Insulin activation of Rheb, a mediator of mTOR/S6K/4E-BP signaling, is inhibited by TSC1 and 2.

By A. Garami, F. Zwartkruis, T. Nobukuni, M. Joaquin, M. Roccio, Hugo Stocker, S. Kozma, E. Hafen, J. Bos, G. Thomas. Molecules and Cells, 2003

1,092 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/c2f694a9c2d57a4eff5e8bb1e21c38c8dbaa808d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

In Molecular Biology

In Physiology

Citations in the corpus

Metformin, Independent of AMPK, Inhibits mTORC1 In a Rag GTPase-Dependent Manner (2010, background): “This allows activation of Ras homolog enriched in brain (Rheb), required for mTORC1 activation (Garami et al., 2003; Long et al., 2005), whereas PRAS40 suppression relieves its inhibitory effects on mTORC1 (Haas and Hagedorn, 1992; Sancak et al., 2007).”
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;”
The TSC1-TSC2 complex: a molecular switchboard controlling cell growth. (2008, background): “A large number of studies have demonstrated that Rheb overexpression can override the effects of amino acid starvation on TORC1 inhibition [58,59,61,62,64,70,75,76].”
Regulation and role of autophagy in mammalian cells. (2004, background): “TSC2 has a GTPase-activating activity towards monomeric Rheb which controls mTOR/p70S6 kinase signaling (Garami et al., 2003; Tabancay et al., 2003).”
The TSC1-2 tumor suppressor controls insulin–PI3K signaling via regulation of IRS proteins (2004, background): “An inhibitory target of TSC1-2 action has been identified as Rheb, a small GTPase (Garami et al., 2003; Saucedo et al., 2003; Stocker et al., 2003; Y. Zhang et al., 2003) with Rheb overexpression resulting in activation of S6K (for review see Li et al.”
A nutrient sensor mechanism controls Drosophila growth. (2003, background): “Furthermore, the TSC (tuberous scleMaulbeerstrasse 66 rosis complex) tumor suppressor, consisting of a TSC1 4058 Basel and TSC2 heterodimer (TSC1/2), as well as the small Switzerland GTPase Rheb, were recently shown to participate to the regulation of TOR function both in vitro and in vivo (Gao et a”
Upstream and downstream of mTOR. (2004, background): “Some studies show that the expression of both TSC2 and TSC1 is required for efficient GAP activity (Garami et al. 2003; Tee et al. 2003b; Zhang et al. 2003b), whereas others show that TSC2 alone is sufficient (Castro et al. 2003; Inoki et al. 2003a).”
Nutrient sensing and TOR signaling in yeast and mammals (2017, positive): “…associates with TSC1 and TBC1D7 to form the TSC complex that functions as GAP (GTPase-activating protein) toward lysosomal RHEB (Gao et al , 2002; Kenerson et al , 2002; Kwiatkowski et al , 2002; Onda et al , 2002; Tee et al , 2002; Garami et al , 2003; Inoki et al , 2003a; Dibble et al , 2012).”
p53 target genes sestrin1 and sestrin2 connect genotoxic stress and mTOR signaling. (2008, positive): “Analysis of Rheb GTP/GDP Content Cells were metabolically labeled with 32 P-orthophosphate and immunoprecipitated with anti-Rheb antibody (Santa Cruz, CA), and guanine nucleotides were extracted and resolved by thin-layer chromatography (Garami et al., 2003).”