Ribosomal protein S6 phosphorylation: from protein synthesis to cell size.
By Igor Ruvinsky, O. Meyuhas. TIBS -Trends in Biochemical Sciences. Regular ed, 2006
814 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/022d38e67a203fc36a91c92fa4aa63c5d50321e0
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In Molecular Biology
Citations in the corpus
- mTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype (2015, neutral): “Whereas S6K1/2 phosphorylation controls translation initiation and elongation 18 , phosphorylation of 4EBPs promotes cap-dependent translation by preventing 4EBP binding to EIF4E (ref.”
- The Ras-ERK and PI3K-mTOR Pathways: Cross-talk and Compensation (2011, background): “These phosphorylations positively regulate rpS6 binding to the 7-methylguanosine cap complex, subsequent cap-dependent translation, and cell size [85, 86].”
- Translational control of long-lasting synaptic plasticity and memory. (2009, neutral): “…documented (Sabatini, 2006; Sancak et al., 2007; Vander Haar et al., 2007) (Table 1). mTORC1 specifically regulates the translation of a subset of mRNAs that contain extensive secondary structure at their 5 0 UTR or an oligopyrimidine tract in their 5 0 end (TOP mRNAs) (Ruvinsky and Meyuhas, 2006).”
- The Molecular Bases of Training Adaptation (2007, background): “The most well-defined effectors of the PI3K-AKT-mTOR signalling pathway are the proteins implicated in translational control: ribosomal protein S6 kinase (S6K), eukaryotic initiation factor 4E-binding protein (4E-BP1) and eukaryotic initiation factor 2B (eIF2B; Bolster et al. 2003a; Ruvinsky and Mey”
- Ecdysone Control of Developmental Transitions: Lessons from Drosophila Research (2012, background): “Because the MAPK and TOR pathways share some common targets (105, 113), it would be interesting to examine in D.”
- Spatially restricting gene expression by local translation at synapses (2010, neutral): “Note, however, that studies of a knock-in mouse with all S6 phosphorylation sites mutated revealed that S6 phosphorylation is dispensable for 5’TOP-dependent translation [51].”
- Inflammatory T cell responses rely on amino acid transporter ASCT2 facilitation of glutamine uptake and mTORC1 kinase activation (2014, neutral): “Stimulation of T cells with anti-CD3 and anti-CD28 triggered the phosphorylation of ribosomal protein S6 (Figure 6A), a well-defined effector molecule of the mTORC1 signaling pathway (Ruvinsky and Meyuhas, 2006).”