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CDH5 is a classical cadherin from the cadherin superfamily and is located in a six-cadherin cluster in a region on the long arm of chromosome 16 that is involved in loss of heterozygosity events in breast and prostate cancer. Additionally we are shipping Cadherin 5 Kits (63) and Cadherin 5 Proteins (17) and many more products for this protein.
Showing 10 out of 231 products:
Human Monoclonal Cadherin 5 Primary Antibody for Func, EIA - ABIN1105885
Martìn-Padura, De Castellarnau, Uccini, Pilozzi, Natali, Nicotra, Ughi, Azzolini, Dejana, Ruco: Expression of VE (vascular endothelial)-cadherin and other endothelial-specific markers in haemangiomas. in The Journal of pathology 1995
Show all 6 references for ABIN1105885
Human Monoclonal Cadherin 5 Primary Antibody for IF, IP - ABIN967857
Corada, Liao, Lindgren, Lampugnani, Breviario, Frank, Muller, Hicklin, Bohlen, Dejana: Monoclonal antibodies directed to different regions of vascular endothelial cadherin extracellular domain affect adhesion and clustering of the protein and modulate endothelial permeability. in Blood 2001
Show all 5 references for ABIN967857
Human Monoclonal Cadherin 5 Primary Antibody for Func, EIA - ABIN1105883
Breviario, Caveda, Corada, Martin-Padura, Navarro, Golay, Introna, Gulino, Lampugnani, Dejana: Functional properties of human vascular endothelial cadherin (7B4/cadherin-5), an endothelium-specific cadherin. in Arteriosclerosis, thrombosis, and vascular biology 1995
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Human Polyclonal Cadherin 5 Primary Antibody for EIA, WB - ABIN357862
Ali, Liao, Martens, Muller: Vascular endothelial cadherin (VE-cadherin): cloning and role in endothelial cell-cell adhesion. in Microcirculation (New York, N.Y. : 1994) 1997
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Human Monoclonal Cadherin 5 Primary Antibody for FACS, ELISA - ABIN1724748
Shrivastava-Ranjan, Rollin, Spiropoulou: Andes virus disrupts the endothelial cell barrier by induction of vascular endothelial growth factor and downregulation of VE-cadherin. in Journal of virology 2010
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Human Monoclonal Cadherin 5 Primary Antibody for FACS, ELISA - ABIN1724747
Pirotte, Lamour, Lambert, Alvarez Gonzalez, Ormenese, Noël, Mottet, Castronovo, Bellahcène: Dentin matrix protein 1 induces membrane expression of VE-cadherin on endothelial cells and inhibits VEGF-induced angiogenesis by blocking VEGFR-2 phosphorylation. in Blood 2011
Show all 2 references for ABIN1724747
Rab11a/Rab11 (show RAB11A Antibodies) family-interacting protein 2 (show RAB11FIP2 Antibodies)-mediated VE-cadherin recycling is required for formation of adherens junctions and restoration of vascular endothelial barrier integrity.
These findings together demonstrate the essential role of KDM4A (show KDM4A Antibodies) and KDM4C (show KDM4C Antibodies) in orchestrating mESC differentiation to endothelial cells through the activation of Flk1 (show KDR Antibodies) and VE-cadherin promoters, respectively
In the absence of Tie-2 (show TEK Antibodies), VE-PTP (show PTPRB Antibodies) inhibition destabilizes endothelial barrier integrity in agreement with the VE-cadherin-supportive effect of VE-PTP (show PTPRB Antibodies).
identification of novel components of the adherens junction complex, and introduction of a novel molecular mechanism through which the VE-cadherin complex controls YAP (show YAP1 Antibodies) transcriptional activity
Endotoxin challenge initiates interrelated changes in microvessel Cx43 (show GJA1 Antibodies), VE-cadherin, and microvessel permeability, with changes in Cx43 (show GJA1 Antibodies) temporally leading the other responses.
Mutating Y731 in the cytoplasmic tail of VE-cadherin, known to selectively affect leukocyte diapedesis, but not the induction of vascular permeability, attenuates bleeding.
mRNA of HIF-2alpha (show EPAS1 Antibodies) and Ets-1 (show ETS1 Antibodies) were significantly increased by HIF-3alpha ablation. Both factors activate the VE-cadherin gene, the transcriptional repression of these factors by HIF-3alpha is important for silencing the irrelevant expression of the VE-cadherin
iPS (show SLC27A4 Antibodies) cell-derived Flk1 (show KDR Antibodies)(+)VE-cadherin(+) cells expressing the Er71 (show ETV2 Antibodies) are as angiogenic as mES (show PTCH1 Antibodies) cell-derived cells and incorporate into CD31 (show PECAM1 Antibodies)(+) neovessels.
