Our VE-Cadherin (Tyr-685) rabbit polyclonal phosphospecific primary antibody from PhosphoSolutions is produced in-house. It detects human, mouse, and rat VE-Cadherin (Tyr-685) and is antigen affinity purified. It is great for use in WB.
Western blot image of human umbilical vein endothelial cells stimulated with pervanadate (1 mM) for 30 min. then the blots were untreated (lanes 1 & 3) or treated with alkaline phosphatase (lanes 2 & 4). The blots were probed with rabbit polyclonal anti-VE-cadherin (Tyr-685) (lanes 1 & 2) or mouse monoclonal anti-VE-cadherin (lanes 3 & 4).
Cadherins are transmembrane glycoproteins vital in calcium-dependent cell-cell adhesion during tissue differentiation. Cadherins cluster to form foci of homophilic binding units. A key determinant to the strength of the cadherin-mediated adhesion may be by the juxtamembrane region in cadherins. VE-cadherin (Cadherin 5) is the major cadherin found in endothelial cells and has important roles during angiogenesis and maintenance of barrier permeability. The cytoplasmic domain of VE-cadherin comprises the juxtamembrane domain that binds to the p120 catenin, and the carboxylterminal domain that interacts with β- or γ-catenins. Modulation of tyrosine phosphorylation on one or more of the nine tyrosine sites in the cytoplasmic domain may be important for regulating both angiogenesis and permeability. Phosphorylation of Tyr-658 and Tyr-731 alters catenin binding, restores cell migration, and decreases barrier permeability. While VEGF-induced phosphorylation of Tyr-685 occurs through c-Src, and regulates endothelial cell migration, but not permeability
Antigen Affinity Purified
Polyclonal
IgG
WB
Rabbit
CDH5
140
Phospho-VE-Cadherin (Tyr-685) synthetic peptide (coupled to carrier protein) corresponding to amino acids surrounding tyrosine 685 in human VE-cadherin. This sequence has significant homology to the conserved site in rat and mouse VE-cadherin, but is not conserved in other cadherins.
Human, Mouse, Rat
Storage at -20°C is recommended, as aliquots may be taken without freeze/thawing due to presence of 50% glycerol. Stable for at least 1 year at -20°C.
Liquid
PBS + 1 mg/ml BSA, 0.05% NaN3 and 50% glycerol
WB: 1:1000
Unconjugated
This antibody was cross-adsorbed to an unrelated phospho-tyrosine peptide and unphosphorylated VE-cadherin (Tyr-685) peptide before affinity purification using phospho-VE-cadherin (Tyr-685) peptide. The purified antibody detects a 140 kDa* band corresponding to VE-cadherin in western blots of human endothelial cells treated with pervanadate, and this band is not detected in untreated cells or after alkaline phosphatase treatment.
Phosphorylated
Tyr-685
Western blots performed on each lot.
For research use only. Not intended for therapeutic or diagnostic use. Use of all products is subject to our terms and conditions, which can be viewed on our website.
United States
After date of receipt, stable for at least 1 year at -20°C.
van der Heijden, M, et al. 2011. Opposing effects of the angiopoietins on the thrombin-induced permeability of human pulmonary microvascular endothelial cells. PLoS One, e23448.
Hiepen, C, et al. 2019. BMPR2 acts as a gatekeeper to protect endothelial cells from increased TGFβ responses and altered cell mechanics. PLoS Biology, e3000557.
Ebrahim, NA, et al. 2016. Transendothelial migration of human umbilical mesenchymal stem cells across uterine endothelial monolayers: Junctional dynamics and putative mechanisms. Placenta, 87-98.
Wylezinski, LS, et al. 2016. Interleukin 2 Activates Brain Microvascular Endothelial Cells Resulting in Destabilization of Adherens Junctions. The Journal of Biological Chemistry, 22913-22923.
Adam, AP, et al. 2010. Src-induced tyrosine phosphorylation of VE-cadherin is not sufficient to decrease barrier function of endothelial monolayers. The Journal of Biological Chemistry, 7045-7055.
Jin, Y, et al. 2022. Tyrosine-protein kinase Yes controls endothelial junctional plasticity and barrier integrity by regulating VE-cadherin phosphorylation and endocytosis. Nature Cardiovascular Research, 1156-1173.
Ziogas, A, et al. 2021. Glycolysis is integral to histamine–induced endothelial hyperpermeability. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, e21425.
Wessel, F, et al. 2014. Leukocyte extravasation and vascular permeability are each controlled in vivo by different tyrosine residues of VE-cadherin. Nature Immunology, 223-230.
Fainaru, O, et al. 2008. Doxycycline induces membrane expression of VE-cadherin on endothelial cells and prevents vascular hyperpermeability. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 3728-3735.
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