5f2e - Revision history

OCA at 08:42, 12 July 2023

2023-07-12T08:42:07Z

← Older revision		Revision as of 08:42, 12 July 2023
Line 1:		Line 1:

	==Crystal Structure of small molecule ARS-853 covalently bound to K-Ras G12C==		==Crystal Structure of small molecule ARS-853 covalently bound to K-Ras G12C==
	<StructureSection load='5f2e' size='340' side='right' caption='[[5f2e]], [[Resolution\|resolution]] 1.40Å' scene=''>		<StructureSection load='5f2e' size='340' side='right'caption='[[5f2e]], [[Resolution\|resolution]] 1.40Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[5f2e]] is a 1 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5F2E OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5F2E FirstGlance]. <br>		<table><tr><td colspan='2'>[[5f2e]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5F2E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5F2E FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=5UT:1-[3-[4-[2-[[4-CHLORANYL-5-(1-METHYLCYCLOPROPYL)-2-OXIDANYL-PHENYL]AMINO]ETHANOYL]PIPERAZIN-1-YL]AZETIDIN-1-YL]PROP-2-EN-1-ONE'>5UT</scene>, <scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>~~</td></tr>~~		</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution\|Resolution]] 1.4Å</td></tr>
	~~<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">KRAS, KRAS2, RASK2 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])~~</td></tr>		<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=5UT:1-[3-[4-[2-[[4-CHLORANYL-5-(1-METHYLCYCLOPROPYL)-2-OXIDANYL-PHENYL]AMINO]ETHANOYL]PIPERAZIN-1-YL]AZETIDIN-1-YL]PROP-2-EN-1-ONE'>5UT</scene>, <scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5f2e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5f2e OCA], [~~http~~://pdbe.org/5f2e PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5f2e RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5f2e PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5f2e ProSAT]</span></td></tr>		<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=5f2e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5f2e OCA], [https://pdbe.org/5f2e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5f2e RCSB], [https://www.ebi.ac.uk/pdbsum/5f2e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5f2e ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
	[~~[http~~://www.uniprot.org/uniprot/RASK_HUMAN RASK_HUMAN]] Defects in KRAS are a cause of acute myelogenous leukemia (AML) [MIM:[~~http~~://omim.org/entry/601626 601626]]. AML is a malignant disease in which hematopoietic precursors are arrested in an early stage of development.<ref>PMID:8955068</ref> Defects in KRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:[~~http~~://omim.org/entry/607785 607785]]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia. It is characterized by leukocytosis with tissue infiltration and in vitro hypersensitivity of myeloid progenitors to granulocyte-macrophage colony stimulating factor. Defects in KRAS are the cause of Noonan syndrome type 3 (NS3) [MIM:[~~http~~://omim.org/entry/609942 609942]]. Noonan syndrome (NS) [MIM:[~~http~~://omim.org/entry/163950 163950]] is a disorder characterized by dysmorphic facial features, short stature, hypertelorism, cardiac anomalies, deafness, motor delay, and a bleeding diathesis. It is a genetically heterogeneous and relatively common syndrome, with an estimated incidence of 1 in 1000-2500 live births. Rarely, NS is associated with juvenile myelomonocytic leukemia (JMML). NS3 inheritance is autosomal dominant.<ref>PMID:16773572</ref> <ref>PMID:16474405</ref> <ref>PMID:17468812</ref> <ref>PMID:17056636</ref> <ref>PMID:19396835</ref> <ref>PMID:20949621</ref> Defects in KRAS are a cause of gastric cancer (GASC) [MIM:[~~http~~://omim.org/entry/613659 613659]]; also called gastric cancer intestinal or stomach cancer. Gastric cancer is a malignant disease which starts in the stomach, can spread to the esophagus or the small intestine, and can extend through the stomach wall to nearby lymph nodes and organs. It also can metastasize to other parts of the body. The term gastric cancer or gastric carcinoma refers to adenocarcinoma of the stomach that accounts for most of all gastric malignant tumors. Two main histologic types are recognized, diffuse type and intestinal type carcinomas. Diffuse tumors are poorly differentiated infiltrating lesions, resulting in thickening of the stomach. In contrast, intestinal tumors are usually exophytic, often ulcerating, and associated with intestinal metaplasia of the stomach, most often observed in sporadic disease.<ref>PMID:3034404</ref> <ref>PMID:7773929</ref> <ref>PMID:14534542</ref> Note=Defects in KRAS are a cause of pylocytic astrocytoma (PA). Pylocytic astrocytomas are neoplasms of the brain and spinal cord derived from glial cells which vary from histologically benign forms to highly anaplastic and malignant tumors.