p53 in the DNA–Damage–Repair Process
Open accessAbstract
The cells in the human body are continuously challenged by a variety of genotoxic attacks. Erroneous repair of the DNA can lead to mutations and chromosomal aberrations that can alter the functions of tumor suppressor genes or oncogenes, thus causing cancer development. As a central tumor suppressor, p53 guards the genome by orchestrating a variety of DNA-damage-response (DDR) mechanisms. Already early in metazoan evolution, p53 started controlling the apoptotic demise of genomically compromised cells. p53 plays a prominent role as a facilitator of DNA repair by halting the cell cycle to allow time for the repair machineries to restore genome stability. In addition, p53 took on diverse roles to also directly impact the activity of various DNA-repair systems. It thus appears as if p53 is multitasking in providing protection from cancer development by maintaining genome stability.
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Transcription factor p53 is the master regulator of the DNA damage response and is stabilized and transactivated in response to DNA damage.
“It is established that transcription factor p53 is the master regulator of the DNA damage response and is stabilized and transactivated in response to DNA damage [ 38 , 39 , 40 , 41 ].”
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- Authors
- Williams, A. B., & Schumacher, B.
- Affiliations
- University of Cologne (DE)
- Corresponding author
- Schumacher, Björn
- Venue
- Cold Spring Harbor Perspectives in Medicine
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2016-04-05
- Volume
- 6
- Issue
- 5
- Pages
- a026070
- ISSN
- 2157-1422 (ISSN-L)
- PMC
- PMC4852800
- OpenAlex
- W2341866865
- Cited by
- 835
- References
- 120
- Citations by year
- 2026: 56 · 2025: 102 · 2024: 114 · 2023: 105 · 2022: 101 · 2021: 128 · 2020: 88 · 2019: 63 · 2018: 47 · 2017: 26 · 2016: 5
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Medicine (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- Funders
- European Commission (316964, 316354, 316390, 239330)
- Deutsche Forschungsgemeinschaft (SFB829, KFO286, SFB 670)
- Deutsche Krebshilfe (109453)
- FP7 Ideas: European Research Council (260383)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- p53, DNA damage response, DNA repair, genome stability, tumor suppressor, apoptosis, cell cycle arrest, genotoxic stress, cancer prevention, chromosomal abnormalities, genetic mutations
- MeSH terms
- Animals, Cell Cycle, DNA Damage, DNA Repair, Humans, Neoplasms, Transcription, Genetic, Tumor Suppressor Protein p53, Genomic Instability
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.
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