Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (511 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The removal of dna lesions and/or restoration of intact DNA strands without base pair mismatches, intrastrand or interstrand crosslinks, or discontinuities in the DNA sugar-phosphate backbones.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: DNA Damage Response.
Where it fits in the MeSH classification
- Broader topics
- Biochemical Phenomena; Genetic Phenomena
- Narrower topics
- DNA End-Joining Repair; DNA Mismatch Repair; Excision Repair; Recombinational DNA Repair; SOS Response, Genetics
- See also
- DNA Damage; DNA Repair Enzymes; DNA Damage Tolerance
Related concepts
- DNA Damage
- Base Pair Mismatches
Research landscape
PubMed indexes 68,054 records tagged with the MeSH heading “DNA Repair” (counts retrieved 2026-10-29). 12,952 of them (19.0%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 20,468 records.
Reviews account for 12,515 records (18.4%) and meta-analyses for 184. Randomized controlled trials number 146 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 18,420 |
| 2000-2009 | 16,214 |
| 2010-2019 | 20,468 |
| 2020 onward | 12,952 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 12,515 | 18.4% |
| Meta-analyses | 184 | 0.3% |
| Randomized controlled trials | 146 | 0.2% |
Method: PubMed query "DNA Repair"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The CIP2A-TOPBP1 axis facilitates mitotic DNA repair via MiDAS and MMEJ | 2025 | Research article Design not recorded in structured metadata | 14 | cc by PMID 41309571 · DOI · PMC12661054 |
| HAT1 functions as a lactyltransferase and mediates RPA1 lactylation to promote DNA repair and radioresistance in lung adenocarcinoma | 2025 | Research article Design not recorded in structured metadata | 8 | cc by PMID 41271679 · DOI · PMC12639135 |
| Hierarchical mechanisms control the clearance of DNA lesion-stalled RNA polymerase II | 2026 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41554717 · DOI · PMC12904859 |
The CIP2A-TOPBP1 axis facilitates mitotic DNA repair via MiDAS and MMEJ [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Mitotic DNA double-strand breaks (DSBs) accumulate in response to replication stress or BRCA1/2 deficiency posing a significant threat to genome stability as repair by non-homologous end-joining (NHEJ) and homologous recombination (HR) is largely inactivated in mitosis.
- Closing excerpt
- These findings position the CIP2A-TOPBP1 axis as a central regulatory hub for mitotic DNA repair, highlighting therapeutic opportunities in tumours characterised by HR deficiency or elevated replication stress.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (182 words)
Mitotic DNA double-strand breaks (DSBs) accumulate in response to replication stress or BRCA1/2 deficiency posing a significant threat to genome stability as repair by non-homologous end-joining (NHEJ) and homologous recombination (HR) is largely inactivated in mitosis. Instead, mitotic cells rely on alternative repair processes such as microhomology-mediated end-joining (MMEJ) and mitotic DNA synthesis (MiDAS). How these mitotic DNA repair pathways are functionally regulated remains unclear. Here we reveal that the CIP2A-TOPBP1 complex plays an essential regulatory role by facilitating the mitotic recruitment of both SMX complex components and Polθ to mitotic chromatin. Recruitment of the SMX complex components is driven by CDK1-dependent phosphorylation of SLX4 at Thr1260, enabling its interaction with TOPBP1 BRCT domains 1/2, thereby promoting MiDAS. Concurrently, CIP2A promotes efficient mitotic localisation of Polθ to facilitate MMEJ. The simultaneous functional disruption of both MiDAS and MMEJ pathways upon CIP2A loss provides rationale for the synthetic lethality observed in BRCA1 or 2-deficient cells. These findings position the CIP2A-TOPBP1 axis as a central regulatory hub for mitotic DNA repair, highlighting therapeutic opportunities in tumours characterised by HR deficiency or elevated replication stress.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41309571 · DOI · PMC12661054
HAT1 functions as a lactyltransferase and mediates RPA1 lactylation to promote DNA repair and radioresistance in lung adenocarcinoma [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Lysine lactylation is a post-translational modification induced by lactate discovered in recent years.
- Closing excerpt
- In conclusion, our research reveals that HAT1-regulated RPA1 lactylation plays an important role in homologous recombination and radioresistance, suggesting that HAT1 may become a potential therapeutic target for reversing the radioresistance caused by lactate accumulation in cancer cells.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (142 words)
Lysine lactylation is a post-translational modification induced by lactate discovered in recent years. Abnormal lysine lactylation contributes to the occurrence and progression of various tumors. However, the mediators and downstream targets of lysine lactylation remain unclear. Here, we report that HAT1 serves as a potential lactyltransferase that can promote homologous recombination and lead to radioresistance by regulating lactylation of RPA1. Lactylation of RPA1 facilitates its binding to single-stranded DNA and MRE11-RAD50-NBS1 (MRN) complexes and promotes homologous recombination. HAT1 knockout inhibits DNA repair in lung adenocarcinoma cells, thereby increasing radiotherapy sensitivity. Interestingly, we also found that K15 auto-lactylation of HAT1 can modulate its lactyltransferase activity. In conclusion, our research reveals that HAT1-regulated RPA1 lactylation plays an important role in homologous recombination and radioresistance, suggesting that HAT1 may become a potential therapeutic target for reversing the radioresistance caused by lactate accumulation in cancer cells.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41271679 · DOI · PMC12639135
Hierarchical mechanisms control the clearance of DNA lesion-stalled RNA polymerase II [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Stalling of elongating RNA polymerase II (RNAPII) at DNA lesions blocks transcription and triggers transcription-coupled repair (TCR).
