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CDC37 — PIK3CA

Pathways - manually collected, often from reviews:

• Reactome Reaction: PIK3CA → CDC37 (reaction) Sordella et al., Science 2004
• Reactome Reaction: PIK3CA → CDC37 (indirect_complex) Sordella et al., Science 2004

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Intact Interaction: Complex of 29 proteins (association, tandem affinity purification) Li et al., Molecular systems biology 2013
• IRef Intact Interaction: Complex of 40 proteins (association, tandem affinity purification) Li et al., Molecular systems biology 2013

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