Tumor-promoting phorbol esters and activated Ras inactivate the tuberous sclerosis tumor suppressor complex via p90 ribosomal S6 kinase.

By Philippe P Roux, Bryan A. Ballif, R. Anjum, Steven P. Gygi, J. Blenis. Proceedings of the National Academy of Sciences of the United States of America, 2004

797 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/ce311d8fe3507707c8c193ce3e4ba49c176a0d65

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Global, in vivo, and site-specific phosphorylation dynamics in signaling networks. (2006, background): “The dynamic phosphoproteome provides a missing link in a global, integrative view of cellular regulation.”
mTOR signaling at a glance (2009, background): “, 2005), and by p90 ribosomal S6 kinase 1 (RSK1) (Roux et al., 2004), and leads”
Phosphorylation and functional inactivation of TSC2 by Erk implications for tuberous sclerosis and cancer pathogenesis. (2005, positive): “On the other hand, although constitutively active RSK1 (myrRSK1) could enhance TSC2 phosphorylation, expression of myrRSK1 alone failed to activate S6K (Roux et al., 2004).”
Ras, PI(3)K and mTOR signalling controls tumour cell growth (2006, background): “and is also a substrate of the downstream ribosomal protein S6 kinase (RSK; Ser 1798”
TSC2 integrates Wnt and energy signals via a coordinated phosphorylation by AMPK and GSK3 to regulate cell growth. (2006, background): “Both TSC1 and TSC2 are phosphorylated by multiple kinases, including Akt, RSK1, ERK, CDC2, MK2, and AMPK (Astrinidis et al., 2003; Fingar and Blenis, 2004; Inoki et al., 2003; Ma et al., 2005; Roux et al., 2004).”
mTOR Signaling in Growth, Metabolism, and Disease (2017, background): “A reduction in cellular energy charge, such as during glucose deprivation, activates the stress responsive metabolic regulator AMPK, which inhibits mTORC1 both indirectly, through phosphorylation and activation of TSC2, as well as directly, through the phosphorylation of Raptor (Gwinn et al., 2008; ”
Defining the role of mTOR in cancer. (2007, background): “One study using siRNA to deplete cells of TSC2 or overexpressing recombinant RHEB finds that in each case, simultaneously overexpressing recombinant PRAS40 suppresses mTORC1 activation (Haar et al., 2007).”
The Ras-ERK and PI3K-mTOR Pathways: Cross-talk and Compensation (2011, background): “Among many other substrates involved in these functions, GSK3 also phosphorylates TSC2, thereby activating TSC2 and inactivating mTORC1 [6].”
The RSK family of kinases: emerging roles in cellular signalling (2008, positive): “Evidence that links RSK to translational control came from studies in our laboratory, as the tumour-suppressor protein tuberous sclerosis complex-2 ( TSC2 ) was regulated by RSK-mediated phosphorylatio”
TOR signaling in growth and metabolism. (2006, background): “The MAPK-activated kinase RSK1 also phosphorylates TSC2 at a unique site (Roux et al., 2004).”
SIN1/MIP1 maintains rictor-mTOR complex integrity and regulates Akt phosphorylation and substrate specificity. (2006, background): “This defect was attributed to a negative feedback regulation of the insulin receptor substrates, IRS, by S6K, whose phosphorylation was augmented in TSC2-deficient cells due to the enhanced TORC1 activity (Harrington et al., 2004; Roux et al., 2004; Shah et al., 2004).”