3tj5 - Revision history

OCA at 13:30, 14 March 2024

OCA — Thu, 14 Mar 2024 13:30:21 GMT

←Older revision		Revision as of 13:30, 14 March 2024
Line 3:		Line 3:
	<StructureSection load='3tj5' size='340' side='right'caption='[[3tj5]], [[Resolution\|resolution]] 1.99Å' scene=''>		<StructureSection load='3tj5' size='340' side='right'caption='[[3tj5]], [[Resolution\|resolution]] 1.99Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3tj5]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/~~Human Human~~] and [https://en.wikipedia.org/wiki/~~Ricro Ricro~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3TJ5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3TJ5 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3tj5]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Rickettsia_rickettsii_str._Iowa Rickettsia rickettsii str. Iowa]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3TJ5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3TJ5 FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=GOL:GLYCEROL'>GOL</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]] 1.99Å</td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max~~-~~height: 3em;'>[[3rf3\|3rf3]]~~, [[~~2ibf~~\|~~2ibf]], [[2hsq\|2hsq]], [[2gww\|2gww]], [[1rkc\|1rkc]], [[3s90\|3s90]], [[3tj6\|3tj6~~]]~~</div>~~</td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
-	<tr id='~~gene~~'><td class="sblockLbl"><b>[[~~Gene~~\|~~Gene~~:]]</b></td><td class="sblockDat">~~VCL ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode~~=~~Info&srchmode~~=~~5&id=9606 HUMAN]), RrIowa_0797, sca4 ([https~~:/~~/www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=452659 RICRO])~~</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=3tj5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3tj5 OCA], [https://pdbe.org/3tj5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3tj5 RCSB], [https://www.ebi.ac.uk/pdbsum/3tj5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3tj5 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=3tj5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3tj5 OCA], [https://pdbe.org/3tj5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3tj5 RCSB], [https://www.ebi.ac.uk/pdbsum/3tj5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3tj5 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Defects in VCL are the cause of cardiomyopathy dilated type 1W (CMD1W) [MIM:[https://omim.org/entry/611407 611407]]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.<ref>PMID:11815424</ref> <ref>PMID:16236538</ref> Defects in VCL are the cause of familial hypertrophic cardiomyopathy type 15 (CMH15) [MIM:[https://omim.org/entry/613255 613255]]. It is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.<ref>PMID:16712796</ref>	+	[https://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN] Defects in VCL are the cause of cardiomyopathy dilated type 1W (CMD1W) [MIM:[https://omim.org/entry/611407 611407]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.<ref>PMID:11815424</ref> <ref>PMID:16236538</ref> Defects in VCL are the cause of familial hypertrophic cardiomyopathy type 15 (CMH15) [MIM:[https://omim.org/entry/613255 613255]. It is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.<ref>PMID:16712796</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Actin filament (F-actin)-binding protein involved in cell-matrix adhesion and cell-cell adhesion. Regulates cell-surface E-cadherin expression and potentiates mechanosensing by the E-cadherin complex. May also play important roles in cell morphology and locomotion.<ref>PMID:20484056</ref>	+	[https://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN] Actin filament (F-actin)-binding protein involved in cell-matrix adhesion and cell-cell adhesion. Regulates cell-surface E-cadherin expression and potentiates mechanosensing by the E-cadherin complex. May also play important roles in cell morphology and locomotion.<ref>PMID:20484056</ref>
-	~~<div style="background-color:#fffaf0;">~~	+
-	~~== Publication Abstract from PubMed ==~~	+
-	Pathogenic Rickettsiae species cause high morbidity and mortality, especially R. prowazekii the causative agent of typhus. Like many intracellular pathogens, Rickettsiae exploit the cytoskeleton to enter and spread within the host cell. Here we report that the cell surface antigen sca4 of Rickettsiae colocalizes with vinculin in cells at sites of focal adhesions, and that sca4 binds to and activates vinculin through two vinculin binding sites (VBSs) that are conserved across all Rickettsia. Remarkably, this occurs through molecular mimicry of the vinculn-talin interaction that is also seen with the IpaA invasin of the intracellular pathogen Shigella, where binding of these VBSs to the vinculin seven-helix bundle head domain (Vh1) displaces intramolecular interactions with the vinculin tail domain that normally clamp vinculin in an inactive state. Finally, the vinculin:sca4-VBS crystal structures reveal that vinculin adopts a new conformation when bound to the C-terminal VBS of sca4. Collectively, our data define the mechanism by which sca4 activates vinculin and interacts with the actin cytoskeleton and they suggest important roles for vinculin in Rickettsia pathogenesis.	+
-		+
-	~~The Rickettsia surface cell antigen 4 applies mimicry to bind to and activate vinculin.,Park H, Lee JH, Cossart P, Gouin E, Izard T J Biol Chem. 2011 Aug 13. PMID:21841197<ref>PMID:21841197</ref>~~	+
-		+
-	~~From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>~~	+
-	~~</div>~~	+
-	~~<div class="pdbe-citations 3tj5" style="background-color:#fffaf0;"></div~~>	+

