mTORC2 Puts Its Shoulder to Krebs’ Wheel

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mTORC2 Puts Its Shoulder to Krebs’ Wheel Sebastian I. Arriola Apelo, Dudley W. Lamming Molecular Cell Volume 63, Issue 5, Pages 723-725 (September 2016) DOI: 10.1016/j.molcel.2016.08.016 Copyright © 2016 Elsevier Inc. Terms and Conditions

Figure 1 mTORC2 Plays a Key Role in Anaplerosis and Protein Glycosylation In the face of decreased glucose and glutamine catabolites, mTORC2 provides substrates for the hexosamine biosynthesis pathway (HBP) by promoting glutaminolysis and anaplerosis. Glucose and α-ketoglutarate promote mTORC2 activity; the exact catabolites sensed by mTORC2 remain to be determined. In the absence of mTORC2, levels of glutamate, α-ketoglutarate, and other TCA intermediates decrease; GFAT1 activity also decreases. Loss of mTORC2 also impairs Gck expression (Lamming et al., 2014), further decreasing the availability of substrates for the HBP. Aberrant protein glycosylation has been linked to several metabolic and neurological disorders. Molecular Cell 2016 63, 723-725DOI: (10.1016/j.molcel.2016.08.016) Copyright © 2016 Elsevier Inc. Terms and Conditions