5l0i - Revision history

OCA at 12:46, 4 October 2023

OCA — Wed, 04 Oct 2023 12:46:21 GMT

←Older revision		Revision as of 12:46, 4 October 2023
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	<StructureSection load='5l0i' size='340' side='right'caption='[[5l0i]], [[Resolution\|resolution]] 2.45Å' scene=''>		<StructureSection load='5l0i' size='340' side='right'caption='[[5l0i]], [[Resolution\|resolution]] 2.45Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5l0i]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5L0I OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=5L0I FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5l0i]] 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=5L0I OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5L0I 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>, <scene name='pdbligand=NA:SODIUM+ION'>NA</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]] 2.45Å</td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://proteopedia.org/fgij/fg.htm?mol=5l0i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5l0i OCA], [~~http~~://pdbe.org/5l0i PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5l0i RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5l0i PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5l0i ProSAT]</span></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>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
		+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=5l0i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5l0i OCA], [https://pdbe.org/5l0i PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5l0i RCSB], [https://www.ebi.ac.uk/pdbsum/5l0i PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5l0i 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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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Chinthalapudi, K]]	+	[[Category: Chinthalapudi K]]
-	[[Category: Izard, T]]	+	[[Category: Izard T]]
-	~~[[Category: 5-helix bundle]]~~	+
-	~~[[Category: Cardiomyopathy]]~~	+
-	~~[[Category: Cell adhesion]]~~	+
-	~~[[Category: Cytoskeletal protein~~]]	+

OCA at 06:38, 5 August 2020

OCA — Wed, 05 Aug 2020 06:38:53 GMT

←Older revision		Revision as of 06:38, 5 August 2020
Line 1:		Line 1:

	==Human metavinculin MVt R975W cardiomyopathy-associated mutant (residues 959-1134)==		==Human metavinculin MVt R975W cardiomyopathy-associated mutant (residues 959-1134)==
-	<StructureSection load='5l0i' size='340' side='right' caption='[[5l0i]], [[Resolution\|resolution]] 2.45Å' scene=''>	+	<StructureSection load='5l0i' size='340' side='right'caption='[[5l0i]], [[Resolution\|resolution]] 2.45Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5l0i]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5L0I OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5L0I FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5l0i]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5L0I OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=5L0I 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>, <scene name='pdbligand=NA:SODIUM+ION'>NA</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>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene></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=5l0i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5l0i OCA], [http://pdbe.org/5l0i PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5l0i RCSB], [http://www.ebi.ac.uk/pdbsum/5l0i PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5l0i ProSAT]</span></td></tr>	+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=5l0i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5l0i OCA], [http://pdbe.org/5l0i PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5l0i RCSB], [http://www.ebi.ac.uk/pdbsum/5l0i PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5l0i ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 20:		Line 20:
	</div>		</div>
	<div class="pdbe-citations 5l0i" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 5l0i" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Vinculin\|Vinculin]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Large Structures]]
	[[Category: Chinthalapudi, K]]		[[Category: Chinthalapudi, K]]
	[[Category: Izard, T]]		[[Category: Izard, T]]

OCA at 23:13, 15 November 2017

OCA — Wed, 15 Nov 2017 23:13:43 GMT

←Older revision		Revision as of 23:13, 15 November 2017
Line 20:		Line 20:
	</div>		</div>
	<div class="pdbe-citations 5l0i" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 5l0i" style="background-color:#fffaf0;"></div>
-
-	==See Also==
-	*[[Vinculin\|Vinculin]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 11:11, 24 August 2017

OCA — Thu, 24 Aug 2017 11:11:50 GMT

←Older revision		Revision as of 11:11, 24 August 2017
Line 20:		Line 20:
	</div>		</div>
	<div class="pdbe-citations 5l0i" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 5l0i" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Vinculin\|Vinculin]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 05:40, 9 September 2016

