Sestrin as a Feedback Inhibitor of TOR That Prevents Age-Related Pathologies-Reference-Cited by-同舟云学术

Sestrin as a Feedback Inhibitor of TOR That Prevents Age-Related Pathologies

Published:2010-03-05 Issue:5970 Volume:327 Page:1223-1228
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Lee Jun Hee¹,Budanov Andrei V.¹,Park Eek Joong¹,Birse Ryan²,Kim Teddy E.³,Perkins Guy A.⁴,Ocorr Karen²,Ellisman Mark H.⁴,Bodmer Rolf²,Bier Ethan³,Karin Michael¹

Affiliation:

1. Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, School of Medicine, University of California San Diego (UCSD), La Jolla, CA 92093–0723, USA.

2. Development and Aging Program, Neuroscience, Aging and Stem Cell Research Center, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037, USA.

3. Section of Cell and Developmental Biology, UCSD, La Jolla, CA 92093–0349, USA.

4. National Center for Microscopy and Imaging Research and Department of Neurosciences, UCSD, La Jolla, CA 92093–0608, USA.

Abstract

Sestrin and the Consequences of Aging The protein kinase TOR (target of rapamycin) plays key roles in the control of fundamental biological processes, including growth, metabolism, aging, and immune function. Sestrin proteins show increased abundance in response to stress and have been implicated in control of TOR activity. Lee et al. (p. 1223 ; see the Perspective by

Topisirovic and Sonenberg

) characterized Drosophila fruit flies lacking sestrins. Sestrins were implicated in a negative feedback loop in which the abundance of sestrins is controlled by TOR activity with sestrins concomitantly also inhibiting activity of TOR. Furthermore, flies lacking sestrins showed accumulation of fat, muscle degeneration, and heart abnormalities similar to those that plague aging humans with a sedentary life-style.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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