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POLDIP2 — VEGFA

Text-mined interactions from Literome

Tokuda et al., J Endocrinol 2001 : These results strongly suggest that p44/p42 MAP kinase activation is not involved in the PGE1 stimulated VEGF synthesis in osteoblasts but that p38 MAP kinase activation is involved
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 )
Kazi et al., Am J Physiol Lung Cell Mol Physiol 2004 (Asthma...) : In addition, stimulation of ASM with VEGF activates ERK, but not p38MAPK , and fibronectin secretion is ERK dependent
Becker et al., Circ Res 2005 (Respiratory Distress Syndrome, Adult) : Npn-1 inhibition also attenuated both VEGF165 mediated pulmonary vascular leak and activation of VEGFR2, p38 , and ERK1/2 MAPK, in inducible lung-specific VEGF transgenic mice
Raidl et al., Cell Biochem Biophys 2007 (Pulmonary Disease, Chronic Obstructive) : VEGF production was dependent on phosphorylation of ERK-1, -2 and p38MAPK , as was shown by examining the effects of PD 098059 ( 10 microM ), an inhibitor of the upstream activator of MAPKkinase (MKK)-1, and SB 203580 ( 10 microM ), an inhibitor of p38MAPK ; there were no differences between non-smokers, smokers without airflow limitation and smokers with COPD in this respect
Nakamura et al., Circ Res 2008 (Disease Models, Animal...) : VEGF induced p38 mitogen activated protein kinase phosphorylation and EC migration are not affected by PTP1B overexpression or knockdown
Abdelsaid et al., J Pharmacol Exp Ther 2010 (Anoxia...) : Expression of vascular endothelial growth factor , caspase-3, and poly ( ADP ribose ) polymerase ( PARP ), activation of Akt and p38 mitogen activated protein kinase ( MAPK ), and tyrosine nitration of the phosphatidylinositol (PI) 3-kinase p85 subunit were analyzed by Western blot
Heo et al., BMB Rep 2009 : Furthermore, a pharmacological inhibitory study revealed that G ( alpha i/o ) -mediated phospholipase C, Akt, Erk, and p38 MAPK signaling are involved in this S1P induced expression of VEGF
Tanaka et al., Phytother Res 2012 : The antiangiogenic mechanism of PRE was evaluated by VEGF induced proliferation and migration of HUVECs and/or human retinal microvascular endothelial cells ( HRMECs ) and phosphorylation of extracellular signal regulated kinase ( ERK ) and p38
Ferrari et al., Mol Cancer Res 2012 : TGF-ß1 activation of p38a is mediated by VEGF , which in the absence of TGF-ß1 activates p38ß
Fu et al., Zhonghua Yi Xue Za Zhi 2013 : PGE1 significantly increased VEGF expression of HUVEC in time and a dose dependent manner with concomitantly increased HUVEC proliferation ; treatment of HUVEC with Bevacizumab apparently suppressed PGE1 stimulated VEGF expression, which led to decreased tube formation, reduced cell proliferation and migration by 41 % and 38 %, respectively, compared with PGE1 treatment alone ; PGE1 time-dependently induced both phosphorylation of ERK and p38 in HUVEC, whereas ERK inhibitor, PD98059, or p38 inhibitor, SB203580, blocked PGE1 induced VEGF expression of HUVEC, resulting in dramatically suppression of HUVEC proliferation and migration compared with PGE1 treatment alone ( 60 % and 55 % by PD98059, 62 % and 51 % by SB203580, respectively ) ; in addition, cAMP dependent protein kinase A inhibitor, H89 or Rp-cAMP blocked PGE1 induced VEGF expression in VSMC