3lq8 - Revision history

OCA at 10:21, 21 February 2024

OCA — Wed, 21 Feb 2024 10:21:50 GMT

←Older revision		Revision as of 10:21, 21 February 2024
Line 1:		Line 1:

	==Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)==		==Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)==
-	<StructureSection load='3lq8' size='340' side='right' caption='[[3lq8]], [[Resolution\|resolution]] 2.02Å' scene=''>	+	<StructureSection load='3lq8' size='340' side='right'caption='[[3lq8]], [[Resolution\|resolution]] 2.02Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3lq8]] 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=3LQ8 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3LQ8 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3lq8]] 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=3LQ8 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3LQ8 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=88Z:N-(3-FLUORO-4-{[6-METHOXY-7-(3-MORPHOLIN-4-YLPROPOXY)QUINOLIN-4-YL]OXY}PHENYL)-N-(4-FLUOROPHENYL)CYCLOPROPANE-1,1-DICARBOXAMIDE'>88Z</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]] 2.02Å</td></tr>
-	~~<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MET ([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=88Z:N-(3-FLUORO-4-{[6-METHOXY-7-(3-MORPHOLIN-4-YLPROPOXY)QUINOLIN-4-YL]OXY}PHENYL)-N-(4-FLUOROPHENYL)CYCLOPROPANE-1,1-DICARBOXAMIDE'>88Z</scene></td></tr>
-	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Receptor_protein-tyrosine_kinase Receptor protein-tyrosine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.10.1 2.7.10.1] </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=3lq8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3lq8 OCA], [https://pdbe.org/3lq8 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3lq8 RCSB], [https://www.ebi.ac.uk/pdbsum/3lq8 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3lq8 ProSAT]</span></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=3lq8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3lq8 OCA], [~~http~~://pdbe.org/3lq8 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3lq8 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3lq8 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3lq8 ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/MET_HUMAN MET_HUMAN]] Note=Activation of MET after rearrangement with the TPR gene produces an oncogenic protein. Note=Defects in MET may be associated with gastric cancer. Defects in MET are a cause of hepatocellular carcinoma (HCC) [MIM:[~~http~~://omim.org/entry/114550 114550]].<ref>PMID:9927037</ref> Defects in MET are a cause of renal cell carcinoma papillary (RCCP) [MIM:[~~http~~://omim.org/entry/605074 605074]]. It is a subtype of renal cell carcinoma tending to show a tubulo-papillary architecture formed by numerous, irregular, finger-like projections of connective tissue. Renal cell carcinoma is a heterogeneous group of sporadic or hereditary carcinoma derived from cells of the proximal renal tubular epithelium. It is subclassified into common renal cell carcinoma (clear cell, non-papillary carcinoma), papillary renal cell carcinoma, chromophobe renal cell carcinoma, collecting duct carcinoma with medullary carcinoma of the kidney, and unclassified renal cell carcinoma.<ref>PMID:9140397</ref> <ref>PMID:9563489</ref> <ref>PMID:10433944</ref> <ref>PMID:10417759</ref> <ref>PMID:10327054</ref> Note=A common allele in the promoter region of the MET shows genetic association with susceptibility to autism in some families. Functional assays indicate a decrease in MET promoter activity and altered binding of specific transcription factor complexes. Note=MET activating mutations may be involved in the development of a highly malignant, metastatic syndrome known as cancer of unknown primary origin (CUP) or primary occult malignancy. Systemic neoplastic spread is generally a late event in cancer progression. However, in some instances, distant dissemination arises at a very early stage, so that metastases reach clinical relevance before primary lesions. Sometimes, the primary lesions cannot be identified in spite of the progresses in the diagnosis of malignancies.<ref>PMID:20949619</ref>	+	[https://www.uniprot.org/uniprot/MET_HUMAN MET_HUMAN] Note=Activation of MET after rearrangement with the TPR gene produces an oncogenic protein. Note=Defects in MET may be associated with gastric cancer. Defects in MET are a cause of hepatocellular carcinoma (HCC) [MIM:[https://omim.org/entry/114550 114550].<ref>PMID:9927037</ref> Defects in MET are a cause of renal cell carcinoma papillary (RCCP) [MIM:[https://omim.org/entry/605074 605074]. It is a subtype of renal cell carcinoma tending to show a tubulo-papillary architecture formed by numerous, irregular, finger-like projections of connective tissue. Renal cell carcinoma is a heterogeneous group of sporadic or hereditary carcinoma derived from cells of the proximal renal tubular epithelium. It is subclassified into common renal cell carcinoma (clear cell, non-papillary carcinoma), papillary renal cell carcinoma, chromophobe renal cell carcinoma, collecting duct carcinoma with medullary carcinoma of the kidney, and unclassified renal cell carcinoma.<ref>PMID:9140397</ref> <ref>PMID:9563489</ref> <ref>PMID:10433944</ref> <ref>PMID:10417759</ref> <ref>PMID:10327054</ref> Note=A common allele in the promoter region of the MET shows genetic association with susceptibility to autism in some families. Functional assays indicate a decrease in MET promoter activity and altered binding of specific transcription factor complexes. Note=MET activating mutations may be involved in the development of a highly malignant, metastatic syndrome known as cancer of unknown primary origin (CUP) or primary occult malignancy. Systemic neoplastic spread is generally a late event in cancer progression. However, in some instances, distant dissemination arises at a very early stage, so that metastases reach clinical relevance before primary lesions. Sometimes, the primary lesions cannot be identified in spite of the progresses in the diagnosis of malignancies.