3myi - Revision history

OCA at 10:27, 21 February 2024

OCA — Wed, 21 Feb 2024 10:27:10 GMT

←Older revision		Revision as of 10:27, 21 February 2024
Line 1:		Line 1:

	==Human metavinculin tail domain==		==Human metavinculin tail domain==
-	<StructureSection load='3myi' size='340' side='right' caption='[[3myi]], [[Resolution\|resolution]] 2.20Å' scene=''>	+	<StructureSection load='3myi' size='340' side='right'caption='[[3myi]], [[Resolution\|resolution]] 2.20Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3myi]] 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=3MYI OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3MYI FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3myi]] 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=3MYI OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3MYI FirstGlance]. <br>
-	</td></tr><tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat"~~>[[1rke\|1rke]], [[1rkc\|1rkc]], [[1syq\|1syq]], [[1ydi\|1ydi]], [[1tr2\|1tr2]], [[2gww\|2gww]]</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]] 2.2Å</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])~~</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=3myi FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3myi OCA], [https://pdbe.org/3myi PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3myi RCSB], [https://www.ebi.ac.uk/pdbsum/3myi PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3myi 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=3myi FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3myi OCA], [~~http~~://pdbe.org/3myi PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3myi RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3myi PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3myi 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>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 22:		Line 21:
	</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=3myi 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=3myi ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
-	<div style="background-color:#fffaf0;">
-	== Publication Abstract from PubMed ==
-	Cells require distinct adhesion complexes to form contacts with their neighbors or the extracellular matrix, and vinculin links these complexes to the actin cytoskeleton. Metavinculin, an isoform of vinculin that harbors a unique 68-residue insert in its tail domain, has distinct actin bundling and oligomerization properties and plays essential roles in muscle development and homeostasis. Moreover, patients with sporadic or familial mutations in the metavinculin-specific insert invariably develop fatal cardiomyopathies. Here we report the high resolution crystal structure of the metavinculin tail domain, as well as the crystal structures of full-length human native metavinculin (1,134 residues) and of the full-length cardiomyopathy-associated DeltaLeu954 metavinculin deletion mutant. These structures reveal that an alpha-helix (H1') and extended coil of the metavinculin insert replace alpha-helix H1 and its preceding extended coil found in the N-terminal region of the vinculin tail domain to form a new five-helix bundle tail domain. Further, biochemical analyses demonstrate that this helix replacement directs the distinct actin bundling and oligomerization properties of metavinculin. Finally, the cardiomyopathy associated DeltaLeu954 and Arg975Trp metavinculin mutants reside on the replaced extended coil and the H1' alpha-helix, respectively. Thus, a helix replacement mechanism directs metavinculin's unique functions.
-
-	A helix replacement mechanism directs metavinculin functions.,Rangarajan ES, Lee JH, Yogesha SD, Izard T PLoS One. 2010 May 19;5(5):e10679. PMID:20502710<ref>PMID:20502710</ref>
-
-	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	</div>
-	<div class="pdbe-citations 3myi" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 38:		Line 28:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
-	[[Category: ~~Izard, T~~]]	+	[[Category: Large Structures]]
-	[[Category: ~~Rangarajan, E S~~]]	+	[[Category: Izard T]]
-	[[Category: ~~Cardiomyopathy]]~~	+	[[Category: Rangarajan ES]]
-	~~[[Category: Cell adhesion]]~~	+
-	~~[[Category: Cytoskeleton]]~~	+
-	~~[[Category: Focal adhesion]]~~	+
-	~~[[Category: Muscle tissue development~~]]	+

OCA at 12:59, 16 January 2019

OCA — Wed, 16 Jan 2019 12:59:10 GMT

←Older revision		Revision as of 12:59, 16 January 2019
Line 16:		Line 16:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/my/3myi_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/my/3myi_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 13:25, 4 August 2016

