PRAS40 is an insulin-regulated inhibitor of the mTORC1 protein kinase.

By Y. Sancak, C. Thoreen, Timothy R. Peterson, Robert A Lindquist, S. A. Kang, E. Spooner, Steven A. Carr, David M. Sabatini. Molecules and Cells, 2007

1,314 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/02893afc14b6eb5619270f6cd32b550f25fbfc00

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In Molecular Biology

1. David M. Sabatini
2. M. Laplante
3. K. Guan
4. R. A. Saxton
5. R. Shaw
6. B. Manning
7. L. Bar-Peled
8. Michael N. Hall

Citations in the corpus

• The 14-3-3 proteins: integrators of diverse signaling cues that impact cell fate and cancer development (2008, background): “With regard to PRAS40, 14-3-3 binding is mediated by pT246, a site phosphorylated by AKT [25,26].”
• 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, Metabolism, and Disease. (2017, background): “TSC is a heterotrimeric complex comprised of TSC1, TSC2, and TBC1D7 (Dibble et al., 2012), and functions as a GTPase activating protein (GAP) for the small GTPase Rheb (Inoki et al., 2003; Tee et al., 2003), which directly binds and activates mTORC1 (Long et al., 2005; Sancak et al., 2007).”
• Hypoxia regulates TSC1/2-mTOR signaling and tumor suppression through REDD1-mediated 14-3-3 shuttling. (2008, background): “Interestingly, recent studies suggest that 14–3–3-dependent pathways may regulate mTORC1 activity both upstream of and downstream from TSC1/2 (Sancak et al. 2007; Vander Haar et al. 2007).”
• The mTOR Signalling Pathway in Human Cancer (2012, background): “AKT also phosphorylates and inhibits PRAS40, which negatively regulates mTORC1 by antagonizing its activation by Rheb [15,50].”
• PI3K/Akt: getting it right matters (2008, background): “Underphosphorylated PRAS40 binds raptor and inhibits mTOR kinase activity (Sancak et al., 2007; Wang et al., 2007).”
• Metformin, Independent of AMPK, Inhibits mTORC1 In a Rag GTPase-Dependent Manner (2010, background): “This allows activation of Ras homolog enriched in brain (Rheb), required for mTORC1 activation (Garami et al., 2003; Long et al., 2005), whereas PRAS40 suppression relieves its inhibitory effects on mTORC1 (Haas and Hagedorn, 1992; Sancak et al., 2007).”
• mTOR signaling in growth control and disease (2012, neutral): “Leading Edge Review mTOR Signaling in Growth”
• Regulation of mTORC1 by amino acids (2014, neutral): “mTORC1 is a 1 MDa (4) homodimer composed of the scaffolding subunit raptor (5, 6); two endogenous kinase inhibitors referred to as DEPTOR (7) and PRAS40 (8); and mLST8 (9) whose function remains cryptic.”
• DEPTOR is an mTOR Inhibitor Whose Frequent Overexpression in Multiple Myeloma Cells Promotes their Survival (2009, methodology): “…lead to hyperactive PI3K signaling, which then overcomes the direct inhibitory effects of DEPTOR on mTORC2, just as the hyperactive rheb found in TSC2 null cells can overcome the inhibitory effects of PRAS40 on mTORC1 880 Cell 137, 873–886, May 29, 2009 ª2009 Elsevier Inc. (Sancak et al., 2007).”
• Nutrient-dependent mTORC1 association with the ULK1-Atg13-FIP200 complex required for autophagy. (2009, methodology): “3% CHAPS) as described previously to maintain the mTOR complex (Sancak et al., 2007).”