mTOR complex 2 (mTORC2) controls hydrophobic motif phosphorylation and activation of serum- and glucocorticoid-induced protein kinase 1 (SGK1).

By J. M. García-Martínez, D. Alessi. Biochemical Journal, 2008

933 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/2c315d851abe172152bed106b0574036f678dbf6

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Citations in the corpus

Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity (2012, neutral): “Phosphorylation of mTORC2 substrates, including the protein kinases PKCa S657 andAkt S473, as well as the serum glucocorticoid– induced protein kinase (SGK) substrate (N-Myc downstream regulated 1) NDRG1 T346 (Fig.”
mTOR Signaling in Growth, Metabolism, and Disease. (2017, background): “Finally, mTORC2 also phosphorylates and activates SGK1, another AGC-kinase that regulates ion transport as well as cell survival (Garcia-Martinez and Alessi, 2008).”
Target of Rapamycin (TOR) in Nutrient Signaling and Growth Control (2011, background): “TORC2 phosphorylates and activates Gad8 and SGK1, the S. pombe and mammalian orthologs of Ypk, respectively, in a similar manner (Matsuo et al. 2003; Garcia-Martinez and Alessi 2008).”
The nuts and bolts of AGC protein kinases (2010, background): “3b ), whereas SGK1 is phosphorylated at its hydrophobic motif (on Ser422) by mTORC2 (Ref”
mTOR signaling in growth control and disease (2012, background): “mTORC2 also directly activates SGK1, a kinase controlling ion transport and growth (Garcı́a-Martı́nez and Alessi, 2008).”
In brief (2011, neutral): “Growth factors activate mTORC2 via PI3K (Frias et al., 2006; Garcı́a-Martı́nez and Alessi, 2008; Yang et al., 2006), but signaling steps beyond PI3K are distinct from those upstream of mTORC1 and unknown (Cybulski and Hall, 2009; Sparks and Guertin, 2010).”
Regulation of Immune Responses by mTOR (2011, background): “SGK1 is similar to Akt and S6K1 in that it is an AGC (cAMP-dependent, cGMPdependent, and protein kinase C) kinase (44).”
mTOR: from growth signal integration to cancer, diabetes and ageing (2010, background): “mTORC2 phosphorylates and activates Akt, serum- and glucocorticoid-regulated kinase (SGK), and protein kinase C (PKC), which regulate cell survival, cell cycle progression and anabolism”
Active-Site Inhibitors of mTOR Target Rapamycin-Resistant Outputs of mTORC1 and mTORC2 (2009, background): “SGK [7] although other kinases, including DNA-PK and Ilk, have also been implicated in Akt hydrophobic motif”
DEPTOR is an mTOR Inhibitor Whose Frequent Overexpression in Multiple Myeloma Cells Promotes their Survival (2009, background): “Because it is still controversial whether SGK1 is an mTORC2 and/or mTORC1 substrate (Garcia-Martinez and Alessi, 2008; Hong et al., 2008), we determined whether DEPTOR-deficient cells could be resensitized to proapoptotic stimuli by inhibiting mTORC1 with rapamycin or by inhibiting both mTORC1 and…”
mTOR Signaling in Growth, Metabolism, and Disease (2017, background): “Finally, mTORC2 also phosphorylates andactivatesSGK1, another AGC-kinase that regulates ion transport as well as cell survival (Garcı́a-Martı́nez and Alessi, 2008).”
mTORC1 controls mitochondrial activity and biogenesis through 4E-BP-dependent translational regulation. (2013, background): “, 2012) by activating AGC kinases including serum- and glucocorticoid-regulated kinase (SGK) and AKT (Garcı́a-Martı́nez and Alessi, 2008; Ikenoue et al., 2008; Sarbassov et al., 2005).”