Differential regulation of transcription and induction of programmed cell death by human p53-family members p63 and p73

被引:59
作者
Dietz, S
Rother, K
Bamberger, C
Schmale, H
Mössner, J
Engeland, K
机构
[1] Univ Leipzig, Max Burger Forschungszentrum, Med Klin & Poliklin 2, D-04103 Leipzig, Germany
[2] Univ Hamburg, Inst Zellbiol & Klin Neurobiol, D-20246 Hamburg, Germany
关键词
p53; p63; p73; transcription; apoptosis;
D O I
10.1016/S0014-5793(02)03093-4
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
The p53 tumor suppressor acts as a transcription factor and has a central function in controlling apoptosis. With p63 and p73 two genes coding for proteins homologous to p53 have been identified. We describe the properties of seven human p63 and p73 proteins as transcriptional activators of p21WAF1/CIP1 expression and apoptotic inducers in direct comparison to p53 in the same assay systems employing DLD-1-tet-off colon cells. Programmed cell death is detected in cells expressing high levels of p53 and p73alpha. Cells overexpressing TAp63alpha, TAp63gamma, TA*p63alpha, TA*p63gamma, DeltaNp63alpha, and DeltaNp63gamma display low or no detectable apoptosis. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:93 / 99
页数:7
相关论文
共 40 条
[1]   Maintenance of genomic integrity by p53:: complementary roles for activated and non-activated p53 [J].
Albrechtsen, N ;
Dornreiter, I ;
Grosse, F ;
Kim, E ;
Wiesmüller, L ;
Deppert, W .
ONCOGENE, 1999, 18 (53) :7706-7717
[2]   Cloning and chromosomal mapping of the human p53-related KET gene to Chromosome 3q27 and its murine homolog Ket to mouse Chromosome 16 [J].
Augustin, M ;
Bamberger, C ;
Paul, D ;
Schmale, H .
MAMMALIAN GENOME, 1998, 9 (11) :899-902
[3]   SUPPRESSION OF HUMAN COLORECTAL-CARCINOMA CELL-GROWTH BY WILD-TYPE-P53 [J].
BAKER, SJ ;
MARKOWITZ, S ;
FEARON, ER ;
WILLSON, JKV ;
VOGELSTEIN, B .
SCIENCE, 1990, 249 (4971) :912-915
[4]   Identification and tissue distribution of novel KET/p63 splice variants [J].
Bamberger, C ;
Schmale, H .
FEBS LETTERS, 2001, 501 (2-3) :121-126
[5]   RADIATION-INDUCED CELL-CYCLE ARREST COMPROMISED BY P21 DEFICIENCY [J].
BRUGAROLAS, J ;
CHANDRASEKARAN, C ;
GORDON, JI ;
BEACH, D ;
JACKS, T ;
HANNON, GJ .
NATURE, 1995, 377 (6549) :552-557
[6]   Requirement for p53 and p21 to sustain G2 arrest after DNA damage [J].
Bunz, F ;
Dutriaux, A ;
Lengauer, C ;
Waldman, T ;
Zhou, S ;
Brown, JP ;
Sedivy, JM ;
Kinzler, KW ;
Vogelstein, B .
SCIENCE, 1998, 282 (5393) :1497-1501
[7]   Heterozygous germline mutations in the p53 homolog p63 are the cause of EEC syndrome [J].
Celli, J ;
Duijf, P ;
Hamel, BCJ ;
Bamshad, M ;
Kramer, B ;
Smits, APT ;
Newbury-Ecob, R ;
Hennekam, RCM ;
Van Buggenhout, G ;
van Haeringen, B ;
Woods, CG ;
van Essen, AJ ;
de Waal, R ;
Vriend, G ;
Haber, DA ;
Yang, A ;
McKeon, F ;
Brunner, HG ;
van Bokhoven, H .
CELL, 1999, 99 (02) :143-153
[8]   A polymorphic microsatellite that mediates induction of PIG3 by p53 [J].
Contente, A ;
Dittmer, A ;
Koch, MC ;
Roth, J ;
Dobbelstein, M .
NATURE GENETICS, 2002, 30 (03) :315-320
[9]   MICE LACKING P21(C/P1/WAF1) UNDERGO NORMAL DEVELOPMENT, BUT ARE DEFECTIVE IN G1 CHECKPOINT CONTROL [J].
DENG, CX ;
ZHANG, PM ;
HARPER, JW ;
ELLEDGE, SJ ;
LEDER, P .
CELL, 1995, 82 (04) :675-684
[10]   p63α and ΔNp63α can induce cell cycle arrest and apoptosis and differentially regulate p53 target genes [J].
Dohn, M ;
Zhang, SZ ;
Chen, XB .
ONCOGENE, 2001, 20 (25) :3193-3205