High expression of vinculin predicts poor prognosis and distant metastasis and associates with influencing tumor-associated NK cell infiltration and epithelial-mesenchymal transition in gastric cancer.
Findings indicate that vinculin resists mechanical fluctuations to maintain the tight junctions paracellular barrier function for ions in epithelial cell sheets.
Integrin engagement during cell attachment activates Poldip2/Nox4 to oxidize actin which modulates filamentous actin assembly and its interaction with vinculin.
Study find that Vinculin is a key downstream target of Linc01060. Vinculin overexpression inhibited Linc01060KD-mediated increases in FAK and paxillin phosphorylation whereas vinculin knockdown reversed the Linc01060-mediated repression of FAK and inactivation of focal adhesion turnover. Vinculin knockdown also accelerated pancreatic cancer cell proliferation by upregulating ERK activity.
EGFR-mediated kinase cascade controls the force-dependent recruitment of vinculin to stressed E-cadherin complexes - a key early signature of cadherin-based mechanotransduction.
Vinculin is necessary to maintain the integrity of the glomerular filtration barrier by modulating podocyte foot processes and stabilizing intercellular junctions.
We report that polyoma small T antigen leads to upregulation of tubulin and vinculin in a time dependent manner with tubulin expression being most significantly affected.
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.
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