OCA at 16:01, 18 October 2023

OCA — Wed, 18 Oct 2023 16:01:37 GMT

←Older revision		Revision as of 16:01, 18 October 2023
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	==Crystal structure of oncogenic KRAS Q61E GMPPCP-bound==		==Crystal structure of oncogenic KRAS Q61E GMPPCP-bound==
-	<StructureSection load='7lz5' size='340' side='right'caption='[[7lz5]]' scene=''>	+	<StructureSection load='7lz5' size='340' side='right'caption='[[7lz5]], [[Resolution\|resolution]] 1.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7LZ5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7LZ5 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[7lz5]] 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=7LZ5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7LZ5 FirstGlance]. <br>
-	</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=7lz5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7lz5 OCA], [https://pdbe.org/7lz5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7lz5 RCSB], [https://www.ebi.ac.uk/pdbsum/7lz5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7lz5 ProSAT]</span></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]] 1.5Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GCP:PHOSPHOMETHYLPHOSPHONIC+ACID+GUANYLATE+ESTER'>GCP</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'>[https://proteopedia.org/fgij/fg.htm?mol=7lz5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7lz5 OCA], [https://pdbe.org/7lz5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7lz5 RCSB], [https://www.ebi.ac.uk/pdbsum/7lz5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7lz5 ProSAT]</span></td></tr>
	</table>		</table>
		+	== Disease ==
		+	[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 ==
		+	[https://www.uniprot.org/uniprot/RASK_HUMAN RASK_HUMAN] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
		+
		+	==See Also==
		+	*[[GTPase KRas 3D structures\|GTPase KRas 3D structures]]
		+	== References ==
		+	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Campbell SL]]		[[Category: Campbell SL]]
	[[Category: Carey LM]]		[[Category: Carey LM]]

OCA at 06:13, 16 March 2022

OCA — Wed, 16 Mar 2022 06:13:25 GMT

←Older revision		Revision as of 06:13, 16 March 2022
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-	'''Unreleased structure'''

-	~~The entry~~ 7lz5 ~~is ON HOLD until Paper Publication~~	+	==Crystal structure of oncogenic KRAS Q61E GMPPCP-bound==
-		+	<StructureSection load='7lz5' size='340' side='right'caption='[[7lz5]]' scene=''>
-	~~Authors~~:	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7LZ5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7LZ5 FirstGlance]. <br>
-	~~Description~~:	+	</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=7lz5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7lz5 OCA], [https://pdbe.org/7lz5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7lz5 RCSB], [https://www.ebi.ac.uk/pdbsum/7lz5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7lz5 ProSAT]</span></td></tr>
-	[[Category: ~~Unreleased~~ Structures]]	+	</table>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Campbell SL]]
		+	[[Category: Carey LM]]

OCA at 05:38, 14 April 2021

OCA — Wed, 14 Apr 2021 05:38:19 GMT

←Older revision		Revision as of 05:38, 14 April 2021
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 7lz5 is ON HOLD	+	The entry 7lz5 is ON HOLD until Paper Publication

	Authors:		Authors:

OCA: Protected "7lz5" [edit=sysop:move=sysop]

OCA — Wed, 17 Mar 2021 05:25:44 GMT

Protected "7lz5" [edit=sysop:move=sysop]

←Older revision

Revision as of 05:25, 17 March 2021

OCA: New page: '''Unreleased structure''' The entry 7lz5 is ON HOLD Authors: Description: Category: Unreleased Structures

OCA — Wed, 17 Mar 2021 05:25:43 GMT

New page: '''Unreleased structure''' The entry 7lz5 is ON HOLD Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 7lz5 is ON HOLD

Authors:

Description:
[[Category: Unreleased Structures]]

7lz5 - Revision history

OCA at 16:01, 18 October 2023

OCA at 06:13, 16 March 2022

OCA at 05:38, 14 April 2021

OCA: Protected "7lz5" [edit=sysop:move=sysop]

OCA: New page: '''Unreleased structure''' The entry 7lz5 is ON HOLD Authors: Description: Category: Unreleased Structures