<ref>PMID:20949619</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/MET_HUMAN MET_HUMAN]] Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to hepatocyte growth factor/HGF ligand. Regulates many physiological processes including proliferation, scattering, morphogenesis and survival. Ligand binding at the cell surface induces autophosphorylation of MET on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1, SRC, GRB2, STAT3 or the adapter GAB1. Recruitment of these downstream effectors by MET leads to the activation of several signaling cascades including the RAS-ERK, PI3 kinase-AKT, or PLCgamma-PKC. The RAS-ERK activation is associated with the morphogenetic effects while PI3K/AKT coordinates prosurvival effects. During embryonic development, MET signaling plays a role in gastrulation, development and migration of muscles and neuronal precursors, angiogenesis and kidney formation. In adults, participates in wound healing as well as organ regeneration and tissue remodeling. Promotes also differentiation and proliferation of hematopoietic cells.<ref>PMID:1846706</ref> <ref>PMID:8182137</ref> <ref>PMID:15314156</ref> Acts as a receptor for Listeria internalin inlB, mediating entry of the pathogen into cells.<ref>PMID:1846706</ref> <ref>PMID:8182137</ref> <ref>PMID:15314156</ref>	+	[https://www.uniprot.org/uniprot/MET_HUMAN MET_HUMAN] Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to hepatocyte growth factor/HGF ligand. Regulates many physiological processes including proliferation, scattering, morphogenesis and survival. Ligand binding at the cell surface induces autophosphorylation of MET on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1, SRC, GRB2, STAT3 or the adapter GAB1. Recruitment of these downstream effectors by MET leads to the activation of several signaling cascades including the RAS-ERK, PI3 kinase-AKT, or PLCgamma-PKC. The RAS-ERK activation is associated with the morphogenetic effects while PI3K/AKT coordinates prosurvival effects. During embryonic development, MET signaling plays a role in gastrulation, development and migration of muscles and neuronal precursors, angiogenesis and kidney formation. In adults, participates in wound healing as well as organ regeneration and tissue remodeling. Promotes also differentiation and proliferation of hematopoietic cells.<ref>PMID:1846706</ref> <ref>PMID:8182137</ref> <ref>PMID:15314156</ref> Acts as a receptor for Listeria internalin inlB, mediating entry of the pathogen into cells.<ref>PMID:1846706</ref> <ref>PMID:8182137</ref> <ref>PMID:15314156</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 23:		Line 22:
	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=3lq8 ConSurf].		</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=3lq8 ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
-	<div style="background-color:#fffaf0;">
-	== Publication Abstract from PubMed ==
-	The Met receptor tyrosine kinase and its ligand, hepatocyte growth factor (HGF), are overexpressed and/or activated in a wide variety of human malignancies. Vascular endothelial growth factor (VEGF) receptors are expressed on the surface of vascular endothelial cells and cooperate with Met to induce tumor invasion and vascularization. EXEL-2880 (XL880, GSK1363089) is a small-molecule kinase inhibitor that targets members of the HGF and VEGF receptor tyrosine kinase families, with additional inhibitory activity toward KIT, Flt-3, platelet-derived growth factor receptor beta, and Tie-2. Binding of EXEL-2880 to Met and VEGF receptor 2 (KDR) is characterized by a very slow off-rate, consistent with X-ray crystallographic data showing that the inhibitor is deeply bound in the Met kinase active site cleft. EXEL-2880 inhibits cellular HGF-induced Met phosphorylation and VEGF-induced extracellular signal-regulated kinase phosphorylation and prevents both HGF-induced responses of tumor cells and HGF/VEGF-induced responses of endothelial cells. In addition, EXEL-2880 prevents anchorage-independent proliferation of tumor cells under both normoxic and hypoxic conditions. In vivo, these effects produce significant dose-dependent inhibition of tumor burden in an experimental model of lung metastasis. Collectively, these data indicate that EXEL-2880 may prevent tumor growth through a direct effect on tumor cell proliferation and by inhibition of invasion and angiogenesis mediated by HGF and VEGF receptors.
-
-	Inhibition of tumor cell growth, invasion, and metastasis by EXEL-2880 (XL880, GSK1363089), a novel inhibitor of HGF and VEGF receptor tyrosine kinases.,Qian F, Engst S, Yamaguchi K, Yu P, Won KA, Mock L, Lou T, Tan J, Li C, Tam D, Lougheed J, Yakes FM, Bentzien F, Xu W, Zaks T, Wooster R, Greshock J, Joly AH Cancer Res. 2009 Oct 15;69(20):8009-16. Epub 2009 Oct 6. PMID:19808973<ref>PMID:19808973</ref>
-
-	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	</div>
-	<div class="pdbe-citations 3lq8" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
-	*[[Hepatocyte growth factor receptor\|Hepatocyte growth factor receptor]]	+	*[[Hepatocyte growth factor receptor 3D structures\|Hepatocyte growth factor receptor 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
-	[[Category: ~~Receptor protein-tyrosine kinase~~]]	+	[[Category: Large Structures]]
-	[[Category: Lougheed~~, J C~~]]	+	[[Category: Lougheed JC]]
-	[[Category: Stout~~, T J]]~~	+	[[Category: Stout TJ]]
-	~~[[Category: Atp-binding]]~~	+
-	~~[[Category: Gsk1363089]]~~	+
-	~~[[Category: Kinase]]~~	+
-	~~[[Category: Kinase domain]]~~	+
-	~~[[Category: Nucleotide-binding]]~~	+
-	~~[[Category: Phosphoprotein]]~~	+
-	~~[[Category: Proto-oncogene]]~~	+
-	~~[[Category: Receptor]]~~	+
-	~~[[Category: Transferase]]~~	+
-	~~[[Category: Transmembrane]]~~	+
-	~~[[Category: Tyrosine-protein kinase]]~~	+
-	~~[[Category: Xl880~~]]	+

