WILD-TYPE P53 IS NOT A NEGATIVE REGULATOR OF SIMIAN-VIRUS 40 DNA-REPLICATION IN INFECTED MONKEY CELLS

被引：18

作者：

VONDERWETH, A ^{[1
]}

DEPPERT, W ^{[1
]}

机构：

[1] HEINRICH PETTE INST EXPTL VIROL & IMMUNOL,MARTINISTR 52,W-2000 HAMBURG 20,GERMANY

来源：

JOURNAL OF VIROLOGY | 1993年 / 67卷 / 02期

关键词：

D O I：

10.1128/JVI.67.2.886-893.1993

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

To analyze the proposed growth-inhibitory function of wild-type p53, we compared simian virus 40 (SV40) DNA replication in primary rhesus monkey kidney (PRK) cells, which express wild-type p53, and in the established rhesus monkey kidney cell line LLC-MK2, which expresses a mutated p53 that does not complex with large T antigen. SV40 DNA replication proceeded identically in both cell types during the course of infection. Endogenously expressed wild-type p53 thus does not negatively modulate SV40 DNA replication in vivo. We suggest that inhibition of SV40 DNA replication by wild-type p53 in in vitro replication assays is due to grossly elevated ratios of p53 to large T antigen, thus depleting the replication-competent free large T antigen in the assay mixtures by complex formation. In contrast, the ratio of p53 to large T antigen in in vivo replication is low, leaving the majority of large T antigen in a free, replication-competent state.

引用

页码：886 / 893

页数：8

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