Vascular endothelial cadherin (VE-cadherin) or CDH5 gene is mapped to human chromosome 16q21. It comprises extracellular cadherin (EC) domains that take up a strand-swapped dimers structure.
Specificity
The antibody detects endogenous level of VE-Cadherin only when phosphorylated at tyrosine 731.
Immunogen
Peptide sequence around phosphorylation site of Tyrosine731 (H-I-Y(p)-G-Y) derived from Human VE-Cadherin.
Application
Anti-phospho-VE-Cadherin (pTyr731) antibody produced in rabbit has been used in western blotting.
Biochem/physiol Actions
Vascular endothelial cadherin (VE-cadherin) plays a key role in maintaining membrane integrity and vascular endothelium. It mediates endothelial cell-cell adhesion in particular at the adherens junctions and participates in leukocyte trafficking. VE-cadherin is also needed for embryonic angiogenesis.
Features and Benefits
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Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Journal of molecular biology, 408(1), 57-73 (2011-01-29)
Vascular endothelial cadherin (VE-cadherin), a divergent member of the type II classical cadherin family of cell adhesion proteins, mediates homophilic adhesion in the vascular endothelium. Previous investigations with a bacterially produced protein suggested that VE-cadherin forms cell surface trimers that
The major hallmarks of Epithelial-Mesenchymal Transition (EMT) is the loss of epithelial cell polarity and loss of expression of the cell- cell adhesion molecule like E-cadherin and acquired mesenchymal cells marker called N-Cadherin. This phenotypical changes of E-M plasticity of
American journal of physiology. Lung cellular and molecular physiology, 315(1), L66-L77 (2018-03-31)
Compromised pulmonary endothelial cell (PEC) barrier function characterizes acute respiratory distress syndrome (ARDS), a cause of substantial morbidity and mortality. Survival from ARDS is greater in children compared with adults. Whether developmental differences intrinsic to PEC barrier function contribute to
Journal of cell science, 123(Pt 7), 1073-1080 (2010-03-25)
Little is known about the molecular mechanisms that regulate the organization of vascular lumen. In this paper we show that lumen formation correlates with endothelial polarization. Adherens junctions (AJs) and VE-cadherin (VEC, encoded by CDH5) are required for endothelial apicobasal
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