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One or more keywords matched the following items that are connected to Guertin, David
Item TypeName
Academic Article An expanding role for mTOR in cancer.
Academic Article Ablation in mice of the mTORC components raptor, rictor, or mLST8 reveals that mTORC2 is required for signaling to Akt-FOXO and PKCalpha, but not S6K1.
Academic Article Postprandial hepatic lipid metabolism requires signaling through Akt2 independent of the transcription factors FoxA2, FoxO1, and SREBP1c.
Academic Article Phosphorylation and regulation of Akt/PKB by the rictor-mTOR complex.
Academic Article Defining the role of mTOR in cancer.
Academic Article mTOR complex 2 is required for the development of prostate cancer induced by Pten loss in mice.
Academic Article Targeting mTOR: prospects for mTOR complex 2 inhibitors in cancer therapy.
Academic Article Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity.
Concept Oncogenes
Concept Proto-Oncogene Proteins c-akt
Concept Proto-Oncogene Proteins
Academic Article Rictor/mTORC2 loss in the Myf5 lineage reprograms brown fat metabolism and protects mice against obesity and metabolic disease.
Academic Article Adipose tissue mTORC2 regulates ChREBP-driven de novo lipogenesis and hepatic glucose metabolism.
Academic Article Systemic insulin sensitivity is regulated by GPS2 inhibition of AKT ubiquitination and activation in adipose tissue.
Academic Article Brown Fat AKT2 Is a Cold-Induced Kinase that Stimulates ChREBP-Mediated De Novo Lipogenesis to Optimize Fuel Storage and Thermogenesis.
Academic Article Oncogenic AKTivation by methylation.
Academic Article Brown fat organogenesis and maintenance requires AKT1 and AKT2.
Academic Article mTORC2/Akt activation in adipocytes is required for adipose tissue inflammation in tuberculosis.
Academic Article Proteome and Phosphoproteome Analysis of Brown Adipocytes Reveals That RICTOR Loss Dampens Global Insulin/AKT Signaling.
Academic Article mTORC2-AKT signaling to ATP-citrate lyase drives brown adipogenesis and de novo lipogenesis.
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  • Oncogenes