|
|
(3 intermediate revisions not shown.) |
Line 1: |
Line 1: |
- | {{STRUCTURE_3rf3| PDB=3rf3 | SCENE= }} | |
- | ===Shigella IpaA-VBS3 in complex with human vinculin=== | |
- | {{ABSTRACT_PUBMED_21525010}} | |
| | | |
- | ==Disease== | + | ==Shigella IpaA-VBS3 in complex with human vinculin== |
- | [[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> | + | <StructureSection load='3rf3' size='340' side='right'caption='[[3rf3]], [[Resolution|resolution]] 1.61Å' scene=''> |
- | | + | == Structural highlights == |
- | ==Function== | + | <table><tr><td colspan='2'>[[3rf3]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Shigella_flexneri Shigella flexneri]. 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 [https://proteopedia.org/fgij/fg.htm?mol=3RF3 FirstGlance]. <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> [[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> | + | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.61Å</td></tr> |
- | | + | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CAC:CACODYLATE+ION'>CAC</scene></td></tr> |
- | ==About this Structure==
| + | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3rf3 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3rf3 OCA], [https://pdbe.org/3rf3 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3rf3 RCSB], [https://www.ebi.ac.uk/pdbsum/3rf3 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3rf3 ProSAT]</span></td></tr> |
- | [[3rf3]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Shigella_flexneri Shigella flexneri]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3RF3 OCA].
| + | </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|Vinculin]] |
- | | + | == References == |
- | ==Reference== | + | <references/> |
- | <ref group="xtra">PMID:021525010</ref><references group="xtra"/><references/>
| + | __TOC__ |
| + | </StructureSection> |
| [[Category: Homo sapiens]] | | [[Category: Homo sapiens]] |
| + | [[Category: Large Structures]] |
| [[Category: Shigella flexneri]] | | [[Category: Shigella flexneri]] |
- | [[Category: Izard, T.]] | + | [[Category: Izard T]] |
- | [[Category: Park, H.]] | + | [[Category: Park H]] |
- | [[Category: Sharff, A.]] | + | [[Category: Sharff A]] |
- | [[Category: Alpha-helix bundle domain]]
| + | |
- | [[Category: Bacterial toxin]]
| + | |
- | [[Category: Cell adhesion]]
| + | |
- | [[Category: Cytoskeletal protein]]
| + | |
- | [[Category: Cytoskeleton]]
| + | |
- | [[Category: Cytosol]]
| + | |
- | [[Category: F-actin]]
| + | |
- | [[Category: Focal adhesion]]
| + | |
- | [[Category: Ipaa]]
| + | |
- | [[Category: Pathogen-host interaction]]
| + | |
- | [[Category: Phosphatidylinositol 4 5-bisphosphate]]
| + | |
- | [[Category: Protein binding-toxin complex]]
| + | |
- | [[Category: Protein-protein interaction]]
| + | |
- | [[Category: Talin]]
| + | |
| Structural highlights
Disease
VINC_HUMAN Defects in VCL are the cause of cardiomyopathy dilated type 1W (CMD1W) [MIM: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.[1] [2] Defects in VCL are the cause of familial hypertrophic cardiomyopathy type 15 (CMH15) [MIM: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.[3]
Function
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.[4]
See Also
References
- ↑ Olson TM, Illenberger S, Kishimoto NY, Huttelmaier S, Keating MT, Jockusch BM. Metavinculin mutations alter actin interaction in dilated cardiomyopathy. Circulation. 2002 Jan 29;105(4):431-7. PMID:11815424
- ↑ Vasile VC, Will ML, Ommen SR, Edwards WD, Olson TM, Ackerman MJ. Identification of a metavinculin missense mutation, R975W, associated with both hypertrophic and dilated cardiomyopathy. Mol Genet Metab. 2006 Feb;87(2):169-74. Epub 2005 Oct 19. PMID:16236538 doi:S1096-7192(05)00258-1
- ↑ Vasile VC, Ommen SR, Edwards WD, Ackerman MJ. A missense mutation in a ubiquitously expressed protein, vinculin, confers susceptibility to hypertrophic cardiomyopathy. Biochem Biophys Res Commun. 2006 Jul 7;345(3):998-1003. Epub 2006 May 4. PMID:16712796 doi:S0006-291X(06)00981-8
- ↑ Le Clainche C, Dwivedi SP, Didry D, Carlier MF. Vinculin is a dually regulated actin filament barbed end-capping and side-binding protein. J Biol Chem. 2010 Jul 23;285(30):23420-32. doi: 10.1074/jbc.M110.102830. Epub, 2010 May 18. PMID:20484056 doi:10.1074/jbc.M110.102830
|