OCA at 07:36, 9 January 2019

OCA — Wed, 09 Jan 2019 07:36:58 GMT

←Older revision		Revision as of 07:36, 9 January 2019
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	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/lq/3lq8_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/lq/3lq8_consurf.spt"</scriptWhenChecked>
	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>		<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>

OCA at 20:40, 5 August 2016

OCA — Fri, 05 Aug 2016 20:40:53 GMT

←Older revision		Revision as of 20:40, 5 August 2016
Line 1:		Line 1:
		+
	==Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)==		==Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)==
	<StructureSection load='3lq8' size='340' side='right' caption='[[3lq8]], [[Resolution\|resolution]] 2.02Å' scene=''>		<StructureSection load='3lq8' size='340' side='right' caption='[[3lq8]], [[Resolution\|resolution]] 2.02Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3lq8]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/~~Homo_sapiens Homo sapiens~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3LQ8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3LQ8 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3lq8]] 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=3LQ8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3LQ8 FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=88Z:N-(3-FLUORO-4-{[6-METHOXY-7-(3-MORPHOLIN-4-YLPROPOXY)QUINOLIN-4-YL]OXY}PHENYL)-N-(4-FLUOROPHENYL)CYCLOPROPANE-1,1-DICARBOXAMIDE'>88Z</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=88Z:N-(3-FLUORO-4-{[6-METHOXY-7-(3-MORPHOLIN-4-YLPROPOXY)QUINOLIN-4-YL]OXY}PHENYL)-N-(4-FLUOROPHENYL)CYCLOPROPANE-1,1-DICARBOXAMIDE'>88Z</scene></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MET ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MET ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Receptor_protein-tyrosine_kinase Receptor protein-tyrosine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.10.1 2.7.10.1] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Receptor_protein-tyrosine_kinase Receptor protein-tyrosine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.10.1 2.7.10.1] </span></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=3lq8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3lq8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3lq8 RCSB], [http://www.ebi.ac.uk/pdbsum/3lq8 PDBsum]</span></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=3lq8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3lq8 OCA], [http://pdbe.org/3lq8 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3lq8 RCSB], [http://www.ebi.ac.uk/pdbsum/3lq8 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3lq8 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 20:		Line 21:
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
	</jmolCheckbox>		</jmolCheckbox>
-	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/~~chain_selection~~.php?pdb_ID=~~2ata~~ ConSurf].	+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=3lq8 ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 30:		Line 31:
	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	</div>		</div>
		+	<div class="pdbe-citations 3lq8" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 37:		Line 39:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Receptor protein-tyrosine kinase]]		[[Category: Receptor protein-tyrosine kinase]]
	[[Category: Lougheed, J C]]		[[Category: Lougheed, J C]]

OCA at 16:23, 18 December 2014

OCA — Thu, 18 Dec 2014 16:23:20 GMT

←Older revision		Revision as of 16:23, 18 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3lq8\| PDB=3lq8 \| SCENE= }}~~	+	==Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)==
-	===Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)===	+	<StructureSection load='3lq8' size='340' side='right' caption='[[3lq8]], [[Resolution\|resolution]] 2.02Å' scene=''>
-	{~~{ABSTRACT_PUBMED_19808973}~~}	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[3lq8]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3LQ8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3LQ8 FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=88Z:N-(3-FLUORO-4-{[6-METHOXY-7-(3-MORPHOLIN-4-YLPROPOXY)QUINOLIN-4-YL]OXY}PHENYL)-N-(4-FLUOROPHENYL)CYCLOPROPANE-1,1-DICARBOXAMIDE'>88Z</scene></td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MET ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
