Transcriptional regulation of the stress response by mTOR

被引:87
作者
Aramburu, Jose [1 ]
Carmen Ortells, M. [2 ,3 ]
Tejedor, Sonia [1 ]
Buxade, Maria [1 ]
Lopez-Rodriguez, Cristina [1 ]
机构
[1] Univ Pompeu Fabra, Dept Expt & Hlth Sci, Barcelona 08003, Spain
[2] Ctr Genom Regulat, Barcelona 08003, Spain
[3] Univ Pompeu Fabra, Barcelona 08003, Spain
关键词
ACTIVATED PROTEIN-KINASE; MAMMALIAN TARGET; CELL-GROWTH; OSMOTIC-STRESS; HEAT-SHOCK; COMPLEX; GENE-EXPRESSION; LIFE-SPAN; PHOSPHATIDYLINOSITOL; 3-KINASE; MEDIATED PHOSPHORYLATION;
D O I
10.1126/scisignal.2005326
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
The kinase mammalian target of rapamycin (mTOR) is a central regulator of cell growth and proliferation that integrates inputs from growth factor receptors, nutrient availability, intracellular ATP (adenosine 5'-triphosphate), and a variety of stressors. Since early works in the mid-1990s uncovered the role of mTOR in stimulating protein translation, this kinase has emerged as a rather multifaceted regulator of numerous processes. Whereas mTOR is generally activated by growth-and proliferation-stimulating signals, its activity can be reduced and even suppressed when cells are exposed to a variety of stress conditions. However, cells can also adapt to stress while maintaining their growth capacity and mTOR function. Despite knowledge accumulated on how stress represses mTOR, less is known about mTOR influencing stress responses. In this review, we discuss the capability of mTOR, in particular mTOR complex 1 (mTORC1), to activate stress-responsive transcription factors, and we outline open questions for future investigation.
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页数:11
相关论文
共 187 条
[1]
Abdelnour-Berchtold E, 2010, ANTICANCER RES, V30, P799
[2]
ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS [J].
Alexander, Angela ;
Cai, Sheng-Li ;
Kim, Jinhee ;
Nanez, Adrian ;
Sahin, Mustafa ;
MacLean, Kirsteen H. ;
Inoki, Ken ;
Guan, Kun-Liang ;
Shen, Jianjun ;
Person, Maria D. ;
Kusewitt, Donna ;
Mills, Gordon B. ;
Kastan, Michael B. ;
Walker, Cheryl Lyn .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2010, 107 (09) :4153-4158
[3]
Regulation of HSF1 Function in the Heat Stress Response: Implications in Aging and Disease [J].
Anckar, Julius ;
Sistonen, Lea .
ANNUAL REVIEW OF BIOCHEMISTRY, VOL 80, 2011, 80 :1089-1115
[4]
Bidirectional crosstalk between endoplasmic reticulum stress and mTOR signaling [J].
Appenzeller-Herzog, Christian ;
Hall, Michael N. .
TRENDS IN CELL BIOLOGY, 2012, 22 (05) :274-282
[5]
Regulation of the hypertonic stress response and other cellular functions by the Rel-like transcription factor NFAT5 [J].
Aramburu, Jose ;
Drews-Elger, Katherine ;
Estrada-Gelonch, Anais ;
Minguillon, Jordi ;
Morancho, Beatriz ;
Santiago, Veronica ;
Lopez-Rodriguez, Cristina .
BIOCHEMICAL PHARMACOLOGY, 2006, 72 (11) :1597-1604
[6]
AKT induces senescence in human cells via mTORC1 and p53 in the absence of DNA damage: implications for targeting mTOR during malignancy [J].
Astle, M. V. ;
Hannan, K. M. ;
Ng, P. Y. ;
Lee, R. S. ;
George, A. J. ;
Hsu, A. K. ;
Haupt, Y. ;
Hannan, R. D. ;
Pearson, R. B. .
ONCOGENE, 2012, 31 (15) :1949-1962
[7]
Hsf1 Activation Inhibits Rapamycin Resistance and TOR Signaling in Yeast Revealed by Combined Proteomic and Genetic Analysis [J].
Bandhakavi, Sricharan ;
Xie, Hongwei ;
O'Callaghan, Brennon ;
Sakurai, Hiroshi ;
Kim, Do-Hyung ;
Griffin, Timothy J. .
PLOS ONE, 2008, 3 (02)
[8]
Ragulator Is a GEF for the Rag GTPases that Signal Amino Acid Levels tomTORC1 [J].
Bar-Peled, Liron ;
Schweitzer, Lawrence D. ;
Zoncu, Roberto ;
Sabatini, David M. .
CELL, 2012, 150 (06) :1196-1208
[9]
TOR controls translation initiation and early G1 progression in yeast [J].
Barbet, NC ;
Schneider, U ;
Helliwell, SB ;
Stansfield, I ;
Tuite, MF ;
Hall, MN .
MOLECULAR BIOLOGY OF THE CELL, 1996, 7 (01) :25-42
[10]
The tuberous sclerosis-1 (TSC1) gene product hamartin suppresses cell growth and augments the expression of the TSC2 product tuberin by inhibiting its ubiquitination [J].
Benvenuto, G ;
Li, SW ;
Brown, SJ ;
Braverman, R ;
Vass, WC ;
Cheadle, JP ;
Halley, DJJ ;
Sampson, JR ;
Wienecke, R ;
DeClue, JE .
ONCOGENE, 2000, 19 (54) :6306-6316