The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Expression of Wild-type p53 Is Required for Efficient Global Genomic Nucleotide Excision Repair in UV-irradiated Human Fibroblasts
Open accessAbstract
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 dimers or 6-4 photoproducts, respectively, to measure their repair in UV-irradiated human fibroblasts. Cells homozygous for p53 mutations were deficient in the repair of both photoproducts, whereas cells heterozygous for mutant p53 exhibited normal repair of 6-4 photoproducts, but decreased initial rates of removal of cyclobutane pyrimidine dimers, compared with normal cells. The specificity of the effect of wild-type p53 on nucleotide excision repair was demonstrated in a p53 homozygous mutant cell line containing a tetracycline-regulated wild-type p53 gene. Wild-type p53 expression and activity were suppressed in the presence of tetracycline, whereas withdrawal of tetracycline resulted in the induction of p53 expression, cell cycle checkpoint activation, and DNA damage-induced apoptosis. The regulated expression of wild-type p53 resulted in the recovery of normal levels of repair of both cyclobutane pyrimidine dimers and 6-4 photoproducts in genomic DNA, but did not alter the transcription-coupled repair of cyclobutane pyrimidine dimers. Therefore, the wild-type p53 gene product is an important determinant of nucleotide excision repair activity in human cells.
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Cites
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Cited by
Molecular mechanism of nucleotide excision repair
de Laat, W. L., Jaspers, N. G. J., & Hoeijmakers, J. H. J. (1999) · Genes & Development · doi:10.1101/gad.13.7.768 · Cited by 1,122
A ribonucleotide reductase gene involved in a p53-dependent cell-cycle checkpoint for DNA damage
Tanaka, H., Arakawa, H., Yamaguchi, T., Shiraishi, K., Fukuda, S., Matsui, K., Takei, Y., & Nakamura, Y. (2000) · Nature · doi:10.1038/35003506 · Cited by 904
p53 in the DNA–Damage–Repair Process
Williams, A. B., & Schumacher, B. (2016) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a026070 · Cited by 835
MDM2 — master regulator of the p53 tumor suppressor protein
Momand, J., Wu, H.-H., & Dasgupta, G. (2000) · Gene · doi:10.1016/s0378-1119(99)00487-4 · Cited by 641
Hwang, B. J., Ford, J. M., Hanawalt, P. C., & Chu, G. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.2.424 · Cited by 581
Self-citation
Metadata
- Authors
- Ford, J. M., & Hanawalt, P. C.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1997-10
- Volume
- 272
- Issue
- 44
- Pages
- 28073-28080
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2015853472
- Cited by
- 358
- References
- 41
- FWCI
- 9.22
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: Expression of Wild-type p53 Is Required for Efficient Global Genomic Nucleotide Excision Repair in UV-irradiated Human Fibroblasts. https://app.cochat.ai/papers/10.1074/jbc.272.44.28073
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- Ford, J. M., & Hanawalt, P. C. (1997). Expression of Wild-type p53 Is Required for Efficient Global Genomic Nucleotide Excision Repair in UV-irradiated Human Fibroblasts. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.272.44.28073
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