Sandbox 465: Difference between revisions

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~~This is a default text for your page '''Kelly Degnon/Sandbox 1'''. Click above on '''edit this page''' to modify. Be careful with the < and > signs.~~

~~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.~~

== Function ==

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" />.

'''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" />.

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== Disease ==

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>.

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>.

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Sandbox 465: Difference between revisions

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 <Structure load='2wtk' size='350' frame='true' align='right' caption=' Serine/Threonine Kinase 11' scene='Insert optional scene name here' />
-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.
-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.
 == Function ==
-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" />.
+'''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" />.
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 == Disease ==
-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>.
+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>.
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