CDH5

(redirected from VE-cadherin)

CDH5

A gene on chromosome 16q22.1 that encodes a calcium-dependent cell–cell adhesion glycoprotein (cadherin), which is involved in regulating cell–cell adhesions, mobility and proliferation of epithelial cells. CDH5 is thought to play a key role in endothelial cell biology by controlling cohesion and organisation of intercellular junctions.
References in periodicals archive ?
2000) reported that VE-cadherin and the armadillo family protein plakoglobin regulated vascular endothelial permeability and growth.
We measured the HUVEC permeability, proliferation, and the secretion of VE-cadherin into culture medium using fluorescein isothiocyanate-dextran assay, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, and enzyme-linked immunosorbent assay, respectively, in response to treatment with MMP9 and/or rhubarb monomers.
In TGF-[beta]1 stimulated HPMECs, treatment with GA resulted in a reduction of EndoMT with a decrease in vimentin, and an increase in VE-cadherin instead.
Data from mTORC2 deficient mice showed that a blocking mTOR or the upstream kinase phosphoinositide 3-kinase (PI3K) dose-dependently decreased VE-cadherin mRNA and protein expression [63].
Chiasson CM, Wittich KB, Vincent PA, Faundez V, Kowalczyk AP p120-catenin inhibits VE-cadherin internalization through a Rho-independent mechanism.
In addition, [beta]-cadherin is found in the placenta (36), VE-cadherin is found in the vascular endothelium, and R-and K-cadherin are found in the retina and kidney, respectively (38).
Vascular endothelial growth factor induces VE-cadherin tyrosine phosphorylation in endothelial cells.
Differential localization of VE- and N-cadherins in human endothelial cells: VE-cadherin competes with N-cadherin for junctional localization.
Recent preclinical research has also shown that CA4P disrupts the molecular engagement of VE-cadherin, a junction protein important for endothelial cell survival and function, and inhibits the associated beta-catenin/AKT signaling pathway, leading to rapid vascular collapse and tumor cell death, or necrosis.
Abbreviations PA Panduratin A HUVECs human umbilical vein endothelial cells iTRAQ isobaric tags for relative and absolute quantification IPA Ingenuity Pathway Analysis mTOR mammalian target of rapamycin protein kinase VEGF vascular endothelial growth factor HIF1[alpha] hypoxia-inducible factor l[alpha] GRB-2 growth factor receptor-bound protein 2 STAB-1 stabilin-1 ICAM-2 Intercellular adhesion molecule-2 CTNND1 p120-catenin ARPC2 actin-related protein 2/3 complex subunit 2 STMN1 stathmin PI propidium iodide ANOVA one-way analysis of variance VE-cadherin vascular endothelial cadherin
Preclinical research has shown that CA4P disrupts the molecular engagement of VE-cadherin, a junction protein important for endothelial cell survival and function, and inhibits the associated (beta)-catenin/AKT signaling pathway, leading to rapid vascular collapse and necrosis.
VE-cadherin and beta-catenin binding dynamics during histamine-induced endothelial hyperpermeability.