='Insert optional scene name here' /> == Function ==...</p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11 complexed with STRADA and MO25' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase 11 (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop. The STK11 alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the active conformation is formed <ref> PMID: 19892943 </ref>. STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process <ref name="loss"> PMID: 12861065</ref>.<br />
P21 inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues <ref> PMID: 9428765 </ref>.<br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11 <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine </ref>. STK11 has a <scene name='72/728131/Atp_binding_site/1'>ATP binding site</scene> located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an <scene name='72/728131/Active_site_1/1'>active site</scene> at Asp176, which serves as a proton acceptor <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref>.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). Individuals with this germline mutation are diagnosed with Peutz-Jeghers Syndrome (PJS), an autosomal dominant mutation caused by a disruption of the kinase domain. This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated with an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). <ref name="PJ"> PMID: 9425897</ref>, particularly p21WAF1 <ref name="loss" />. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase 2 to regulate apoptosis <ref> PMID: 25329316 </ref>. Therefore, a mutation in STK11 leads to CDKN1A malfunction resulting in uncontrolled growth. In addition to cancerous growth, PJS is also characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="PJ" />. <br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=User:Kelly_Degnon/STK11&diff=2588781User:Kelly Degnon/STK112016-04-28T03:44:44Z<p>Kelly Degnon: New page: <Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11 complexed with STRADA and MO25' scene='Insert optional scene name here' /> == Function ==...</p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11 complexed with STRADA and MO25' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase 11 (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop. The STK11 alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the active conformation is formed <ref> PMID: 19892943 </ref>. STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process <ref name="loss"> PMID: 12861065</ref>.<br />
P21 inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues <ref> PMID: 9428765 </ref>.<br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11 <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine </ref>. STK11 has a <scene name='72/728131/Atp_binding_site/1'>ATP binding site</scene> located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an <scene name='72/728131/Active_site_1/1'>active site</scene> at Asp176, which serves as a proton acceptor <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref>.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). Individuals with this germline mutation are diagnosed with Peutz-Jeghers Syndrome (PJS), an autosomal dominant mutation caused by a disruption of the kinase domain. This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated with an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). <ref name="PJ"> PMID: 9425897</ref>, particularly p21WAF1 <ref name="loss" />. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase 2 to regulate apoptosis <ref> PMID: 25329316 </ref>. Therefore, a mutation in STK11 leads to CDKN1A malfunction resulting in uncontrolled growth. In addition to cancerous growth, PJS is also characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="PJ" />. <br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588767Sandbox 4652016-04-28T02:38:37Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11 complexed with STRADA and MO25' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase 11 (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop. The STK11 alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the active conformation is formed <ref> PMID: 19892943 </ref>. STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process <ref name="loss"> PMID: 12861065</ref>.<br />
P21 inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues <ref> PMID: 9428765 </ref>.<br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11 <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine </ref>. STK11 has a <scene name='72/728131/Atp_binding_site/1'>ATP binding site</scene> located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an <scene name='72/728131/Active_site_1/1'>active site</scene> at Asp176, which serves as a proton acceptor <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref>.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). Individuals with this germline mutation are diagnosed with Peutz-Jeghers Syndrome (PJS), an autosomal dominant mutation caused by a disruption of the kinase domain. This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated with an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). <ref name="PJ"> PMID: 9425897</ref>, particularly p21WAF1 <ref name="loss" />. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase 2 to regulate apoptosis <ref> PMID: 25329316 </ref>. Therefore, a mutation in STK11 leads to CDKN1A malfunction resulting in uncontrolled growth. In addition to cancerous growth, PJS is also characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="PJ" />. <br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588474Sandbox 4652016-04-26T15:43:30Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase 11 (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop. The STK11 alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the active conformation is formed <ref> PMID: 19892943 </ref>. STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process <ref name="loss"> PMID: 12861065</ref>.<br />
