The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
p53 regulation of DNA excision repair pathways
Abstract
The regulation of DNA excision repair pathways by p53 and its downstream genes is an emerging body of literature, largely distinct and separable from the more-studied cell cycle arrest and apoptosis responses regulated by p53. Regulation of nucleotide excision repair of UV-damage by p53 and its downstream genes Gadd45 and p48XPE has been well-documented, but much remains to be done in elucidating mechanisms. Moreover, p53 also participates in base excision repair of hydrogen peroxide-induced damage, still at an early stage of investigation. In human cancers carrying inactivating mutations in p53, especially those wherein p53 mutation occurs early, accelerated mutagenesis by exogenous and endogenous DNA damage is predicted. At the same time, the excision repair pathways could provide a useful target for DNA-damaging chemotherapeutics against p53-defective cancers, having decreased ability to repair chemotherapeutic damage. To our knowledge, this is the first review to address this emerging field.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Kastan, M. B., Zhan, Q., El-Deiry, W. S., Carrier, F., Jacks, T., Walsh, W. V., Plunkett, B. S., Vogelstein, B., & Fornace, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90593-2 · Cited by 3,047 · cited 3×
“In order to specifically address a role for p53 in the observed DNA damage responses, matched pairs of p53 wild-type and p53 mutant cell lines were used (Kastan et al., 1992).”
BackgroundMethodInfluentialDefinition of a consensus binding site for p53
El-Deiry, W. S., Kern, S. E., Pietenpol, J. A., Kinzler, K. W., & Vogelstein, B. (1992) · Nature Genetics · doi:10.1038/ng0492-45 · Cited by 1,985
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
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
UCN-01: a potent abrogator of G2 checkpoint function in cancer cells with disrupted p53
Wang, Q., Fan, S., Eastman, A., Worland, P. J., Sausville, E. A., & O'Connor, P. M. (1996) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/88.14.956 · Cited by 453
Cited by
A Mechanistic Perspective on the Chemistry of DNA Repair Glycosylases
Stivers, J. T., & Jiang, Y. L. (2003) · Chemical Reviews · doi:10.1021/cr010219b · Cited by 447
Ultraviolet radiation and cutaneous malignant melanoma
Jhappan, C., Noonan, F. P., & Merlino, G. (2003) · Oncogene · doi:10.1038/sj.onc.1206450 · Cited by 283
Intracellular Aβ42 activates p53 promoter: a pathway to neurodegeneration in Alzheimer's disease
Ohyagi, Y., Asahara, H., Chui, D.-H., Tsuruta, Y., Sakae, N., Miyoshi, K., Yamada, T., Kikuchi, H., Taniwaki, T., Murai, H., et al. (2005) · The FASEB Journal · doi:10.1096/fj.04-2637fje · Cited by 281
p53 and regulation of DNA damage recognition during nucleotide excision repair
Adimoolam, S., & Ford, J. M. (2003) · DNA Repair · doi:10.1016/s1568-7864(03)00087-9 · Cited by 181
Mechanisms of mutation formation with long‐wave ultraviolet light (UVA)
Rünger, T. M., & Kappes, U. P. (2008) · Photodermatology, Photoimmunology & Photomedicine · doi:10.1111/j.1600-0781.2008.00319.x · Cited by 171
Metadata
- Authors
- Smith, M. L.
- Venue
- Mutagenesis
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-03-01
- Volume
- 17
- Issue
- 2
- Pages
- 149-156
- ISSN
- 0267-8357 (ISSN-L)
- 1464-3804
- OpenAlex
- W2097572806
- Cited by
- 162
- References
- 5
- FWCI
- 4.75
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: p53 regulation of DNA excision repair pathways. https://app.cochat.ai/papers/10.1093/mutage/17.2.149
- The paper
- Smith, M. L. (2002). p53 regulation of DNA excision repair pathways. Mutagenesis. https://doi.org/10.1093/mutage/17.2.149
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