	==See Also==		==See Also==
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: ~~Ricro~~]]	+	[[Category: Rickettsia rickettsii str. Iowa]]
-	[[Category: Cossart, P]]	+	[[Category: Cossart P]]
-	[[Category: Gouin, E]]	+	[[Category: Gouin E]]
-	[[Category: Izard, T]]	+	[[Category: Izard T]]
-	[[Category: Lee~~, J H~~]]	+	[[Category: Lee JH]]
-	[[Category: Park, H]]	+	[[Category: Park H]]
-	~~[[Category: Alpha-helix bundle domain]]~~	+
-	~~[[Category: Cell adhesion]]~~	+
-	~~[[Category: Cytoskeleton]]~~	+
-	~~[[Category: Cytosol]]~~	+
-	~~[[Category: Epidemic typhus]]~~	+
-	~~[[Category: Focal adhesion]]~~	+
-	~~[[Category: Protein binding-toxin complex]]~~	+
-	~~[[Category: Protein-protein interaction]]~~	+
-	~~[[Category: Sca4]]~~	+
-	~~[[Category: Spotted fever~~]]	+

OCA at 17:00, 6 July 2022

OCA — Wed, 06 Jul 2022 17:00:23 GMT

←Older revision		Revision as of 17:00, 6 July 2022
Line 1:		Line 1:

	==human vinculin head domain (Vh1, residues 1-258) in complex with the vinculin binding site of the surface cell antigen 4 (sca4-VBS-N; residues 412-434) from Rickettsia rickettsii==		==human vinculin head domain (Vh1, residues 1-258) in complex with the vinculin binding site of the surface cell antigen 4 (sca4-VBS-N; residues 412-434) from Rickettsia rickettsii==
-	<StructureSection load='3tj5' size='340' side='right' caption='[[3tj5]], [[Resolution\|resolution]] 1.99Å' scene=''>	+	<StructureSection load='3tj5' size='340' side='right'caption='[[3tj5]], [[Resolution\|resolution]] 1.99Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3tj5]] is a 2 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/Human Human] and [~~http~~://en.wikipedia.org/wiki/Ricro Ricro]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3TJ5 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3TJ5 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3tj5]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human] and [https://en.wikipedia.org/wiki/Ricro Ricro]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3TJ5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3TJ5 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3rf3\|3rf3]], [[2ibf\|2ibf]], [[2hsq\|2hsq]], [[2gww\|2gww]], [[1rkc\|1rkc]], [[3s90\|3s90]], [[3tj6\|3tj6]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[3rf3\|3rf3]], [[2ibf\|2ibf]], [[2hsq\|2hsq]], [[2gww\|2gww]], [[1rkc\|1rkc]], [[3s90\|3s90]], [[3tj6\|3tj6]]</div></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">VCL ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), RrIowa_0797, sca4 ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=452659 RICRO])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">VCL ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), RrIowa_0797, sca4 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=452659 RICRO])</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=3tj5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3tj5 OCA], [~~http~~://pdbe.org/3tj5 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3tj5 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3tj5 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3tj5 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=3tj5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3tj5 OCA], [https://pdbe.org/3tj5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3tj5 RCSB], [https://www.ebi.ac.uk/pdbsum/3tj5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3tj5 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Defects in VCL are the cause of cardiomyopathy dilated type 1W (CMD1W) [MIM:[~~http~~://omim.org/entry/611407 611407]]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.<ref>PMID:11815424</ref> <ref>PMID:16236538</ref> Defects in VCL are the cause of familial hypertrophic cardiomyopathy type 15 (CMH15) [MIM:[~~http~~://omim.org/entry/613255 613255]]. It is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.<ref>PMID:16712796</ref>	+	[[https://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Defects in VCL are the cause of cardiomyopathy dilated type 1W (CMD1W) [MIM:[https://omim.org/entry/611407 611407]]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.<ref>PMID:11815424</ref> <ref>PMID:16236538</ref> Defects in VCL are the cause of familial hypertrophic cardiomyopathy type 15 (CMH15) [MIM:[https://omim.org/entry/613255 613255]]. It is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.<ref>PMID:16712796</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Actin filament (F-actin)-binding protein involved in cell-matrix adhesion and cell-cell adhesion. Regulates cell-surface E-cadherin expression and potentiates mechanosensing by the E-cadherin complex. May also play important roles in cell morphology and locomotion.<ref>PMID:20484056</ref>	+	[[https://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Actin filament (F-actin)-binding protein involved in cell-matrix adhesion and cell-cell adhesion. Regulates cell-surface E-cadherin expression and potentiates mechanosensing by the E-cadherin complex. May also play important roles in cell morphology and locomotion.<ref>PMID:20484056</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
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	</div>		</div>
	<div class="pdbe-citations 3tj5" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 3tj5" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Vinculin\|Vinculin]]
	== References ==		== References ==
	<references/>		<references/>
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	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Ricro]]		[[Category: Ricro]]
	[[Category: Cossart, P]]		[[Category: Cossart, P]]

OCA at 09:52, 8 November 2017

OCA — Wed, 08 Nov 2017 09:52:11 GMT

←Older revision		Revision as of 09:52, 8 November 2017
Line 22:		Line 22:
	</div>		</div>
	<div class="pdbe-citations 3tj5" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 3tj5" style="background-color:#fffaf0;"></div>
-
-	==See Also==
-	*[[Vinculin\|Vinculin]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 23:16, 5 August 2016

OCA — Fri, 05 Aug 2016 23:16:15 GMT

←Older revision		Revision as of 23:16, 5 August 2016
Line 1:		Line 1:
		+
	==human vinculin head domain (Vh1, residues 1-258) in complex with the vinculin binding site of the surface cell antigen 4 (sca4-VBS-N; residues 412-434) from Rickettsia rickettsii==		==human vinculin head domain (Vh1, residues 1-258) in complex with the vinculin binding site of the surface cell antigen 4 (sca4-VBS-N; residues 412-434) from Rickettsia rickettsii==
	<StructureSection load='3tj5' size='340' side='right' caption='[[3tj5]], [[Resolution\|resolution]] 1.99Å' scene=''>		<StructureSection load='3tj5' size='340' side='right' caption='[[3tj5]], [[Resolution\|resolution]] 1.99Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3tj5]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/~~Homo_sapiens Homo sapiens~~] and [http://en.wikipedia.org/wiki/~~Rickettsia_rickettsii Rickettsia rickettsii~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3TJ5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3TJ5 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3tj5]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human] and [http://en.wikipedia.org/wiki/Ricro Ricro]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3TJ5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3TJ5 FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3rf3\|3rf3]], [[2ibf\|2ibf]], [[2hsq\|2hsq]], [[2gww\|2gww]], [[1rkc\|1rkc]], [[3s90\|3s90]], [[3tj6\|3tj6]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3rf3\|3rf3]], [[2ibf\|2ibf]], [[2hsq\|2hsq]], [[2gww\|2gww]], [[1rkc\|1rkc]], [[3s90\|3s90]], [[3tj6\|3tj6]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">VCL ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~]), RrIowa_0797, sca4 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=~~783 Rickettsia rickettsii~~])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">VCL ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), RrIowa_0797, sca4 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=452659 RICRO])</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=3tj5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3tj5 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3tj5 RCSB], [http://www.ebi.ac.uk/pdbsum/3tj5 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=3tj5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3tj5 OCA], [http://pdbe.org/3tj5 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3tj5 RCSB], [http://www.ebi.ac.uk/pdbsum/3tj5 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3tj5 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
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	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 3tj5" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 27:		Line 29:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
-	[[Category: ~~Rickettsia rickettsii~~]]	+	[[Category: Ricro]]
	[[Category: Cossart, P]]		[[Category: Cossart, P]]
	[[Category: Gouin, E]]		[[Category: Gouin, E]]