P21 inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues <ref> PMID: 9428765 </ref>.<br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11 <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine </ref>. STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref>.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A) <ref name="PJ"> PMID: 9425897</ref>, particularly p21WAF1 <ref name="loss" />. Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="PJ" />. <br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588436Sandbox 4652016-04-26T13:30:54Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase 11 (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop. The STK11 alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the active conformation is formed <ref> PMID: 19892943 </ref>. STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process <ref name="loss"> PMID: 12861065</ref>.<br />
P21 inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues <ref> PMID: 9428765 </ref>.<br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11 <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine </ref>. STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref>.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588416Sandbox 4652016-04-26T06:29:49Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase 11 (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop. The STK11 alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the active conformation is formed <ref> PMID: 19892943 </ref> STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process <ref name="loss"> PMID: 12861065</ref> <br />
P21 inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref> STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. <br />
<ref name="loss" /><br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588410Sandbox 4652016-04-26T01:16:16Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase ([[AMPK]]). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop. The STK11 alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the active conformation is formed <ref> PMID: 19892943 </ref> STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process <ref name="loss"> PMID: 12861065</ref> <br />
P21 inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref> STK11 also interacts with brahma-related gene-1 ([[Brg1]]), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. <br />
<ref name="loss" /><br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588407Sandbox 4652016-04-26T01:10:22Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoptosis. It controls the activity of [[adenine monophosphate-activated protein kinase]] (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop. The STK11 alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the active conformation is formed <ref> PMID: 19892943 </ref> STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process <ref name="loss"> PMID: 12861065</ref> <br />
P21 inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref> STK11 also interacts with [[brahma-related gene-1]] (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. <br />
<ref name="loss" /><br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588406Sandbox 4652016-04-26T01:05:16Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop. The STK11 alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the active conformation is formed <ref> PMID: 19892943 </ref> STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process <ref name="loss"> PMID: 12861065</ref> <br />
P21 inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref> STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. <br />
<ref name="loss" /><br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588403Sandbox 4652016-04-26T00:54:07Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoptosis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop <ref> PMID: 19892943 </ref> The STK11 alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the active conformation is formed <ref> PMID: 19892943 </ref> STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process <ref name="loss"> PMID: 12861065</ref> <br />
P21 inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref> STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. <br />
<ref name="loss" /><br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588401Sandbox 4652016-04-26T00:37:50Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoposis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). The STK11 alpha helix is rotated into a closed conformation, conserving salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the active conformation is formed (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13) P21 inhibits apoptosis and may promote cell proliferation in some tumors (http://www.ncbi.nlm.nih.gov/pubmed/19449443). STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13)<br />
<br />
<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588400Sandbox 4652016-04-26T00:37:36Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoposis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 interacting with the STK11 activation loop . The STK11 alpha helix is rotated into a closed conformation, forming the consevered salt bridge between <scene name='72/728131/Lys/1'>lys78</scene> and <scene name='72/728131/Glu/2'>glu98</scene>. This is where the active conformation is formed <ref> PMID: 19892943</ref>. STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process <ref name="loss"> PMID: 12861065 </ref><br />
<br />
