Roles for p53 in growth arrest and apoptosis: putting on the brakes after genotoxic stress
Abstract
The tumor suppressor gene p53 plays a major role in regulation of the mammalian cellular stress response, in part through the transcriptional activation of genes involved in cell cycle control, DNA repair, and apoptosis. Many factors contribute to control of the activation of p53, and the downstream response to its activation may also vary depending on the cellular environment or other modifying factors in the cell. The complexity of the p53 response makes this an ideal system for application of newly emerging rapid throughput analysis techniques and informatics analysis.
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Arsenic results in cytotoxicity by affecting the status of tumor-suppressor protein 53.
“Arsenic results in cytotoxicity by affecting the status of tumor-suppressor protein 53 [92, 93].”
From Arsenic Contamination of Groundwater: A Review of Sources, Prevalence, Health Risks, and Strategies for Mitigation (2014) · cites this paper as [92]
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“Protein 53 plays a very crucial role in a wide range of cellular functions by modulation of transformation and regulation of cell growth and control of cell cycle, DNA synthesis, DNA repair and differentiation, and apoptosis [94, 95].”
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Cellular senescence and apoptosis: how cellular responses might influence aging phenotypes
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MdmX Protects p53 from Mdm2-Mediated Degradation
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Cancer and aging: the importance of telomeres in genome maintenance
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p53 is dispensable for UV-induced cell cycle arrest at late G1 in mammalian cells
Al-Mohanna, M. A., Al-Khodairy, F. M., Krezolek, Z., Bertilsson, P.-A., Al-Houssein, K. A., & Aboussekhra, A. (2001) · Carcinogenesis · doi:10.1093/carcin/22.4.573 · Cited by 30 · see citing works
DNA damage response in proliferating Müller glia in the mammalian retina
Nomura-Komoike, K., Saitoh, F., Komoike, Y., & Fujieda, H. (2016) · Investigative Opthalmology & Visual Science · doi:10.1167/iovs.15-18101 · Cited by 25 · see citing works
- Authors
- Amundson, S. A., Myers, T. G., & Fornace, A. J.
- Affiliations
- National Institutes of Health (US)
- Venue
- Oncogene
- Published
- 1998-12-24
- Volume
- 17
- Issue
- 25
- Pages
- 3287-3299
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2318612270
- Cited by
- 424
- References
- 0
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 4 · 2023: 6 · 2022: 1 · 2021: 5 · 2020: 11 · 2019: 6 · 2018: 6 · 2017: 7 · 2016: 10 · 2015: 14 · 2014: 28 · 2013: 20 · 2012: 12
- FWCI
- 14.67
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- p53, tumor suppressor, genotoxic stress, cell cycle arrest, apoptosis, DNA repair, transcriptional activation, cellular stress response, p53 activation, cell cycle regulation
- MeSH terms
- Animals, Cell Cycle, Cell Division, Computer Simulation, DNA, DNA Damage, Gene Expression Regulation, Humans, Spindle Apparatus, Mutagens, Transcription, Genetic, Tumor Suppressor Protein p53, Apoptosis, Computational Biology
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