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: 4 complete abstracts (721 words), 10 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
A major DNA repair mechanism in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand.
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: Nucleotide Excision Repair; Excision Repair, Nucleotide; Base Excision Repair; Excision Repair, Base; Transcription Coupled Excision Repair; Transcription Coupled Repair; Transcription-Coupled Excision Repair; Excision Repair, Transcription-Coupled.
Where it fits in the MeSH classification
- Broader topics
- DNA Repair
Research landscape
PubMed indexes 323 records tagged with the MeSH heading “Excision Repair” (counts retrieved 2026-10-29). 322 of them (99.7%) were published from 2020 onward, and the busiest period so far is 2020 onward with 322 records.
Reviews account for 60 records (18.6%) and meta-analyses for 0. Randomized controlled trials number 1 (0.3%) 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 | 1 |
| 2000-2009 | 0 |
| 2010-2019 | 0 |
| 2020 onward | 322 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 60 | 18.6% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 1 | 0.3% |
Method: PubMed query "Excision 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 |
|---|---|---|---|---|
| Covalent PARylation of DNA base excision repair proteins regulates DNA demethylation | 2024 | Research article Design not recorded in structured metadata | 30 | cc by PMID 38167803 · DOI · PMC10762122 |
| Trabectedin derails transcription-coupled nucleotide excision repair to induce DNA breaks in highly transcribed genes | 2024 | Research article Design not recorded in structured metadata | 25 | cc by PMID 38360910 · DOI · PMC10869700 |
| Elf1 promotes Rad26's interaction with lesion-arrested Pol II for transcription-coupled repair | 2024 | Research article Design not recorded in structured metadata | 22 | cc by PMID 38194460 · DOI · PMC10801861 |
| Mitochondrial DNA Instability and Neuroinflammation: Connecting the Dots Between Base Excision Repair and Neurodegenerative Disease | 2026 | Review article Design not recorded in structured metadata | 5 | cc by PMID 41595502 · DOI · PMC12841323 |
Covalent PARylation of DNA base excision repair proteins regulates DNA demethylation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The intracellular ATP-ribosyltransferases PARP1 and PARP2, contribute to DNA base excision repair (BER) and DNA demethylation and have been implicated in epigenetic programming in early mammalian development.
- Closing excerpt
- Our findings establish a critical function of covalent protein PARylation in coordinating molecular processes associated with dynamic DNA methylation.
- 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 (133 words)
The intracellular ATP-ribosyltransferases PARP1 and PARP2, contribute to DNA base excision repair (BER) and DNA demethylation and have been implicated in epigenetic programming in early mammalian development. Recently, proteomic analyses identified BER proteins to be covalently poly-ADP-ribosylated by PARPs. The role of this posttranslational modification in the BER process is unknown. Here, we show that PARP1 senses AP-sites and SSBs generated during TET-TDG mediated active DNA demethylation and covalently attaches PAR to each BER protein engaged. Covalent PARylation dissociates BER proteins from DNA, which accelerates the completion of the repair process. Consistently, inhibition of PARylation in mESC resulted both in reduced locus-specific TET-TDG-targeted DNA demethylation, and in reduced general repair of random DNA damage. Our findings establish a critical function of covalent protein PARylation in coordinating molecular processes associated with dynamic DNA methylation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38167803 · DOI · PMC10762122
Trabectedin derails transcription-coupled nucleotide excision repair to induce DNA breaks in highly transcribed genes [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Most genotoxic anticancer agents fail in tumors with intact DNA repair.
- Closing excerpt
- This work advances the use of trabectedin for precision oncology and for studying TC-NER and transcription.
