Gene interactions and pathways from curated databases and text-mining

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KDR — NOS3

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Shen et al., J Biol Chem 1999 : A KDR receptor-selective mutant increased eNOS expression, whereas an Flt-1 receptor-selective mutant did not
Tanimoto et al., J Biol Chem 2002 : These data are the first to establish a critical role of Flk-1/KDR in S1P stimulated eNOS phosphorylation and activation
Duval et al., J Biol Chem 2003 : Moreover, expression of Cbl in contrast to 70Z/3-Cbl inhibits the Flk-1 dependent activation of eNOS and, thus, NO release
Miura et al., Hypertension 2003 : Our results showed that, in HCECs, stimulation of the B2 receptor leads to the transactivation of KDR/Flk-1 , as well as to eNOS activation , which induces tube formation
Jin et al., Circ Res 2003 : Flow stimulated VEGFR2 recruits phosphoinositide 3-kinase and mediates activation of Akt and eNOS ... Decreasing VEGFR2 expression with antisense VEGFR2 oligonucleotides significantly attenuates activation of Akt and eNOS
Escribano et al., Clin Sci (Lond) 2004 (Colonic Neoplasms) : Overexpression of eNOS , VEGF and its receptor Flk-1 occurred early after azoxymethane administration in rat colonic tissue, even before morphological changes associated with tumour generation were observed, and aspirin prevented the overexpression of both eNOS and VEGF receptor Flk-1
Jin et al., J Biol Chem 2005 : Gab1 phosphorylation as well as activation of Akt and eNOS by flow was inhibited by the Src kinase inhibitor PP2 ( 4-amino-5- ( 4-chlorophenyl ) -7- ( t-butyl ) pyrazolo [ 3,4-d ] pyrimidine ) and VEGFR2 kinase inhibitors SU1498 and VTI, suggesting that flow mediated Gab1 phosphorylation is Src kinase dependent and VEGFR2 dependent
Cai et al., Microvasc Res 2006 : Suppression of eNOS expression only abolished endothelial cell proliferation at VEGF concentrations above 20 ng/ml. Taken together, these results indicate that activation of VEGFR-2 by VEGF enhances SH-PTP1 activity and eNOS expression, which in turn lead to two diverse events : one is that SH-PTP1 dephosphorylates VEGFR-2 and ERK/MAPK, which weaken VEGF mitogenic activity, and the other is that eNOS increases nitric oxide production which in turn lowers SH-PTP1 activity via S-nitrosylation
Grummer et al., Biochem J 2009 : The selective VEGFR-1 agonist PlGF ( placental growth factor ) -1 elicits only a modest activation of eNOS in P-UAECs compared with VEGF ( 165 ), whereas the VEGFR-2 kinase inhibitor blocks VEGF ( 165 ) -stimulated eNOS activation, suggesting VEGF ( 165 ) predominantly activates eNOS via VEGFR-2 ... Although VEGF ( 165 ) also activates ERK ( extracellular-signal regulated kinase ) -1/2, this is not necessary for eNOS activation since U0126 blocks ERK-1/2 phosphorylation, but not eNOS activation, and the VEGFR-2 kinase inhibitor inhibits eNOS activation, but not ERK-1/2 phosphorylation