Anti-VE-Cadherin (Tyr-685), Phosphospecific Antibody

Name: Anti-VE-Cadherin (Tyr-685), Phosphospecific Antibody
Brand: PhosphoSolutions
SKU: CP1981
Price: 329.0 USD
Availability: InStock

16 Citations

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.

Phosphorylation of CDH5 Y658, CDH5 Y685 (cat. CP1981) and VEGFR2 (Tyr1054/1059) in cultured human LECs after Yoda1 (0.3 µM) treatment for the indicated periods. Image from publication CC-BY-4.0. PMID: 38528202

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).

Species Reactivity

Human, Mouse, Rat

Applications

Host Species

Rabbit

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SKU: CP1981

Volume: 100 µL

Variant

Price:

$329.00

Quantity:

Product Details

Target

VE-Cadherin (Tyr-685)

Target Description

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

Format

Antigen Affinity Purified

Clonality

Polyclonal

Isotype

IgG

Applications

Host Species

Rabbit

Gene Name

CDH5

Molecular Weight

140

Antigen

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.

Species Reactivity

Human, Mouse, Rat

Storage

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.

Physical State

Liquid

Buffer

PBS + 1 mg/ml BSA, 0.05% NaN3 and 50% glycerol

Dilution Ranges

WB: 1:1000

Conjugate

Unconjugated

Specificity

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.

Post Translational Modification Type

Phosphorylated

Post Translational Modification Residue

Tyr-685

Quality Control

Western blots performed on each lot.

Usage Statement

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.

Country of Origin

United States

Expiration

After date of receipt, stable for at least 1 year at -20°C.

Shipping

Blue Ice

Synonyms

Cadherin-5, vascular endothelial Cadherin, CD144

UniProt Details

UniProt (Human): P33151
UniProt (Immunogen Species): P33151

Product Specific References for Applications and Species

Immunocytochemistry: Human
Immunohistochemistry: Mouse
Western Blot: Human | Mouse

Immunocytochemistry: Human
PMID	Dilution	Publication
21858121	1:200	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.

Immunohistochemistry: Mouse
PMID	Dilution	Publication
26272756	not listed	Sivaraj, KK, et al. 2015. Endothelial Gαq/11 is required for VEGF-induced vascular permeability and angiogenesis. Cardiovascular Research, 171-180.

Western Blot: Human
PMID	Dilution	Publication
31826007	1:1000	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.
27871478	2 ug/ml	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.
27601468	not listed	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.
26598555	1:1000	Benn, A, et al. 2016. VE-cadherin facilitates BMP-induced endothelial cell permeability and signaling. Journal of Cell Science, 206-218.
21123455	not listed	Lo, CW, et al. 2011. IL-6 trans-signaling in formation and progression of malignant ascites in ovarian cancer. Cancer Research, 424-434.
20048167	not listed	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.

Western Blot: Mouse
PMID	Dilution	Publication
38940198	1:1000	Shan, KZ, et al. 2024. TMEM16F scramblase regulates angiogenesis via endothelial intracellular signaling. Journal of cell science, .
38528202	not listed	Choi, D, et al. 2024. Piezo1 regulates meningeal lymphatic vessel drainage and alleviates excessive CSF accumulation. Nature Neuroscience, 0.
37936984	1:1000	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.
34376570	1:100	Kataru, RP, et al. 2021. Lymphatic-specific intracellular modulation of receptor tyrosine kinase signaling improves lymphatic growth and function. Science signaling, eabc0836.
33566443	not listed	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.
26272756	not listed	Sivaraj, KK, et al. 2015. Endothelial Gαq/11 is required for VEGF-induced vascular permeability and angiogenesis. Cardiovascular Research, 171-180.
24487320	not listed	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.
18606869	not listed	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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Anti-VE-Cadherin (Tyr-685), Phosphospecific Antibody

SKU: CP1981

Product Details

Product Specific References for Applications and Species

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