VE-cadherin tyrosine phosphorylation at Y685 is a physiological and hormonally regulated process in female reproductive organs.
Conclude that the site Y685 in VE-cadherin is involved in the physiological regulation of capillary permeability in mouse ovary/uterus.
VE-cadherin/amotL2 (show AMOTL2 Antibodies) complex is responsible for transmitting mechanical force between endothelial cells for the coordination of cellular morphogenesis consistent with aortic lumen expansion and function.
Cdh5 organizes junctional and cortical actin cytoskeletons and F-actin polymerization during endothelial cell elongation.
Regulatory pathways affecting vascular stabilization via VE-cadherin dynamics
suggest that Ve-cadherin and Moesin1 (show MSN Antibodies) function to establish and maintain apical/basal polarity during multicellular lumen formation in the intersegmental vessels
results demonstrate a significant role for VE-cadherin in cardiac development independent of its effects on the formation of the peripheral vasculature
fli1 (show FLI1 Antibodies), and etsrp (show ETV2 Antibodies), demonstrated that erg (show KCNH2 Antibodies) and fli1 (show FLI1 Antibodies) act cooperatively and are required for angiogenesis possibly via direct regulation of an endothelial cell junction molecule, VE-cadherin
VE-cadherin plays an essential role in vascular development
S-nitrosylation regulates endothelial cell VE-cadherin phosphorylation and internalization in microvascular permeability.
Data indicate that monoclonal antibody (mAb) against vascular endothelial cadherin 5 (VECDH5) has good binding ability and specificity.
our data show the importance of spatio-temporal regulation of the actin cytoskeleton through Trio (show TRIO Antibodies) and Rac1 at VE-cadherin-based cell-cell junctions in the maintenance of the endothelial barrier.
ankyrin-G (show ANK3 Antibodies) associates with and inhibits the endocytosis of VE-cadherin cis (show CISH Antibodies) dimers.
VE-cadherin complexes are central force transducers in endothelial barrier in response to force.
Demonstrate that TrkB (show NTRK2 Antibodies) protects endothelial integrity during atherogenesis by promoting Ets1 (show ETS1 Antibodies)-mediated VE-cadherin expression and plays a previously unknown protective role in the development of coronary artery disease.
homophilic interactions of VE-cadherin stabilize it at cell borders and prevent entry into the lateral border recycling compartment.
The number of CD34 (show CD34 Antibodies)/144 positive circulating endothelial cells was high in patients with large artery atherosclerosis who experienced chronic ischemic stroke. And this number may reflect severity of carotid atherosclerosis.
Breast cancer cell incorporation into the vascular endothelium initiates by dislocating VE-cadherin at endothelial cell junctions.
VE-cadherin induces opposing growth signals.
investigated the role of catenin p120 (show CTNND1 Antibodies)-VE-cadherin interaction in regulation of barrier function in confluent endothelial monolayers
Vascular endothelial-cadherin regulates cytoskeletal tension, cell spreading, and focal adhesions by stimulating RhoA (show RHOA Antibodies)
a VE-cadherin-dependent pathway may link T2-TrpRS (show WARS Antibodies) to inhibition of new blood vessel formation
results indicate that integrin engagement disrupts VE-cadherin-containing adherens junctions via the activation of Src, but not Ras, possibly as a result of modulation of the actin network
exposure of BAECs to hydrostatic pressure (PHYSIOLOGIC PRESSURE) may downregulate the expression of VE-cadherin, resulting in loss of contact inhibition followed by increased proliferation and formation of a multilayered structure
In all, these results demonstrate that cell-cell contact signals through VE-cadherin, RhoA, and intracellular tension in the actin cytoskeleton to regulate proliferation.
Low expressions of eNOS3 and Ve-cadherin in the salvaged sub-healthy microvascular endothelium of infarcted and marginal areas suggest that endothelial system is impaired at 7-day of reperfused acute myocardial infarction.
This gene is a classical cadherin from the cadherin superfamily and is located in a six-cadherin cluster in a region on the long arm of chromosome 16 that is involved in loss of heterozygosity events in breast and prostate cancer. The encoded protein is a calcium-dependent cell-cell adhesion glycoprotein comprised of five extracellular cadherin repeats, a transmembrane region and a highly conserved cytoplasmic tail. Functioning as a classic cadherin by imparting to cells the ability to adhere in a homophilic manner, the protein may play an important role in endothelial cell biology through control of the cohesion and organization of the intercellular junctions. An alternative splice variant has been described but its full length sequence has not been determined.
cadherin 5, type 2, VE-cadherin (vascular endothelium)
, cadherin 5, type 2, VE-cadherin (vascular epithelium)
, vascular endothelial cadherin
, VE-cadherin (vascular epithelium)
, type 2
, 7B4 antigen
, cd144 antigen
, endothelial-specific cadherin
, VE cadherin