Rheb is a direct target of the tuberous sclerosis tumour suppressor proteins

By Yong Zhang, Xinsheng Gao, L. Saucedo, B. Ru, Bruce Edgar, Duojia Pan. Nature Cell Biology, 2003

974 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/5963448a3f686021cfe151d2e319f491a53b4306

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In Immunology

1. David M. Sabatini
2. L. Bar-Peled
3. B. Manning
4. N. Hay
5. Arnold J. Levine
6. P. Pandolfi
7. Arkaitz Carracedo
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In Molecular Biology

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In Physiology

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6. J. Blenis
7. P. Pandolfi
8. K. Inoki

Citations in the corpus

• Phosphorylation and functional inactivation of TSC2 by Erk implications for tuberous sclerosis and cancer pathogenesis. (2005, positive): “GTP bound Rheb is elevated in TSC2 null cells and is reduced by TSC1TSC2 add-back (Garami et al., 2003; Inoki et al., 2003a; Tee et al., 2003; Zhang et al., 2003b).”
• Target of rapamycin (TOR): an integrator of nutrient and growth factor signals and coordinator of cell growth and cell cycle progression (2004, background): “…toward Rheb: TSC2 catalyses the conversion of Rheb-GTP into Rheb-GDP in vitro (Tee et al., 2003a; Zhang et al., 2003), and expression of TSC2 or the TSC1/2 complex in vivo increases the ratio of GDP:GTP-bound Rheb (Castro et al., 2003; Garami et al., 2003; Inoki et al., 2003a; Zhang et al., 2003).”
• The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “…and inactivates the GTPase-activating protein (GAP) TSC2 (Dan et al., 2002; Inoki et al., 2002; Potter et al., 2002), which forms a complex with TSC1 to inhibit a small GTPase, Rheb (Ras-homolog enriched in brain) (Garami et al., 2003; Inoki et al., 2003; Tee et al., 2003; Zhang et al., 2003b).”
• The TSC1-2 tumor suppressor controls insulin–PI3K signaling via regulation of IRS proteins (2004, background): “Although the full range of consequences of activation of the mTOR/S6K pathway remain to be determined, it appears that a reduced responsiveness to growth factors may not be restricted to insulin signaling (H. Zhang et al., 2003).”
• 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).”
• Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1/TSC2 tumor suppressor complex. (2004, background): “1A) (Jaeschke et al. 2002; H. Zhang et al. 2003).”