		+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Receptor_protein-tyrosine_kinase Receptor protein-tyrosine kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.10.1 2.7.10.1] </span></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=3lq8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3lq8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3lq8 RCSB], [http://www.ebi.ac.uk/pdbsum/3lq8 PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/MET_HUMAN MET_HUMAN]] Note=Activation of MET after rearrangement with the TPR gene produces an oncogenic protein. Note=Defects in MET may be associated with gastric cancer. Defects in MET are a cause of hepatocellular carcinoma (HCC) [MIM:[http://omim.org/entry/114550 114550]].<ref>PMID:9927037</ref> Defects in MET are a cause of renal cell carcinoma papillary (RCCP) [MIM:[http://omim.org/entry/605074 605074]]. It is a subtype of renal cell carcinoma tending to show a tubulo-papillary architecture formed by numerous, irregular, finger-like projections of connective tissue. Renal cell carcinoma is a heterogeneous group of sporadic or hereditary carcinoma derived from cells of the proximal renal tubular epithelium. It is subclassified into common renal cell carcinoma (clear cell, non-papillary carcinoma), papillary renal cell carcinoma, chromophobe renal cell carcinoma, collecting duct carcinoma with medullary carcinoma of the kidney, and unclassified renal cell carcinoma.<ref>PMID:9140397</ref> <ref>PMID:9563489</ref> <ref>PMID:10433944</ref> <ref>PMID:10417759</ref> <ref>PMID:10327054</ref> Note=A common allele in the promoter region of the MET shows genetic association with susceptibility to autism in some families. Functional assays indicate a decrease in MET promoter activity and altered binding of specific transcription factor complexes. Note=MET activating mutations may be involved in the development of a highly malignant, metastatic syndrome known as cancer of unknown primary origin (CUP) or primary occult malignancy. Systemic neoplastic spread is generally a late event in cancer progression. However, in some instances, distant dissemination arises at a very early stage, so that metastases reach clinical relevance before primary lesions. Sometimes, the primary lesions cannot be identified in spite of the progresses in the diagnosis of malignancies.<ref>PMID:20949619</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/MET_HUMAN MET_HUMAN]] Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to hepatocyte growth factor/HGF ligand. Regulates many physiological processes including proliferation, scattering, morphogenesis and survival. Ligand binding at the cell surface induces autophosphorylation of MET on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1, SRC, GRB2, STAT3 or the adapter GAB1. Recruitment of these downstream effectors by MET leads to the activation of several signaling cascades including the RAS-ERK, PI3 kinase-AKT, or PLCgamma-PKC. The RAS-ERK activation is associated with the morphogenetic effects while PI3K/AKT coordinates prosurvival effects. During embryonic development, MET signaling plays a role in gastrulation, development and migration of muscles and neuronal precursors, angiogenesis and kidney formation. In adults, participates in wound healing as well as organ regeneration and tissue remodeling. Promotes also differentiation and proliferation of hematopoietic cells.<ref>PMID:1846706</ref> <ref>PMID:8182137</ref> <ref>PMID:15314156</ref> Acts as a receptor for Listeria internalin inlB, mediating entry of the pathogen into cells.<ref>PMID:1846706</ref> <ref>PMID:8182137</ref> <ref>PMID:15314156</ref>
		+	== Evolutionary Conservation ==
		+	[[Image:Consurf_key_small.gif\|200px\|right]]
		+	Check<jmol>
		+	<jmolCheckbox>
		+	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/lq/3lq8_consurf.spt"</scriptWhenChecked>
		+	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
		+	<text>to colour the structure by Evolutionary Conservation</text>
		+	</jmolCheckbox>
		+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf].
		+	<div style="clear:both"></div>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	The Met receptor tyrosine kinase and its ligand, hepatocyte growth factor (HGF), are overexpressed and/or activated in a wide variety of human malignancies. Vascular endothelial growth factor (VEGF) receptors are expressed on the surface of vascular endothelial cells and cooperate with Met to induce tumor invasion and vascularization. EXEL-2880 (XL880, GSK1363089) is a small-molecule kinase inhibitor that targets members of the HGF and VEGF receptor tyrosine kinase families, with additional inhibitory activity toward KIT, Flt-3, platelet-derived growth factor receptor beta, and Tie-2. Binding of EXEL-2880 to Met and VEGF receptor 2 (KDR) is characterized by a very slow off-rate, consistent with X-ray crystallographic data showing that the inhibitor is deeply bound in the Met kinase active site cleft. EXEL-2880 inhibits cellular HGF-induced Met phosphorylation and VEGF-induced extracellular signal-regulated kinase phosphorylation and prevents both HGF-induced responses of tumor cells and HGF/VEGF-induced responses of endothelial cells. In addition, EXEL-2880 prevents anchorage-independent proliferation of tumor cells under both normoxic and hypoxic conditions. In vivo, these effects produce significant dose-dependent inhibition of tumor burden in an experimental model of lung metastasis. Collectively, these data indicate that EXEL-2880 may prevent tumor growth through a direct effect on tumor cell proliferation and by inhibition of invasion and angiogenesis mediated by HGF and VEGF receptors.