<ref> PMID: 12861065 </ref> P21 inhibits apoptosis and may promote cell proliferation in some tumors <ref> PMID: 19449443 </ref>. STK11 also interacts with brahma-related gene-1 (BRG1), an ATPase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation <ref name="loss" /><br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588397Sandbox 4652016-04-26T00:33:47Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoposis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 intracting with the STK11 activation loop (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). The STK11 alpha helix is rotated into a closed conformation, forming the consevered salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the activite conformation is formed (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13) P21 inhibits apoptosis and may promote cell proliferation in some tumors (http://www.ncbi.nlm.nih.gov/pubmed/19449443). STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13)<br />
<br />
<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 gene is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588396Sandbox 4652016-04-26T00:31:52Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoposis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 intracting with the STK11 activation loop (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). The STK11 alpha helix is rotated into a closed conformation, forming the consevered salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/3'>glu98</scene> . This is where the activite conformation is formed (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13) P21 inhibits apoptosis and may promote cell proliferation in some tumors (http://www.ncbi.nlm.nih.gov/pubmed/19449443). STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13)<br />
<br />
<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588393Sandbox 4652016-04-26T00:23:04Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoposis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 intracting with the STK11 activation loop (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). The STK11 alpha helix is rotated into a closed conformation, forming the consevered salt bridge between <scene name='72/728131/Lys/2'>lys78</scene> and <scene name='72/728131/Glu/2'>glu98</scene>. This is where the activite conformation is formed (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13) P21 inhibits apoptosis and may promote cell proliferation in some tumors (http://www.ncbi.nlm.nih.gov/pubmed/19449443). STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13)<br />
<br />
<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588392Sandbox 4652016-04-26T00:18:36Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoposis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 intracting with the STK11 activation loop (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). The STK11 alpha helix is rotated into a closed conformation, forming the consevered salt bridge between <scene name='72/728131/Lys/2'>TextToBeDisplayed</scene> and <scene name='72/728131/Glu/2'>glu98</scene>. This is where the activite conformation is formed (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13) P21 inhibits apoptosis and may promote cell proliferation in some tumors (http://www.ncbi.nlm.nih.gov/pubmed/19449443). STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13)<br />
<br />
<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588382Sandbox 4652016-04-25T21:00:39Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoposis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 intracting with the STK11 activation loop (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). The STK11 alpha helix is rotated into a closed conformation, forming the consevered salt bridge between <scene name='72/728131/Lys/1'>lys78</scene> and <scene name='72/728131/Glu/2'>glu98</scene>. This is where the activite conformation is formed (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13) P21 inhibits apoptosis and may promote cell proliferation in some tumors (http://www.ncbi.nlm.nih.gov/pubmed/19449443). STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13)<br />
<br />
<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588381Sandbox 4652016-04-25T20:59:44Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoposis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 intracting with the STK11 activation loop (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). The STK11 alpha helix is rotated into a closed conformation, forming the consevered salt bridge between <scene name='72/728131/Lys/1'>lys78</scene> lys78 and <scene name='72/728131/Glu/2'>glu98</scene> glu98. This is where the activite conformation is formed (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13) P21 inhibits apoptosis and may promote cell proliferation in some tumors (http://www.ncbi.nlm.nih.gov/pubmed/19449443). STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13)<br />
<br />
<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588380Sandbox 4652016-04-25T20:56:53Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoposis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 intracting with the STK11 activation loop (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). The STK11 alpha helix is rotated into a closed conformation, forming the consevered salt bridge between <scene name='72/728131/Lys/1'>lys78</scene> lys78 and glu98. This is where the activite conformation is formed (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13) P21 inhibits apoptosis and may promote cell proliferation in some tumors (http://www.ncbi.nlm.nih.gov/pubmed/19449443). STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13)<br />
<br />
