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TM, especially TME45, maintains vascular integrity, at least in part, via Src (zeige SRC Proteine) signaling.
These results suggest that SHP-2-via association with ICAM-1-mediates ICAM-1-induced Src activation and modulates VE-cadherin switching association with ICAM-1 or actin, thereby negatively regulating neutrophil adhesion to endothelial cells and enhancing their transendothelial migration.
Galphas (zeige GNAS Proteine) depletion blocks the S1PR1 (zeige S1PR1 Proteine)-activation induced VE-cadherin stabilization at junctions.
Rab11a/Rab11 (zeige RAB11A Proteine) family-interacting protein 2 (zeige RAB11FIP2 Proteine)-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 (zeige KDM4A Proteine) and KDM4C (zeige KDM4C Proteine) in orchestrating mESC differentiation to endothelial cells through the activation of Flk1 (zeige KDR Proteine) and VE-cadherin promoters, respectively
In the absence of Tie-2 (zeige TEK Proteine), VE-PTP (zeige PTPRB Proteine) inhibition destabilizes endothelial barrier integrity in agreement with the VE-cadherin-supportive effect of VE-PTP (zeige PTPRB Proteine).
identification of novel components of the adherens junction complex, and introduction of a novel molecular mechanism through which the VE-cadherin complex controls YAP (zeige YAP1 Proteine) transcriptional activity
Endotoxin challenge initiates interrelated changes in microvessel Cx43 (zeige GJA1 Proteine), VE-cadherin, and microvessel permeability, with changes in Cx43 (zeige GJA1 Proteine) 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 (zeige EPAS1 Proteine) and Ets-1 (zeige ETS1 Proteine) 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
VE-cadherin and Esama (zeige ESAM Proteine) have distinct and redundant functions during blood vessel morphogenesis
C1qr (zeige CD93 Proteine) and c1qrl regulate angiogenesis through controlling endothelial cdh5 expression.
the conserved targeting of VE-cadherin by miR (zeige MYLIP Proteine)-22 regulates endothelial inflammation, tissue injury, and angiogenesis.
VE-cadherin/amotL2 (zeige AMOTL2 Proteine) 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 (zeige MSN Proteine) 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 (zeige FLI1 Proteine), and etsrp (zeige ETV2 Proteine), demonstrated that erg (zeige KCNH2 Proteine) and fli1 (zeige FLI1 Proteine) 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
Data suggest that cadherin 5 (CDH5) may play a key role in hematogenous recurrence of advanced gastric cancer and may be a viable treatment target.
The present study investigated the interplay of VEGF (zeige VEGFA Proteine)-A165a isoform, the anti-angiogenic VEGF (zeige VEGFA Proteine)-A165b, placental growth factor (PIGF) and their receptors, VEGFR1 (zeige FLT1 Proteine) and VEGFR2 (zeige KDR Proteine).on junctional occupancy of VE-cadherin and macromolecular leakage in human endothelial monolayers and the perfused placental microvascular bed.
CDH5 and FABP1 (zeige FABP1 Proteine) expression levels were both elevated in drug-induced liver injury.
Varenicline promotes HUVEC migration by lowering VE-cadherin expression due to activated ERK/p38 (zeige MAPK1 Proteine)/JNK (zeige MAPK8 Proteine) signaling through alpha7 nAChR (zeige CHRNA7 Proteine). These processes probably contribute to varenicline-aggravated atherosclerotic plaque.
Plakoglobin (zeige JUP Proteine) maintains the integrity of vascular endothelial cell junctions and regulates VEGF (zeige VEGFA Proteine)-induced phosphorylation of VE-cadherin
Endothelial Tspan5 (zeige TSPAN5 Proteine)- and Tspan17-ADAM10 (zeige ADAM10 Proteine) 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 (zeige HBA1 Proteine) and VE-cadherin, and a significant increase in that of alpha-SMA (zeige SMN1 Proteine) 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
VE-cadherin induces opposing growth signals.
investigated the role of catenin p120 (zeige CTNND1 Proteine)-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 (zeige RHOA Proteine)
a VE-cadherin-dependent pathway may link T2-TrpRS (zeige WARS Proteine) 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