SIN1/MIP1 maintains rictor-mTOR complex integrity and regulates Akt phosphorylation and substrate specificity.

By E. Jacinto, V. Facchinetti, Dou Liu, Nelyn Soto, Shiniu Wei, S. Jung, Qiaojia Huang, J. Qin, B. Su. Cell, 2006

1,478 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/afb897c173d616655f61a6c2048ae91a9b43f328

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Citations in the corpus

Insulin Resistance: From Mechanisms to Therapeutic Strategies (2021, background): “org lated to gluconeogenesis, such as FOXO, and these activations might be suppressed in a background of insulin resistance, while other Akt substrates, such as GSK3β and tuberous sclerosis complex 2 (TSC2), which requires AKT phosphorylation at Thr308, might not be disrupted [41,42].”
mTOR signaling at a glance (2009, background): “Other studies have subsequently observed that ablation of various mTORC2 components specifically blocks AKT phosphorylation at Ser473 and the downstream phosphorylation of some, but not all, AKT substrates (Guertin et al., 2006; Jacinto et al., 2006 ).”
Energy Metabolism in the Liver (2014, neutral): “Insulin stimulates mTORC2, which phosphorylates Akt at Ser473 and enhances Akt activity (96).”
Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, background): “Increasing data seem to suggest a role for TORC2 in phosphorylating ser 473 on Akt (116).”
The mTOR Signalling Pathway in Human Cancer (2012, background): “In mammalian cells, mTORC2 phosphorylates AKT upon serum stimulation, namely growth factors such as insulin and IGF1 (insulin-like growth factor 1), suggesting that mTORC2 is regulated by the PI3K pathway [35,92].”
CD28− T cells: their role in the age-associated decline of immune function (2009, background): “Phosphorylation of Akt at two different sites (Ser473 and Thr308) is associated with activation [75,76] and a progressive decline in Akt phosphorylation at the Ser473 site was observed as T cells differentiated from CD28+CD27+ to CD28−CD27+ to CD28−CD27− and this could not be reversed by the additio”
PHLPP and a second isoform, PHLPP2, differentially attenuate the amplitude of Akt signaling by regulating distinct Akt isoforms. (2007, background): “In particular, the phosphorylation state of FoxO1 on Ser256 was reported to be the same in normal cells and in SIN1 knockdown cells (where Ser473 phosphorylation is abolished) (Jacinto et al., 2006).”
Proliferation, survival and metabolism: the role of PI3K/AKT/mTOR signalling in pluripotency and cell fate determination (2016, background): “5-11.5 (Jacinto et al., 2006) *Pi3kr1 gene.”
In brief (2011, positive): “For mSIN1, mNIP7, Rpl7, Rps16, PTEN, or Bad knockdown, a pool of four different synthetic siRNA or of the appropriate control siRNA (Dharmacon) was used as described (Thedieck et al., 2007).”
Insulin signalling to mTOR mediated by the Akt/PKB substrate PRAS40 (2007, result): “The Sin1–mTOR interaction has also been identified in recent studies by other group”
TNF‐mediated inflammatory disease (2008, background): “Etk is a novel regulator of epithelial cell junctions and mediates the TNF-induced phosphatidylinositol 3-kinase (PI3K)–Akt angiogenic pathway in vascular endothelial cells through Etkmediated cross-talk with vascular endothelial growth factor receptor 2 (VEGFR2) [37].”
mTOR Signaling in Growth, Metabolism, and Disease (2017, background): “, 2009), aswell as the regulatory subunitsmSin1 (Frias et al., 2006; Jacinto et al., 2006; Yang et al., 2006) and Protor1/2 (Pearce et al.”