<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588379Sandbox 4652016-04-25T20:39:42Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoposis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 intracting with the STK11 activation loop (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). The STK11 alpha helix is rotated into a closed conformation, forming the consevered salt bridge between lys78 and glu98. This is where the activite conformation is formed (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/). STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13) P21 inhibits apoptosis and may promote cell proliferation in some tumors (http://www.ncbi.nlm.nih.gov/pubmed/19449443). STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13)<br />
<br />
<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588378Sandbox 4652016-04-25T20:14:06Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
Serine-threonine kinase (STK11) is a tumor suppressor gene that plays an important role in regulating cell growth, cell polarity and apoposis. It controls the activity of adenine monophosphate-activated protein kinase (AMPK). STK11 is regulated by the pseudokinase STRADA and the protein MO25. Both STRADA and MO25 allosterically promote the activation of STK11, which is also stabilized by MO25 intracting with the STK11 activation loop. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/) STK11 facilitates cell cycle arrest through induction of cyclin-dependent kinase inhibitor p21WAF1, through a p53-dependent process. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13) P21 inhibits apoptosis and may promote cell proliferation in some tumors (http://www.ncbi.nlm.nih.gov/pubmed/19449443). STK11 also interacts with brahma-related gene-1 (BRG1), an ATpase that is associated with SWI/SNF chromatin-remodeling complexes. Exogenous express of brg1 is able to induce cell cycle arrest and loss of cell power of division and growth in a retinoblastoma-dependent fashion. The tumor suppression function of STK11 lies within its ability to affect the cell cycle proliferation. (http://www.nature.com/modpathol/journal/v16/n7/full/3880825a.html#bib13)<br />
<br />
<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a <scene name='72/728131/Nucleotide_binding_site/1'>nucleotide binding site</scene> (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588359Sandbox 4652016-04-25T13:36:52Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
<br />
== Function ==<br />
'''Serine/Threonine-protein kinase''' (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity of the [[AMP-activated protein kinase]] (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop within AMPK and non AMPK members. The non AMPK family proteins that it phosphorylates are STRADA, [[PTEN]] and possibly [[p53]]/TP53. The AMPK family members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as an upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of [[PI3K]]/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton. <ref name="Uniprot" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a nucleotide binding site (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). Therefore a mutation in SKT11 leads to CDKN1A malfunction. CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588077Sandbox 4652016-04-21T20:21:41Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' /><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity of the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop within AMPK and non AMPK members. The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. The AMPK family members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as an upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton. <ref name="Uniprot" />.<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over expressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref> PMID: 9428765 </ref><br />
<br />
----<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> <br />
STK11. Genetics Home Reference. National Library of Medicine. </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a nucleotide binding site (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. </ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas (cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract). This is due to improper DNA repair mechanisms and resistance to apoptosis which are both associated to an accumulation of cyclin-dependent kinase inhibitor 1A (CDKN1A). CDKN1A regulates cell development during the G1 and S phase of interphase and activates cyclin-dependent kinase2 to regulate apoptosis. <ref> PMID: 25329316 </ref>. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers (PJ) syndrome, an autosomal genetic dominant mutation caused by a disruption of the kinase domain function. PJ syndrome is characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. <ref> PMID: 9425897 </ref>. <br />
<br />
----<br />
<br />
<br />
== References ==<br />
<references/></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2588060Sandbox 4652016-04-21T15:41:49Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption='Insert caption here' scene='Insert optional scene name here' /><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change in STK11 to form the catalytically active state which transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the interaction between STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref name="STK11" />STK11 has a ATP binding site located at Lys78, a basic amino acid, and a nucleotide binding site (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref name="LKB1" /><br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is overexpressed it is mostly located in the nucleus, having limited amounts in the cytoplasm. When a cell is undergoing apoptosis, STK11 translocates into the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref name ="Nature" /><br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity of the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop within AMPK and non AMPK members. The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. The AMPK family members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as an upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton. <ref name="Uniprot" />.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="Uniprot"/>. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown. <ref name="OMIM" /><br />
