◀ Back to MTOR
MTOR — SREBF1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Guo et al., Science signaling 2009
(Brain Neoplasms...) :
This response was mediated by Akt ; however, clinical data from rapamycin treated patients showed that
SREBP-1 activation was
independent of the
mammalian target of rapamycin complex 1, possibly explaining rapamycin 's poor efficacy in the treatment of such tumors
Yue et al., BMB Rep 2010
:
Moreover, inhibition of
mTOR activity by rapamycin
resulted in a reduction of
SREBP-1c protein expression and adipogenesis in cells
Wong et al., Curr Opin Pharmacol 2010
(Metabolic Diseases) :
SREBP-1c can be
induced by
mTORC1 , bifurcating lipogenesis from AKT activated gluconeogenesis
Yecies et al., Cell Metab 2011
:
To further define the
role of
mTORC1 in the regulation of
SREBP1c in the liver, we generated mice with liver-specific deletion of TSC1 ( LTsc1KO ), which results in insulin independent activation of mTORC1 ... Therefore,
mTORC1 activation is not
sufficient to stimulate hepatic
SREBP1c in the absence of Akt signaling, revealing the existence of an additional downstream pathway also required for this induction
Li et al., Biochem Biophys Res Commun 2011
(Fatty Liver...) :
Evidence suggests that
mammalian target of rapamycin (mTOR) complex 1 ( mTORC1 )
contributes to the regulation of
SREBP1c expression, but signaling downstream of mTORC1 remains unclear
Bakan et al., Curr Opin Lipidol 2012
:
Recent studies indicate that
mTORC1 regulates
SREBP-1 activation at multiple levels