<ref>PMID:8439212</ref> Defects in KRAS are a cause of cardiofaciocutaneous syndrome (CFC syndrome) [MIM:[~~http~~://omim.org/entry/115150 115150]]; also known as cardio-facio-cutaneous syndrome. CFC syndrome is characterized by a distinctive facial appearance, heart defects and mental retardation. Heart defects include pulmonic stenosis, atrial septal defects and hypertrophic cardiomyopathy. Some affected individuals present with ectodermal abnormalities such as sparse, friable hair, hyperkeratotic skin lesions and a generalized ichthyosis-like condition. Typical facial features are similar to Noonan syndrome. They include high forehead with bitemporal constriction, hypoplastic supraorbital ridges, downslanting palpebral fissures, a depressed nasal bridge, and posteriorly angulated ears with prominent helices. The inheritance of CFC syndrome is autosomal dominant. Note=KRAS mutations are involved in cancer development.		[https://www.uniprot.org/uniprot/RASK_HUMAN RASK_HUMAN] Defects in KRAS are a cause of acute myelogenous leukemia (AML) [MIM:[https://omim.org/entry/601626 601626]. AML is a malignant disease in which hematopoietic precursors are arrested in an early stage of development.<ref>PMID:8955068</ref> Defects in KRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:[https://omim.org/entry/607785 607785]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia. It is characterized by leukocytosis with tissue infiltration and in vitro hypersensitivity of myeloid progenitors to granulocyte-macrophage colony stimulating factor. Defects in KRAS are the cause of Noonan syndrome type 3 (NS3) [MIM:[https://omim.org/entry/609942 609942]. Noonan syndrome (NS) [MIM:[https://omim.org/entry/163950 163950] is a disorder characterized by dysmorphic facial features, short stature, hypertelorism, cardiac anomalies, deafness, motor delay, and a bleeding diathesis. It is a genetically heterogeneous and relatively common syndrome, with an estimated incidence of 1 in 1000-2500 live births. Rarely, NS is associated with juvenile myelomonocytic leukemia (JMML). NS3 inheritance is autosomal dominant.<ref>PMID:16773572</ref> <ref>PMID:16474405</ref> <ref>PMID:17468812</ref> <ref>PMID:17056636</ref> <ref>PMID:19396835</ref> <ref>PMID:20949621</ref> Defects in KRAS are a cause of gastric cancer (GASC) [MIM:[https://omim.org/entry/613659 613659]; also called gastric cancer intestinal or stomach cancer. Gastric cancer is a malignant disease which starts in the stomach, can spread to the esophagus or the small intestine, and can extend through the stomach wall to nearby lymph nodes and organs. It also can metastasize to other parts of the body. The term gastric cancer or gastric carcinoma refers to adenocarcinoma of the stomach that accounts for most of all gastric malignant tumors. Two main histologic types are recognized, diffuse type and intestinal type carcinomas. Diffuse tumors are poorly differentiated infiltrating lesions, resulting in thickening of the stomach. In contrast, intestinal tumors are usually exophytic, often ulcerating, and associated with intestinal metaplasia of the stomach, most often observed in sporadic disease.<ref>PMID:3034404</ref> <ref>PMID:7773929</ref> <ref>PMID:14534542</ref> Note=Defects in KRAS are a cause of pylocytic astrocytoma (PA). Pylocytic astrocytomas are neoplasms of the brain and spinal cord derived from glial cells which vary from histologically benign forms to highly anaplastic and malignant tumors.<ref>PMID:8439212</ref> Defects in KRAS are a cause of cardiofaciocutaneous syndrome (CFC syndrome) [MIM:[https://omim.org/entry/115150 115150]; also known as cardio-facio-cutaneous syndrome. CFC syndrome is characterized by a distinctive facial appearance, heart defects and mental retardation. Heart defects include pulmonic stenosis, atrial septal defects and hypertrophic cardiomyopathy. Some affected individuals present with ectodermal abnormalities such as sparse, friable hair, hyperkeratotic skin lesions and a generalized ichthyosis-like condition. Typical facial features are similar to Noonan syndrome. They include high forehead with bitemporal constriction, hypoplastic supraorbital ridges, downslanting palpebral fissures, a depressed nasal bridge, and posteriorly angulated ears with prominent helices. The inheritance of CFC syndrome is autosomal dominant. Note=KRAS mutations are involved in cancer development.
	== Function ==		== Function ==
	[~~[http~~://www.uniprot.org/uniprot/RASK_HUMAN RASK_HUMAN]] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.		[https://www.uniprot.org/uniprot/RASK_HUMAN RASK_HUMAN] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 21:		Line 21:
	</div>		</div>
	<div class="pdbe-citations 5f2e" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 5f2e" style="background-color:#fffaf0;"></div>