-	~~==Disease==~~	+	Inhibition of tumor cell growth, invasion, and metastasis by EXEL-2880 (XL880, GSK1363089), a novel inhibitor of HGF and VEGF receptor tyrosine kinases.,Qian F, Engst S, Yamaguchi K, Yu P, Won KA, Mock L, Lou T, Tan J, Li C, Tam D, Lougheed J, Yakes FM, Bentzien F, Xu W, Zaks T, Wooster R, Greshock J, Joly AH Cancer Res. 2009 Oct 15;69(20):8009-16. Epub 2009 Oct 6. PMID:19808973<ref>PMID:19808973</ref>
-	~~[[http://www.uniprot.org/uniprot/MET_HUMAN MET_HUMAN]] Note=Activation~~ of MET after rearrangement with the TPR gene produces an oncogenic protein. Note=Defects in MET may be associated with gastric cancer. Defects in MET are a cause of hepatocellular carcinoma (HCC) [MIM:[http://omim.org/entry/114550 114550]].<ref>PMID:9927037</ref> Defects in MET are a cause of renal cell ~~carcinoma papillary~~ (~~RCCP~~) ~~[MIM:[http://omim.org/entry/605074 605074]]. It is a subtype of renal cell carcinoma tending to show a tubulo-papillary architecture formed by numerous~~, ~~irregular, finger-like projections of connective tissue. Renal cell carcinoma is~~ a ~~heterogeneous group~~ of ~~sporadic or hereditary carcinoma derived from cells of the proximal renal tubular epithelium~~. ~~It is subclassified into common renal cell carcinoma (clear cell~~, ~~non-papillary carcinoma)~~, ~~papillary renal cell carcinoma~~, ~~chromophobe renal cell carcinoma~~, ~~collecting duct carcinoma with medullary carcinoma of the kidney~~, and unclassified renal cell carcinoma.<ref>PMID:9140397</ref><ref>PMID:9563489</ref><ref>PMID:10433944</ref><ref>PMID:10417759</ref><ref>PMID:10327054</ref> Note=A common allele in the promoter region of the MET shows genetic association with susceptibility to autism in some families. Functional assays indicate a decrease in MET promoter activity and altered binding of specific transcription factor complexes. Note=MET activating mutations may be involved in the development of a highly malignant, ~~metastatic syndrome known as cancer of unknown primary origin (CUP) or primary occult malignancy. Systemic neoplastic spread is generally a late event in cancer progression. However~~, ~~in some instances~~, ~~distant dissemination arises at a very early stage~~, ~~so that metastases reach clinical relevance before primary lesions. Sometimes~~, ~~the primary lesions cannot be identified in spite of the progresses in the diagnosis of malignancies~~.<ref>PMID:~~20949619~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~//www.uniprot.org/uniprot/MET_HUMAN MET_HUMAN]] Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to hepatocyte growth factor/HGF ligand. Regulates many physiological processes including proliferation, ~~scattering, morphogenesis and survival. Ligand binding at the cell surface induces autophosphorylation~~ of ~~MET on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1, SRC, GRB2, STAT3 or~~ the ~~adapter GAB1~~. ~~Recruitment of these downstream effectors by MET leads to the activation of several signaling cascades including the RAS-ERK, PI3 kinase-AKT, or PLCgamma-PKC~~. The RAS-ERK activation is associated with the morphogenetic effects while PI3K/AKT coordinates prosurvival effects. During embryonic development, MET signaling plays a role in gastrulation, development and migration of muscles and neuronal precursors, angiogenesis and kidney formation. In adults, participates in wound healing as well as organ regeneration and tissue remodeling. Promotes also differentiation and proliferation of hematopoietic cells.<~~ref~~>~~PMID:1846706~~</~~ref~~><ref>PMID:8182137</ref><ref>PMID:15314156</ref> Acts as a receptor for Listeria internalin inlB, mediating entry of the pathogen into cells.<ref>PMID:1846706</ref><ref>PMID:8182137</ref><ref>PMID:15314156</ref>	+	</div>
-		+
-	~~==About this Structure==~~	+
-	[[3lq8]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3LQ8 OCA].	+

