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Article

Expression of wild-type p53 is required for efficient global genomic nucleotide excision repair in UV-irradiated human fibroblasts.

The Journal of biological chemistry - 31 Oct 1997

Ford J M, Hanawalt P C

Abstract excerpt

We have shown previously that Li-Fraumeni syndrome fibroblasts homozygous for p53 mutations are deficient in the removal of UV-induced cyclobutane pyrimidine dimers from genomic DNA, but still proficient in the transcription-coupled repair pathway (Ford, J. M., and Hanawalt, P. C. (1995) Proc. Natl. Acad. Sci. U. S. A. 92, 8876-8880). We have now utilized monoclonal antibodies specific for cyclobutane pyrimidine...

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Source

Identifiers

PMID: 9346961
DOI: 10.1074/jbc.272.44.28073

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Expression of wild-type p53 is required for efficient global genomic nucleotide excision repair in UV-irradiated human fibroblasts.PMID 9346961Read ↗

Li-Fraumeni syndrome fibroblasts homozygous for p53 mutations are deficient in global DNA repair but exhibit normal transcription-coupled repair and enhanced UV resistance.Semantic proximity Read ↗

Decreased DNA Repair Efficiency by Loss or Disruption of p53 Function Preferentially Affects Removal of Cyclobutane Pyrimidine Dimers from Non-transcribed Strand and Slow Repair Sites in Transcribed StrandSemantic proximity Read ↗

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