7scw - Revision history

OCA at 09:34, 25 October 2023

OCA — Wed, 25 Oct 2023 09:34:35 GMT

←Older revision		Revision as of 09:34, 25 October 2023
Line 4:		Line 4:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[7scw]] is a 2 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=7SCW OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7SCW FirstGlance]. <br>		<table><tr><td colspan='2'>[[7scw]] is a 2 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=7SCW OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7SCW FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GSP:5-GUANOSINE-DIPHOSPHATE-MONOTHIOPHOSPHATE'>GSP</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]] 1.98Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GSP:5-GUANOSINE-DIPHOSPHATE-MONOTHIOPHOSPHATE'>GSP</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=7scw FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7scw OCA], [https://pdbe.org/7scw PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7scw RCSB], [https://www.ebi.ac.uk/pdbsum/7scw PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7scw 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=7scw FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7scw OCA], [https://pdbe.org/7scw PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7scw RCSB], [https://www.ebi.ac.uk/pdbsum/7scw PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7scw ProSAT]</span></td></tr>
	</table>		</table>
Line 20:		Line 21:
	</div>		</div>
	<div class="pdbe-citations 7scw" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 7scw" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[GTPase KRas 3D structures\|GTPase KRas 3D structures]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 11:02, 30 November 2022

OCA — Wed, 30 Nov 2022 11:02:15 GMT

←Older revision		Revision as of 11:02, 30 November 2022
Line 1:		Line 1:

-	====	+	==KRAS full length wild-type in complex with RGL1 Ras association domain==
-	<StructureSection load='7scw' size='340' side='right'caption='[[7scw]]' scene=''>	+	<StructureSection load='7scw' size='340' side='right'caption='[[7scw]], [[Resolution\|resolution]] 1.98Å' 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= OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol= FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[7scw]] is a 2 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=7SCW OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7SCW 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=7scw FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7scw OCA], [https://pdbe.org/7scw PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7scw RCSB], [https://www.ebi.ac.uk/pdbsum/7scw PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7scw ProSAT]</span></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GSP:5-GUANOSINE-DIPHOSPHATE-MONOTHIOPHOSPHATE'>GSP</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=7scw FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7scw OCA], [https://pdbe.org/7scw PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7scw RCSB], [https://www.ebi.ac.uk/pdbsum/7scw PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7scw 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.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Ral Guanine Nucleotide Dissociation Stimulator Like 1 (RGL1) is a RAS effector protein that activates Ral GTPase by stimulating nucleotide exchange. Most structures of RAS-effector complexes are for the HRAS isoform; relatively few KRAS-effector structures have been solved, even though KRAS mutations are more frequent in human cancers. We determined crystal structures of KRAS/RGL1-RAS-association (RA) domain complexes and characterized the interaction in solution using nuclear magnetic resonance spectroscopy, size-exclusion chromatography combined with multi-angle light scattering and biolayer interferometry. We report structures of wild-type KRAS and the oncogenic G12V mutant in complex with the RA domain of RGL1 at < 2 A resolution. KRAS(WT)/RGL1-RA crystallized as a 1:1 heterodimer, whilst KRAS(G12V)/RGL1-RA crystallized as a heterotetrameric structure in which RGL1-RA dimerized via domain-swapping the C-terminal beta-strand. Solution data indicated that KRAS(WT) and KRAS(G12V) in complex with RGL1-RA both exist predominantly as 1:1 dimers, while tetramerization occurs through very slow association. Through detailed structural analyses, the distance and angle between RAS alpha1 helix and RBD/RA alpha1 helix were found to differ significantly among RAS and RBD/RA complexes. The KRAS/RGL1-RA structures possess some of the largest alpha1(RAS)/alpha1(Effector) distances (21.7-22.2 A), whereas the corresponding distances in previously reported RAS/RAF complexes are significantly shorter (15.2-17.7 A). Contact map analysis identified unique structural signatures involving contacts between the beta1-beta2 loop of RA and the alpha1 helix of RAS, clearly distinguishing the KRAS/RGL1-RA (and other RAS/RA complexes) from RAS/RBD complexes. These results demonstrate that RAS effectors employ an assortment of finely-tuned docking surfaces to achieve optimal interactions with RAS.
		+
		+	Structures of RGL1 RAS-Association Domain in Complex with KRAS and the Oncogenic G12V Mutant.,Eves BJ, Gebregiworgis T, Gasmi-Seabrook GMC, Kuntz DA, Prive GG, Marshall CB, Ikura M J Mol Biol. 2022 May 15;434(9):167527. doi: 10.1016/j.jmb.2022.167527. Epub 2022 , Mar 4. PMID:35257782<ref>PMID:35257782</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 7scw" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: ~~Z-disk~~]]	+	[[Category: Eves BJ]]
		+	[[Category: Ikura M]]
		+	[[Category: Kuntz DA]]
		+	[[Category: Marshall CB]]

OCA at 10:16, 18 May 2022

OCA — Wed, 18 May 2022 10:16:37 GMT

←Older revision		Revision as of 10:16, 18 May 2022
Line 1:		Line 1:
-	'''Unreleased structure'''

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

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

OCA — Wed, 06 Oct 2021 04:16:49 GMT

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

←Older revision

Revision as of 04:16, 6 October 2021

OCA: New page: '''Unreleased structure''' The entry 7scw is ON HOLD until Paper Publication Authors: Description: Category: Unreleased Structures

OCA — Wed, 06 Oct 2021 04:16:48 GMT

New page: '''Unreleased structure''' The entry 7scw is ON HOLD until Paper Publication Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 7scw is ON HOLD until Paper Publication

Authors:

Description:
[[Category: Unreleased Structures]]