◀ Back to MAPK1

GPI — MAPK1

Text-mined interactions from Literome

Rebsamen et al., J Mol Cell Cardiol 2003 : Investigating the role of MAPK in the stimulation of prostacyclin induced by these three agonists, we found that both the p42/44 MAPK inhibitor PD 98059 ( 50 microM ) and the p38 MAPK blocker SB 203580 ( 5 microM ) prevented agonist induced PGI ( 2 ) secretion without affecting COX-2 activity or synthesis
Martínez-González et al., Atherosclerosis 2004 : Pertussis toxin ( an inhibitor of Galphai/Galphao proteins ) prevented MAPK activation and inhibited both Cox-2 up-regulation and PGI ( 2 ) release
Brooks et al., Vet Immunol Immunopathol 2009 : This study has demonstrated that clinically relevant concentrations of LPS activate p38 MAPK in equine endothelial cells and that both neutrophil adhesion to LPS activated EDVEC and PGI ( 2 ) release are dependent upon p38 MAPK phosphorylation
Jackson et al., Thromb Res 2010 (MAP Kinase Signaling System) : PGI ( 2 ) inhibited ERK/p38 ( MAPK ) phosphorylation in response to both agonists which was unaffected by a cPLA(2) inhibitor ( AACOCF ( 3 ) )
Kho et al., Cancer Res 2013 (Breast Neoplasms) : Mechanistic investigations indicated that interaction of AMF with HER2 triggers HER2 phosphorylation and metalloprotease mediated ectodomain shedding, activating phosphoinositide-3-kinase (PI3K) and mitogen activated protein kinase signaling and ablating the ability of trastuzumab to inhibit breast carcinoma cell growth
Patel et al., Biochem J 1996 : These results provide direct evidence for the involvement of p42 and p44 MAPK in the PGI2 response of intact endothelial cells : we have shown that both the endothelial P2Y purinoceptors are linked to activation of MAPK, and that activation of this pathway is a requirement for the stimulation by ATP/ADP of endothelial PGI2 production
Braconi Quintaje et al., J Mol Cell Cardiol 1998 : Investigating the role of MAPK in EGF- and in PMA promoted PGI2-formation , we found that the MAPK-inhibitor 6-thioguanine ( 500 microM ), as well as the MAPK-kinase-inhibitor PD98059 ( 50 microM ) abolished both EGF- and PMA stimulated PGI2 production in cardiomyocytes