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MTOR — TESC

Text-mined interactions from Literome

El-Hashemite et al., Cancer Res 2003 : Tuberous sclerosis complex (TSC) gene products negatively regulate mammalian target of rapamycin (mTOR) activity
Tee et al., Semin Cell Dev Biol 2005 (Disease...) : Recent studies reveal that the tuberous sclerosis complex (TSC)-1/2 , PTEN, and LKB1 tumor suppressor proteins tightly control mTOR
Sofer et al., Mol Cell Biol 2005 : We have recently identified the stress response REDD1 gene as a mediator of tuberous sclerosis complex (TSC) dependent mTOR regulation by hypoxia
Arvisais et al., J Biol Chem 2006 : Treatment with PGF2alpha did not increase AKT phosphorylation but increased the phosphorylation of Erk and the tumor suppressor protein tuberous sclerosis complex 2 (TSC2) , an upstream regulator of mTOR
Marshall et al., Science signaling 2009 : Tuberous sclerosis complex 2 (TSC2) , whose gene is frequently mutated in tuberous sclerosis, increases the guanosine triphosphatase ( GTPase ) activity of the small heterotrimeric GTP binding protein (G protein) Rheb, thus resulting in the decreased activity of the mammalian target of rapamycin (mTOR) , the master regulator of cell growth
Acosta-Jaquez et al., Mol Cell Biol 2009 : Here we focus on mTORC1 and show that TSC/Rheb signaling promotes mTOR S1261 phosphorylation in an amino acid dependent, rapamycin-insensitive, and autophosphorylation independent manner
Haidinger et al., Transpl Int 2010 (Lymphangioleiomyomatosis...) : Tuberous sclerosis complex (TSC) is caused by constitutively activated mammalian target of rapamycin (mTOR) resulting in nonmalignant tumours of several organs and consequently renal failure
Peces et al., Nephrol Dial Transplant 2010 (Angiomyolipoma...) : Tuberous sclerosis complex (TSC) is caused by constitutively activated mammalian target of rapamycin (mTOR) resulting in non-malignant tumours of several organs including renal angiomyolipomas ( AMLs )
Hsu et al., Science 2011 : The adaptor protein Grb10 was identified as an mTORC1 substrate that mediates the inhibition of phosphoinositide 3-kinase typical of cells lacking tuberous sclerosis complex 2 (TSC2) , a tumor suppressor and negative regulator of mTORC1
Jung et al., Autophagy 2011 : The stimulatory effect of ULK1 knockdown on mTORC1 signaling occurred even in the absence of tuberous sclerosis complex 2 (TSC2) , the negative regulator of mTORC1 signaling