Gene interactions and pathways from curated databases and text-mining

◀ Back to MAPK8

KDR — MAPK8

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: MAPK8 → KDR (increases, KDR Activity, MAPK8 Activity) Soldi et al., EMBO J 1999
    Evidence: The formed transductosome mediates the activation of MAP kinase, PI 3-kinase, Jun kinase, cGMP-dependent kinase and focal adhesion kinase

Text-mined interactions from Literome

Hata et al., Diabetes 1999 : MAPK inhibitor PD98059 reduced KDR mRNA expression 72 % at concentrations that inhibited bFGF induced MAPK phosphorylation 100 %, suggesting that pathways in addition to MAPK might also be involved
Wu et al., J Biol Chem 2000 : MEK, PLCgamma, and to a lesser extent PKC, are in the pathway through which KDR activates MAPK
Kim et al., J Biol Chem 2002 : Endostatin blocked VEGF induced tyrosine phosphorylation of KDR/Flk-1 and activation of ERK, p38 MAPK , and p125(FAK) in human umbilical vein endothelial cells
Zeng et al., J Biol Chem 2003 : Our results further indicate that Gq/11 proteins specifically mediate KDR signaling such as intracellular Ca2+ mobilization rather than Flt-1 induced CDC42 activation and that a Gq/11 antisense oligonucleotide completely inhibits MAPK phosphorylation induced by KDR but has no effect on Flt-1 induced MAPK activation
Ferrari et al., Proc Natl Acad Sci U S A 2006 : Inhibition of p38 ( MAPK ) blocks TGF-beta1 induced apoptosis, showing that VEGF/flk-1 mediated activation of p38 ( MAPK ) is required for TGF-beta1 induction of apoptosis ... However, in context with TGF-beta1, VEGF/flk-1 mediated activation of p38 ( MAPK ) results in apoptosis
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
Samuel et al., Diabetes 2010 (Diabetes Mellitus, Experimental...) : We also observed increased phosphorylated mitogen activated protein kinase activated protein kinase-2, 2 days after the treatment and increased expression of vascular endothelial growth factor ( VEGF ), Flk-1 , angiopoietin-1 (Ang-1), Tie-2, and survivin, 4 days after treatment in the diabetic animals
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
Belugali Nataraj et al., Cell Signal 2013 (Breast Neoplasms...) : NAP is phosphorylated by VEGF induced activation of MAPK and JNK pathways through VEGFR2 phosphorylation