ReviewNeuroscience2007
The case for 8,5'-cyclopurine-2'-deoxynucleosides as endogenous DNA lesions that cause neurodegeneration in xeroderma pigmentosum.
Review in Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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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.
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Who cites it
57 citing papers in PubMed, 123 citations in OpenAlex.
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- Biochemical Battle: Influence of Omega-6 Fatty Acids on the Formation of DNA Adducts with 4-HNE.Current issues in molecular biology · 2025Review
- Transcription-Coupled Nucleotide Excision Repair: A Faster Solution or the Only Option?Biomolecules · 2025Review
- Biological Models of Oxidative Purine DNA Damage in Neurodegenerative Disorders.Antioxidants (Basel, Switzerland) · 2025Review
- Keep calm and reboot - how cells restart transcription after DNA damage and DNA repair.FEBS letters · 2025Review
- Nucleolar reorganization after cellular stress is orchestrated by SMN shuttling between nuclear compartments.Nature communications · 2023Article
- Review
- Requirement of transcription-coupled nucleotide excision repair for the removal of a specific type of oxidatively induced DNA damage.Nucleic acids research · 2023Article
- The Influence of 5',8-Cyclo-2'-Deoxyguanosine on ds-DNA Charge Transfer Depends on Its Diastereomeric Form: A Theoretical Study.Antioxidants (Basel, Switzerland) · 2023Article
- Cell migration is impaired in XPA-deficient cells.FASEB bioAdvances · 2023Article
- A matter of delicate balance: Loss and gain of Cockayne syndrome proteins in premature aging and cancer.Frontiers in aging · 2022Review
- When UDG and hAPE1 Meet Cyclopurines. How (5'Molecules (Basel, Switzerland) · 2021Article
- The Influence of 5'Molecules (Basel, Switzerland) · 2021Article
- Nucleotide Excision Repair: From Molecular Defects to Neurological Abnormalities.International journal of molecular sciences · 2021Review
- 5',8-Cyclopurine Lesions in DNA Damage: Chemical, Analytical, Biological, and Diagnostic Significance.Cells · 2019Review
- Macular and Retinal Nerve Fibre Layer Thinning in Xeroderma Pigmentosum: A Cross-sectional Study.Neuro-ophthalmology (Aeolus Press) · 2018Article
- Xeroderma pigmentosum-Cockayne syndrome complex.Orphanet journal of rare diseases · 2017Review
- Noise Stress Induces an Epidermal Growth Factor Receptor/Xeroderma Pigmentosum-A Response in the Auditory Nerve.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2017Article
- Occurrence, Biological Consequences, and Human Health Relevance of Oxidative Stress-Induced DNA Damage.Chemical research in toxicology · 2016Review
- Comprehensive Assessment of Oxidatively Induced Modifications of DNA in a Rat Model of Human Wilson's Disease.Molecular & cellular proteomics : MCP · 2016Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Patients with the genetic disease xeroderma pigmentosum (XP) lack the capacity to carry out a specific type of DNA repair process called nucleotide excision repair (NER). The NER pathway plays a critical role in the repair of DNA damage resulting from ultraviolet (UV) radiation. A subset of XP patients develops a profound neurodegenerative condition known as XP neurological disease. Robbins and colleagues [Andrews A, Barrett S, Robbins J (1978) Xeroderma pigmentosum neurological abnormalities correlate with the colony forming ability after ultraviolet irradiation. Proc Natl Acad Sci U S A 75:1984-1988] hypothesized that since UV light cannot reach into the human brain, XP neurological disease results from some form of endogenous DNA damage that is normally repaired by the NER pathway. In the absence of NER, the damage accumulates, causing neuronal death by blocking transcription. In this manuscript, I consider the evidence that a particular class of oxidative DNA lesions, the 8,5'-cyclopurine-2'-deoxynucleosides, fulfills many of the criteria expected of neurodegenerative DNA lesions in XP. Specifically, these lesions are chemically stable, endogenous DNA lesions that are repaired by the NER pathway but not by any other known process, and strongly block transcription by RNA polymerase II in cells from XP patients. A similar set of criteria might be used to evaluate other candidate DNA lesions responsible for neurological diseases resulting from defects in other DNA repair mechanisms as well.
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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.