Loss of wild-type p53 function is responsible for upregulated homologous recombination in immortal rodent fibroblasts.

doi:10.1080/09553000050111523

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Article

Loss of wild-type p53 function is responsible for upregulated homologous recombination in immortal rodent fibroblasts.

International journal of radiation biology - 1 Aug 2000

Willers H, McCarthy E E, Alberti W, Dahm-Daphi J, Powell S N

Abstract excerpt

PURPOSE: A correlation between mutations in the tumour suppressor gene p53 and high rates of homologous recombination were previously found in immortal rodent fibroblasts. In the current study, direct evidence was sought that loss of p53 function is mainly responsible for upregulated levels of homologous recombination. MATERIALS AND METHODS: Homologous recombination was assessed in vitro using DNA plasmid...

Topics

Animals
Cell Division
Cell Transformation, Neoplastic
Cells, Cultured
Fibroblasts
Genes, p53
Mice
Mutation
Plasmids
Rats
Recombination, Genetic
Up-Regulation

Source

Open in PubMed

Identifiers

PMID: 10947118
DOI: 10.1080/09553000050111523

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026.

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