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Human Vinculin Protein expressed in HEK-293 Cells - ABIN2735299
Beppu, Sawai, Satoh, Mori, Kazami, Misawa, Shibuya, Ishibashi, Sogawa, Kado, Kodera, Nomura, Kuwabara: Autoantibodies against vinculin in patients with chronic inflammatory demyelinating polyneuropathy. in Journal of neuroimmunology 2015
We report that polyoma small T antigen leads to upregulation of tubulin (show TUBB Proteins) and vinculin in a time dependent manner with tubulin (show TUBB Proteins) expression being most significantly affected.
Differential phosphatidylinositol 4,5-diphosphate binding of vinculin isoforms promotes quasi-equivalent dimerization.
Study used an all-heavy-atom structure-based model to study vinculin activation by talin in a high-tension context mechanically driven by F-actin, showed that vinculin activation may proceed from an intermediate state stabilized by partial talin-vinculin association. There is a low-force regime and a high-force regime where vinculin activation is dominated by two different pathways with distinct responses to force.
Vinculin head-tail interaction is required on soft substrates to destabilize vinculin and talin in FAs (show FAS Proteins), and to allow hMSCs branching. Another module involves paxillin (show PXN Proteins) and FAK (show PTK2 Proteins), which soft substrates also destabilize, but independently of vinculin head-tail interaction. This multi-modularity may be key to allow a versatile response to complex biomechanical cues.
The central role of talin and vinculin in cell adhesions suggests that the disintegration of the tissue in atherosclerosis could be partially driven by downregulation of these genes, leading to loosening of cell-ECM (show MMRN1 Proteins) interactions and remodeling of the tissue.
East Asian common VCL variant p.Asp841His (D841H) was associated with sudden unexplained nocturnal death syndrome (SUNDS) in the Chinese Han population.
We identified mutations in VCL associated with Short segment Hirschsprung disease. Correction of this mutation in induced pluripotent stem cells using CRISPR/Cas9 editing, as well as the RET (show RET Proteins) G731del mutation that causes Hirschsprung disease with total colonic aganglionosis, restored enteric neural crest cell function.
This review discusses the current understanding of the roles of vinculin in cell-cell and cell-matrix adhesions. Emphasis is placed on the how vinculin is recruited, activated and regulated. [review]
Study predicted the structure of the MAPK1 (show MAPK3 Proteins)-vinculin binding interface using a combination of flexible docking and molecular dynamics simulations, and confirmed that the MAPK1 (show MAPK3 Proteins)-vinculin interaction is mechanically regulated, and implicated a change in the vinculin D3-D4 cleft size upon vinculin activation as the basis for the conformational selectivity of MAPK1 (show MAPK3 Proteins) binding toward open vinculin.
These results suggest that vinculin promotes the nuclear localization of transcription factor TAZ (show TAZ Proteins) to inhibit the adipocyte differentiation on rigid extracellular matrix.
Study show that zebrafish contain two homologous vinculin isoforms, of which the sequence of key functional domains is conserved with several higher vertebrate. Loss of both zygotic vcla and maternal contribution of vcla did not result in notable defects, while the additional loss of zygotic vclb is lethal only after embryonic stages. These data indicate that embryonic development in zebrafish can occur without vinculin.
Results suggest that myosin VI (show MYO6 Proteins) and vinculin form a molecular apparatus that generates cohesive cell-cell contacts in cultured mammalian epithelia.
Lipid binding increases vinculin activation and turnover at focal adhesions.
results suggest that the vinculin-actin interaction participates in FA-mediated mechanotransduction
The results indicate that lipid rafts play an important role in extracellular matrix stiffness regulation of cell migration via expression vinculin and its interaction with vinexin alpha (show Sorbs3 Proteins).
Binding of vinculin to the R1-R3 region of the talin rod is important for focal adhesion stability.
These data demonstrate that Src-mediated phosphorylation is necessary for vinculin activation, and that phosphorylation controls cytoskeletal mechanics by regulating force transmission between the actin cytoskeleton and focal adhesion proteins.
results suggest that vinculin promotes directionally persistent cell migration and tension-dependent ECM (show MMRN1 Proteins) remodeling in complex 3D environments by increasing cell-ECM (show MMRN1 Proteins) adhesion and traction force generation.
Force-dependent conformational switch of alpha-catenin (show CTNNA1 Proteins) controls vinculin binding.
Mutant vinculin expressing cells are altered in cell migration, which is accompanied by changes in cell adhesion.
show that Src (show SRC Proteins) phosphorylation of Y1065 within the C-terminal hairpin regulates Vt-mediated actin bundling and provide a detailed characterization of vinculin Y1065 mutations
These findings demonstrate the crucial importance of the tight control of the activity of vinculin.
Syndecan-4 (show SDC4 Proteins) acts as a central mediator that bridges fibronectin (show FN1 Proteins), integrin and intracellular components (actin and vinculin) and once silenced, the cytoskeleton protein network is disrupted, highlighting Syn4 (show SNTG1 Proteins) relevance for balanced cell behavior.
Vinculin is a cytoskeletal protein associated with cell-cell and cell-matrix junctions, where it is thought to function as one of several interacting proteins involved in anchoring F-actin to the membrane. Defects in VCL are the cause of cardiomyopathy dilated type 1W. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Multiple alternatively spliced transcript variants have been found for this gene, but the biological validity of some variants has not been determined.
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