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Human Cadherin 5 ELISA Kit for Sandwich ELISA - ABIN416976
Kaban, Salva, Akbuga: The effects of chitosan/miR-200c nanoplexes on different stages of cancers in breast cancer cell lines. in European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences 2016
Galphas (show GNAS ELISA Kits) depletion blocks the S1PR1 (show S1PR1 ELISA Kits)-activation induced VE-cadherin stabilization at junctions.
Rab11a/Rab11 (show RAB11A ELISA Kits) family-interacting protein 2-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 ELISA Kits) and KDM4C (show KDM4C ELISA Kits) in orchestrating mESC differentiation to endothelial cells through the activation of Flk1 (show KDR ELISA Kits) and VE-cadherin promoters, respectively
In the absence of Tie-2 (show TEK ELISA Kits), VE-PTP (show PTPRB ELISA Kits) inhibition destabilizes endothelial barrier integrity in agreement with the VE-cadherin-supportive effect of VE-PTP (show PTPRB ELISA Kits).
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 ELISA Kits) transcriptional activity
Endotoxin challenge initiates interrelated changes in microvessel Cx43 (show GJA1 ELISA Kits), VE-cadherin, and microvessel permeability, with changes in Cx43 (show GJA1 ELISA Kits) 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 ELISA Kits) and Ets-1 (show ETS1 ELISA Kits) 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 ELISA Kits) cell-derived Flk1 (show KDR ELISA Kits)(+)VE-cadherin(+) cells expressing the Er71 are as angiogenic as mES (show PTCH1 ELISA Kits) cell-derived cells and incorporate into CD31 (show PECAM1 ELISA Kits)(+) neovessels.
VE-cadherin tyrosine phosphorylation at Y685 is a physiological and hormonally regulated process in female reproductive organs.
VE-cadherin and Esama (show ESAM ELISA Kits) have distinct and redundant functions during blood vessel morphogenesis
C1qr (show CD93 ELISA Kits) and c1qrl regulate angiogenesis through controlling endothelial cdh5 expression.
the conserved targeting of VE-cadherin by miR (show MYLIP ELISA Kits)-22 regulates endothelial inflammation, tissue injury, and angiogenesis.
VE-cadherin/amotL2 (show AMOTL2 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits), and etsrp, demonstrated that erg (show KCNH2 ELISA Kits) and fli1 (show FLI1 ELISA Kits) 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
Plakoglobin (show JUP ELISA Kits) maintains the integrity of vascular endothelial cell junctions and regulates VEGF (show VEGFA ELISA Kits)-induced phosphorylation of VE-cadherin
Endothelial Tspan5 (show TSPAN5 ELISA Kits)- and Tspan17-ADAM10 (show ADAM10 ELISA Kits) complexes may regulate inflammation by maintaining normal VE-cadherin expression and promoting T lymphocyte transmigration.
Study found that high VE-cadherin gene expression levels were associated with low expression of miR (show MLXIP ELISA Kits)-27b and that the latter directly bound to its 3'UTR (show UTS2R ELISA Kits) to regulate its expression.
Cells in high glucose for 7 days showed a significant decrease in mRNA expression of CD31 (show HBA1 ELISA Kits) and VE-cadherin, and a significant increase in that of alpha-SMA (show SMN1 ELISA Kits) and collagen I.
AngII could induce pulmonary injury by triggering endothelial barrier injury, and such process may be related to the dephosphorylation of Y685-VE-cadherin and the endothelial skeletal rearrangement
Breast cancer-secreted miR (show MLXIP ELISA Kits)-939 downregulates VE-cadherin and destroys the barrier function of endothelial monolayers.
EGFR (show EGFR ELISA Kits) genes are associated with overexpression of CDH5 through increased phosphorylation of EGFR (show EGFR ELISA Kits) and downstream Akt (show AKT1 ELISA Kits) pathways.
We found that patients with chronic spontaneous urticaria (CSU) had significantly higher CDH5 serum levels compared with patients with atopic dermatitis and control subjects. Moreover, serum levels ofCDH5 were closely associated with the severity of CSU.
Results indicate that the posthemorrhagic shock mesenteric lymph in vitro increases the cellular permeability of human umbilical vein endothelial cells through suppression of F-actin and VE-cadherin.
CMTM3 (show CMTM3 ELISA Kits) mediates cell-cell adhesion at adherens junctions and contributes to the control of vascular sprouting by regulation VE-cadherin turnover.
VE-cadherin induces opposing growth signals.
investigated the role of catenin p120 (show CTNND1 ELISA Kits)-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 ELISA Kits)
a VE-cadherin-dependent pathway may link T2-TrpRS (show WARS ELISA Kits) 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