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AKT3 — KDR

Text-mined interactions from Literome

Wick et al., J Neurosci 2002 : Inhibition of VEGFR-2 blocked the activation of Akt/PKB
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
Zhang et al., J Biol Chem 2003 : Phosphorylation of VEGFR2 at Tyr-801 and Tyr-1175, the critical sites for VEGF induced PI3K-Akt signaling, was not involved in TNF mediated Akt activation
Endo et al., J Recept Signal Transduct Res 2003 : Inhibition of VEGFR-2 blocked activation of extracellular regulated-kinase, p38, Akt , and endothelial nitric oxide synthetase ( eNOS ) by VEGF, but did not inhibit p38 activation by the VEGFR-1-specific ligand, placental growth factor ( PIGF )
Cho et al., Biochem Biophys Res Commun 2005 : Thus, atRA decreases eNOS-Ser ( 1179 ) phosphorylation through a mechanism that depends on VEGF-KDR/Flk-1 mediated Akt phosphorylation but is independent of RARE, leading to reduction in NO production
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
Ling et al., Biochem Biophys Res Commun 2007 (Carcinoma, Lewis Lung) : Endostar suppressed the VEGF induced tyrosine phosphorylation of KDR/Flk-1 ( VEGFR-2 ) as well as the overall VEGFR-2 expression and the activation of ERK, p38 MAPK, and AKT in HUVECs
Silva et al., Int J Cancer 2011 (Carcinoid Tumor...) : The purpose of our study was to : ( i ) assess the expression of VEGFR-2 in the novel human carcinoid cell line BON, ( ii ) to determine the role of PI3K/Akt signaling on VEGFR-2 expression and ( iii ) to assess the effect of VEGFR-2 on BON cell invasion, migration and proliferation
Geretti et al., Mol Cancer Res 2010 (Melanoma) : It antagonized VEGF induced VEGFR-2/NRP2 complex formation and inhibited VEGF induced activation of AKT , a mediator of cell survival, without affecting activation of VEGFR-2
Ricciardi et al., Chemotherapy 2010 (Pancreatic Neoplasms) : Sorafenib reduced c-Kit, ERK and VEGFR2 activation and on the other hand, gemcitabine inhibited Akt phosphorylation
Garonna et al., PloS one 2011 : Inhibition of VEGFR2 tyrosine kinase activity reduced leptin stimulated p38 ( MAPK ) and Akt activation, COX-2 induction, and pro-angiogenic EC responses, and blockade of VEGFR2 or COX-2 activities abolished leptin-driven neo-angiogenesis in a chick chorioallantoic membrane vascularisation assay in vivo
Li et al., Exp Cell Res 2012 : Taken together, VEGFR-2 is expressed on primary human hair follicle DP cells and VEGF induces proliferation of DP cells through VEGFR-2/ERK pathway, but not p38, JNK or AKT signaling
Song et al., Angiogenesis 2012 (Breast Neoplasms...) : Usnic acid inhibits breast tumor angiogenesis and growth by suppressing VEGFR2 mediated AKT and ERK1/2 signaling pathways
Edelstein et al., Neurosci Lett 2012 (Neuroblastoma) : Notably, rapamycin augmented the OA-induced hyperphosphorylation of Akt by suppressing a negative feedback loop of Akt activation through VEGFR2 and its downstream target phosphatidylinositol 3-kinase (PI3K)
Gerber et al., J Biol Chem 1998 : Endothelial cells cultured in the presence of VEGF and the Flk-1/KDR-selective VEGF mutant induced phosphorylation of the serine-threonine kinase Akt in a PI3-kinase dependent manner