Nutrient overload, insulin resistance, and ribosomal protein S6 kinase 1, S6K1.

By S. Um, D. D’Alessio, G. Thomas. Cell Metabolism, 2006

721 citations recorded by the source corpus.

Subfields: Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/fe5a47b29f05c38e6e41875cf2ed6e1b75ec68b8

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In Molecular Biology

1. David M. Sabatini
2. K. Copps
3. J. Blenis
4. X. Ma
5. M. Wymann
6. R. Schneiter
7. Bruce E. Kemp
8. G. Thomas

In Surgery

1. K. Copps
2. M. Wymann
3. R. Schneiter
4. Bruce E. Kemp
5. J. Blenis
6. B. Viollet
7. D. Hardie
8. Jongsoon Lee

Citations in the corpus

• Regulation of insulin sensitivity by serine/threonine phosphorylation of insulin receptor substrate proteins IRS1 and IRS2 (2012, background): “Increased plasma BCAA levels in obese, insulin-resistant persons have long been regarded as part of an insulin-resistant metabolic ‘signature’ [110, 111], but supplementation of rodent diets with mixed BCAA or leucine has not clarified that this is diabetogenic [111, 112].”
• Lipid signalling in disease (2008, background): “Control over insulin signalling is achieved by an autoregulatory feedback loop whereby the S6 kinase-1 (S6K1), a downstream effector of mTOR, inhibits upstream elements (a process known as homologous desensitizatio”
• Metformin, Independent of AMPK, Inhibits mTORC1 In a Rag GTPase-Dependent Manner (2010, background): “S6K1 have been implicated in suppressing insulin signaling by the phosphorylation of IRS1 (Um et al., 2006).”
• Translational regulation of gene expression during conditions of cell stress. (2010, background): “Similarly, under fed conditions, S6K phosphorylates several proteins that control overall translation rates, including components of the small ribosomal subunit rpS6, eukaryotic elongation factor 2 kinase (eEF2K; thus inactivating this kinase, which negatively regulates eIF2), and eIF4B (which activ”
• Branched-chain amino acids in health and disease: metabolism, alterations in blood plasma, and as supplements (2018, background): “However, several researchers have suggested that excessive intake of amino acids could lead to inhibition of insulin signaling [22, 23].”
• A Branched-Chain Amino Acid-Related Metabolic Signature that Differentiates Obese and Lean Humans and Contributes to Insulin Resistance (2009, background): “It has been known for some time that obesity is accompanied by an increase in circulating levels of multiple amino acids, including BCAA (Felig et al., 1974; Chevalier et al., 2005; Um et al., 2006; Tremblay et al., 2007b; Krebs et al., 2007).”
• Mechanisms of Life Span Extension by Rapamycin in the Fruit Fly Drosophila melanogaster (2010, background): “Thus, under favorable conditions, such as an amino acid-rich diet, when TORC1 is active, phosphorylated S6K functions as a positive mediator of the TOR pathway by promoting C cellular and organismal growth, and additionally by altering metabolism (Montagne et al., 1999; Um et al., 2006).”
• The mTOR Signalling Pathway in Human Cancer (2012, background): “produces the second messenger PtdIns(3,4,5)P3 [40].”
• Time restricted feeding without reducing caloric intake prevents metabolic diseases in mice fed a high fat diet (2012, positive): “Hepatic CREB phosphorylation is elevated during fasting, consistent with the role of active pCREB in gluconeogenesis (Herzig et al., 2001), while insulin and mTOR-stimulated pS6 levels (Um et al., 2006) are elevated during feeding.”
• Molecular mechanisms of mTOR-mediated translational control (2009, background): “It is becoming increasingly appreciated that this negative-feedback loop has an important role in insulin-resistant diabetes and in cance”