SAB4504676
Anti-phospho-VE-Cadherin (pTyr731) antibody produced in rabbit
affinity isolated antibody
Synonym(s):
Anti-7B4, Anti-CD144
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About This Item
UNSPSC Code:
12352203
NACRES:
NA.41
Recommended Products
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 87 kDa
species reactivity
human, rat, mouse
concentration
~1 mg/mL
technique(s)
ELISA: 1:20000
immunohistochemistry: 1:50-1:100
western blot: 1:500-1:1000
NCBI accession no.
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
phosphorylation (pTyr731)
Gene Information
human ... CDH5(1003)
Related Categories
General description
Cadherin 5 (CDH5) is encoded by the gene mapped to long arm of human chromosome 16. The encoded protein is expressed in endothelial cells, but it is absent in normal epithelium.
Immunogen
The antiserum was produced against synthesized peptide derived from human VE-Cadherin around the phosphorylation site of Tyr731.
Immunogen Range: 697-746
Immunogen Range: 697-746
Application
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Western Blotting (1 paper)
Western Blotting (1 paper)
Biochem/physiol Actions
Cadherin 5 (CDH5) plays an essential role in various cellular processes, such as regulation of cell adhesion, cell proliferation, cell survival, cell shape, cell motility, modulation of signaling pathways and transcriptional gene regulation. Cdh5/VE(vascular endothelial)-cadherin is a core component of endothelial adherens junction, which plays a vital role in angiogenic sprouting by enhancing cell migration and cell elongation. CDH5 expressed in glioblastoma multiforme (GBM), facilitates the transdifferentiation of glioblastoma stem-like cells (GSCs) to endothelial cells and to form blood vessels, under hypoxia condition. VE-cadherin induces endothelial cell-cell adhesion at adherens junctions (AJs). CDH5 gene knockout results in loss of cell polarity and modification in vascular lumenal structure. CDH5 inhibits the synthesis of CDH2 (also known as N-cadherin) in the endothelium.
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.
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Maria Grazia Lampugnani et al.
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
Loïc Sauteur et al.
Cell reports, 9(2), 504-513 (2014-11-07)
Organ morphogenesis requires the coordination of cell behaviors. Here, we have analyzed dynamic endothelial cell behaviors underlying sprouting angiogenesis in vivo. Two different mechanisms contribute to sprout outgrowth: tip cells show strong migratory behavior, whereas extension of the stalk is dependent upon
Frans van Roy
Nature reviews. Cancer, 14(2), 121-134 (2014-01-21)
Loss of cadherin 1 (CDH1; also known as epithelial cadherin (E-cadherin)) is used for the diagnosis and prognosis of epithelial cancers. However, it should not be ignored that the superfamily of transmembrane cadherin proteins encompasses more than 100 members in
Junwen Zhang et al.
Molecular medicine reports, 13(3), 2918-2924 (2016-02-06)
Changes in pulmonary microvascular permeability following cardiopulmonary bypass (CPB) and the underlying mechanisms have not yet been established. Therefore, the aim of the present study was to elucidate the alterations in pulmonary microvascular permeability following CPB and the underlying mechanism.
Xing-Gang Mao et al.
Neuro-oncology, 15(7), 865-879 (2013-05-07)
A proportion of glioblastoma stemlike cells (GSCs) expressing endothelial cell marker CDH5 (vascular-endothelial-cadherin or CD144) can transdifferentiate into endothelial cells and form blood vessels. However, the implications of CDH5 expression in gliomas and how it is regulated in GSCs remain
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