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MTOR — STAT3
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Yokogami et al., Curr Biol 2000
(MAP Kinase Signaling System) :
Serine phosphorylation and maximal activation of
STAT3 during CNTF signaling is
mediated by the rapamycin target
mTOR
Kusaba et al., J Biol Chem 2005
:
In accordance with this, reduction in the
mTOR protein level by small interfering RNA
resulted in suppression of
Stat3 phosphorylation and decreased production of IFN-gamma after IL-12 stimulation
Riemenschneider et al., Cancer Res 2006
(Glioblastoma) :
mTOR activation
results in subsequent activation of S6K and
STAT3 , as well as suppression ( i.e., phosphorylation ) of 4E-BP1, leading to cell cycle progression and inhibition of apoptosis
Kim et al., J Biol Chem 2008
(Carcinoma, Hepatocellular...) :
Interestingly, we find that the phosphorylation of STAT3 on Ser ( 727 ) and STAT3 transcriptional activity are regulated by
mTOR upon IL-6 stimulation and that
STAT3 is
required for IL-6 inhibition of insulin signaling
Kim et al., J Biol Chem 2009
(Diabetes Mellitus, Type 2...) :
Our results also indicated that
mammalian target of rapamycin was likely
responsible for the phosphorylation of
STAT3 at Ser ( 727 ) in response to excess amino acids
Magri et al., Cell stem cell 2011
(Epilepsy...) :
Notably,
mTORC1 dependent Akt inhibition and
STAT3 activation were involved in the reduced self-renewal and earlier neuronal and astroglial differentiation of mutant NSCs
Yang et al., J Biol Chem 2013
(Neoplasms...) :
The interaction of Gadd45a with
mTOR suppresses
STAT3 phosphorylation at Ser-727 and leads to down-regulated expression of VEGFa