OCA — Thu, 04 Aug 2016 13:25:33 GMT

←Older revision		Revision as of 13:25, 4 August 2016
Line 1:		Line 1:
		+
	==Human metavinculin tail domain==		==Human metavinculin tail domain==
	<StructureSection load='3myi' size='340' side='right' caption='[[3myi]], [[Resolution\|resolution]] 2.20Å' scene=''>		<StructureSection load='3myi' size='340' side='right' caption='[[3myi]], [[Resolution\|resolution]] 2.20Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3myi]] 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=3MYI OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3MYI FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3myi]] 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=3MYI OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3MYI FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rke\|1rke]], [[1rkc\|1rkc]], [[1syq\|1syq]], [[1ydi\|1ydi]], [[1tr2\|1tr2]], [[2gww\|2gww]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rke\|1rke]], [[1rkc\|1rkc]], [[1syq\|1syq]], [[1ydi\|1ydi]], [[1tr2\|1tr2]], [[2gww\|2gww]]</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~~])</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])</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=3myi FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3myi OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3myi RCSB], [http://www.ebi.ac.uk/pdbsum/3myi 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=3myi FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3myi OCA], [http://pdbe.org/3myi PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3myi RCSB], [http://www.ebi.ac.uk/pdbsum/3myi PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3myi ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 19:		Line 20:
	<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=3myi ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 29:		Line 30:
	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 3myi" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 36:		Line 38:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Izard, T]]		[[Category: Izard, T]]
	[[Category: Rangarajan, E S]]		[[Category: Rangarajan, E S]]

OCA at 15:49, 18 December 2014

OCA — Thu, 18 Dec 2014 15:49:33 GMT

←Older revision		Revision as of 15:49, 18 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3myi~~\| ~~PDB~~=3myi \| ~~SCENE~~= }}	+	==Human metavinculin tail domain==
-	===~~Human metavinculin tail domain~~===	+	<StructureSection load='3myi' size='340' side='right' caption='[[3myi]], [[Resolution\|resolution]] 2.20Å' scene=''>
-	~~{{ABSTRACT_PUBMED_20502710}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[3myi]] 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=3MYI OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3MYI FirstGlance]. <br>
		+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1rke\|1rke]], [[1rkc\|1rkc]], [[1syq\|1syq]], [[1ydi\|1ydi]], [[1tr2\|1tr2]], [[2gww\|2gww]]</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])</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=3myi FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3myi OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3myi RCSB], [http://www.ebi.ac.uk/pdbsum/3myi 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>
		+	== 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>
		+	== 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/my/3myi_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 ==
		+	Cells require distinct adhesion complexes to form contacts with their neighbors or the extracellular matrix, and vinculin links these complexes to the actin cytoskeleton. Metavinculin, an isoform of vinculin that harbors a unique 68-residue insert in its tail domain, has distinct actin bundling and oligomerization properties and plays essential roles in muscle development and homeostasis. Moreover, patients with sporadic or familial mutations in the metavinculin-specific insert invariably develop fatal cardiomyopathies. Here we report the high resolution crystal structure of the metavinculin tail domain, as well as the crystal structures of full-length human native metavinculin (1,134 residues) and of the full-length cardiomyopathy-associated DeltaLeu954 metavinculin deletion mutant. These structures reveal that an alpha-helix (H1') and extended coil of the metavinculin insert replace alpha-helix H1 and its preceding extended coil found in the N-terminal region of the vinculin tail domain to form a new five-helix bundle tail domain. Further, biochemical analyses demonstrate that this helix replacement directs the distinct actin bundling and oligomerization properties of metavinculin. Finally, the cardiomyopathy associated DeltaLeu954 and Arg975Trp metavinculin mutants reside on the replaced extended coil and the H1' alpha-helix, respectively. Thus, a helix replacement mechanism directs metavinculin's unique functions.