<br />
----<br />
<br />
<br />
== References ==<br />
<ref name="STK11"> [1] </ref> STK11. Genetics Home Reference. <br />
<ref name="LKB1"> 10.3390/ijms150916698 </ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. <br />
<ref name="Nature"> [3] </ref> Hemminki A, Markie D, Tomlinson I, Avizienyte E, Roth S, Loukola A, Bignell G, Warren W, Aminoff M, Höglund P, Järvinen H, Kristo P, Pelin K, Ridanpää M, Salovaara R, Toro T, Bodmer W, Olschwang S, Olsen AS, Stratton MR, de la Chapelle A, Aaltonen LA. A serine/threonine kinase gene defective in Peutz-Jeghers syndrome. Nature. 1998 Jan8;391(6663):184-7.<br />
<ref name="Uniprot"> [4] </ref> Boutet E, Lieberherr D, Tognolli M, Schneider M, Bansal P, Bridge AJ, Poux S, Bougueleret L, Xenarios I. UniProtKB/Swiss-Prot, the Manually Annotated Section of the UniProt KnowledgeBase: How to Use the Entry View Methods Mol. Biol. 2016; 1374:23-54.<br />
<ref name="OMIM"> [5] </ref> McKusick, VA, and O’Neill, MJF, Online Mendelian Inheritance in Man, OMIM®, Johns Hopkins University. 2008.</div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2587154Sandbox 4652016-04-13T23:03:47Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption='Insert caption here' scene='Insert optional scene name here' /><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref name="STK11" />STK11 has a ATP binding site located at Lys78, a basic amino acid, and a nucleotide binding site (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref name="LKB1" /><br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues. <ref name ="Nature" /><br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton. <ref name="Uniprot" />.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref name="Uniprot"/>. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown. <ref name="OMIM" /><br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
<br />
== References ==<br />
<ref name="STK11"> [1] </ref> STK11. Genetics Home Reference. <br />
<ref name="LKB1"> 10.3390/ijms150916698 </ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. <br />
<ref name="Nature"> [3] </ref> Hemminki A, Markie D, Tomlinson I, Avizienyte E, Roth S, Loukola A, Bignell G, Warren W, Aminoff M, Höglund P, Järvinen H, Kristo P, Pelin K, Ridanpää M, Salovaara R, Toro T, Bodmer W, Olschwang S, Olsen AS, Stratton MR, de la Chapelle A, Aaltonen LA. A serine/threonine kinase gene defective in Peutz-Jeghers syndrome. Nature. 1998 Jan8;391(6663):184-7.<br />
<ref name="Uniprot"> [4] </ref> Boutet E, Lieberherr D, Tognolli M, Schneider M, Bansal P, Bridge AJ, Poux S, Bougueleret L, Xenarios I. UniProtKB/Swiss-Prot, the Manually Annotated Section of the UniProt KnowledgeBase: How to Use the Entry View Methods Mol. Biol. 2016; 1374:23-54.<br />
<ref name="OMIM"> [5] </ref> McKusick, VA, and O’Neill, MJF, Online Mendelian Inheritance in Man, OMIM®, Johns Hopkins University. 2008.</div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2587143Sandbox 4652016-04-13T22:36:33Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption='Insert caption here' scene='Insert optional scene name here' /><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
STK11 has a molecular mass of approximately 50kDa and is the catalytically active unit of a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances the kinase activity of STK11. <ref> [1] </ref> STK11 has a ATP binding site located at Lys78, a basic amino acid, and a nucleotide binding site (9 residues) consisting of hydrophobic amino acids (such as Gly, Leu, and Val), hydrophilic amino acids (such as Ser and Tyr), a basic amino acid (Lys), and an acidic amino acid (Glu). STK11 also has an active site at Asp176, which serves as a proton acceptor. <ref> 10.3390/ijms150916698 </ref><br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton. <ref>[4]</ref><br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth <ref>[3]</ref>. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown. <ref> [4] </ref><br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
<br />
== References ==<br />
<ref>[1] </ref> STK11. Genetics Home Reference. <br />
<ref> 10.3390/ijms150916698 </ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. <br />
<ref> [3] </ref> Boutet E, Lieberherr D, Tognolli M, Schneider M, Bansal P, Bridge AJ, Poux S, Bougueleret L, Xenarios I. <br />
UniProtKB/Swiss-Prot, the Manually Annotated Section of the UniProt KnowledgeBase: How to Use the Entry View<br />
Methods Mol. Biol. 2016; 1374:23-54.<br />
<ref> [4] </ref> McKusick, VA, and O’Neill, MJF, Online Mendelian Inheritance in Man, OMIM®, Johns Hopkins University. 2008.</div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2587091Sandbox 4652016-04-13T19:25:11Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption='Insert caption here' scene='Insert optional scene name here' /><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
To carry out enzymatic activities, STK11 forms a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances STRAD’s effect on STK11’s kinase activity. <br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown. <ref>PMCID:PMC4200829 </ref><br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
<br />
== References ==<br />
<references/><br />
<br />
<ref> 10.3390/ijms150916698 </ref> Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. <br />
#<ref>[2] </ref> STK11. Genetics Home Reference. <br />
