5o2q
From Proteopedia
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==p130Cas SH3 domain Vinculin peptide chimera== | ==p130Cas SH3 domain Vinculin peptide chimera== | ||
| - | <StructureSection load='5o2q' size='340' side='right'caption='[[5o2q | + | <StructureSection load='5o2q' size='340' side='right'caption='[[5o2q]]' scene=''> |
== Structural highlights == | == Structural highlights == | ||
| - | <table><tr><td colspan='2'>[[5o2q]] is a 1 chain structure with sequence from [ | + | <table><tr><td colspan='2'>[[5o2q]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5O2Q OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5O2Q FirstGlance]. <br> |
| - | </td></tr><tr id=' | + | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</td></tr> |
| - | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | + | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=5o2q FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5o2q OCA], [https://pdbe.org/5o2q PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5o2q RCSB], [https://www.ebi.ac.uk/pdbsum/5o2q PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5o2q 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> [https://www.uniprot.org/uniprot/BCAR1_HUMAN BCAR1_HUMAN] Docking protein which plays a central coordinating role for tyrosine kinase-based signaling related to cell adhesion. Implicated in induction of cell migration. Overexpression confers antiestrogen resistance on breast cancer cells.<ref>PMID:12832404</ref> <ref>PMID:17038317</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: | + | [[Category: Homo sapiens]] |
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
| - | [[Category: Hexnerova | + | [[Category: Hexnerova R]] |
| - | [[Category: Veverka | + | [[Category: Veverka V]] |
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Current revision
p130Cas SH3 domain Vinculin peptide chimera
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