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F2RL1 — PIK3R1

Text-mined interactions from Literome

Wang et al., Biochemistry 2006 : Here we demonstrate that PAR-2 can increase PI3K activity through a Galphaq/Ca ( 2+ ) -dependent pathway involving PYK2 and a Src-family kinase, while inhibiting PI3K activity through a beta-arrestin dependent mechanism, and that beta-arrestin-1 can directly associate with and inhibit the catalytic activity of p110alpha
Wang et al., Biochem J 2007 : We have shown previously that PAR-2 simultaneously promotes Galphaq/Ca2+ dependent activation and beta-arrestin-1 dependent inhibition of class IA PI3K ( phosphoinositide 3-kinase ), and we sought to characterize further the role of beta-arrestins in the regulation of PI3K activity ... In the present study we have demonstrated that : ( i ) PAR-2 increases p110alpha- and p110beta associated lipid kinase activities, and both p110alpha and p110beta are inhibited by over-expression of either beta-arrestin-1 or -2 ; ( ii ) both beta-arrestin-1 and -2 directly inhibit the p110alpha catalytic subunit in vitro, whereas only beta-arrestin-2 directly inhibited p110beta ; ( iii ) examination of upstream pathways revealed that PAR-2 induced PI3K activity required the small GTPase Cdc ( cell-division cycle)42, but not tyrosine phosphorylation of p85 ; and ( iv ) beta-arrestins inhibit PAR-2 induced Cdc42 activation
Saito et al., Hum Reprod 2011 (Endometriosis...) : The TGF-ß1 induced increase in PAR2 gene expression was repressed by inhibition of p38 MAPK, p42/44 MAPK or PI3K , but not by knockdown of Smad4 expression