<br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2587076Sandbox 4652016-04-13T18:47:36Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption='Insert caption here' scene='Insert optional scene name here' /><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
To carry out enzymatic activities, STK11 forms a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances STRAD’s effect on STK11’s kinase activity. <br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
<br />
== References ==<br />
<references/><br />
<ref>Gan RY, Li HB. Recent Progress on Liver Kinase B1 (LKB1): Expression, Regulation, Downstream Signaling and Cancer Suppressive Function. International Journal of Molecular Science. 2014 Sep; 15(9):16698-16718. PMCID:PMC4200829 doi:10.3390/ijms150916698 </fef><br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2587073Sandbox 4652016-04-13T18:31:54Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption='Insert caption here' scene='Insert optional scene name here' /><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
To carry out enzymatic activities, STK11 forms a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances STRAD’s effect on STK11’s kinase activity. <br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2587072Sandbox 4652016-04-13T18:29:39Z<p>Kelly Degnon: </p>
<hr />
<div><StructureSection load='2WTK'' size='350' frame='true' align='right' side='right' caption='Structure of the STK11 Protein' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
To carry out enzymatic activities, STK11 forms a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances STRAD’s effect on STK11’s kinase activity. <br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2587071Sandbox 4652016-04-13T18:28:33Z<p>Kelly Degnon: </p>
<hr />
<div><br />
<StructureSection load='2WTK'' size='350' frame='true' align='right' side='right' caption='Structure of the STK11 Protein' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
To carry out enzymatic activities, STK11 forms a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances STRAD’s effect on STK11’s kinase activity. <br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2587065Sandbox 4652016-04-13T18:23:45Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption='Insert caption here' scene='Insert optional scene name here' />==Serine/Threonine-Protein Kinase STK11==<br />
<StructureSection load='Final.casp (2).pdb' size='340' side='right' caption='Structure of the STK11 Protein' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
To carry out enzymatic activities, STK11 forms a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances STRAD’s effect on STK11’s kinase activity. <br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2587063Sandbox 4652016-04-13T18:22:12Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption='Insert caption here' scene='Insert optional scene name here' />==Serine/Threonine-Protein Kinase STK11==<br />
<StructureSection load='Final.casp (2).pdb' size='340' side='right' caption='Structure of the STK11 Protein' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
To carry out enzymatic activities, STK11 forms a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances STRAD’s effect on STK11’s kinase activity. <br />
<br />
<scene name='72/728131/Stk11/5'>TextToBeDisplayed</scene><br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2587061Sandbox 4652016-04-13T18:20:23Z<p>Kelly Degnon: </p>
<hr />
<div><Structure load='2wtk' size='350' frame='true' align='right' caption='Insert caption here' scene='Insert optional scene name here' />==Serine/Threonine-Protein Kinase STK11==<br />
<StructureSection load='Final.casp (2).pdb' size='340' side='right' caption='Structure of the STK11 Protein' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
To carry out enzymatic activities, STK11 forms a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances STRAD’s effect on STK11’s kinase activity. <br />
<br />
<scene name='72/728131/Stk11/5'>TextToBeDisplayed</scene><br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
[[Image:STK11.jpeg]]<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=Sandbox_465&diff=2586789Sandbox 4652016-04-12T14:37:20Z<p>Kelly Degnon: New page: ==Serine/Threonine-Protein Kinase STK11== <StructureSection load='Final.casp (2).pdb' size='340' side='right' caption='Structure of the STK11 Protein' scene=''> This is a default text for ...</p>
<hr />
<div>==Serine/Threonine-Protein Kinase STK11==<br />
<StructureSection load='Final.casp (2).pdb' size='340' side='right' caption='Structure of the STK11 Protein' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
To carry out enzymatic activities, STK11 forms a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances STRAD’s effect on STK11’s kinase activity. <br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
[[Image:STK11.jpeg]]<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=User:Kelly_Degnon/Sandbox_1&diff=2586599User:Kelly Degnon/Sandbox 12016-04-12T03:16:09Z<p>Kelly Degnon: </p>
<hr />
<div>==Serine/Threonine-Protein Kinase STK11==<br />
<StructureSection load='Final.casp (2).pdb' size='340' side='right' caption='Structure of the STK11 Protein' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
To carry out enzymatic activities, STK11 forms a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances STRAD’s effect on STK11’s kinase activity. <br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
[[Image:STK11.jpeg]]<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=File:Final.casp_(2).pdb&diff=2586598File:Final.casp (2).pdb2016-04-12T03:10:41Z<p>Kelly Degnon: PDB of STK11 found through Phyre2</p>
<hr />
<div>== Summary ==<br />
PDB of STK11 found through Phyre2<br />
== Licensing ==<br />
{{subst:No license from license selector|Don't know}}</div>Kelly Degnonhttps://proteopedia.org/index.php?title=User:Kelly_Degnon/Sandbox_1&diff=2586574User:Kelly Degnon/Sandbox 12016-04-11T20:54:51Z<p>Kelly Degnon: </p>
