Gene interactions and pathways from curated databases and text-mining

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Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Briaud et al., J Biol Chem 2005 (Diabetes Mellitus, Type 2) : Moreover, adenoviral mediated expression of constitutively active mTOR ( mTORDelta ) further increased glucose/IGF-1 induced Ser/Thr phosphorylation of IRS-2 and decreased IRS-2 protein levels, whereas adenoviral mediated expression of `` kinase-dead '' mTOR ( mTOR-KD ) conversely reduced Ser/Thr phosphorylation of IRS-2 and maintained IRS-2 protein levels ... In adenoviral infected beta-cells expressing mTORDelta, the decrease in IRS-2 protein levels was also prevented by rapamycin or lactacystin, further indicating a proteasomal mediated degradation of IRS-2 mediated via mTOR induced Ser/Thr phosphorylation of IRS-2 ... Thus, chronic activation of mTOR by glucose ( and/or IGF-1 ) in beta-cells leads to increased Ser/Thr phosphorylation of IRS-2 that targets it for proteasomal degradation, resulting in decreased IRS-2 expression and increased beta-cell apoptosis
Ma et al., Mol Cell Biol 2006 (Breast Neoplasms...) : In support of this mechanism, reduction of Irs-2 expression in Irs1 ( -/- ) tumor cells restored mTor signaling to wild-type levels
Huypens et al., Med Hypotheses 2007 (Overweight) : However, sustained activation leads to negative feedback via the mTOR induced proteasomal degradation of IRS-2 ... Considering that AMPK prevents mTOR induced degradation of IRS-2 , we propose that adiponectin and leptin cooperatively achieve compensatory beta cell growth in accordance to adiposity
Pankratz et al., J Biol Chem 2009 (Breast Neoplasms...) : Irs-2 was shown to be important for mammalian target of rapamycin (mTor) activation, and Irs-2 dependent regulation of Glut1 surface expression is rapamycin-sensitive