Article
Li-Fraumeni syndrome fibroblasts homozygous for p53 mutations are deficient in global DNA repair but exhibit normal transcription-coupled repair and enhanced UV resistance.
Proceedings of the National Academy of Sciences of the United States of America - 12 Sept 1995
Ford J M, Hanawalt P C
Abstract excerpt
We investigated whether mutations in the p53 tumor suppressor gene alter UV sensitivity and/or repair of UV-induced DNA damage in primary human skin fibroblasts from patients with Li-Fraumeni syndrome, heterozygous for mutations in one allele of the p53 gene (p53 wt/mut) and sublines expressing only mutant p53 (p53 mut). The p53 mut cells were more resistant than the p53 wt/mut cells to UV cytotoxicity and...
Topics
- Apoptosis
- Cell Survival
- Clone Cells
- DNA Repair
- Dose-Response Relationship, Radiation
- Fibroblasts
- Homozygote
- Humans
- Li-Fraumeni Syndrome
- Microscopy, Fluorescence