-	~~==Disease==~~	+	A helix replacement mechanism directs metavinculin functions.,Rangarajan ES, Lee JH, Yogesha SD, Izard T PLoS One. 2010 May 19;5(5):e10679. PMID:20502710<ref>PMID:20502710</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==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[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>
-		+
-	~~==About this Structure==~~	+
-	[[3myi]] 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=3MYI OCA].	+

	==See Also==		==See Also==
	*[[Vinculin\|Vinculin]]		*[[Vinculin\|Vinculin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:020502710</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Izard, T.]]	+	[[Category: Izard, T]]
-	[[Category: Rangarajan, E S.]]	+	[[Category: Rangarajan, E S]]
	[[Category: Cardiomyopathy]]		[[Category: Cardiomyopathy]]
	[[Category: Cell adhesion]]		[[Category: Cell adhesion]]

OCA at 19:22, 24 March 2013

OCA — Sun, 24 Mar 2013 19:22:58 GMT

←Older revision		Revision as of 19:22, 24 March 2013
Line 1:		Line 1:
-	[[Image:3myi.png\|left\|200px]]
-
	{{STRUCTURE_3myi\| PDB=3myi \| SCENE= }}		{{STRUCTURE_3myi\| PDB=3myi \| SCENE= }}
-
	===Human metavinculin tail domain===		===Human metavinculin tail domain===
		+	{{ABSTRACT_PUBMED_20502710}}

-	~~{{ABSTRACT_PUBMED_20502710}}~~	+	==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:020502710</ref><references group="xtra"/>	+	<ref group="xtra">PMID:020502710</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Izard, T.]]		[[Category: Izard, T.]]

OCA at 06:37, 20 October 2012

OCA — Sat, 20 Oct 2012 06:37:00 GMT

←Older revision		Revision as of 06:37, 20 October 2012
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	==About this Structure==		==About this Structure==
-	[[3myi]] is a 1 chain structure ~~of [[Vinculin]]~~ 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=3MYI OCA].	+	[[3myi]] 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=3MYI OCA].

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

OCA at 13:44, 25 July 2012

OCA — Wed, 25 Jul 2012 13:44:47 GMT

←Older revision		Revision as of 13:44, 25 July 2012
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	[[Image:3myi.png\|left\|200px]]		[[Image:3myi.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_3myi", 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_3myi\| PDB=3myi \| SCENE= }}		{{STRUCTURE_3myi\| PDB=3myi \| SCENE= }}

	===Human metavinculin tail domain===		===Human metavinculin tail domain===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_20502710}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 20502710 is the PubMed ID number.
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	{{ABSTRACT_PUBMED_20502710}}		{{ABSTRACT_PUBMED_20502710}}

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	==See Also==		==See Also==
-	*[[Vinculin]]	+	*[[Vinculin\|Vinculin]]

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~20502710~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:020502710</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Izard, T.]]		[[Category: Izard, T.]]

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

OCA — Mon, 27 Dec 2010 00:58:47 GMT

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

←Older revision

Revision as of 00:58, 27 December 2010

OCA at 00:58, 27 December 2010

OCA — Mon, 27 Dec 2010 00:58:46 GMT

←Older revision		Revision as of 00:58, 27 December 2010
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-	{{Seed}}
	[[Image:3myi.png\|left\|200px]]		[[Image:3myi.png\|left\|200px]]

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	==About this Structure==		==About this Structure==
-	~~3MYI~~ 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=3MYI OCA].	+	[[3myi]] is a 1 chain structure of [[Vinculin]] 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=3MYI OCA].
		+
		+	==See Also==
		+	*[[Vinculin]]

	==Reference==		==Reference==
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	[[Category: Focal adhesion]]		[[Category: Focal adhesion]]
	[[Category: Muscle tissue development]]		[[Category: Muscle tissue development]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Jun 23 08:45:21 2010''

OCA at 04:40, 23 June 2010

OCA — Wed, 23 Jun 2010 04:40:05 GMT

←Older revision		Revision as of 04:40, 23 June 2010
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	-->		-->
	{{ABSTRACT_PUBMED_20502710}}		{{ABSTRACT_PUBMED_20502710}}
-
-	==Disease==
-	Known disease associated with this structure: Cardiomyopathy, dilated, 1W OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=193065 193065]]

	==About this Structure==		==About this Structure==
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	[[Category: Muscle tissue development]]		[[Category: Muscle tissue development]]

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on ~~Thu~~ Jun ~~10 10~~:53:55 2010''	+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Jun 23 08:45:21 2010''