- 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 (151 words)
Most genotoxic anticancer agents fail in tumors with intact DNA repair. Therefore, trabectedin, anagent more toxic to cells with active DNA repair, specifically transcription-coupled nucleotide excision repair (TC-NER), provides therapeutic opportunities. To unlock the potential of trabectedin and inform its application in precision oncology, an understanding of the mechanism of the drug's TC-NER-dependent toxicity is needed. Here, we determine that abortive TC-NER of trabectedin-DNA adducts forms persistent single-strand breaks (SSBs) as the adducts block the second of the two sequential NER incisions. We map the 3'-hydroxyl groups of SSBs originating from the first NER incision at trabectedin lesions, recording TC-NER on a genome-wide scale. Trabectedin-induced SSBs primarily occur in transcribed strands of active genes and peak near transcription start sites. Frequent SSBs are also found outside gene bodies, connecting TC-NER to divergent transcription from promoters. This work advances the use of trabectedin for precision oncology and for studying TC-NER and transcription.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38360910 · DOI · PMC10869700
Elf1 promotes Rad26's interaction with lesion-arrested Pol II for transcription-coupled repair [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Transcription-coupled nucleotide excision repair (TC-NER) is a highly conserved DNA repair pathway that removes bulky lesions in the transcribed genome.
- Closing excerpt
- Together, our results provide important mechanistic insights into how two conserved transcription-coupled repair factors, Rad26/CSB and Elf1/ELOF1, work together at the initial lesion recognition steps of transcription-coupled repair.
- 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 (196 words)
Transcription-coupled nucleotide excision repair (TC-NER) is a highly conserved DNA repair pathway that removes bulky lesions in the transcribed genome. Cockayne syndrome B protein (CSB), or its yeast ortholog Rad26, has been known for decades to play important roles in the lesion-recognition steps of TC-NER. Another conserved protein ELOF1, or its yeast ortholog Elf1, was recently identified as a core transcription-coupled repair factor. How Rad26 distinguishes between RNA polymerase II (Pol II) stalled at a DNA lesion or other obstacles and what role Elf1 plays in this process remains unknown. Here, we present cryo-EM structures of Pol II-Rad26 complexes stalled at different obstacles that show that Rad26 uses a common mechanism to recognize a stalled Pol II, with additional interactions when Pol II is arrested at a lesion. A cryo-EM structure of lesion-arrested Pol II-Rad26 bound to Elf1 revealed that Elf1 induces further interactions between Rad26 and a lesion-arrested Pol II. Biochemical and genetic data support the importance of the interplay between Elf1 and Rad26 in TC-NER initiation. Together, our results provide important mechanistic insights into how two conserved transcription-coupled repair factors, Rad26/CSB and Elf1/ELOF1, work together at the initial lesion recognition steps of transcription-coupled repair.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38194460 · DOI · PMC10801861
Mitochondrial DNA Instability and Neuroinflammation: Connecting the Dots Between Base Excision Repair and Neurodegenerative Disease [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Neurons have exceptionally high energy demands, sustained by thousands to millions of mitochondria per cell.
- Closing excerpt
- We also explore emerging therapeutic strategies to enhance mtDNA repair, optimize its mitochondrial environment, and modulate neuroimmune pathways to counteract neurodegeneration.
