TSC1-2 tumour suppressor and regulation of mTOR signalling: linking cell growth and proliferation?
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References (67)
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TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling
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The TSC1-2 tumor suppressor controls insulin–PI3K signaling via regulation of IRS proteins
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The LKB1 tumor suppressor negatively regulates mTOR signaling
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Insulin Activation of Rheb, a Mediator of mTOR/S6K/4E-BP Signaling, Is Inhibited by TSC1 and 2
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mTOR inhibition reverses Akt-dependent prostate intraepithelial neoplasia through regulation of apoptotic and HIF-1-dependent pathways
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Akt regulates growth by directly phosphorylating Tsc2
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mTOR Controls Cell Cycle Progression through Its Cell Growth Effectors S6K1 and 4E-BP1/Eukaryotic Translation Initiation Factor 4E
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Inappropriate Activation of the TSC/Rheb/mTOR/S6K Cassette Induces IRS1/2 Depletion, Insulin Resistance, and Cell Survival Deficiencies
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Rheb promotes cell growth as a component of the insulin/TOR signalling network
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Drosophila myc Regulates Cellular Growth during Development
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Rheb fills a GAP between TSC and TOR
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TSC1 and TSC2 tumor suppressors antagonize insulin signaling in cell growth
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DrosophilaRheb GTPase is required for cell cycle progression and cell growth
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Pathological mutations in TSC1 and TSC2 disrupt the interaction between hamartin and tuberin
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Negative Regulation of dE2F1 by Cyclin-Dependent Kinases Controls Cell Cycle Timing
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Tsc2 is not a critical target of Akt during normal Drosophila development
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Regulation of B-Raf Kinase Activity by Tuberin and Rheb Is Mammalian Target of Rapamycin (mTOR)-independent
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Cdc42 Promotes G1 Progression through p70 S6 Kinase-mediated Induction of Cyclin E Expression
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