Tsc tumour suppressor proteins antagonize amino-acid–TOR signalling

By Xinsheng Gao, Yong Zhang, Peter Arrazola, O. Hino, Toshiyuki Kobayashi, R. Yeung, B. Ru, Duojia Pan. Nature Cell Biology, 2002

709 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/63ec755f97ab611bdf07af0e655859b15b2ae68b

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Citations in the corpus

The AMP-activated protein kinase pathway – new players upstream and downstream (2004, background): “Studies in Drosophila suggest that the TSC1-TSC2 complex negatively regulates cell growth, and acts upstream of TOR to cause its inhibition (Gao et al., 2002).”
Upstream and downstream of mTOR. (2004, background): “For instance, overexpression of TSC1 and TSC2 blocks amino acid-induced activation of mTOR (Tee et al. 2002), and deletion of TSC2 renders mTOR resistant to amino acid deprivation (Gao et al. 2002).”
Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1/TSC2 tumor suppressor complex. (2004, background): “Whereas mTOR regulation by growth factors and energy stores requires an intact Tsc1/Tsc2 complex, amino acids seem to regulate mTOR function through both Tsc1/Tsc2-dependent and independent pathways (Gao et al. 2002; H. Zhang et al. 2003).”
Insulin signalling to mTOR mediated by the Akt/PKB substrate PRAS40 (2007, background): “Hyperactivation of mTOR caused by abrogation of its negative regulators (such as phosphatase and tension homolog (PTEN) and TSC2) has been identified in a number of human cancers, including prostate cancers, multiple myeloma and several hamartoma syndromes (including TSC, Cowden's disease and Peutz-”
Rheb GTPase is a direct target of TSC2 GAP activity and regulates mTOR signaling. (2003, background): “Phosphorylation of S6K and 4EBP1 enhances translation (Gingras et al. 1999).”
PRAS40 is an insulin-regulated inhibitor of the mTORC1 protein kinase. (2007, result): “…other hand, the sequential knockdown of dRheb and then dTSC2 completely blocked the increase in cell size caused by the knockdown of dTSC2 alone, in accord with the established placement of dRheb downstream of dTSC2 (Gao et al., 2002; Saucedo et al., 2003; Stocker et al., 2003; Zhang et al., 2003).”
TSC2 mediates cellular energy response to control cell growth and survival. (2003, neutral): “The above tions that nutrient depletion-induced S6K dephosphorylation is compromised in TSC2 / cells (Gao et al., 2002).”
Metformin, Independent of AMPK, Inhibits mTORC1 In a Rag GTPase-Dependent Manner (2010, background): “As previously reported (Gao et al., 2002; Radimerski et al., 2002), depletion of either protein enhanced dS6K activity but did not alter inhibition by oligomycin (Figure 1C).”
Nutrient sensing and TOR signaling in yeast and mammals (2017, positive): “We note that yeast contains a protein, termed Rhb1 (Urano et al , 2000), that resembles RHEB, but is not a functional RHEB homolog. mTORC1 inactivation is an active process that requires translocation of TSC2 to the lysosome to inhibit RHEB upon growth factor deprivation (Menon et al , 2014; Fawal e”
Regulation of immune responses by L-arginine metabolism (2005, background): “Nitrogen sources (such as urea), amino-acid limitation and rapamycin suppress MTOR activity, which is essential for directing translation initiation in mammalian cells, through ribosomal protein S6 kinas”