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FAS — PI3

Text-mined interactions from Literome

Chang et al., J Lipid Res 2005 : Induction of SREBP-1, SCD-1, and FAS by KGF was inhibited by the JNK inhibitor SP600125 and the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 but not by the ERK inhibitor PD98059
Letellier et al., Immunity 2010 (Inflammation...) : CD95L stimulation of CD95 on these cells activated phosphoinositide 3-kinase (PI3K) and metalloproteinase-9 ( MMP-9 ) via recruitment and activation of Syk kinase, ultimately leading to increased migration
Gulbins et al., Pflugers Arch 1998 (Glioma) : Here, we demonstrate that CD95 ligation induces a rapid and transient tyrosine phosphorylation and activation of phosphoinositide-3-kinase (PI-3-K) in Jurkat T lymphocytes or CD95-sensitive glioma cells ... Experiments using p56lck-deficient or p56lck reconstituted Jurkat clones and the tyrosine kinase inhibitor herbimycin A revealed that tyrosine phosphorylation and activation of PI-3-K by CD95 depends on expression of Src-like tyrosine kinases, in particular p56lck
Gulbins et al., J Leukoc Biol 1998 : We demonstrate a rapid and transient activation of phosphoinositide-3-kinase (PI-3-K) by Fas receptor triggering or cellular treatment with synthetic C6-ceramide ... The stimulation of PI-3-K is critical for Fas or C6-ceramide induced programmed cell death because transfection with a transdominant inhibitory PI-3-K construct or pre-treatment with the PI-3-K inhibitor wortmannin almost completely prevented Fas or C6-ceramide mediated apoptosis ... Treatment with the caspase inhibitor Ac-YVAD-cmk or cellular transfection with transdominant inhibitory N17Ras prevented PI-3-K stimulation by Fas , suggesting that Fas activates PI-3-K via caspases and Ras