Acidosis, Respiratory
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
This study initially shows both physical and functional interaction between VCL and cardiac sodium channel, and suggests an important role for respiratory acidosis in triggering the fatal arrhythmia underlying SUNDS.
|
28218286 |
2017 |
Acute Coronary Syndrome
|
0.300 |
Biomarker
|
disease |
CTD_human |
The expression levels of proteins involved in cellular cytoskeleton (F-actin capping, β-tubulin, α-tubulin isotypes 1 and 2, vinculin, vimentin and two Ras-related protein Rab-7b isotypes), glycolysis pathway (glyceraldehyde-3-phosphate dehydrogenase, lactate dehydrogenase and two pyruvate kinase isotypes) and cellular-related antioxidant system (manganese superoxide dismutase) and even the expression and activity of glutathione-S-transferase were significantly reduced in platelets from ACS patients compared to CAD patients.
|
21751358 |
2011 |
Adult Glioblastoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Moreover, global transcriptional profiling revealed that adhesion and cytoskeletal proteins such as Vinculin, Talin and signaling pathways including focal adhesion kinase (FAK), extracellular martrix (ECM) receptor interaction, and cellular motility were significantly enriched in U87 and T98 glioblastoma cells upon LKB1 knockdown.
|
31497348 |
2019 |
Arteriosclerosis
|
0.020 |
Biomarker
|
disease |
BEFREE |
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 interactions and remodeling of the tissue.
|
27816808 |
2016 |
Arteriosclerosis
|
0.020 |
Biomarker
|
disease |
BEFREE |
The present review discusses the substrates of FXIIIa (activated FXIII) involved in thrombosis and wound healing with a particular focus on: (i) the influence of plasma FXIIIa on the formation of stable fibrin clots able to withstand mechanical and enzymatic breakdown through fibrin-fibrin cross-linking and cross-linking of fibrinolysis inhibitors, in particular α2-antiplasmin; (ii) the role of intracellular FXIIIa in clot retraction through cross-linking of platelet cytoskeleton proteins, including actin, myosin, filamin and vinculin; (iii) the role of intracellular FXIIIa in cross-linking the cytoplasmic tails of monocyte AT1Rs (angiotensin type 1 receptors) and potential effects on the development of atherosclerosis; and (iv) the role of FXIIIa on matrix deposition and tissue repair, including cross-linking of extracellular matrix proteins, such as fibronectin, collagen and von Willebrand factor, and the effects on matrix deposition and cell-matrix interactions.
|
23075332 |
2013 |
Atherosclerosis
|
0.020 |
Biomarker
|
disease |
BEFREE |
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 interactions and remodeling of the tissue.
|
27816808 |
2016 |
Atherosclerosis
|
0.020 |
Biomarker
|
disease |
BEFREE |
The present review discusses the substrates of FXIIIa (activated FXIII) involved in thrombosis and wound healing with a particular focus on: (i) the influence of plasma FXIIIa on the formation of stable fibrin clots able to withstand mechanical and enzymatic breakdown through fibrin-fibrin cross-linking and cross-linking of fibrinolysis inhibitors, in particular α2-antiplasmin; (ii) the role of intracellular FXIIIa in clot retraction through cross-linking of platelet cytoskeleton proteins, including actin, myosin, filamin and vinculin; (iii) the role of intracellular FXIIIa in cross-linking the cytoplasmic tails of monocyte AT1Rs (angiotensin type 1 receptors) and potential effects on the development of atherosclerosis; and (iv) the role of FXIIIa on matrix deposition and tissue repair, including cross-linking of extracellular matrix proteins, such as fibronectin, collagen and von Willebrand factor, and the effects on matrix deposition and cell-matrix interactions.
|
23075332 |
2013 |
Benign Prostatic Hyperplasia
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Further analysis of 443 specimens from across all stages of prostate cancer progression showed that vinculin expression was highest in castration-resistant prostate cancers, but negative or very low in benign prostatic hyperplasia (p < 0.0001).
|
21294127 |
2011 |
Bladder Neoplasm
|
0.010 |
Biomarker
|
disease |
BEFREE |
Furthermore, ACTN1 and VCL may play roles in bladder cancer development, partly via the focal adhesion pathway.
