Gene regulation associated with apoptosis

被引:31
作者
Jehn, BM
Osborne, BA
机构
[1] UNIV MASSACHUSETTS,DEPT VET & ANIM SCI,AMHERST,MA 01003
[2] UNIV MASSACHUSETTS,PROGRAM MOL BIOL,PAIGE LAB,AMHERST,MA 01003
来源
CRITICAL REVIEWS IN EUKARYOTIC GENE EXPRESSION | 1997年 / 7卷 / 1-2期
关键词
AP-1; glucocorticocoid receptor; nur77; nuclear receptor; thymocytes;
D O I
10.1615/CritRevEukarGeneExpr.v7.i1-2.100
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Apoptosis, one of the best-studied forms of programmed cell death processes, plays an important role during the development and life-cycle of most multicellular organisms. The mechanisms underlying the initiation and manifestation of apoptotic cell death are the focus of the most recent cell death research. Generally, it is believed that cells are eliminated via a highly ordered and controlled program. This program might consist of the successive activation of unique apoptosis-specific genes, which are solely involved in the regulation of the programmed cell, death. However, more and more evidence is accumulating that novel genes are not activated or induced during apoptosis, but rather many well-known genes previously described for their roles in processes such as proliferation and differentiation and belonging, for example, to the protein families of immediate-early genes and transcription factors become activated. The death-specific feature is achieved thereby by the extent, combination, and specific timing of gene expression. The involvement of the three different transcription factors glucocorticoid receptor (GR), nur77, and activator protein 1 (AP-1) in such a scenario is the focus of this review.
引用
收藏
页码:179 / 193
页数:15
相关论文
共 103 条
[31]  
DEGROOT RP, 1992, ONCOGENE, V7, P2281
[32]   PROTOONCOGENE C-FOS EXPRESSION IN GROWTH REGIONS OF FETAL BONE AND MESODERMAL WEB TISSUE [J].
DONY, C ;
GRUSS, P .
NATURE, 1987, 328 (6132) :711-714
[33]   EVIDENCE THAT GLUCOCORTICOID-INDUCED AND CYCLIC AMP-INDUCED APOPTOTIC PATHWAYS IN LYMPHOCYTES SHARE DISTAL EVENTS [J].
DOWD, DR ;
MIESFELD, RL .
MOLECULAR AND CELLULAR BIOLOGY, 1992, 12 (08) :3600-3608
[34]   IMMEDIATE-EARLY GENE PROTEIN EXPRESSION IN NEURONS UNDERGOING DELAYED DEATH, BUT NOT NECROSIS, FOLLOWING HYPOXIC-ISCHEMIC INJURY TO THE YOUNG-RAT BRAIN [J].
DRAGUNOW, M ;
BEILHARZ, E ;
SIRIMANNE, E ;
LAWLOR, P ;
WILLIAMS, C ;
BRAVO, R ;
GLUCKMAN, P .
MOLECULAR BRAIN RESEARCH, 1994, 25 (1-2) :19-33
[35]   ALTERED GENE-EXPRESSION IN NEURONS DURING PROGRAMMED CELL-DEATH - IDENTIFICATION OF C-JUN AS NECESSARY FOR NEURONAL APOPTOSIS [J].
ESTUS, S ;
ZAKS, WJ ;
FREEMAN, RS ;
GRUDA, M ;
BRAVO, R ;
JOHNSON, EM .
JOURNAL OF CELL BIOLOGY, 1994, 127 (06) :1717-1727
[36]  
FARHNER TJ, 1990, MOL CELL BIOL, V10, P6454
[37]   GLUCOCORTICOID AND PROGESTERONE INHIBIT INVOLUTION AND PROGRAMMED CELL-DEATH IN THE MOUSE MAMMARY-GLAND [J].
FENG, ZW ;
MARTI, A ;
JEHN, B ;
ALTERMATT, HJ ;
CHICAIZA, G ;
JAGGI, R .
JOURNAL OF CELL BIOLOGY, 1995, 131 (04) :1095-1103
[38]   Ionizing radiation-induced apoptosis is associated with c-Jun expression and c-Jun/AP-1 activation in the developing cerebellum of the rat [J].
Ferrer, I ;
Barron, S ;
RodriquezFarre, E ;
Planas, AM .
NEUROSCIENCE LETTERS, 1995, 202 (1-2) :105-108
[39]   THE MAMMARY-GLAND [J].
FORSYTH, IA .
BAILLIERES CLINICAL ENDOCRINOLOGY AND METABOLISM, 1991, 5 (04) :809-832
[40]   THE NEUROENDOCRINE THYMUS - COEXISTENCE OF OXYTOCIN AND NEUROPHYSIN IN THE HUMAN THYMUS [J].
GEENEN, V ;
LEGROS, JJ ;
FRANCHIMONT, P ;
BAUDRIHAYE, M ;
DEFRESNE, MP ;
BONIVER, J .
SCIENCE, 1986, 232 (4749) :508-511