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CRK — PI3

Text-mined interactions from Literome

Chun et al., Biochem Biophys Res Commun 2000 : In addition, expression of a constitutively active form of PI3-kinase ( p110* ) enhanced myotube formation and p38 MAPK activation, while expression of a dominant negative form of PI3-kinase ( Deltap85 ) attenuated these responses
Canesi et al., Dev Comp Immunol 2002 : Interestingly, the PI3-kinase ( phosphatidylinositol-3-OH-kinase ) inhibitor, Wortmannin, reduced both p38 activation and bacterial killing, indicating a critical role also for this lipid kinase in the hemocyte immune response
Lee et al., Circulation 2004 : Simvastatin activated p38 and Akt in VSMCs, and the respective inhibitors of p38 and phosphoinositide 3-kinase (PI3K) greatly reduced the level of simvastatin induced HO-1, which suggests the involvement of p38 and the PI3K-Akt pathway in HO-1 induction
Tassi et al., Immunity 2007 : p110gamma played a major role in receptor induced interferon-gamma (IFN-gamma) production through a pathway that involved the kinase ERK and 5-Lipoxigenase, which most likely generates lipid mediators activating GPRCs. Conversely, PI3Ks negatively regulated interleukin-12 (IL-12) and IL-18 induced IFN-gamma by modulating p38 kinase activation
Blank et al., Exp Cell Res 2013 : We also showed that PKCd and p38 activation stimulated by the peptide was inhibited by a specific pharmacological inhibitor of phosphatidylinositol 3-kinase (PI3K) or by a dominant negative p85 PI3K-regulatory subunit, suggesting that PI3K is upstream in the signaling cascade