			==See Also==
			*[[GTPase KRas 3D structures\|GTPase KRas 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
	[[Category: ~~Human~~]]		[[Category: Homo sapiens]]
	[[Category: Babbar, A]]		[[Category: Large Structures]]
	[[Category: Chen~~, J H~~]]		[[Category: Babbar A]]
	[[Category: Chen, Y]]		[[Category: Chen JH]]
	[[Category: Ely, T]]		[[Category: Chen Y]]
	[[Category: Feng, J]]		[[Category: Ely T]]
	[[Category: Firdaus~~, S J~~]]		[[Category: Feng J]]
	[[Category: Hansen, R]]		[[Category: Firdaus SJ]]
	[[Category: Janes~~, M R~~]]		[[Category: Hansen R]]
	[[Category: Kessler~~, L V~~]]		[[Category: Janes MR]]
	[[Category: Kucharski~~, J M~~]]		[[Category: Kessler LV]]
	[[Category: Li, L S]]		[[Category: Kucharski JM]]
	[[Category: Liu, Y]]		[[Category: Li L-S]]
	[[Category: Patricelli~~, M P~~]]		[[Category: Liu Y]]
	[[Category: Peters, U]]		[[Category: Patricelli MP]]
	[[Category: Ren, P]]		[[Category: Peters U]]
	~~[[Category: Covalent inhibitor bound]]~~		[[Category: Ren P]]
	~~[[Category: Gdp bound]]~~
	~~[[Category: Hydrolase]]~~
	~~[[Category: Small gtpase domain]]~~
	~~[[Category: Switch ii pocket~~]]

