Human tumor suppressor p53 and DNA viruses

被引:58
作者
Collot-Teixeira, S [1 ]
Bass, J [1 ]
Denis, F [1 ]
Ranger-Rogez, S [1 ]
机构
[1] Univ Limoges, Teaching Hosp, CHRU Dupuytren, Dept Virol, F-87042 Limoges, France
关键词
D O I
10.1002/rmv.431
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Human tumor suppressor protein p53 plays a major role in the cell cycle, orchestrating a number of important genes involved in cell-cycle control and apoptosis, and seems to be one of the most important molecules protecting cells from malignant transformation. Mutations in the p53 gene are observed in about 50% of primary tumors, inducing defective p53 protein no longer capable of binding DNA and of activating transcription. Certain DNA viruses are thought to act in a similar way and may also contribute to the progression of invasive cancer in infected tissue. One of the most effective strategies employed by these viruses is the inhibition of p53 protein by interaction with viral oncoproteins, implying a direct but also an indirect role of these viruses in the impairment of p53 structure and function. This article provides a summary of current knowledge concerning p53 tumor suppressor protein and reviews the different mechanisms adopted by different DNA viruses in undermining p53 function. Copyright (C) 2004 John Wiley Sons, Ltd.
引用
收藏
页码:301 / 319
页数:19
相关论文
共 193 条
[1]   Downregulation of the cdc2/cyclin B protein kinase activity by binding of p53 to p34cdc2 [J].
Ababneh, M ;
Götz, C ;
Montenarh, M .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2001, 283 (02) :507-512
[2]   MALIGNANT TRANSFORMATION OF HAMSTER EMBRYO FIBROBLASTS FOLLOWING EXPOSURE TO ULTRAVIOLET-IRRADIATED HUMAN CYTOMEGALOVIRUS [J].
ALBRECHT, T ;
RAPP, F .
VIROLOGY, 1973, 55 (01) :53-61
[3]  
Appella E, 2000, PATHOL BIOL, V48, P227
[4]   Transcriptional regulation of the mdm2 oncogene by p53 requires TRRAP acetyltransferase complexes [J].
Ard, PG ;
Chatterjee, C ;
Kunjibettu, S ;
Adside, LR ;
Gralinski, LE ;
McMahon, SB .
MOLECULAR AND CELLULAR BIOLOGY, 2002, 22 (16) :5650-5661
[5]   NQ01 stabilizes p53 through a distinct pathway [J].
Asher, G ;
Lotem, J ;
Kama, R ;
Sachs, L ;
Shaul, Y .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (05) :3099-3104
[6]   Mdm-2 and ubiquitin-independent p53 proteasomal degradation regulated by NQ01 [J].
Asher, G ;
Lotem, J ;
Sachs, L ;
Kahana, C ;
Shaul, Y .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (20) :13125-13130
[7]  
Azzam EI, 1997, CELL GROWTH DIFFER, V8, P1161
[8]   THE RETINOBLASTOMA PROTEIN COPURIFIES WITH E2F-I, AN E1A-REGULATED INHIBITOR OF THE TRANSCRIPTION FACTOR E2F [J].
BAGCHI, S ;
WEINMANN, R ;
RAYCHAUDHURI, P .
CELL, 1991, 65 (06) :1063-1072
[9]   Suppression of mismatched mutation by p53: a mechanism for guarding genomic integrity [J].
Ballal, K ;
Zhang, W ;
Mukhopadyay, T ;
Huang, P .
JOURNAL OF MOLECULAR MEDICINE-JMM, 2002, 80 (01) :25-32
[10]   SITE-SPECIFIC BINDING OF WILD-TYPE-P53 TO CELLULAR DNA IS INHIBITED BY SV40-T ANTIGEN AND MUTANT P53 [J].
BARGONETTI, J ;
REYNISDOTTIR, I ;
FRIEDMAN, PN ;
PRIVES, C .
GENES & DEVELOPMENT, 1992, 6 (10) :1886-1898