	==See Also==		==See Also==
	*[[Hepatocyte growth factor receptor\|Hepatocyte growth factor receptor]]		*[[Hepatocyte growth factor receptor\|Hepatocyte growth factor receptor]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:019808973</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Receptor protein-tyrosine kinase]]		[[Category: Receptor protein-tyrosine kinase]]
-	[[Category: Lougheed, J C.]]	+	[[Category: Lougheed, J C]]
-	[[Category: Stout, T J.]]	+	[[Category: Stout, T J]]
	[[Category: Atp-binding]]		[[Category: Atp-binding]]
	[[Category: Gsk1363089]]		[[Category: Gsk1363089]]

OCA: Protected "3lq8" [edit=sysop:move=sysop]

OCA — Mon, 25 Mar 2013 05:01:42 GMT

Protected "3lq8" [edit=sysop:move=sysop]

←Older revision

Revision as of 05:01, 25 March 2013

OCA at 05:01, 25 March 2013

OCA — Mon, 25 Mar 2013 05:01:40 GMT

←Older revision		Revision as of 05:01, 25 March 2013
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-	{{Seed}}
-	[[Image:3lq8.jpg\|left\|200px]]
-
-	<!--
-	The line below this paragraph, containing "STRUCTURE_3lq8", creates the "Structure Box" on the page.
-	You may change the PDB parameter (which sets the PDB file loaded into the applet)
-	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
-	or leave the SCENE parameter empty for the default display.
-	-->
	{{STRUCTURE_3lq8\| PDB=3lq8 \| SCENE= }}		{{STRUCTURE_3lq8\| PDB=3lq8 \| SCENE= }}
-
	===Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)===		===Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)===
-
-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_19808973}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 19808973 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_19808973}}		{{ABSTRACT_PUBMED_19808973}}