OCA at 09:56, 22 November 2017

2017-11-22T09:56:02Z

← Older revision		Revision as of 09:56, 22 November 2017
Line 3:		Line 3:
	<StructureSection load='5f2e' size='340' side='right' caption='[[5f2e]], [[Resolution\|resolution]] 1.40Å' scene=''>		<StructureSection load='5f2e' size='340' side='right' caption='[[5f2e]], [[Resolution\|resolution]] 1.40Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[5f2e]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5F2E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5F2E FirstGlance]. <br>		<table><tr><td colspan='2'>[[5f2e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5F2E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5F2E FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=5UT:1-[3-[4-[2-[[4-CHLORANYL-5-(1-METHYLCYCLOPROPYL)-2-OXIDANYL-PHENYL]AMINO]ETHANOYL]PIPERAZIN-1-YL]AZETIDIN-1-YL]PROP-2-EN-1-ONE'>5UT</scene>, <scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=5UT:1-[3-[4-[2-[[4-CHLORANYL-5-(1-METHYLCYCLOPROPYL)-2-OXIDANYL-PHENYL]AMINO]ETHANOYL]PIPERAZIN-1-YL]AZETIDIN-1-YL]PROP-2-EN-1-ONE'>5UT</scene>, <scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5f2e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5f2e OCA], [http://pdbe.org/5f2e PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5f2e RCSB], [http://www.ebi.ac.uk/pdbsum/5f2e PDBsum]</span></td></tr>		<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">KRAS, KRAS2, RASK2 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
			<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5f2e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5f2e OCA], [http://pdbe.org/5f2e PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5f2e RCSB], [http://www.ebi.ac.uk/pdbsum/5f2e PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5f2e ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 24:		Line 25:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
			[[Category: Human]]
	[[Category: Babbar, A]]		[[Category: Babbar, A]]
	[[Category: Chen, J H]]		[[Category: Chen, J H]]

OCA at 17:44, 10 May 2016

2016-05-10T17:44:05Z

@@ Line 1: / Line 1: @@
 ==Crystal Structure of small molecule ARS-853 covalently bound to K-Ras G12C==
 <StructureSection load='5f2e' size='340' side='right' caption='[[5f2e]], [[Resolution|resolution]] 1.40&Aring;' scene=''>
@@ Line 10: / Line 11: @@
 == Function ==
 [[http://www.uniprot.org/uniprot/RASK_HUMAN RASK_HUMAN]] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
 == References ==
 <references/>

