Disease relevance of LOC503620

• Hypoxia increased VEGF receptor number 50% in BREC without altering affinity [1].

High impact information on LOC503620

• TGF-beta1 potently induces VEGF receptor 1 (VEGFR-1) expression in endothelial cells and thereby prevents oxygen-induced vessel loss in vivo [2].
• This study shows that shear stress induces a rapid induction as well as nuclear translocation of the vascular endothelial growth factor (VEGF) receptor 2 and promotes the binding of the VEGF receptor 2 and the adherens junction molecules, VE-cadherin and beta-catenin, to the endothelial cytoskeleton [3].
• VEGF receptor 2 and the adherens junction as a mechanical transducer in vascular endothelial cells [3].
• These results suggest that VEGF receptor 2 and the adherens junction act as shear-stress cotransducers, mediating the transduction of shear-stress signals into vascular endothelial cells [3].
• In endothelial cells lacking VE-cadherin, shear stress did not augment nuclear translocation of the VEGF receptor 2 and phosphorylation of Akt1 and P38 as well as transcriptional induction of a reporter gene regulated by a shear stress-responsive promoter [3].

Biological context of LOC503620

• The stimulation of endothelial cells with CNF1 resulted in a marked increase in the tyrosine phosphorylation of the VEGF receptor (VEGFR)-2, which was correlated with a stimulation of its kinase activity and with its association with downstream tyrosine phosphorylated proteins [4].
• The objective of the present study was to demonstrate the expression of VEGF, VEGF receptor (R)-1, and VEGFR-2 in detail by different methodological approaches in bovine corpora lutea (CL) obtained from different stages of the estrous cycle and during pregnancy [5].
• We found that chemical inhibition of TrxR in Se-sufficient endothelial cells (ECs) was associated with increases in VEGF and VEGF receptor expression, cell migration, proliferation, and angiogenesis to levels similar to those seen in Se-deficient ECs [6].

Anatomical context of LOC503620

• Characterization of VEGF receptor (VEGFR) expression revealed that BME, BAE, and BLE cell lines express VEGFR-1 and -2, whereas of the three cell lines assessed, only BAE cells express VEGFR-3 [7].

Associations of LOC503620 with chemical compounds

• These findings suggest that Ang II might potentiate VEGF-induced angiogenic activity through an increase of the VEGF receptor KDR/Flk-1 [8].
• Antiphosphotyrosine immunoblotting showed VEGF-stimulated tyrosine autophosphorylation of VEGF receptor bands at 225 and 220 kDa and another band at 80 kDa within 1 min.(ABSTRACT TRUNCATED AT 250 WORDS)[1]
• 6. Tranilast did not affect VEGF binding or VEGF-induced phosphorylation of tyrosine residues of VEGF receptor- and phospholipase Cgamma and their associated proteins [9].
• Taken together, these results are consistent with the hypothesis that interactions between cell surface heparan sulfate proteoglycans and the VEGF receptor contribute to allowing maximal VEGF binding [10].
• Involvement of VEGF in fibrinogen-dependent in vitro tube formation was evaluated using anti-VEGF neutralizing antibody or VEGF receptor 2-selective inhibitor (SU5416) [11].

Physical interactions of LOC503620

• Northern blot analysis and 125I-VEGF binding analysis were used to identify hypoxia-induced alterations of VEGF receptor at mRNA and protein levels [12].

Regulatory relationships of LOC503620

• Basic fibroblast growth factor induces expression of VEGF receptor KDR through a protein kinase C and p44/p42 mitogen-activated protein kinase-dependent pathway [13].

Other interactions of LOC503620

• These results indicated that inhibition of VEGF interaction with VEGF receptor 2 is the mechanism serves A. cinnamomea as a protective mechanism composing the anti-angiogenesis function [14].
• VEGF and VEGF receptor transcripts were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and ribonuclease protection assay [5].

References