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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