The common and distinct target genes of the p53 family transcription factors

被引:248
作者
Harms, K [1 ]
Nozell, S [1 ]
Chen, X [1 ]
机构
[1] Univ Alabama Birmingham, Dept Cell Biol, Birmingham, AL 35294 USA
关键词
p53; p63; p73; transcription; cell cycle arrest; apoptosis; development;
D O I
10.1007/s00018-003-3304-4
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
p53 is the most commonly mutated gene in human cancer. After activation by cellular stresses such as DNA damage or oncogene activation, p53, a sequence-specific DNA-binding protein, induces the expression of target genes which mediate tumor suppression. Two recently identified p53 homologues, p63 and p73, appear to function similarly to p53, that is, they both activate target gene expression and suppress cell growth when overexpressed; however, the p63 and p73 genes are rarely mutated in human cancer and do not adhere to Knudson's classical model of a tumor suppressor gene. Recently, exciting observations suggest nonoverlapping functions for the family members. Herein, we outline the recent literatures identifying and characterizing both the common and distinct target genes of the p53 family transcription factors in relation to their signaling pathways.
引用
收藏
页码:822 / 842
页数:21
相关论文
共 222 条
  • [41] Inactivation of the p53-homologue p73 by the mdm2-oncoprotein
    Dobbelstein, M
    Wienzek, S
    König, C
    Roth, J
    [J]. ONCOGENE, 1999, 18 (12) : 2101 - 2106
  • [42] Receptor tyrosine kinase EphA2 is regulated by p53-family proteins and induces apoptosis
    Dohn, M
    Jiang, JY
    Chen, XB
    [J]. ONCOGENE, 2001, 20 (45) : 6503 - 6515
  • [43] p63α and ΔNp63α can induce cell cycle arrest and apoptosis and differentially regulate p53 target genes
    Dohn, M
    Zhang, SZ
    Chen, XB
    [J]. ONCOGENE, 2001, 20 (25) : 3193 - 3205
  • [44] Donald SP, 2001, CANCER RES, V61, P1810
  • [45] MICE DEFICIENT FOR P53 ARE DEVELOPMENTALLY NORMAL BUT SUSCEPTIBLE TO SPONTANEOUS TUMORS
    DONEHOWER, LA
    HARVEY, M
    SLAGLE, BL
    MCARTHUR, MJ
    MONTGOMERY, CA
    BUTEL, JS
    BRADLEY, A
    [J]. NATURE, 1992, 356 (6366) : 215 - 221
  • [46] Overexpression of the p53-inducible brain-specific angiogenesis inhibitor 1 suppresses efficiently tumour angiogenesis
    Duda, DG
    Sunamura, M
    Lozonschi, L
    Yokoyama, T
    Yatsuoka, T
    Motoi, F
    Horii, A
    Tani, K
    Asano, S
    Nakamura, Y
    Matsuno, S
    [J]. BRITISH JOURNAL OF CANCER, 2002, 86 (03) : 490 - 496
  • [47] WAF1, A POTENTIAL MEDIATOR OF P53 TUMOR SUPPRESSION
    ELDEIRY, WS
    TOKINO, T
    VELCULESCU, VE
    LEVY, DB
    PARSONS, R
    TRENT, JM
    LIN, D
    MERCER, WE
    KINZLER, KW
    VOGELSTEIN, B
    [J]. CELL, 1993, 75 (04) : 817 - 825
  • [48] Elkeles A, 1999, MOL CELL BIOL, V19, P2594
  • [49] REDD1, a developmentally regulated transcriptional target of p63 and p53, links p63 to regulation of reactive oxygen species
    Ellisen, LW
    Ramsayer, KD
    Johannessen, CM
    Yang, A
    Beppu, H
    Minda, K
    Oliner, JD
    McKeon, F
    Haber, DA
    [J]. MOLECULAR CELL, 2002, 10 (05) : 995 - 1005
  • [50] p53 induction of heparin-binding EGF-like growth factor counteracts p53 growth suppression through activation of MAPK and PI3K/Akt signaling cascades
    Fang, L
    Li, GN
    Liu, GZ
    Lee, SW
    Aaronson, SA
    [J]. EMBO JOURNAL, 2001, 20 (08) : 1931 - 1939