OCA — Fri, 09 Sep 2016 05:40:35 GMT

←Older revision		Revision as of 05:40, 9 September 2016
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 5l0i is ~~ON HOLD~~	+	==Human metavinculin MVt R975W cardiomyopathy-associated mutant (residues 959-1134)==
		+	<StructureSection load='5l0i' size='340' side='right' caption='[[5l0i]], [[Resolution\|resolution]] 2.45Å' scene=''>
		+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[5l0i]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5L0I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5L0I 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>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene></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=5l0i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5l0i OCA], [http://pdbe.org/5l0i PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5l0i RCSB], [http://www.ebi.ac.uk/pdbsum/5l0i PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5l0i ProSAT]</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>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	The main cause of death globally remains debilitating heart conditions, such as dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM), which are often due to mutations of specific components of adhesion complexes. Vinculin regulates these complexes and plays essential roles in intercalated discs that are necessary for muscle cell function and coordinated movement and in the development and function of the heart. Humans bearing familial or sporadic mutations in vinculin suffer from chronic, progressively debilitating DCM that ultimately leads to cardiac failure and death, whereas autosomal dominant mutations in vinculin can also provoke HCM, causing acute cardiac failure. The DCM/HCM-associated mutants of vinculin occur in the 68-residue insert unique to the muscle-specific, alternatively spliced isoform of vinculin, termed metavinculin (MV). Contrary to studies that suggested that phosphoinositol-4,5-bisphosphate (PIP2) only induces vinculin homodimers, which are asymmetric, we show that phospholipid binding results in a domain-swapped symmetric MV dimer via a quasi-equivalent interface compared with vinculin involving R975. Although one of the two PIP2 binding sites is preserved, the symmetric MV dimer that bridges two PIP2 molecules differs from the asymmetric vinculin dimer that bridges only one PIP2 Unlike vinculin, wild-type MV and the DCM/HCM-associated R975W mutant bind PIP2 in their inactive conformations, and R975W MV fails to dimerize. Mutating selective vinculin residues to their corresponding MV residues, or vice versa, switches the isoform's dimeric constellation and lipid binding site. Collectively, our data suggest that MV homodimerization modulates microfilament attachment at muscular adhesion sites and furthers our understanding of MV-mediated cardiac remodeling.

-	~~Authors: Chinthalapudi~~, K., ~~Izard~~, T.	+	Differential lipid binding of vinculin isoforms promotes quasi-equivalent dimerization.,Chinthalapudi K, Rangarajan ES, Brown DT, Izard T Proc Natl Acad Sci U S A. 2016 Aug 23;113(34):9539-44. doi:, 10.1073/pnas.1600702113. Epub 2016 Aug 8. PMID:27503891<ref>PMID:27503891</ref>

-	~~Description: Human metavinculin MVt R975W cardiomyopathy~~-~~associated mutant (residues 959~~-~~1134)~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[Category~~: ~~Unreleased Structures]]~~	+	</div>
		+	<div class="pdbe-citations 5l0i" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
	[[Category: Chinthalapudi, K]]		[[Category: Chinthalapudi, K]]
	[[Category: Izard, T]]		[[Category: Izard, T]]
		+	[[Category: 5-helix bundle]]
		+	[[Category: Cardiomyopathy]]
		+	[[Category: Cell adhesion]]
		+	[[Category: Cytoskeletal protein]]

OCA: Protected "5l0i" [edit=sysop:move=sysop]

OCA — Thu, 04 Aug 2016 02:20:04 GMT

Protected "5l0i" [edit=sysop:move=sysop]

←Older revision

Revision as of 02:20, 4 August 2016

OCA: New page: '''Unreleased structure''' The entry 5l0i is ON HOLD Authors: Chinthalapudi, K., Izard, T. Description: Human metavinculin MVt R975W cardiomyopathy-associated mutant (residues 959-1134...

OCA — Thu, 04 Aug 2016 02:20:02 GMT

New page: '''Unreleased structure''' The entry 5l0i is ON HOLD Authors: Chinthalapudi, K., Izard, T. Description: Human metavinculin MVt R975W cardiomyopathy-associated mutant (residues 959-1134...

New page

'''Unreleased structure'''

The entry 5l0i is ON HOLD

Authors: Chinthalapudi, K., Izard, T.

Description: Human metavinculin MVt R975W cardiomyopathy-associated mutant (residues 959-1134)
[[Category: Unreleased Structures]]
[[Category: Chinthalapudi, K]]
[[Category: Izard, T]]