- 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 (241 words)
Neurons have exceptionally high energy demands, sustained by thousands to millions of mitochondria per cell. Each mitochondrion depends on the integrity of its mitochondrial DNA (mtDNA), which encodes essential electron transport chain (ETC) subunits required for oxidative phosphorylation (OXPHOS). The continuous, high-level ATP production by OXPHOS generates reactive oxygen species (ROS) that pose a significant threat to the nearby mtDNA. To counter these insults, neurons rely on base excision repair (BER), the principal mechanism for removing oxidative and other small, non-bulky base lesions in nuclear and mtDNA. BER involves a coordinated enzymatic pathway that excises damaged bases and restores DNA integrity, helping maintain mitochondrial genome stability, which is vital for neuronal bioenergetics and survival. When mitochondrial BER is impaired, mtDNA becomes unstable, leading to ETC dysfunction and a self-perpetuating cycle of bioenergetic failure, elevated ROS levels, and continued mtDNA damage. Damaged mtDNA fragments can escape into the cytosol or extracellular space, where they act as damage-associated molecular patterns (DAMPs) that activate innate immune pathways and inflammasome complexes. Chronic activation of these pathways drives sustained neuroinflammation, exacerbating mitochondrial dysfunction and neuronal loss, and functionally links genome instability to innate immune signaling in neurodegenerative diseases. This review summarizes recent advancements in understanding how BER preserves mitochondrial genome stability, affects neuronal health when dysfunctional, and contributes to damage-driven neuroinflammation and neurodegenerative disease progression. We also explore emerging therapeutic strategies to enhance mtDNA repair, optimize its mitochondrial environment, and modulate neuroimmune pathways to counteract neurodegeneration.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41595502 · DOI · PMC12841323
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 A half century of exploring DNA excision repair in chromatin [5]
- Research article Protein-protein interactions in the core nucleotide excision repair pathway [6]
- Research article The role of Transcription Factor IIH complex in nucleotide excision repair [7]
- Research article Novel Processes Associated with the Repair of Interstrand Cross-Links Derived from Abasic Sites in Duplex DNA: Roles for the Base Excision Repair Glycosylase NEIL3 and the SRAP Protein HMCES [8]
- Research article Global genome and transcription-coupled nucleotide excision repair pathway in prokaryotes [9]
- Research article Methods for Assessment of Nucleotide Excision Repair Efficiency [10]
References
- Schwarz SD, Xu J, Gunasekera K, Schürmann D, Vågbø CB, Ferrari E, et al.. Covalent PARylation of DNA base excision repair proteins regulates DNA demethylation. . 2024. PMID 38167803 · DOI · PMC10762122
- Son K, Takhaveev V, Mor V, Yu H, Dillier E, Zilio N, et al.. Trabectedin derails transcription-coupled nucleotide excision repair to induce DNA breaks in highly transcribed genes. . 2024. PMID 38360910 · DOI · PMC10869700
- Sarsam RD, Xu J, Lahiri I, Gong W, Li Q, Oh J, et al.. Elf1 promotes Rad26's interaction with lesion-arrested Pol II for transcription-coupled repair. . 2024. PMID 38194460 · DOI · PMC10801861
- Pittman MN, Nelsen MB, Thompson MK, Prakash A. Mitochondrial DNA Instability and Neuroinflammation: Connecting the Dots Between Base Excision Repair and Neurodegenerative Disease. . 2026. PMID 41595502 · DOI · PMC12841323
- Smerdon MJ, Wyrick JJ, Delaney S. A half century of exploring DNA excision repair in chromatin. J Biol Chem. 2023. PMID 37527775 · DOI · PMC10498010
- D'Souza A, Kim M, Chazin WJ, Schärer OD. Protein-protein interactions in the core nucleotide excision repair pathway. DNA Repair (Amst). 2024. PMID 39029374 · DOI · PMC11330345
- Hoag A, Duan M, Mao P. The role of Transcription Factor IIH complex in nucleotide excision repair. Environ Mol Mutagen. 2024. PMID 37545038 · DOI · PMC10903506
- Price NE, Gates KS. Novel Processes Associated with the Repair of Interstrand Cross-Links Derived from Abasic Sites in Duplex DNA: Roles for the Base Excision Repair Glycosylase NEIL3 and the SRAP Protein HMCES. Chem Res Toxicol. 2024. PMID 38198604 · DOI
- Thakur M, Muniyappa K. Global genome and transcription-coupled nucleotide excision repair pathway in prokaryotes. J Biosci. 2023. PMID 38088378 · DOI
- Popov AA, Petruseva IO, Naumenko NV, Lavrik OI. Methods for Assessment of Nucleotide Excision Repair Efficiency. Biochemistry (Mosc). 2023. PMID 38105203 · DOI
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.