	==Disease==		==Disease==
-	~~Known disease associated with this structure: Hepatocellular carcinoma, childhood type OMIM:~~[[http://www.~~ncbi~~.~~nlm~~.~~nih~~.~~gov~~/~~entrez~~/~~dispomim~~.~~cgi?id=164860 164860~~]]~~, Renal~~ cell carcinoma, papillary~~, familial and sporadic OMIM~~:[[http://~~www~~.~~ncbi~~.~~nlm~~.~~nih~~.~~gov~~/~~entrez~~/~~dispomim~~.~~cgi?id~~=~~164860 164860]]~~, ~~Autism~~, ~~suseptibility to~~, ~~9 OMIM~~:[[http://www.~~ncbi~~.~~nlm~~.~~nih~~.~~gov~~/~~entrez~~/~~dispomim~~.~~cgi?id=164860 164860]]~~	+	[[http://www.uniprot.org/uniprot/MET_HUMAN MET_HUMAN]] Note=Activation of MET after rearrangement with the TPR gene produces an oncogenic protein. Note=Defects in MET may be associated with gastric cancer. Defects in MET are a cause of hepatocellular carcinoma (HCC) [MIM:[http://omim.org/entry/114550 114550]].<ref>PMID:9927037</ref> Defects in MET are a cause of renal cell carcinoma papillary (RCCP) [MIM:[http://omim.org/entry/605074 605074]]. It is a subtype of renal cell carcinoma tending to show a tubulo-papillary architecture formed by numerous, irregular, finger-like projections of connective tissue. Renal cell carcinoma is a heterogeneous group of sporadic or hereditary carcinoma derived from cells of the proximal renal tubular epithelium. It is subclassified into common renal cell carcinoma (clear cell, non-papillary carcinoma), papillary renal cell carcinoma, chromophobe renal cell carcinoma, collecting duct carcinoma with medullary carcinoma of the kidney, and unclassified renal cell carcinoma.<ref>PMID:9140397</ref><ref>PMID:9563489</ref><ref>PMID:10433944</ref><ref>PMID:10417759</ref><ref>PMID:10327054</ref> Note=A common allele in the promoter region of the MET shows genetic association with susceptibility to autism in some families. Functional assays indicate a decrease in MET promoter activity and altered binding of specific transcription factor complexes. Note=MET activating mutations may be involved in the development of a highly malignant, metastatic syndrome known as cancer of unknown primary origin (CUP) or primary occult malignancy. Systemic neoplastic spread is generally a late event in cancer progression. However, in some instances, distant dissemination arises at a very early stage, so that metastases reach clinical relevance before primary lesions. Sometimes, the primary lesions cannot be identified in spite of the progresses in the diagnosis of malignancies.<ref>PMID:20949619</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/MET_HUMAN MET_HUMAN]] Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to hepatocyte growth factor/HGF ligand. Regulates many physiological processes including proliferation, scattering, morphogenesis and survival. Ligand binding at the cell surface induces autophosphorylation of MET on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1, SRC, GRB2, STAT3 or the adapter GAB1. Recruitment of these downstream effectors by MET leads to the activation of several signaling cascades including the RAS-ERK, PI3 kinase-AKT, or PLCgamma-PKC. The RAS-ERK activation is associated with the morphogenetic effects while PI3K/AKT coordinates prosurvival effects. During embryonic development, MET signaling plays a role in gastrulation, development and migration of muscles and neuronal precursors, angiogenesis and kidney formation. In adults, participates in wound healing as well as organ regeneration and tissue remodeling. Promotes also differentiation and proliferation of hematopoietic cells.<ref>PMID:1846706</ref><ref>PMID:8182137</ref><ref>PMID:15314156</ref> Acts as a receptor for Listeria internalin inlB, mediating entry of the pathogen into cells.<ref>PMID:1846706</ref><ref>PMID:8182137</ref><ref>PMID:15314156</ref>

	==About this Structure==		==About this Structure==
-	~~3LQ8~~ is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3LQ8 OCA].	+	[[3lq8]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3LQ8 OCA].
		+
		+	==See Also==
		+	*[[Hepatocyte growth factor receptor\|Hepatocyte growth factor receptor]]