|
28552713 |
2017 |
Breast Carcinoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, we find that ERα is a novel regulator of vinculin expression in breast cancer.
|
28266545 |
2017 |
Brugada Syndrome (disorder)
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
The aggravation of loss of function of SCN5A caused by VCL-D841H under acidosis supports that nocturnal sleep respiratory disorders with acidosis may play a key role in the pathogenesis of SUNDS.
|
28373245 |
2017 |
Brugada Syndrome (disorder)
|
0.020 |
Biomarker
|
disease |
BEFREE |
This study initially shows both physical and functional interaction between VCL and cardiac sodium channel, and suggests an important role for respiratory acidosis in triggering the fatal arrhythmia underlying SUNDS.
|
28218286 |
2017 |
Carcinoma
|
0.020 |
Biomarker
|
group |
BEFREE |
The data identify the kidney as a new organ site for ALK-associated carcinomas and VCL as a novel ALK fusion partner.
|
21076462 |
2011 |
Carcinoma
|
0.020 |
AlteredExpression
|
group |
BEFREE |
Here we show that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. p38-mediated EZH2 phosphorylation at T367 promotes EZH2 cytoplasmic localization and potentiates EZH2 binding to vinculin and other cytoskeletal regulators of cell migration and invasion.
|
30022044 |
2018 |
Carcinoma of bladder
|
0.010 |
Biomarker
|
disease |
BEFREE |
Furthermore, ACTN1 and VCL may play roles in bladder cancer development, partly via the focal adhesion pathway.
|
28552713 |
2017 |
Carcinoma of lung
|
0.010 |
Biomarker
|
disease |
BEFREE |
Together, we demonstrate that reduced NME2 levels lead to transcriptional de-repression of vinculin and regulate lung cancer metastasis.
|
25249619 |
2014 |
Cardiac Arrhythmia
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
This study initially shows both physical and functional interaction between VCL and cardiac sodium channel, and suggests an important role for respiratory acidosis in triggering the fatal arrhythmia underlying SUNDS.
|
28218286 |
2017 |
Cardiomegaly
|
0.010 |
AlteredExpression
|
phenotype |
LHGDN |
Obstructive hypertrophic cardiomyopathy is associated with reduced expression of vinculin in the intercalated disc.
|
16949038 |
2006 |
Cardiomyopathies
|
0.480 |
GeneticVariation
|
group |
BEFREE |
The VCL-encoding protein was involved in cardiomyopathy that associated with hypertension, therefore our results suggest the rs4746172 of VCL may be a novel target for clinical interventions to reduce CVD risk by regulating blood pressure in male Chinese.
|
26487440 |
2015 |
Cardiomyopathies
|
0.480 |
GeneticVariation
|
group |
BEFREE |
Cardiomyopathy Mutations in Metavinculin Disrupt Regulation of Vinculin-Induced F-Actin Assemblies.
|
30844403 |
2019 |
Cardiomyopathies
|
0.480 |
GeneticVariation
|
group |
BEFREE |
Metavinculin mutations are pathogenic substrates for both HCM and DCM, further highlighting the allelic nature of these cardiomyopathies.
|
16236538 |
2006 |
Cardiomyopathies
|
0.480 |
GeneticVariation
|
group |
BEFREE |
Mutations in the MVcn insert are linked to various cardiomyopathies.
|
31483833 |
2019 |
Cardiomyopathies
|
0.480 |
GeneticVariation
|
group |
BEFREE |
We have identified the cardiomyopathy-susceptibility gene vinculin (<i>VCL</i>) mutation M94I may account for a sudden unexplained nocturnal death syndrome (SUNDS) case.
|
28373245 |
2017 |
Cardiomyopathies
|
0.480 |
Biomarker
|
group |
BEFREE |
Vinculin (VCL) was linked to sudden arrhythmia death in VCL knockout mice prior to the appearance of cardiomyopathy.
|
28218286 |
2017 |
Cardiomyopathies
|
0.480 |
GeneticVariation
|
group |
BEFREE |
We provide the first report of a cardiomyopathy associated mutation in vinculin.
|
16712796 |
2006 |