S6K1−/−/S6K2−/− Mice Exhibit Perinatal Lethality and Rapamycin-Sensitive 5′-Terminal Oligopyrimidine mRNA Translation and Reveal a Mitogen-Activated Protein Kinase-Dependent S6 Kinase Pathway

By M. Pende, S. Um, Virginie Mieulet, Melanie Sticker, V. Goss, J. Mestan, Matthias Mueller, S. Fumagalli, S. Kozma, G. Thomas. Molecular and Cellular Biology, 2004

796 citations recorded by the source corpus.

Subfields: Molecular Biology, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/7da40d672a68ba184f558c81df0111ac97b8f597

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In Molecular Biology

In Radiology, Nuclear Medicine and Imaging

Nahum Sonenberg

Citations in the corpus

Growing roles for the mTOR pathway. (2005, background): “It was thought to act by controlling the translation of an abundant class of mRNAs containing a 50TOP sequence, but more recent work does not support this conclusion [22,31].”
Molecular mechanisms of mTOR-mediated translational control (2009, background): “Consistently, RPS6 phosphorylation levels are nearly normal in S6K1-deficient mic”
Upstream and downstream of mTOR. (2004, background): “Moreover, Pende et al. (2004) recently generated embryonic stem cells and MEF cells lacking S6K1 and S6K2 and showed that serum enhances the recruitment of the 5!”
mTOR and S6K1 mediate assembly of the translation preinitiation complex through dynamic protein interchange and ordered phosphorylation events. (2005, positive): “It now appears that S6K1, but not S6K2 and S6 phosphorylation, is linked to cellular growth control (Pende et al., 2004).”
Antitumor Activity of Rapamycin in a Phase I Trial for Patients with Recurrent PTEN-Deficient Glioblastoma (2008, background): “In comparing the two antibodies, changes in pSer235/236 were statistically more significantly linked to Ki67 response, even though this site is believed to be less specific for S6K1 activity than pSer240/244 due to phosphorylation by other kinases [20].”
mTOR, translation initiation and cancer (2006, background): “A role for the S6 kinases in controlling the cell size has been suggested as their deletion results in smaller animals (Pende et al., 2004).”
The nuts and bolts of AGC protein kinases (2010, neutral): “Moreover, RSK phosphorylates ribosomal protein S6 (Ref”
How cells coordinate growth and division. (2004, background): “The mechanisms that control ribosome production in response to growth factors are highly complex and need much further exploration [187].”
The RSK family of kinases: emerging roles in cellular signalling (2008, background): “Studies from S6k1/S6k2 -knockout mice with phosphosite-specific antibodies showed that there was minimal phosphorylation of rpS6 at Ser240/244, but there was persistent phosphorylation at Ser235/236 (Ref”
Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1/TSC2 tumor suppressor complex. (2004, background): “While the importance of S6K in the phosphorylation of S6 is well documented (Pende et al. 2004), Tsc1/Tsc2 might conceivably also regulate S6 phosphorylation in an mTORindependent/S6K-independent manner.”
Ingested protein dose response of muscle and albumin protein synthesis after resistance exercise in young men. (2009, background): “phosphorylation, because this site is phosphorylated by S6K1 and is responsive to feeding after resistance exercise (16, 30).”
Nutrient overload, insulin resistance, and ribosomal protein S6 kinase 1, S6K1. (2006, background): “phosphorylation, as the major S6 kinase appears to be S6K2 in all tissues examined to date ( Pende et al., 2004 ), including pancreas (M. Pende, S.H.U., and S.C.”
Regulation of cardiac hypertrophy by intracellular signalling pathways (2006, background): “Indeed, further analysis of S6 phosphorylation and cellular growth effects in S6k1 -and S6k2 -null mice indicated a potential disconnection in the proposed mechanism whereby S6Ks directly regulate growth through translational control involving S6 (Ref”