mTOR Signaling in Growth, Metabolism, and Disease

Robert A Saxton; David M Sabatini

doi:10.1016/j.cell.2017.02.004

mTOR Signaling in Growth, Metabolism, and Disease

Cell. 2017 Mar 9;168(6):960-976. doi: 10.1016/j.cell.2017.02.004.

Authors

Robert A Saxton¹, David M Sabatini²

Affiliations

¹ Whitehead Institute for Biomedical Research, 455 Main Street, Cambridge, MA 02142, USA; Department of Biology, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Koch Institute for Integrative Cancer Research, 77 Massachusetts Avenue, Cambridge, MA 02139, USA; Broad Institute of Harvard and Massachusetts Institute of Technology, 415 Main Street, Cambridge, MA 02142, USA.
² Whitehead Institute for Biomedical Research, 455 Main Street, Cambridge, MA 02142, USA; Department of Biology, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Koch Institute for Integrative Cancer Research, 77 Massachusetts Avenue, Cambridge, MA 02139, USA; Broad Institute of Harvard and Massachusetts Institute of Technology, 415 Main Street, Cambridge, MA 02142, USA. Electronic address: sabatini@wi.mit.edu.

Abstract

The mechanistic target of rapamycin (mTOR) coordinates eukaryotic cell growth and metabolism with environmental inputs, including nutrients and growth factors. Extensive research over the past two decades has established a central role for mTOR in regulating many fundamental cell processes, from protein synthesis to autophagy, and deregulated mTOR signaling is implicated in the progression of cancer and diabetes, as well as the aging process. Here, we review recent advances in our understanding of mTOR function, regulation, and importance in mammalian physiology. We also highlight how the mTOR signaling network contributes to human disease and discuss the current and future prospects for therapeutically targeting mTOR in the clinic.

Keywords: aging; cancer; cell growth; diabetes; mTOR; mTORC1; mTORC2; metabolism; nutrients; signaling.

Publication types

Review

MeSH terms

Aging / metabolism
Animals
Diabetes Mellitus / metabolism
Glucose / metabolism
Humans
Muscles / metabolism
Neoplasms / metabolism
Signal Transduction*
TOR Serine-Threonine Kinases / metabolism*

Substances

TOR Serine-Threonine Kinases
Glucose

Abstract

Publication types

MeSH terms

Substances

Grants and funding