Rheb promotes cell growth as a component of the insulin/TOR signalling network

By L. Saucedo, Xinsheng Gao, Dominic A. Chiarelli, Ling Li, Duoija Pan, Bruce Edgar. Nature Cell Biology, 2003

708 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/20d4d1df5e5d1b741a8ac498ba3b9134ccdd0607

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In Immunology

1. David M. Sabatini
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6. P. Pandolfi
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In Molecular Biology

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Citations in the corpus

• mTOR Controls Cell Cycle Progression through Its Cell Growth Effectors S6K1 and 4E-BP1/Eukaryotic Translation Initiation Factor 4E (2004, background): “A novel positive regulator of TOR, the small GTPase Rheb (named for Ras homologue enriched in brain), has recently been shown to function as an integrator of both nutrient and mitogenic signals (14, 43 , 49, 54, 62).”
• mTOR: a pharmacologic target for autophagy regulation. (2015, neutral): “Since GTP-bound Rheb is a potent mTORC1 activator, inhibition of TSC1/2 by AKT-dependent phosphorylation results in mTORC1 activation (25, 26).”
• TSC2 integrates Wnt and energy signals via a coordinated phosphorylation by AMPK and GSK3 to regulate cell growth. (2006, background): “Genetic and biochemical data indicate that Rheb functions downstream of TSC2 and upstream of mTOR (mammalian target of rapamycin (Gao et al., 2002; Saucedo et al., 2003; Stocker et al., 2003).”
• mTOR: from growth signal integration to cancer, diabetes and ageing (2010, background): “This relocalization may enable mTORC1 to interact with the small GTPase Ras homologue enriched in brain (RHEB) (in its GTP-bound state), an essential activator of mTORC1 that is controlled by growth factor input”
• Upstream and downstream of mTOR. (2004, background): “Epistasis analyses in Drosophila suggest that Rheb functions downstream of PI3K/Akt and upstream of TOR and is epistatic over TSC1 and TSC2 (Saucedo et al. 2003; Stocker et al. 2003).”
• Phosphorylation and functional inactivation of TSC2 by Erk implications for tuberous sclerosis and cancer pathogenesis. (2005, positive): “Rheb can act as a protooncogene and, as demonstrated by genetic analysis in Drosophila, is epistatic to dPI3k, dAkt, dTsc1, and dTsc2, while dTOR and dS6k are epistatic to Rheb (Saucedo et al., 2003; Stocker et al., 2003).”
• Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1/TSC2 tumor suppressor complex. (2004, background): “Tsc2 functions as a GTPase-activating protein (GAP) toward the small G protein Rheb, which through a poorly understood mechanism controls mammalian target of rapamycin (mTOR), a central regulator of protein translation (Castro et al. 2003; Garami et al. 2003; Inoki et al. 2003a; Saucedo et al. 2003;”