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Galphas (show GNAS Proteins) depletion blocks the S1PR1 (show S1PR1 Proteins)-activation induced VE-cadherin stabilization at junctions.
Rab11a/Rab11 (show RAB11A Proteins) family-interacting protein 2 (show RAB11FIP2 Proteins)-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 Proteins) and KDM4C (show KDM4C Proteins) in orchestrating mESC differentiation to endothelial cells through the activation of Flk1 (show KDR Proteins) and VE-cadherin promoters, respectively
In the absence of Tie-2 (show TEK Proteins), VE-PTP (show PTPRB Proteins) inhibition destabilizes endothelial barrier integrity in agreement with the VE-cadherin-supportive effect of VE-PTP (show PTPRB Proteins).
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 Proteins) transcriptional activity
Endotoxin challenge initiates interrelated changes in microvessel Cx43 (show GJA1 Proteins), VE-cadherin, and microvessel permeability, with changes in Cx43 (show GJA1 Proteins) 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 Proteins) and Ets-1 (show ETS1 Proteins) 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 Proteins) cell-derived Flk1 (show KDR Proteins)(+)VE-cadherin(+) cells expressing the Er71 (show ETV2 Proteins) are as angiogenic as mES (show PTCH1 Proteins) cell-derived cells and incorporate into CD31 (show PECAM1 Proteins)(+) neovessels.
VE-cadherin tyrosine phosphorylation at Y685 is a physiological and hormonally regulated process in female reproductive organs.
VE-cadherin and Esama (show ESAM Proteins) have distinct and redundant functions during blood vessel morphogenesis
C1qr (show CD93 Proteins) and c1qrl regulate angiogenesis through controlling endothelial cdh5 expression.
the conserved targeting of VE-cadherin by miR (show MYLIP Proteins)-22 regulates endothelial inflammation, tissue injury, and angiogenesis.
VE-cadherin/amotL2 (show AMOTL2 Proteins) 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 Proteins) 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 Proteins), and etsrp (show ETV2 Proteins), demonstrated that erg (show KCNH2 Proteins) and fli1 (show FLI1 Proteins) 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
CDH5 and FABP1 (show FABP1 Proteins) expression levels were both elevated in drug-induced liver injury.
Varenicline promotes HUVEC migration by lowering VE-cadherin expression due to activated ERK/p38 (show MAPK1 Proteins)/JNK (show MAPK8 Proteins) signaling through alpha7 nAChR (show CHRNA7 Proteins). These processes probably contribute to varenicline-aggravated atherosclerotic plaque.
Plakoglobin (show JUP Proteins) maintains the integrity of vascular endothelial cell junctions and regulates VEGF (show VEGFA Proteins)-induced phosphorylation of VE-cadherin
Endothelial Tspan5 (show TSPAN5 Proteins)- and Tspan17-ADAM10 (show ADAM10 Proteins) 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-27b and that the latter directly bound to its 3'UTR to regulate its expression.
Cells in high glucose for 7 days showed a significant decrease in mRNA expression of CD31 (show HBA1 Proteins) and VE-cadherin, and a significant increase in that of alpha-SMA (show SMN1 Proteins) 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 Proteins)-939 downregulates VE-cadherin and destroys the barrier function of endothelial monolayers.
EGFR (show EGFR Proteins) genes are associated with overexpression of CDH5 through increased phosphorylation of EGFR (show EGFR Proteins) and downstream Akt (show AKT1 Proteins) 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.
VE-cadherin induces opposing growth signals.
investigated the role of catenin p120 (show CTNND1 Proteins)-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 Proteins)
a VE-cadherin-dependent pathway may link T2-TrpRS (show WARS Proteins) 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