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Text-mined interactions from Literome

Rousseau et al., J Biol Chem 2000 : Vascular endothelial growth factor ( VEGF ) -driven actin based motility is mediated by VEGFR2 and requires concerted activation of stress activated protein kinase 2 ( SAPK2/p38 ) and geldanamycin-sensitive phosphorylation of focal adhesion kinase ... Using porcine endothelial cells expressing one or the other type of the VEGF receptors, VEGFR1 or VEGFR2, or human umbilical vein endothelial cells pretreated with a VEGFR2 neutralizing antibody, we show that VEGFR2 is responsible for VEGF induced activation of the stress activated protein kinase-2/p38 ( SAPK2/p38 ), phosphorylation of focal adhesion kinase ( FAK ), and enhanced migratory activity
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 )
Ferrari et al., Proc Natl Acad Sci U S A 2006 : However, in context with TGF-beta1, VEGF/flk-1 mediated activation of p38 ( MAPK ) results in apoptosis
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