Insulin signalling to mTOR mediated by the Akt/PKB substrate PRAS40

By E. V. Haar, Seong-il Lee, S. Bandhakavi, T. Griffin, Do-Hyung Kim. Nature Cell Biology, 2007

1,262 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/bf5982e8acd79ce09a758311f2d4e98ae8d4094e

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Citations in the corpus

Autophagy Induction and Autophagosome Clearance in Neurons: Relationship to Autophagic Pathology in Alzheimer's Disease (2008, background): “…of the mTOR kinase pathway: rapamycin, a direct inhibitor of the mTOR complex (Blommaart et al., 1995; Sabers et al., 1995), and nutrient deprivation, which inactivates the PI3K (phosphoinositide 3-kinase)–AKT pathway leading to mTOR suppression (Barber et al., 2001; Vander Haar et al., 2007).”
Antitumor Activity of Rapamycin in a Phase I Trial for Patients with Recurrent PTEN-Deficient Glioblastoma (2008, background): “PRAS40 has also been recently shown to inhibit mTOR, and this inhibition is relieved by Akt phosphorylation [29–31].”
Regulation of the mTOR complex 1 pathway by nutrients, growth factors, and stress (2010, background): “…of mTORC1 phosphorylates both PRAS40 and Deptor, which weakens their association with the remainder of mTORC1 and promotes the kinase activity of the complex (Oshiro et al., 2007; Peterson et al., 2009; Sancak et al., 2007; Thedieck et al., 2007; Vander Haar et al., 2007; Wang et al., 2008).”
Regulation of mTORC1 and its impact on gene expression at a glance (2013, background): “…by two means: (1) reducing the interaction of proline-rich AKT substrate 40 kDa (PRAS40) with mTORC1 (Sancak et al., 2007; Thedieck et al., 2007; Vander Haar et al., 2007; Wang et al., 2007), and (2) phosphorylating and inactivating the tuberous sclerosis complex (TSC), a protein complex…”
Trends in insulin resistance: insights into mechanisms and therapeutic strategy (2022, background): “Further, PRAS40 and mTOR also exerts negative feedbacks on proximal insulin signaling, PRAS40 knockdown significantly decreases Akt phosphorylation, mTORC1 binds and inhibits INSR by inducing destabilization of IRS1.(28) The signaling system of IR are multifactorial including different metabolic pat”
PRAS40 is an insulin-regulated inhibitor of the mTORC1 protein kinase. (2007, background): “A recent parallel study also identifies PRAS40 as an mTORC1-interacting protein (Haar et al., 2007) and r Inc. focuses on its role in modulating the feedback loop between mTORC1 and the IRS/PI3K pathway.”
ULK-Atg13-FIP200 complexes mediate mTOR signaling to the autophagy machinery. (2009, methodology): “Lentiviral shRNA transduction was performed as described previously (Vander Haar et al., 2007).”
mTOR Signaling in Growth, Metabolism, and Disease (2017, background): “In addition to these three core components, mTORC1 also contains the two inhibitory subunits PRAS40 (proline-rich Akt substrate of 40 kDa) (Sancak et al., 2007; Vander Haar et al., 2007; Wang et al., 2007) and DEPTOR (DEP domain containing mTOR interacting protein) (Peterson et al., 2009).”
mTOR signaling at a glance (2009, background): “Additionally, AKT activation by growth factors can activate mTORC1 in a TSC1/2-independent manner by promoting the phosphorylation and dissociation of PRAS40 from mTORC1 (Sancak et al., 2007; Vander Haar et al., 2007; Wang et al., 2007).”
mTOR signaling in growth control and disease (2012, positive): “…(raptor) (Hara et al., 2002; Kim et al., 2002) and proline-rich Akt substrate 40 kDa (PRAS40) (Sancak et al., 2007; Thedieck et al., 2007; Vander Haar et al., 2007; Wang et al., 2007) are specific to mTORC1, whereas rapamycin-insensitive companion of mTOR (rictor) (Jacinto et al., 2004;…”