THE GENETIC-REGULATION OF APOPTOSIS

被引:256
作者
WYLLIE, AH
机构
[1] Cancer Research Campaign Laboratories, Department of Pathology, The University of Edinburgh Medical School, Edinburgh, EH8 9AG, Teviot Place
关键词
D O I
10.1016/S0959-437X(95)90060-8
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Dramatic advances, most of them within the past two years, have provided a picture of the genetic regulation of apoptosis in mammalian cells. Although much detail remains to be filled in, the general structure-concordant with programmed death in invertebrates - includes signalling systems, genetic determination of susceptibility, critical proteins capable of reversing or re-affirming the death sentence, and a common effector pathway driven by specific proteases.
引用
收藏
页码:97 / 104
页数:8
相关论文
共 87 条
[1]   THE C-MYC PROTEIN INDUCES CELL-CYCLE PROGRESSION AND APOPTOSIS THROUGH DIMERIZATION WITH MAX [J].
AMATI, B ;
LITTLEWOOD, TD ;
EVAN, GI ;
LAND, H .
EMBO JOURNAL, 1993, 12 (13) :5083-5087
[2]   SUSCEPTIBILITY TO APOPTOSIS IS DIFFERENTIALLY REGULATED BY C-MYC AND MUTATED HA-RAS ONCOGENES AND IS ASSOCIATED WITH ENDONUCLEASE AVAILABILITY [J].
ARENDS, MJ ;
MCGREGOR, AH ;
TOFT, NJ ;
BROWN, EJH ;
WYLLIE, AH .
BRITISH JOURNAL OF CANCER, 1993, 68 (06) :1127-1133
[3]  
BELLAMY COC, 1995, IN PRESS SEMIN CANCE
[4]   CELL-PROLIFERATION, DNA-REPAIR, AND P53 FUNCTION ARE NOT REQUIRED FOR PROGRAMMED DEATH OF PROSTATIC GLANDULAR CELLS INDUCED BY ANDROGEN ABLATION [J].
BERGES, RR ;
FURUYA, Y ;
REMINGTON, L ;
ENGLISH, HF ;
JACKS, T ;
ISAACS, JT .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (19) :8910-8914
[5]   BCL-X, A BCL-2-RELATED GENE THAT FUNCTIONS AS A DOMINANT REGULATOR OF APOPTOTIC CELL-DEATH [J].
BOISE, LH ;
GONZALEZGARCIA, M ;
POSTEMA, CE ;
DING, LY ;
LINDSTEN, T ;
TURKA, LA ;
MAO, XH ;
NUNEZ, G ;
THOMPSON, CB .
CELL, 1993, 74 (04) :597-608
[6]   THE PROTEIN BCL-2-ALPHA DOES NOT REQUIRE MEMBRANE ATTACHMENT, BUT 2 CONSERVED DOMAINS TO SUPPRESS APOPTOSIS [J].
BORNER, C ;
MARTINOU, I ;
MATTMANN, C ;
IRMLER, M ;
SCHAERER, E ;
MARTINOU, JC ;
TSCHOPP, J .
JOURNAL OF CELL BIOLOGY, 1994, 126 (04) :1059-1068
[7]   ADENOVIRUS-E1B 19-KDA AND BCL-2 PROTEINS INTERACT WITH A COMMON SET OF CELLULAR PROTEINS [J].
BOYD, JM ;
MALSTROM, S ;
SUBRAMANIAN, T ;
VENKATESH, LK ;
SCHAEPER, U ;
ELANGOVAN, B ;
DSAEIPPER, C ;
CHINNADURAI, G .
CELL, 1994, 79 (02) :341-351
[8]   P53-DEPENDENT APOPTOSIS IN THE ABSENCE OF TRANSCRIPTIONAL ACTIVATION OF P53-TARGET GENES [J].
CAELLES, C ;
HELMBERG, A ;
KARIN, M .
NATURE, 1994, 370 (6486) :220-223
[9]   PROTECTION FROM FAS-MEDIATED APOPTOSIS BY A SOLUBLE FORM OF THE FAS MOLECULE [J].
CHENG, JH ;
ZHOU, T ;
LIU, CD ;
SHAPIRO, JP ;
BRAUER, MJ ;
KIEFER, MC ;
BARR, PJ ;
MOUNTZ, JD .
SCIENCE, 1994, 263 (5154) :1759-1762
[10]   BCL-2 BLOCKS P53-DEPENDENT APOPTOSIS [J].
CHIOU, SK ;
RAO, L ;
WHITE, E .
MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (04) :2556-2563