The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
p53 protein at the hub of cellular DNA damage response pathways through sequence-specific and non-sequence-specific DNA binding
Abstract
Our environment contains physical, chemical and pathological agents that challenge the integrity of our DNA. In addition to DNA repair, higher multicellular organisms have evolved multiple pathways of response to damage including programmed cell death-apoptosis. The p53 protein appears to sense multiple types of DNA damage and coordinate with multiple options for cellular response. The p53 protein activities depend upon its DNA binding. Specific p53 protein post-translational modifications are required for efficient sequence-specific binding and transcriptional activities. Non-sequence-specific DNA binding may involve a wide spectrum of p53 proteins and predominate as DNA damage is more severe or p53 protein is more highly induced. p53 protein is not strictly required for DNA damage sensing and repair. Rather, p53 protein may govern an apoptosis checkpoint through competition with DNA repair proteins for non-sequence-specific binding to exposed single-stranded regions in the DNA duplex. This model provides a framework for testing mechanisms of p53-mediated apoptosis dependent upon the p53 protein modification state, the level of p53 protein accumulation, the level of DNA damage and the capacity of the damaged cell to repair.
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Cites
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Crystal Structure of a p53 Tumor Suppressor-DNA Complex: Understanding Tumorigenic Mutations
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DNA damage-induced phosphorylation of p53 alleviates inhibition by MDM2
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Definition of a consensus binding site for p53
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DNA damage activates p53 through a phosphorylation–acetylation cascade
Sakaguchi, K., Herrera, J. E., Saito, S., Miki, T., Bustin, M., Vassilev, A., Anderson, C. W., & Appella, E. (1998) · Genes & Development · doi:10.1101/gad.12.18.2831 · Cited by 1,204
A role for ATR in the DNA damage-induced phosphorylation of p53
Tibbetts, R. S., Brumbaugh, K. M., Williams, J. M., Sarkaria, J. N., Cliby, W. A., Shieh, S.-Y., Taya, Y., Prives, C., & Abraham, R. T. (1999) · Genes & Development · doi:10.1101/gad.13.2.152 · Cited by 1,046
Chk2/hCds1 functions as a DNA damage checkpoint in G1by stabilizing p53
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p53 Sites Acetylated In Vitro by PCAF and p300 Are Acetylated In Vivo in Response to DNA Damage
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Cited by
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
DNA damage response to different surface chemistry of silver nanoparticles in mammalian cells
Ahamed, M., Karns, M., Goodson, M., Rowe, J., Hussain, S. M., Schlager, J. J., & Hong, Y. (2008) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2008.09.015 · Cited by 730
p53: traffic cop at the crossroads of DNA repair and recombination
Sengupta, S., & Harris, C. C. (2005) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1546 · Cited by 544
Ahamed, M., Posgai, R., Gorey, T. J., Nielsen, M., Hussain, S. M., & Rowe, J. J. (2010) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2009.10.016 · Cited by 494
Copper Oxide Nanoparticles Induced Mitochondria Mediated Apoptosis in Human Hepatocarcinoma Cells
Siddiqui, M. A., Alhadlaq, H. A., Ahmad, J., Al-Khedhairy, A. A., Musarrat, J., & Ahamed, M. (2013) · PLoS ONE · doi:10.1371/journal.pone.0069534 · Cited by 366
Metadata
- Authors
- Liu, Y.
- Venue
- Carcinogenesis
- Publisher
- Oxford University Press (OUP)
- Published
- 2001-06-01
- Volume
- 22
- Issue
- 6
- Pages
- 851-860
- ISSN
- 0143-3334 (ISSN-L)
- 1460-2180
- OpenAlex
- W2106493014
- Cited by
- 184
- References
- 8
- FWCI
- 3.53
- Type
- journal article
- Language
- en
- Open access
- closed
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- Liu, Y. (2001). p53 protein at the hub of cellular DNA damage response pathways through sequence-specific and non-sequence-specific DNA binding. Carcinogenesis. https://doi.org/10.1093/carcin/22.6.851
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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).
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