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IRF6 — MTOR
Text-mined interactions from Literome
Kristof et al., J Biol Chem 2003
(Inflammation) :
The
role of
mTOR and PI3K in the activation of human inducible nitric oxide synthase transcription by cytokines and
lipopolysaccharide (LPS) was investigated in lung epithelial adenocarcinoma ( A549 ) cells
Mandal et al., J Immunol 2007
:
The
mammalian target of rapamycin activity ( measured as phospho-p70S6 kinase ) was
activated by
LPS but not significantly blocked by LY2
Donahue et al., Eur J Immunol 2007
:
We used flow cytometry and magnetic cell sorting to examine the requirement for PI3K and
mTOR in
responses of splenic B cell subsets to BCR and
LPS stimulation ... In contrast,
LPS induced
mTOR signaling is strikingly resistant to wortmannin in both subsets
Lorne et al., Am J Respir Cell Mol Biol 2009
(Acute Lung Injury) :
Rapamycin pretreatment inhibited PAM- or
LPS induced
mTORC1 activation in the lungs
Lang et al., Am J Physiol Endocrinol Metab 2010
(Body Weight...) :
These data support the idea that the
LPS induced reduction in
mTOR activity is relatively more important in regulating skeletal muscle mass in response to nutrient stimulation than under basal conditions
Meng et al., J Cell Physiol 2010
:
To understand the mechanism by which LPS triggers the cell autophagy, we first investigated the
effects of
LPS on the expression of BIRC2 ( cIAP1 ), a well-known apoptosis inhibitor, and on the kinase activity of
mammalian target of rapamycin (mTOR) and nuclear translocation of p53
Lee et al., PloS one 2010
(Endotoxemia) :
Furthermore, in vitro cellular studies demonstrated that
LPS ( lipopolysaccharide )
activation of
mTORC1-S6K still occurs in the presence of PI3K-Akt inhibition alone, but can be suppressed by concurrent inhibition of PI3K-Akt and MEK-ERK pathways
Zhang et al., Mol Med 2012
(Endotoxemia) :
LPS induced the activation of
mTOR in WT peritoneal macrophages, but not in IRF-1 KO macrophages
Zhang et al., Basic Res Cardiol 2012
(Calcium Signaling...) :
Furthermore,
LPS rapidly
increased mTOR phosphorylation in cardiomyocytes, which was blocked by Rac1N17 and an inhibitor of calmodulin dependent protein kinases ( CaMKs ) KN93, but enhanced by ouabain
Jeong et al., Biol Pharm Bull 2013
:
Ginsenoside Rh1 significantly inhibited
LPS/CHX induced Akt phosphorylation, as well as
mammalian target of rapamycin and Bcl-2 associated death promoter activation in both cell types