AMPK phosphorylation of raptor mediates a metabolic checkpoint.
By Dana M. Gwinn, D. Shackelford, Daniel F Egan, Maria M. Mihaylova, A. Méry, Debbie S. Vasquez, B. Turk, R. Shaw. Molecules and Cells, 2008
3,890 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/7e555e629f7efc8c3e86aea297ce0674fdd8cf2a
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cell Biology
In Molecular Biology
Citations in the corpus
- AMP-activated protein kinase: an energy sensor that regulates all aspects of cell function. (2011, methodology): “This was elucidated using various approaches, including synthetic peptides (Weekes et al. 1993; Dale et al. 1995), site-directed mutagenesis with an recombinant substrate (Scott et al. 2002), and a peptide library approach (Gwinn et al. 2008).”
- The nuts and bolts of AGC protein kinases (2010, background): “A rise in cellular AMP levels causes activation of the AMP-activated protein kinase (AMPK), which suppresses mTORC1 activity by phosphorylating TSC2 and RAPTO”
- AMPK Phosphorylates and Inhibits SREBP Activity to Attenuate Hepatic Steatosis and Atherosclerosis in Diet-induced Insulin Resistant Mice (2011, positive): “AMPK Directly Phosphorylates SREBP-1c at Ser372 In Vitro and In Vivo In vitro AMPK kinase assays were performed using recombinant SREBP-1c or -2 as a substrate in the presence of ATP, as described previously (Inoki et al., 2003; Gwinn et al., 2008).”
- mTOR: from growth signal integration to cancer, diabetes and ageing (2010, background): “Moreover, AMPK phosphorylates RAPTOR, causing it to bind 14-3-3 proteins, which leads to the inhibition of mTORC1 through allosteric mechanism”
- Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models (2011, background): “(AMPK), an energy status sensor activated by ATP depletion, inhibits mTORC1 by phosphorylating and inactivating Raptor [23], and by phosphorylating and activating TSC2 [24].”
- LKB1 and AMPK control of mTOR signalling and growth (2009, background): “We demonstrated that this G2/M arrest is ablated in cells reconstituted with raptor cDNA mutated at the two AMPK phosphorylation sites (Gwinn et al. 2008).”
- The androgen receptor fuels prostate cancer by regulating central metabolism and biosynthesis (2011, background): “AMPK activity promotes glycolysis by phosphorylation of PFK2 and negatively regulates protein synthesis by phos- phorylating the TSC1/TSC2 complex upstream of mTOR (Marsin et al, 2000; Gwinn et al, 2008).”
- Cancer Cell Metabolism: One Hallmark, Many Faces (2012, background): “Moreover, anabolic mTORC1 activity can be suppressed through either of two AMPK-mediated phosphorylation events: (i) activation of the TSC1/2 complex, or (ii) inactivation of the mTORC1 scaffold protein, RAPTOR (46, 47).”
- An Overview of Autophagy: Morphology, Mechanism, and Regulation (2014, background): “Alternatively, AMPK can directly inhibit MTORC1 (35, 154).”
- mTOR Signaling in Growth, Metabolism, and Disease. (2017, background): “A reduction in cellular energy charge, for example during glucose deprivation, activates the stress responsive metabolic regulator AMPK, which inhibits mTORC1 both indirectly, through phosphorylation and activation of TSC2, as well as directly through the phosphorylation of Raptor (Gwinn et al., 200”
- mTOR- and HIF-1α–mediated aerobic glycolysis as metabolic basis for trained immunity (2014, methodology): “We first assessed whether metformin—which acts through AMPK activation and subsequently mTOR inhibition (28) and is commonly used for the treatment of type 2 diabetes (29)—abrogates the protective effects in these experimental models.”
- Rapamycin passes the torch: a new generation of mTOR inhibitors (2011, neutral): “114 ), or directly by phosphorylating and inactivating RAPTO”