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GRAP2 — VEGFA

Text-mined interactions from Literome

Zhang et al., Am J Reprod Immunol 2003 : We found that up-regulation of the expression of MMPs was induced by FN and VEGF through the focal adhesion kinase ( FAK ) /mitogen activated protein kinase ( MAPK ) and Flt-1/p38SAPK/MAPKAPK2 signaling pathways, respectively
Ouchi et al., Circ Res 2005 (MAP Kinase Signaling System) : The p38 MAPK inhibitor SB203580 blocked AICAR induced increase in VEGF mRNA and protein levels, indicating that AICAR mediated VEGF induction is dependent on p38 MAPK signaling
Ali et al., J Pharmacol Sci 2005 : M475271 inhibited VEGF induced extracellular signal regulated kinase1/2 ( ERK1/2 ) and p38 but not Akt activation in a concentration dependent manner
Kilic et al., FASEB J 2006 (Brain Ischemia) : Following 90-min episodes of middle cerebral artery occlusion, VEGF increased phosphorylated ( but not total ) Akt and ERK-1/-2 and reduced phosphorylated mitogen activated protein kinase/p38 and c-Jun NH2-terminal kinase (JNK)-1/-2 levels, at the same time decreasing inducible NO synthase expression in ischemic neurons
Murata et al., J Orthop Res 2006 (Anoxia...) : In contrast, IL-1 induced VEGF secretion was blocked by JNK inhibitor, and not by p38MAPK inhibitor
Awasthi et al., Lab Invest 2009 (Neoplasm Metastasis...) : Although VEGF induced phosphorylation of Akt, Erk1/2, p38 and Raf 2.8-, 1.5-, 2.2- and 3.6-fold, respectively, EMAP II preincubation blocked this induction in phosphorylation to control levels
Fontijn et al., Cell Oncol 2009 (Melanoma) : PI-3K, p38 MAPK and ERK1/2 MAPK pathways were activated, while inhibition of PI-3K or p38 resulted in, respectively, 55 % and up to 70 % reduction of VEGF mRNA overexpression
Kim et al., J Clin Immunol 2009 (Asthma...) : Inhibition of p38 suppressed CCL20 and VEGF secretion, as did a NADPH oxidase blocker and an antioxidant, in C. pneumoniae infected BECs
O'Sullivan et al., World journal of surgical oncology 2009 (Adenocarcinoma) : Therfore inhibition of these pathways may reduce tumour growth We set out to examine the effects of P38-MAPK inhibition on apoptosis, proliferation, VEGF release and cell cycle effects in-vitro and on primary tumour growth in-vivo ... P38-MAPK inhibition in-vitro resulted in a significant reduction in proliferation ( 75.2 +/- 8.4 % vs. 100 +/- 4.3 %, p < 0.05 ) and G1 cell cycle phase ( 35.9 +/- 1.1 % vs. 32.5 +/- 0.6 %, p < 0.05 ) but no significant changes in apoptosis or VEGF levels
Alleva et al., Toxicol In Vitro 2011 (MAP Kinase Signaling System) : APM treatment induces VEGF-pathway activation by erk1/2 and p38 phosphorylation
Demyanets et al., Basic Res Cardiol 2011 (Atherosclerosis...) : STAT3 inhibitor WP1066, p38 MAPK inhibitors SB-202190 and BIRB 0796, extracellular signal regulated kinase1/2 ( Erk1/2 ) inhibitor U0126, and phosphatidylinositol 3-kinase (PI3K) inhibitors LY-294002 and PI-103 reduced OSM induced VEGF synthesis
Ferrari et al., Mol Cancer Res 2012 : Therefore, we hypothesized that different p38 ( MAPK ) isoforms control endothelial cell apoptosis or survival, and that TGF-ß1 directs VEGF activation of p38 ( MAPK ) from a prosurvival to a proapoptotic isoform
Pin et al., Angiogenesis 2012 : In addition, the lentivirus mediated expression of miR-20a precursor ( pmiR-20a ) is associated with a decrease in the VEGF induced activation of p38