OCA at 07:25, 21 December 2014

OCA — Sun, 21 Dec 2014 07:25:29 GMT

←Older revision		Revision as of 07:25, 21 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3tj5\| PDB=3tj5 \| SCENE= }}~~	+	==human vinculin head domain (Vh1, residues 1-258) in complex with the vinculin binding site of the surface cell antigen 4 (sca4-VBS-N; residues 412-434) from Rickettsia rickettsii==
-	===human vinculin head domain (Vh1, residues 1-258) in complex with the vinculin binding site of the surface cell antigen 4 (sca4-VBS-N; residues 412-434) from Rickettsia rickettsii===	+	<StructureSection load='3tj5' size='340' side='right' caption='[[3tj5]], [[Resolution\|resolution]] 1.99Å' scene=''>
-	~~{{ABSTRACT_PUBMED_21841197}}~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[3tj5]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Rickettsia_rickettsii Rickettsia rickettsii]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3TJ5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3TJ5 FirstGlance]. <br>
-	==Disease==	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3rf3\|3rf3]], [[2ibf\|2ibf]], [[2hsq\|2hsq]], [[2gww\|2gww]], [[1rkc\|1rkc]], [[3s90\|3s90]], [[3tj6\|3tj6]]</td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">VCL ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), RrIowa_0797, sca4 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=783 Rickettsia rickettsii])</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=3tj5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3tj5 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3tj5 RCSB], [http://www.ebi.ac.uk/pdbsum/3tj5 PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
	[[http://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Defects in VCL are the cause of cardiomyopathy dilated type 1W (CMD1W) [MIM:[http://omim.org/entry/611407 611407]]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.<ref>PMID:11815424</ref> <ref>PMID:16236538</ref> Defects in VCL are the cause of familial hypertrophic cardiomyopathy type 15 (CMH15) [MIM:[http://omim.org/entry/613255 613255]]. It is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.<ref>PMID:16712796</ref>		[[http://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Defects in VCL are the cause of cardiomyopathy dilated type 1W (CMD1W) [MIM:[http://omim.org/entry/611407 611407]]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.<ref>PMID:11815424</ref> <ref>PMID:16236538</ref> Defects in VCL are the cause of familial hypertrophic cardiomyopathy type 15 (CMH15) [MIM:[http://omim.org/entry/613255 613255]]. It is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.<ref>PMID:16712796</ref>
-		+	== Function ==
-	==Function==	+
	[[http://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Actin filament (F-actin)-binding protein involved in cell-matrix adhesion and cell-cell adhesion. Regulates cell-surface E-cadherin expression and potentiates mechanosensing by the E-cadherin complex. May also play important roles in cell morphology and locomotion.<ref>PMID:20484056</ref>		[[http://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Actin filament (F-actin)-binding protein involved in cell-matrix adhesion and cell-cell adhesion. Regulates cell-surface E-cadherin expression and potentiates mechanosensing by the E-cadherin complex. May also play important roles in cell morphology and locomotion.<ref>PMID:20484056</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Pathogenic Rickettsiae species cause high morbidity and mortality, especially R. prowazekii the causative agent of typhus. Like many intracellular pathogens, Rickettsiae exploit the cytoskeleton to enter and spread within the host cell. Here we report that the cell surface antigen sca4 of Rickettsiae colocalizes with vinculin in cells at sites of focal adhesions, and that sca4 binds to and activates vinculin through two vinculin binding sites (VBSs) that are conserved across all Rickettsia. Remarkably, this occurs through molecular mimicry of the vinculn-talin interaction that is also seen with the IpaA invasin of the intracellular pathogen Shigella, where binding of these VBSs to the vinculin seven-helix bundle head domain (Vh1) displaces intramolecular interactions with the vinculin tail domain that normally clamp vinculin in an inactive state. Finally, the vinculin:sca4-VBS crystal structures reveal that vinculin adopts a new conformation when bound to the C-terminal VBS of sca4. Collectively, our data define the mechanism by which sca4 activates vinculin and interacts with the actin cytoskeleton and they suggest important roles for vinculin in Rickettsia pathogenesis.