OCA at 20:35, 13 January 2016

2016-01-13T20:35:11Z

← Older revision		Revision as of 20:35, 13 January 2016
Line 1:		Line 1:
	'''~~Unreleased structure~~'''		==Crystal Structure of small molecule ARS-853 covalently bound to K-Ras G12C==
			<StructureSection load='5f2e' size='340' side='right' caption='[[5f2e]], [[Resolution\|resolution]] 1.40Å' scene=''>
	~~The entry~~ 5f2e is ~~ON HOLD until Paper Publication~~		== Structural highlights ==
			<table><tr><td colspan='2'>[[5f2e]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5F2E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5F2E FirstGlance]. <br>
	~~Authors~~: ~~Patricelli~~, M.P., ~~Janes~~, M.R., ~~Li, L~~.-S., ~~Hansen~~, R., ~~Peters~~, U., ~~Kessler~~, L.V., ~~Chen~~, Y., ~~Kucharski~~, J.M., ~~Feng~~, J., ~~Ely~~, T., ~~Chen~~, J.H.~~, Firdaus, S~~.J., Babbar, A., ~~Ren, P., Liu~~, Y.		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=5UT:1-[3-[4-[2-[[4-CHLORANYL-5-(1-METHYLCYCLOPROPYL)-2-OXIDANYL-PHENYL]AMINO]ETHANOYL]PIPERAZIN-1-YL]AZETIDIN-1-YL]PROP-2-EN-1-ONE'>5UT</scene>, <scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</scene>, <scene name='pdbligand=GLY:GLYCINE'>GLY</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
			<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5f2e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5f2e OCA], [http://pdbe.org/5f2e PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5f2e RCSB], [http://www.ebi.ac.uk/pdbsum/5f2e PDBsum]</span></td></tr>
	~~Description~~: ~~Crystal Structure of small molecule ARS-853 covalently bound to K-Ras G12C~~		</table>
	[[Category: ~~Unreleased Structures~~]]		== Disease ==
			[[http://www.uniprot.org/uniprot/RASK_HUMAN RASK_HUMAN]] Defects in KRAS are a cause of acute myelogenous leukemia (AML) [MIM:[http://omim.org/entry/601626 601626]]. AML is a malignant disease in which hematopoietic precursors are arrested in an early stage of development.<ref>PMID:8955068</ref> Defects in KRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:[http://omim.org/entry/607785 607785]]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia. It is characterized by leukocytosis with tissue infiltration and in vitro hypersensitivity of myeloid progenitors to granulocyte-macrophage colony stimulating factor. Defects in KRAS are the cause of Noonan syndrome type 3 (NS3) [MIM:[http://omim.org/entry/609942 609942]]. Noonan syndrome (NS) [MIM:[http://omim.org/entry/163950 163950]] is a disorder characterized by dysmorphic facial features, short stature, hypertelorism, cardiac anomalies, deafness, motor delay, and a bleeding diathesis. It is a genetically heterogeneous and relatively common syndrome, with an estimated incidence of 1 in 1000-2500 live births. Rarely, NS is associated with juvenile myelomonocytic leukemia (JMML). NS3 inheritance is autosomal dominant.<ref>PMID:16773572</ref> <ref>PMID:16474405</ref> <ref>PMID:17468812</ref> <ref>PMID:17056636</ref> <ref>PMID:19396835</ref> <ref>PMID:20949621</ref> Defects in KRAS are a cause of gastric cancer (GASC) [MIM:[http://omim.org/entry/613659 613659]]; also called gastric cancer intestinal or stomach cancer. Gastric cancer is a malignant disease which starts in the stomach, can spread to the esophagus or the small intestine, and can extend through the stomach wall to nearby lymph nodes and organs. It also can metastasize to other parts of the body. The term gastric cancer or gastric carcinoma refers to adenocarcinoma of the stomach that accounts for most of all gastric malignant tumors. Two main histologic types are recognized, diffuse type and intestinal type carcinomas. Diffuse tumors are poorly differentiated infiltrating lesions, resulting in thickening of the stomach. In contrast, intestinal tumors are usually exophytic, often ulcerating, and associated with intestinal metaplasia of the stomach, most often observed in sporadic disease.<ref>PMID:3034404</ref> <ref>PMID:7773929</ref> <ref>PMID:14534542</ref> Note=Defects in KRAS are a cause of pylocytic astrocytoma (PA). Pylocytic astrocytomas are neoplasms of the brain and spinal cord derived from glial cells which vary from histologically benign forms to highly anaplastic and malignant tumors.<ref>PMID:8439212</ref> Defects in KRAS are a cause of cardiofaciocutaneous syndrome (CFC syndrome) [MIM:[http://omim.org/entry/115150 115150]]; also known as cardio-facio-cutaneous syndrome. CFC syndrome is characterized by a distinctive facial appearance, heart defects and mental retardation. Heart defects include pulmonic stenosis, atrial septal defects and hypertrophic cardiomyopathy. Some affected individuals present with ectodermal abnormalities such as sparse, friable hair, hyperkeratotic skin lesions and a generalized ichthyosis-like condition. Typical facial features are similar to Noonan syndrome. They include high forehead with bitemporal constriction, hypoplastic supraorbital ridges, downslanting palpebral fissures, a depressed nasal bridge, and posteriorly angulated ears with prominent helices. The inheritance of CFC syndrome is autosomal dominant. Note=KRAS mutations are involved in cancer development.
			== Function ==
			[[http://www.uniprot.org/uniprot/RASK_HUMAN RASK_HUMAN]] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
			== References ==
			<references/>
			__TOC__
			</StructureSection>
			[[Category: Babbar, A]]
			[[Category: Chen, J H]]
			[[Category: Chen, Y]]
			[[Category: Ely, T]]
			[[Category: Feng, J]]
			[[Category: Firdaus, S J]]
	[[Category: Hansen, R]]		[[Category: Hansen, R]]
	[[Category: ~~Kucharski~~, J.M]]		[[Category: Janes, M R]]
	[[Category: ~~Janes~~, ~~M.R~~]]		[[Category: Kessler, L V]]
	[[Category: ~~Chen~~, Y]]		[[Category: Kucharski, J M]]
	[[Category: ~~Babbar~~, A]]		[[Category: Li, L S]]
	[[Category: Liu, Y]]		[[Category: Liu, Y]]
	~~[[Category: Chen, J.H]]~~		[[Category: Patricelli, M P]]
	~~[[Category: Feng, J]]~~
	~~[[Category: Kessler, L.V]]~~
	~~[[Category: Li, L.-S]]~~
	~~[[Category: Ely, T]]~~
	[[Category: Patricelli, M.P]]
	[[Category: Peters, U]]		[[Category: Peters, U]]
	[[Category: Ren, P]]		[[Category: Ren, P]]
	[[Category: ~~Firdaus, S.J~~]]		[[Category: Covalent inhibitor bound]]
			[[Category: Gdp bound]]
			[[Category: Hydrolase]]
			[[Category: Small gtpase domain]]
			[[Category: Switch ii pocket]]

