p53 in recombination and repair
Abstract
Convergent studies demonstrated that p53 regulates homologous recombination (HR) independently of its classic tumour-suppressor functions in transcriptionally transactivating cellular target genes that are implicated in growth control and apoptosis. In this review, we summarise the analyses of the involvement of p53 in spontaneous and double-strand break (DSB)-triggered HR and in alternative DSB repair routes. Molecular characterisation indicated that p53 controls the fidelity of Rad51-dependent HR and represses aberrant processing of replication forks after stalling at unrepaired DNA lesions. These findings established a genome stabilising role of p53 in counteracting error-prone DSB repair. However, recent work has also unveiled a stimulatory role for p53 in topoisomerase I-induced recombinative repair events that may have implications for a gain-of-function phenotype of cancer-related p53 mutants. Additional evidence will be discussed which suggests that p53 and/or p53-regulated gene products also contribute to nucleotide excision, base excision, and mismatch repair.
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Several p53 target genes encode DNA repair proteins.
“Given that p53 is activated in response to DNA damage, it is not surprising that several of its target genes encode for DNA repair proteins.162, 163”
From Census and evaluation of p53 target genes (2017) · cites this paper as [163]
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p53 Inhibits Strand Exchange and Replication Fork Regression Promoted by Human Rad51
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Self-citationPotential roles for p53 in nucleotide excision repair
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Wild-type p53 inhibits replication-associated homologous recombination
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Association of p53 and MSH2 with recombinative repair complexes during S phase
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Self-citationAnalysis of the Binding of p53 to DNAs Containing Mismatched and Bulged Bases
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Self-citationP53 Activates Fanconi Anemia Group C Gene Expression
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Regulation of DNA double-strand break repair pathway choice
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Census and evaluation of p53 target genes
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Thioredoxin and Related Molecules–From Biology to Health and Disease
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Coping with stress: multiple ways to activate p53
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Self-citation
- Authors
- Gatz, S. A., & Wiesmüller, L.
- Affiliations
- University Hospital Ulm (DE)
- Corresponding author
- Wiesmüller, L
- Venue
- Cell Death & Differentiation
- Published
- 2006-03-17
- Volume
- 13
- Issue
- 6
- Pages
- 1003-1016
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- OpenAlex
- W2036179093
- Cited by
- 242
- References
- 176
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 8 · 2023: 4 · 2022: 16 · 2021: 7 · 2020: 12 · 2019: 7 · 2018: 16 · 2017: 6 · 2016: 6 · 2015: 13 · 2014: 9 · 2013: 12 · 2012: 16
- FWCI
- 1.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cell Death and Differentiation (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- p53, homologous recombination, DNA double-strand break repair, RAD51, replication fork stalling, topoisomerase I, nucleotide excision repair, base excision repair, DNA mismatch repair, genome stability, tumor suppressor function
- MeSH terms
- Animals, Cell Transformation, Neoplastic, DNA, DNA Damage, DNA Repair, Humans, Mutation, Recombination, Genetic, Transcription, Genetic, Tumor Suppressor Protein p53, Apoptosis, Cell Cycle Proteins, DNA Repair Enzymes, Cell Proliferation, Apoptosis Regulatory Proteins
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