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~19808973~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:019808973</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Receptor protein-tyrosine kinase]]		[[Category: Receptor protein-tyrosine kinase]]
Line 43:		Line 33:
	[[Category: Tyrosine-protein kinase]]		[[Category: Tyrosine-protein kinase]]
	[[Category: Xl880]]		[[Category: Xl880]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu May 20 09:29:59 2010''

OCA at 06:30, 20 May 2010

OCA — Thu, 20 May 2010 06:30:01 GMT

←Older revision		Revision as of 06:30, 20 May 2010
Line 1:		Line 1:
-	~~'''Unreleased structure'''~~	+	{{Seed}}
		+	[[Image:3lq8.jpg\|left\|200px]]

-	The ~~entry 3lq8~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_3lq8", creates the "Structure Box" on the page.
		+	You may change the PDB parameter (which sets the PDB file loaded into the applet)
		+	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
		+	or leave the SCENE parameter empty for the default display.
		+	-->
		+	{{STRUCTURE_3lq8\| PDB=3lq8 \| SCENE= }}

-	~~Authors: Lougheed, J.C., Stout, T.J.~~	+	===Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)===

-	Description: Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on ~~Wed Mar 3 15~~:27:59 2010''	+	<!--
		+	The line below this paragraph, {{ABSTRACT_PUBMED_19808973}}, adds the Publication Abstract to the page
		+	(as it appears on PubMed at http://www.pubmed.gov), where 19808973 is the PubMed ID number.
		+	-->
		+	{{ABSTRACT_PUBMED_19808973}}
		+
		+	==Disease==
		+	Known disease associated with this structure: Hepatocellular carcinoma, childhood type OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=164860 164860]], Renal cell carcinoma, papillary, familial and sporadic OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=164860 164860]], Autism, suseptibility to, 9 OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=164860 164860]]
		+
		+	==About this Structure==
		+	3LQ8 is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3LQ8 OCA].
		+
		+	==Reference==
		+	<ref group="xtra">PMID:19808973</ref><references group="xtra"/>
		+	[[Category: Homo sapiens]]
		+	[[Category: Receptor protein-tyrosine kinase]]
		+	[[Category: Lougheed, J C.]]
		+	[[Category: Stout, T J.]]
		+	[[Category: Atp-binding]]
		+	[[Category: Gsk1363089]]
		+	[[Category: Kinase]]
		+	[[Category: Kinase domain]]
		+	[[Category: Nucleotide-binding]]
		+	[[Category: Phosphoprotein]]
		+	[[Category: Proto-oncogene]]
		+	[[Category: Receptor]]
		+	[[Category: Transferase]]
		+	[[Category: Transmembrane]]
		+	[[Category: Tyrosine-protein kinase]]
		+	[[Category: Xl880]]
		+
		+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu May 20 09:29:59 2010''

OCA at 13:28, 3 March 2010

OCA — Wed, 03 Mar 2010 13:28:00 GMT

←Older revision		Revision as of 13:28, 3 March 2010
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 3lq8 is ON HOLD	+	The entry 3lq8 is ON HOLD until Paper Publication

	Authors: Lougheed, J.C., Stout, T.J.		Authors: Lougheed, J.C., Stout, T.J.
Line 7:		Line 7:
	Description: Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)		Description: Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed ~~Feb 17 10~~:11:37 2010''	+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Mar 3 15:27:59 2010''

OCA: New page: '''Unreleased structure''' The entry 3lq8 is ON HOLD Authors: Lougheed, J.C., Stout, T.J. Description: Structure of the kinase domain of c-Met bound to XL880 (GSK1363089) ''Page seede...

OCA — Wed, 17 Feb 2010 08:11:37 GMT

New page: '''Unreleased structure''' The entry 3lq8 is ON HOLD Authors: Lougheed, J.C., Stout, T.J. Description: Structure of the kinase domain of c-Met bound to XL880 (GSK1363089) ''Page seede...

New page

'''Unreleased structure'''

The entry 3lq8 is ON HOLD

Authors: Lougheed, J.C., Stout, T.J.

Description: Structure of the kinase domain of c-Met bound to XL880 (GSK1363089)

''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Feb 17 10:11:37 2010''