Gene interactions and pathways from curated databases and text-mining

◀ Back to MTOR


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
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
Wong et al., Curr Opin Pharmacol 2010 (Metabolic Diseases) : SREBP-1c can be induced by mTORC1 , bifurcating lipogenesis from AKT activated gluconeogenesis
Bakan et al., Curr Opin Lipidol 2012 : Recent studies indicate that mTORC1 regulates SREBP-1 activation at multiple levels
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