3rf3: Difference between revisions

<StructureSection load='3rf3' size='340' side='right' caption='[[3rf3]], [[Resolution|resolution]] 1.61&Aring;' scene=''>

<table><tr><td colspan='2'>[[3rf3]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/"shigella_paradysenteriae"_weldin_1927 "shigella paradysenteriae" weldin 1927] and [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3RF3 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3RF3 FirstGlance]. <br>

</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CAC:CACODYLATE+ION'>CAC</scene></td></tr>

<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[2gww|2gww]], [[2hsq|2hsq]], [[2ibf|2ibf]]</td></tr>

<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">VCL, vinculin ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), CP0125, ipaA ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=623 "Shigella paradysenteriae" Weldin 1927])</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=3rf3 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3rf3 OCA], [http://pdbe.org/3rf3 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3rf3 RCSB], [http://www.ebi.ac.uk/pdbsum/3rf3 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3rf3 ProSAT]</span></td></tr>

[[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]] 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/IPAA_SHIFL IPAA_SHIFL]] Rapidly associates with the first 265 amino acids of vinculin after bacteria-cell contact. This interaction is critical for efficient Shigella uptake. IpaA acts as a potent activator of vinculin and increase its ability to interact with F-actin. The complex IpaA-vinculin induces F-actin depolymerization along with the occasional formation of actin filament bundles.<ref>PMID:9184218</ref> <ref>PMID:10545097</ref>