Translational responses to growth factors and stress.
Cellular stresses can induce a wide range of biological responses, depending on the type of stress, the type of cell and the cellular environment. Stress-mediated changes in translational output cover a broad spectrum of potential responses, including an overall decrease in translation or an increase in the translation of specific mRNAs. Many of these changes involve post-translational modifications of components of the translational machinery. The mTOR (mammalian target of rapamycin) pathway is a critical regulator of growth and translation in response to a wide variety of signals, including growth factors, amino acids and energy availability. Through its kinase activity, mTOR activation results in the phosphorylation of translational components and an increase in translation. As stress-mediated changes in translational output are context-dependent, the interplay between stress and mTOR in the control of translation is also likely to depend on factors such as the strength and type of incident stress. In the present paper, we review mTOR-dependent and -independent translational responses, and discuss their regulation by stress.
Cully
Megan
M
Signal Transduction Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3PX, UK. megan.cully@cancer.org.uk
Downward
Julian
J
D000818:Animals; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism*; D010442:Peptide Chain Initiation, Translational; D014176:Protein Biosynthesis; D011494:Protein Kinases / Q000378:metabolism; D013312:Stress, Physiological; D058570:TOR Serine-Threonine Kinases
D036341:Intercellular Signaling Peptides and Proteins; D011494:Protein Kinases; C546842:MTOR protein, human; D058570:TOR Serine-Threonine Kinases; D048049:Extracellular Signal-Regulated MAP Kinases