<hr />
<div>==Serine/Threonine-Protein Kinase STK11==<br />
<StructureSection load='1stp' size='340' side='right' caption='Caption for this structure' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
To carry out enzymatic activities, STK11 forms a heterotrimeric complex with STE20-related adaptor (STRAD) and mouse protein 25 (MO25). STRAD, a pseudokinase, induces a conformational change of STK11 into its catalytically active state and transports STK11 from the nucleus to the cytoplasm. MO25, a scaffold protein, strengthens the binding of STK11 and STRAD, and as a result enhances STRAD’s effect on STK11’s kinase activity. <br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
[[Image:STK11.jpeg]]<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=User:Kelly_Degnon/Sandbox_1&diff=2586572User:Kelly Degnon/Sandbox 12016-04-11T20:42:42Z<p>Kelly Degnon: </p>
<hr />
<div>==Serine/Threonine-Protein Kinase STK11==<br />
<StructureSection load='1stp' size='340' side='right' caption='Caption for this structure' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
[[Image:STK11.jpeg]]<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11><br />
#<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200829/><br />
#<http://www.uniprot.org/uniprot/Q15831></div>Kelly Degnonhttps://proteopedia.org/index.php?title=User:Kelly_Degnon/Sandbox_1&diff=2586350User:Kelly Degnon/Sandbox 12016-04-10T21:47:38Z<p>Kelly Degnon: </p>
<hr />
<div>==Serine/Threonine-Protein Kinase STK11==<br />
<StructureSection load='1stp' size='340' side='right' caption='Caption for this structure' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
[[Image:STK11.jpeg]]<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11></div>Kelly Degnonhttps://proteopedia.org/index.php?title=User:Kelly_Degnon/Sandbox_1&diff=2586342User:Kelly Degnon/Sandbox 12016-04-10T21:41:18Z<p>Kelly Degnon: </p>
<hr />
<div>==Serine/Threonine-Protein Kinase STK11==<br />
<StructureSection load='1stp' size='340' side='right' caption='Caption for this structure' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
[[Image:STK11.jpeg]]<br />
<br />
----<br />
<br />
== Function ==<br />
Serine/Threonine-protein kinase (STK11) is a tumor suppressor that plays a role in cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 controls the activity or the AMP-activated protein kinase (AMPK) family members as well as other non AMPK family members. This enzyme acts by phosphorylating the T-loop of AMPK and non AMPK members.The non AMPK family proteins that it phosphorylates are STRADA, PTEN and possibly p53/TP53. While the AMPK members it phosphorylates are PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2 and others but not MELK. STK11 acts as a upstream regulator by mediating phosphorylation and activation of the AMPK catalytic subunits PRKAA1 and PRKAA2. It also regulates activation of autophagy when cells undergo nutrient deprivation, B-cell differentiation in the germinal center in response to DNA damage and inhibition of signaling pathway that promotes cell growth and proliferation when energy levels are low. Its inhibition of PI3K/Akt signaling activity in vein endothelial cells induces apoptosis in response to the oxidant peroxynitrite (in vitro). This enzyme also regulates UV-radiation induced DNA damage response and cell polarity by remodeling the actin cytoskeleton.<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11></div>Kelly Degnonhttps://proteopedia.org/index.php?title=User:Kelly_Degnon/Sandbox_1&diff=2586337User:Kelly Degnon/Sandbox 12016-04-10T21:31:46Z<p>Kelly Degnon: </p>
<hr />
<div>==Serine/Threonine-Protein Kinase STK11==<br />
<StructureSection load='1stp' size='340' side='right' caption='Caption for this structure' scene=''><br />
This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the &lt; and &gt; signs.<br />
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.<br />
<br />
== Structure ==<br />
<br />
<br />
----<br />
<br />
== Location ==<br />
The STK11 gene is located on chromosome 19 on the p arm of the chromosome, also known as the short arm. The exact location is between base pair 1,205,799 and 1,228,435. Location is found in both the nucleus and the cytoplasm. In humans, when STK11 is over express it is mostly located in the nucleus, having limited portions in the cytoplasm. When a cell is undergoing apoptosis, STK11 is found to translocate to the mitochondria. STK11 is mostly expressed in the seminiferous tubules of the testes, showing higher expression in the fetal tissues than in adult tissues.<br />
<br />
[[Image:STK11.jpeg]]<br />
<br />
----<br />
<br />
== Function ==<br />
<br />
<br />
----<br />
<br />
== Disease ==<br />
The function of the STK11 is to suppress tumors. A mutation in this protein increases the risk of cancer and carcinomas, cancer arising from the epithelial tissue of internal organs primarily in the gastrointestinal (GI) tract. The risk of cancer and carcinomas not only increases with mutation, but is influenced by old age as well. In addition to cancer, a germline mutation of STK11 also increases the chances of Peutz-Jeghers syndrome, an autosomal genetic dominant mutation characterized by the growth of hamartomatous polyps in the GI tract, neoplasm, and discoloration of the skin and mouth. Polyps are masses of tissues that arise in the bowl and penetrates the lumen, which can be removed though endoscopic technology. Neoplasm is abnormal growth of tissues that can be categorized into four categories- benign, institu, malignant, and unknown.<br />
<br />
----<br />
<br />
This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.<br />
<br />
</StructureSection><br />
== References ==<br />
#<https://ghr.nlm.nih.gov/gene/STK11></div>Kelly Degnon