Gene expression and the thiol redox state

被引:393
作者
Arrigo, AP [1 ]
机构
[1] Univ Lyon 1, CNRS, UMR 106, Lab Stress Cellulaire,Ctr Genet Mol & Cellulaire, F-69622 Villeurbanne, France
关键词
thiol redox state; glutathione; reactive oxygen species; free radicals; gene expression; transcription factors;
D O I
10.1016/S0891-5849(99)00175-6
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The intracellular redox status is a tightly regulated parameter which provides the cell with an optimal ability to counteract the highly oxidizing extracellular environment. Intracellular redox homeostasis is regulated by thiol-containing molecules, such as glutathione and thioredoxin. Essential cellular functions, such as gene expression, are influenced by the balance between pro- and antioxidant conditions. The mechanism by which the transcription of specific eukaryotic genes is redox regulated is complex, however, recent findings suggest that redox-sensitive transcription factors play an essential role in this process. This review is focused on the recent knowledge concerning some eukaryotic transcription factors, whose activation and DNA binding is controlled by the thiol redox status of the cell. (C) 1999 Elsevier Science Inc.
引用
收藏
页码:936 / 944
页数:9
相关论文
共 102 条
[71]   MODULATION OF TRANSCRIPTION FACTOR NF-KAPPA-B ACTIVITY BY INTRACELLULAR GLUTATHIONE LEVELS AND BY VARIATIONS OF THE EXTRACELLULAR CYSTEINE SUPPLY [J].
MIHM, S ;
GALTER, D ;
DROGE, W .
FASEB JOURNAL, 1995, 9 (02) :246-252
[72]   Regulation of the heat shock transcriptional response: cross talk between a family of heat shock factors, molecular chaperones, and negative regulators [J].
Morimoto, RI .
GENES & DEVELOPMENT, 1998, 12 (24) :3788-3796
[73]   TRANSCRIPTIONAL ACTIVATION OF EARLY-RESPONSE GENES BY HYDROGEN-PEROXIDE IN A MOUSE OSTEOBLASTIC CELL-LINE [J].
NOSE, K ;
SHIBANUMA, M ;
KIKUCHI, K ;
KAGEYAMA, H ;
SAKIYAMA, S ;
KUROKI, T .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1991, 201 (01) :99-106
[74]   HUMAN THIOREDOXIN ADULT T-CELL LEUKEMIA-DERIVED FACTOR ACTIVATES THE ENHANCER BINDING-PROTEIN OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 BY THIOL REDOX CONTROL MECHANISM [J].
OKAMOTO, T ;
OGIWARA, H ;
HAYASHI, T ;
MITSUI, A ;
KAWABE, T ;
YODOI, J .
INTERNATIONAL IMMUNOLOGY, 1992, 4 (07) :811-819
[75]   Redox state regulates binding of p53 to sequence-specific DNA, but not to non-specific or mismatched DNA [J].
Parks, D ;
Bolinger, R ;
Mann, K .
NUCLEIC ACIDS RESEARCH, 1997, 25 (06) :1289-1295
[76]   Deletion of the Saccharomyces cerevisiae TRR1 gene encoding thioredoxin reductase inhibits p53-dependent reporter gene expression [J].
Pearson, GD ;
Merrill, GF .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (10) :5431-5434
[77]  
POGNONEC P, 1992, J BIOL CHEM, V267, P24563
[78]   REDOX SIGNALING AND THE CONTROL OF CELL-GROWTH AND DEATH [J].
POWIS, G ;
BRIEHL, M ;
OBLONG, J .
PHARMACOLOGY & THERAPEUTICS, 1995, 68 (01) :149-173
[79]   STIMULATION OF GLUTATHIONE-PEROXIDASE ACTIVITY DECREASES HIV TYPE-1 ACTIVATION AFTER OXIDATIVE STRESS [J].
SAPPEY, C ;
LEGRANDPOELS, S ;
BESTBELPOMME, M ;
FAVIER, A ;
RENTIER, B ;
PIETTE, J .
AIDS RESEARCH AND HUMAN RETROVIRUSES, 1994, 10 (11) :1451-1461
[80]   DISTINCT EFFECTS OF THIOREDOXIN AND ANTIOXIDANTS ON THE ACTIVATION OF TRANSCRIPTION FACTORS NF-KAPPA-B AND AP-1 [J].
SCHENK, H ;
KLEIN, M ;
ERDBRUGGER, W ;
DROGE, W ;
SCHULZEOSTHOFF, K .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (05) :1672-1676