- Closing excerpt
- This mechanistic framework explains how cells resolve DNA lesion-stalled RNAPII during normal and compromised TCR.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (187 words)
Stalling of elongating RNA polymerase II (RNAPII) at DNA lesions blocks transcription and triggers transcription-coupled repair (TCR). However, the mechanisms determining the fate of stalled RNAPII remain incompletely understood. Here, we develop a time-resolved assay to track RNAPII clearance and degradation at UV-induced lesions. We show that RNAPII ubiquitylation by CSB and the CRL4CSA ubiquitin ligase is essential, as loss of these proteins causes persistent RNAPII accumulation at damage sites. Downstream of CSB/CRL4CSA-mediated ubiquitylation, two distinct pathways mediate RNAPII removal. The primary rapid route relies on TFIIH, with its XPD helicase activity driving RNAPII dissociation after proper recruitment and positioning by ELOF1, UVSSA, and STK19. A secondary slow pathway is mediated by the ubiquitin-dependent segregase VCP, which compensates for impaired TFIIH function. While VCP contributes only minimally in TCR-proficient cells, inhibition of VCP in TFIIH-deficient contexts completely abrogates RNAPII clearance. Together, these findings establish a hierarchical program in which CSB/CRL4CSA-mediated ubiquitylation initiates RNAPII processing, TFIIH/XPD helicase activity provides the main clearance mechanism, and VCP-dependent extraction acts as a backup when TFIIH fails. This mechanistic framework explains how cells resolve DNA lesion-stalled RNAPII during normal and compromised TCR.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41554717 · DOI · PMC12904859
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article DNA damage response inhibitors in cancer therapy: lessons from the past, current status and future implications [4]
- Research article H2AX: A key player in DNA damage response and a promising target for cancer therapy [5]
- Research article Pathogenesis of DNA repair-deficient cancers: a statistical meta-analysis of putative Real Common Target genes [6]
- Research article Causes and consequences of DNA single-strand breaks [7]
- Research article Systematic review and meta-analysis of ovarian cancers: estimation of microsatellite-high frequency and characterization of mismatch repair deficient tumor histology [8]
- Research article How Do ROS Induce NETosis? Oxidative DNA Damage, DNA Repair, and Chromatin Decondensation [9]
References
- Martin PR, Nieminuszczy J, Kozik Z, Jakub N, Kowalski S, Lecot M, et al.. The CIP2A-TOPBP1 axis facilitates mitotic DNA repair via MiDAS and MMEJ. . 2025. PMID 41309571 · DOI · PMC12661054
- He J, Lai T, Zhao Y, Zhou Z, Zhou L, Tao D, et al.. HAT1 functions as a lactyltransferase and mediates RPA1 lactylation to promote DNA repair and radioresistance in lung adenocarcinoma. . 2025. PMID 41271679 · DOI · PMC12639135
- van der Meer PJ, Yakoub G, Tsukada K, Nakazawa Y, Ogi T, Luijsterburg MS. Hierarchical mechanisms control the clearance of DNA lesion-stalled RNA polymerase II. . 2026. PMID 41554717 · DOI · PMC12904859
- Drew Y, Zenke FT, Curtin NJ. DNA damage response inhibitors in cancer therapy: lessons from the past, current status and future implications. Nat Rev Drug Discov. 2025. PMID 39533099 · DOI
- Prabhu KS, Kuttikrishnan S, Ahmad N, Habeeba U, Mariyam Z, Suleman M, et al.. H2AX: A key player in DNA damage response and a promising target for cancer therapy. Biomed Pharmacother. 2024. PMID 38688170 · DOI
- Woerner SM, Benner A, Sutter C, Schiller M, Yuan YP, Keller G, et al.. Pathogenesis of DNA repair-deficient cancers: a statistical meta-analysis of putative Real Common Target genes. Oncogene. 2003. PMID 12700659 · DOI
- Caldecott KW. Causes and consequences of DNA single-strand breaks. Trends Biochem Sci. 2024. PMID 38040599 · DOI
- Pal T, Permuth-Wey J, Kumar A, Sellers TA. Systematic review and meta-analysis of ovarian cancers: estimation of microsatellite-high frequency and characterization of mismatch repair deficient tumor histology. Clin Cancer Res. 2008. PMID 18980979 · DOI · PMC2655731
- Azzouz D, Palaniyar N. How Do ROS Induce NETosis? Oxidative DNA Damage, DNA Repair, and Chromatin Decondensation. Biomolecules. 2024. PMID 39456240 · DOI · PMC11505619
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.