OCA at 17:26, 30 December 2015

2015-12-30T17:26:39Z

← Older revision		Revision as of 17:26, 30 December 2015
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

	The entry 5f2e is ON HOLD		The entry 5f2e is ON HOLD until Paper Publication

	Authors: Patricelli, M.P., Janes, M.R., Li, L.-S., Hansen, R., Peters, U., Kessler, L.V., Chen, Y., Kucharski, J.M., Feng, J., Ely, T., Chen, J.H., Firdaus, S.J., Babbar, A., Ren, P., Liu, Y.		Authors: Patricelli, M.P., Janes, M.R., Li, L.-S., Hansen, R., Peters, U., Kessler, L.V., Chen, Y., Kucharski, J.M., Feng, J., Ely, T., Chen, J.H., Firdaus, S.J., Babbar, A., Ren, P., Liu, Y.

OCA: Protected "5f2e" [edit=sysop:move=sysop]

2015-12-09T12:31:25Z

Protected "5f2e" [edit=sysop:move=sysop]

← Older revision	Revision as of 12:31, 9 December 2015
(No difference)

OCA: New page: '''Unreleased structure''' The entry 5f2e is ON HOLD Authors: Patricelli, M.P., Janes, M.R., Li, L.-S., Hansen, R., Peters, U., Kessler, L.V., Chen, Y., Kucharski, J.M., Feng, J., Ely, ...

2015-12-09T12:31:23Z

New page: '''Unreleased structure''' The entry 5f2e is ON HOLD Authors: Patricelli, M.P., Janes, M.R., Li, L.-S., Hansen, R., Peters, U., Kessler, L.V., Chen, Y., Kucharski, J.M., Feng, J., Ely, ...

New page

'''Unreleased structure'''

The entry 5f2e is ON HOLD

Authors: Patricelli, M.P., Janes, M.R., Li, L.-S., Hansen, R., Peters, U., Kessler, L.V., Chen, Y., Kucharski, J.M., Feng, J., Ely, T., Chen, J.H., Firdaus, S.J., Babbar, A., Ren, P., Liu, Y.

Description: Crystal Structure of small molecule ARS-853 covalently bound to K-Ras G12C
[[Category: Unreleased Structures]]
[[Category: Hansen, R]]
[[Category: Kucharski, J.M]]
[[Category: Janes, M.R]]
[[Category: Chen, Y]]
[[Category: Babbar, A]]
[[Category: Liu, Y]]
[[Category: Chen, J.H]]
[[Category: Feng, J]]
[[Category: Kessler, L.V]]
[[Category: Li, L.-S]]
[[Category: Ely, T]]
[[Category: Patricelli, M.P]]
[[Category: Peters, U]]
[[Category: Ren, P]]
[[Category: Firdaus, S.J]]