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Sci. Signal., 18 February 2014
Vol. 7, Issue 313, p. ra17
[DOI: 10.1126/scisignal.2004785]


Editor's Summary

Negatively Adapting Metabolism
Deficiency of the adaptor protein p66Shc, which inhibits signaling through receptor tyrosine kinases, improves the glucose tolerance of mice that are a genetic model of obesity. Soliman et al. found that in both transformed and nontransformed cells, p66Shc silencing enhanced glucose metabolism, increased the abundance of intermediates in various biosynthetic pathways, and increased cell size. The change in metabolism required the mTOR pathway, which couples energy, nutrient, and growth factor (including insulin) signals to processes that mediate cellular growth and proliferation. Thus, p66Shc suppresses mTOR signaling, and manipulating the abundance of p66Shc or interfering with p66Shc function could be used to treat diseases characterized by disruptions in this pathway, including diabetes and cancer.

Citation: M. A. Soliman, A. M. Abdel Rahman, D. W. Lamming, K. Birsoy, J. Pawling, M. E. Frigolet, H. Lu, I. G. Fantus, A. Pasculescu, Y. Zheng, D. M. Sabatini, J. W. Dennis, T. Pawson, The Adaptor Protein p66Shc Inhibits mTOR-Dependent Anabolic Metabolism. Sci. Signal. 7, ra17 (2014).

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Science Signaling Podcast: 18 February 2014.
J. W. Dennis, M. A. Soliman, and A. M. VanHook (2014)
Science Signaling 7, pc6
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