Wild-type P53 is Not a Negative Regulator of Simian Virus 40 DNA Replication in Infected Monkey Cells

Overview

Journal J Virol

Publisher American Society for Microbiology

Date 1993 Feb 1

PMID 8380470

Citations 5

Authors

A von der Weth

W Deppert

Affiliations

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Abstract

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.

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In vivo assay of p53 function in homologous recombination between simian virus 40 chromosomes.

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Structural requirements for simian virus 40 replication and virion maturation.

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