Gene interactions and pathways from curated databases and text-mining

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CDC73 — PIK3CA

Text-mined interactions from Literome

Zeng et al., J Biol Chem 2002 : As expected, CDC42 and Rac1 activation mediated by EGLT can be completely inhibited by PI3K inhibitors, wortmannin and LY294002, and the p85 dominant negative mutant but not by either the phospholipase C inhibitor, or an intracellular Ca ( 2+ ) chilator BAPTA/AM
Wang et al., Biochem J 2007 : 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
Stephens et al., J Biol Chem 1993 : A number of characteristics of these responses, including their relative sensitivities to inhibition by pertussis toxin and guanosine 5'-beta- ( thio ) diphosphate, suggested that fMLP and PAF increased this PI3K activity via the actions of heterotrimeric G-proteins