学术探索
学术期刊
新闻热点
数据分析
智能评审

THE GENETIC-REGULATION OF APOPTOSIS

被引：255
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
来源：
CURRENT OPINION IN GENETICS & DEVELOPMENT | 1995年 / 5卷 / 01期
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
    AMATI, B
    LITTLEWOOD, TD
    EVAN, GI
    LAND, H
    [J]. 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
    ARENDS, MJ
    MCGREGOR, AH
    TOFT, NJ
    BROWN, EJH
    WYLLIE, AH
    [J]. 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
    BERGES, RR
    FURUYA, Y
    REMINGTON, L
    ENGLISH, HF
    JACKS, T
    ISAACS, JT
    [J]. 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
    BOISE, LH
    GONZALEZGARCIA, M
    POSTEMA, CE
    DING, LY
    LINDSTEN, T
    TURKA, LA
    MAO, XH
    NUNEZ, G
    THOMPSON, CB
    [J]. CELL, 1993, 74 (04) : 597 - 608
  • [6] THE PROTEIN BCL-2-ALPHA DOES NOT REQUIRE MEMBRANE ATTACHMENT, BUT 2 CONSERVED DOMAINS TO SUPPRESS APOPTOSIS
    BORNER, C
    MARTINOU, I
    MATTMANN, C
    IRMLER, M
    SCHAERER, E
    MARTINOU, JC
    TSCHOPP, J
    [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
    BOYD, JM
    MALSTROM, S
    SUBRAMANIAN, T
    VENKATESH, LK
    SCHAEPER, U
    ELANGOVAN, B
    DSAEIPPER, C
    CHINNADURAI, G
    [J]. CELL, 1994, 79 (02) : 341 - 351
  • [8] P53-DEPENDENT APOPTOSIS IN THE ABSENCE OF TRANSCRIPTIONAL ACTIVATION OF P53-TARGET GENES
    CAELLES, C
    HELMBERG, A
    KARIN, M
    [J]. NATURE, 1994, 370 (6486) : 220 - 223
  • [9] PROTECTION FROM FAS-MEDIATED APOPTOSIS BY A SOLUBLE FORM OF THE FAS MOLECULE
    CHENG, JH
    ZHOU, T
    LIU, CD
    SHAPIRO, JP
    BRAUER, MJ
    KIEFER, MC
    BARR, PJ
    MOUNTZ, JD
    [J]. SCIENCE, 1994, 263 (5154) : 1759 - 1762
  • [10] BCL-2 BLOCKS P53-DEPENDENT APOPTOSIS
    CHIOU, SK
    RAO, L
    WHITE, E
    [J]. MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (04) : 2556 - 2563
123456789