ArticleGenes & development2003
Recognition and repair of the cyclobutane thymine dimer, a major cause of skin cancers, by the human excision nuclease.
Article in Genes & development, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
86 citing papers in PubMed, 173 citations in OpenAlex.
- Assessment and detection of nucleotide excision repair capability in human cells: a critical review of current functional methods.Molecular biology reports · 2026Review
- Uncovering the Genetic Landscape of Spinal Dysraphism: A Retrospective Analysis of 150 Fetal Cases.Prenatal diagnosis · 2026Article
- Plant tolerance mechanisms to DNA-damaging UV stress.Journal of experimental botany · 2025Review
- Transcription-Coupled Nucleotide Excision Repair: A Faster Solution or the Only Option?Biomolecules · 2025Review
- Dynamics of transcription-coupled repair of cyclobutane pyrimidine dimers and (6-4) photoproducts inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Structure-specific nucleases in genome dynamics and strategies for targeting cancers.Journal of molecular cell biology · 2024Review
- Article
- Differing structures and dynamics of two photolesions portray verification differences by the human XPD helicase.Nucleic acids research · 2023Article
- Structural polymorphism of the PH domain in TFIIH.Bioscience reports · 2023Article
- Nucleotide excision repair in Human cell lines lacking both XPC and CSB proteins.Nucleic acids research · 2023Article
- Requirement of transcription-coupled nucleotide excision repair for the removal of a specific type of oxidatively induced DNA damage.Nucleic acids research · 2023Article
- A scanning-to-incision switch in TFIIH-XPG induced by DNA damage licenses nucleotide excision repair.Nucleic acids research · 2023Article
- XPC-PARP complexes engage the chromatin remodeler ALC1 to catalyze global genome DNA damage repair.Nature communications · 2022Article
- XPG in the Nucleotide Excision Repair and Beyond: a study on the different functional aspects of XPG and its associated diseases.Molecular biology reports · 2022Review
- CSB-independent, XPC-dependent transcription-coupled repair inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- DNA Repair in Haploid Context.International journal of molecular sciences · 2021Review
- Nucleotide Excision Repair: From Molecular Defects to Neurological Abnormalities.International journal of molecular sciences · 2021Review
- Regulation of ddb2 expression in blind cavefish and zebrafish reveals plasticity in the control of sunlight-induced DNA damage repair.PLoS genetics · 2021Article
- The Dark Side of UV-Induced DNA Lesion Repair.Genes · 2020Review
- The DNA damage-sensing NER repair factor XPC-RAD23B does not recognize bulky DNA lesions with a missing nucleotide opposite the lesion.DNA repair · 2020Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The cyclobutane thymine dimer is the major DNA lesion induced in human skin by sunlight and is a primary cause of skin cancer, the most prevalent form of cancer in the Northern Hemisphere. In humans, the only known cellular repair mechanism for eliminating the dimer from DNA is nucleotide excision repair. Yet the mechanism by which the dimer is recognized and removed by this repair system is not known. Here we demonstrate that the six-factor human excision nuclease recognizes and removes the dimer at a rate consistent with the in vivo rate of removal of this lesion, even though none of the six factors alone is capable of efficiently discriminating the dimer from undamaged DNA. We propose a recognition mechanism by which the low-specificity recognition factors, RPA, XPA, and XPC, act in a cooperative manner to locate the lesion and, aided by the kinetic proofreading provided by TFIIH, form a high-specificity complex at the damage site that initiates removal of thymine dimers at a physiologically relevant rate and specificity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.