-	~~==About this Structure==~~	+	The Rickettsia surface cell antigen 4 applies mimicry to bind to and activate vinculin.,Park H, Lee JH, Cossart P, Gouin E, Izard T J Biol Chem. 2011 Aug 13. PMID:21841197<ref>PMID:21841197</ref>
-	~~[[3tj5]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]~~ and ~~[http://en~~.~~wikipedia~~.~~org/wiki/Rickettsia_rickettsii Rickettsia rickettsii]~~. ~~Full crystallographic information is available from [http~~://~~oca~~.~~weizmann~~.ac.il/~~oca-bin/ocashort?id=3TJ5 OCA].~~	+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>

	==See Also==		==See Also==
	*[[Vinculin\|Vinculin]]		*[[Vinculin\|Vinculin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:021841197</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Rickettsia rickettsii]]		[[Category: Rickettsia rickettsii]]
-	[[Category: Cossart, P.]]	+	[[Category: Cossart, P]]
-	[[Category: Gouin, E.]]	+	[[Category: Gouin, E]]
-	[[Category: Izard, T.]]	+	[[Category: Izard, T]]
-	[[Category: Lee, J H.]]	+	[[Category: Lee, J H]]
-	[[Category: Park, H.]]	+	[[Category: Park, H]]
	[[Category: Alpha-helix bundle domain]]		[[Category: Alpha-helix bundle domain]]
	[[Category: Cell adhesion]]		[[Category: Cell adhesion]]

OCA at 06:34, 2 May 2013

OCA — Thu, 02 May 2013 06:34:58 GMT

←Older revision		Revision as of 06:34, 2 May 2013
Line 4:		Line 4:

	==Disease==		==Disease==
-	[[http://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Defects in VCL are the cause of cardiomyopathy dilated type 1W (CMD1W) [MIM:[http://omim.org/entry/611407 611407]]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.<ref>PMID:11815424</ref><ref>PMID:16236538</ref> Defects in VCL are the cause of familial hypertrophic cardiomyopathy type 15 (CMH15) [MIM:[http://omim.org/entry/613255 613255]]. It is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.<ref>PMID:16712796</ref>	+	[[http://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Defects in VCL are the cause of cardiomyopathy dilated type 1W (CMD1W) [MIM:[http://omim.org/entry/611407 611407]]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.<ref>PMID:11815424</ref> <ref>PMID:16236538</ref> Defects in VCL are the cause of familial hypertrophic cardiomyopathy type 15 (CMH15) [MIM:[http://omim.org/entry/613255 613255]]. It is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.<ref>PMID:16712796</ref>

	==Function==		==Function==
-	[[http://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Actin filament (F-actin)-binding protein involved in cell-matrix adhesion and cell-cell adhesion. Regulates cell-surface E-cadherin expression and potentiates mechanosensing by the E-cadherin complex. May also play important roles in cell morphology and locomotion.<ref>PMID:20484056</ref>	+	[[http://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Actin filament (F-actin)-binding protein involved in cell-matrix adhesion and cell-cell adhesion. Regulates cell-surface E-cadherin expression and potentiates mechanosensing by the E-cadherin complex. May also play important roles in cell morphology and locomotion.<ref>PMID:20484056</ref>

