p53 protein is a suppressor of papillomavirus DNA amplificational replication

被引:37
作者
Lepik, D
Ilves, I
Kristjuhan, A
Maimets, T
Ustav, M
机构
[1] Tartu State Univ, Inst Mol & Cell Biol, Dept Microbiol & Virol, EE-2400 Tartu, Estonia
[2] Tartu State Univ, Inst Mol & Cell Biol, Dept Cell Biol, EE-2400 Tartu, Estonia
[3] Estonian Bioctr, EE-2400 Tartu, Estonia
关键词
D O I
10.1128/JVI.72.8.6822-6831.1998
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
p53 protein was able to block human and bovine papillomavirus DNA amplificational replication while not interfering with Epstein-Barr virus oriP once-per-cell cycle replication. Oligomerization, intact DNA-binding, replication protein A-binding, and proline-rich domains of the p53 protein were essential for efficient inhibition, while the N-terminal transcriptional activation and C-terminal regulatory domains were dispensable for the suppressor activity of the p53 protein. The inhibition of replication was caused neither by the downregulation of expression of the E1 and E2 proteins nor by cell cycle block or apoptosis. Our data suggest that the intrinsic activity of p53 to suppress amplificational replication of the papillomavirus origin may have an important role in the virus life cycle and in virus-cell interactions.
引用
收藏
页码:6822 / 6831
页数:10
相关论文
共 69 条
[1]   Interaction between replication protein A and p53 is disrupted after UV damage in a DNA repair-dependent manner [J].
Abramova, NA ;
Russell, J ;
Botchan, M ;
Li, R .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (14) :7186-7191
[2]   Transcriptional and replicational activation functions in the bovine papillomavirus type 1 E2 protein are encoded by different structural determinants [J].
Abroi, A ;
Kurg, R ;
Ustav, M .
JOURNAL OF VIROLOGY, 1996, 70 (09) :6169-6179
[3]   THE HUMAN RIBOSOMAL-PROTEIN S7-ENCODING GENE - ISOLATION, STRUCTURE AND LOCALIZATION IN 2P25 [J].
ANNILO, T ;
LAAN, M ;
STAHL, J ;
METSPALU, A .
GENE, 1995, 165 (02) :297-302
[4]   P53 BINDS SINGLE-STRANDED-DNA ENDS THROUGH THE C-TERMINAL DOMAIN AND INTERNAL DNA SEGMENTS VIA THE MIDDLE DOMAIN [J].
BAKALKIN, G ;
SELIVANOVA, G ;
YAKOVLEVA, T ;
KISELEVA, E ;
KASHUBA, E ;
MAGNUSSON, KP ;
SZEKELY, L ;
KLEIN, G ;
TERENIUS, L ;
WIMAN, KG .
NUCLEIC ACIDS RESEARCH, 1995, 23 (03) :362-369
[5]   P53 BINDS SINGLE-STRANDED-DNA ENDS AND CATALYZES DNA RENATURATION AND STRAND TRANSFER [J].
BAKALKIN, G ;
YAKOVLEVA, T ;
SELIVANOVA, G ;
MAGNUSSON, KP ;
SZEKELY, L ;
KISELEVA, E ;
KLEIN, G ;
TERENIUS, L ;
WIMAN, KG .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (01) :413-417
[6]   A PROTEOLYTIC FRAGMENT FROM THE CENTRAL REGION OF P53 HAS MARKED SEQUENCE-SPECIFIC DNA-BINDING ACTIVITY WHEN GENERATED FROM WILD-TYPE BUT NOT FROM ONCOGENIC MUTANT P53-PROTEIN [J].
BARGONETTI, J ;
MANFREDI, JJ ;
CHEN, XB ;
MARSHAK, DR ;
PRIVES, C .
GENES & DEVELOPMENT, 1993, 7 (12B) :2565-2574
[7]  
BOTCHAN MR, 1986, PAPILLOMAVIRUSES, P53
[8]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[9]  
BRAIN R, 1994, ONCOGENE, V9, P1775
[10]   p53 levels, functional domains, and DNA damage determine the extent of the apoptotic response of tumor cells [J].
Chen, XB ;
Ko, LJ ;
Jayaraman, L ;
Prives, C .
GENES & DEVELOPMENT, 1996, 10 (19) :2438-2451