7ktu
From Proteopedia
(Difference between revisions)
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<StructureSection load='7ktu' size='340' side='right'caption='[[7ktu]], [[Resolution|resolution]] 4.15Å' scene=''> | <StructureSection load='7ktu' size='340' side='right'caption='[[7ktu]], [[Resolution|resolution]] 4.15Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
| - | <table><tr><td colspan='2'> | + | <table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7KTU OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7KTU FirstGlance]. <br> |
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution|Resolution]] 4.15Å</td></tr> | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution|Resolution]] 4.15Å</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=7ktu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7ktu OCA], [https://pdbe.org/7ktu PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7ktu RCSB], [https://www.ebi.ac.uk/pdbsum/7ktu PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7ktu 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=7ktu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7ktu OCA], [https://pdbe.org/7ktu PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7ktu RCSB], [https://www.ebi.ac.uk/pdbsum/7ktu PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7ktu ProSAT]</span></td></tr> | ||
</table> | </table> | ||
| - | == 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> | ||
| - | == 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> | ||
==See Also== | ==See Also== | ||
| - | *[[Vinculin|Vinculin]] | + | *[[Vinculin 3D structures|Vinculin 3D structures]] |
| - | + | ||
| - | + | ||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
| - | [[Category: Homo sapiens]] | ||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: Izard T]] | [[Category: Izard T]] | ||
[[Category: Rangarajan ES]] | [[Category: Rangarajan ES]] | ||
Current revision
Cryogenic electron microscopy model of full-length human metavinculin H1'-parallel conformation 1
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