	==About this Structure==		==About this Structure==

OCA at 07:12, 25 March 2013

OCA — Mon, 25 Mar 2013 07:12:16 GMT

←Older revision		Revision as of 07:12, 25 March 2013
Line 1:		Line 1:
-	[[Image:3tj5.png\|left\|200px]]
-
	{{STRUCTURE_3tj5\| PDB=3tj5 \| SCENE= }}		{{STRUCTURE_3tj5\| PDB=3tj5 \| SCENE= }}
-
	===human vinculin head domain (Vh1, residues 1-258) in complex with the vinculin binding site of the surface cell antigen 4 (sca4-VBS-N; residues 412-434) from Rickettsia rickettsii===		===human vinculin head domain (Vh1, residues 1-258) in complex with the vinculin binding site of the surface cell antigen 4 (sca4-VBS-N; residues 412-434) from Rickettsia rickettsii===
		+	{{ABSTRACT_PUBMED_21841197}}

-	~~{{ABSTRACT_PUBMED_21841197}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Defects in VCL are the cause of cardiomyopathy dilated type 1W (CMD1W) [MIM:[http://omim.org/entry/611407 611407]]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.<ref>PMID:11815424</ref><ref>PMID:16236538</ref> Defects in VCL are the cause of familial hypertrophic cardiomyopathy type 15 (CMH15) [MIM:[http://omim.org/entry/613255 613255]]. It is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.<ref>PMID:16712796</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/VINC_HUMAN VINC_HUMAN]] Actin filament (F-actin)-binding protein involved in cell-matrix adhesion and cell-cell adhesion. Regulates cell-surface E-cadherin expression and potentiates mechanosensing by the E-cadherin complex. May also play important roles in cell morphology and locomotion.<ref>PMID:20484056</ref>

	==About this Structure==		==About this Structure==
Line 14:		Line 16:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:021841197</ref><references group="xtra"/>	+	<ref group="xtra">PMID:021841197</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Rickettsia rickettsii]]		[[Category: Rickettsia rickettsii]]

OCA at 22:34, 20 October 2012

OCA — Sat, 20 Oct 2012 22:34:04 GMT

←Older revision		Revision as of 22:34, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[3tj5]] is a 2 chain structure ~~of [[Vinculin]]~~ with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Rickettsia_rickettsii Rickettsia rickettsii]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3TJ5 OCA].	+	[[3tj5]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Rickettsia_rickettsii Rickettsia rickettsii]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3TJ5 OCA].

	==See Also==		==See Also==

OCA at 16:45, 27 July 2012

OCA — Fri, 27 Jul 2012 16:45:52 GMT

←Older revision		Revision as of 16:45, 27 July 2012
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	[[Image:3tj5.png\|left\|200px]]		[[Image:3tj5.png\|left\|200px]]

-	<!--
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	{{STRUCTURE_3tj5\| PDB=3tj5 \| SCENE= }}		{{STRUCTURE_3tj5\| PDB=3tj5 \| SCENE= }}

	===human vinculin head domain (Vh1, residues 1-258) in complex with the vinculin binding site of the surface cell antigen 4 (sca4-VBS-N; residues 412-434) from Rickettsia rickettsii===		===human vinculin head domain (Vh1, residues 1-258) in complex with the vinculin binding site of the surface cell antigen 4 (sca4-VBS-N; residues 412-434) from Rickettsia rickettsii===

-
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	{{ABSTRACT_PUBMED_21841197}}		{{ABSTRACT_PUBMED_21841197}}

	==About this Structure==		==About this Structure==
-	[[3tj5]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Rickettsia_rickettsii Rickettsia rickettsii]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3TJ5 OCA].	+	[[3tj5]] is a 2 chain structure of [[Vinculin]] with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Rickettsia_rickettsii Rickettsia rickettsii]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3TJ5 OCA].
		+
		+	==See Also==
		+	*[[Vinculin\|Vinculin]]

	==Reference==		==Reference==

OCA at 07:29, 2 November 2011

OCA — Wed, 02 Nov 2011 07:29:28 GMT

←Older revision		Revision as of 07:29, 2 November 2011
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-	[[Image:3tj5.~~jpg~~\|left\|200px]]	+	[[Image:3tj5.png\|left\|200px]]

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