ReviewDNA repair2008
The 8,5'-cyclopurine-2'-deoxynucleosides: candidate neurodegenerative DNA lesions in xeroderma pigmentosum, and unique probes of transcription and nucleotide excision repair.
Review in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 126 citations in OpenAlex.
- The role of HECT-type E3 ubiquitin ligases in DNA damage response and repair.Cell death discovery · 2025Review
- Biochemical Battle: Influence of Omega-6 Fatty Acids on the Formation of DNA Adducts with 4-HNE.Current issues in molecular biology · 2025Review
- Biological Models of Oxidative Purine DNA Damage in Neurodegenerative Disorders.Antioxidants (Basel, Switzerland) · 2025Review
- Impact of double-strand breaks induced by uv radiation on neuroinflammation and neurodegenerative disorders.Molecular biology reports · 2024Review
- Neurological disease in xeroderma pigmentosum: prospective cohort study of its features and progression.Brain : a journal of neurology · 2023Article
- Incorporation of 5',8-cyclo-2'deoxyadenosines by DNA repair polymerases via base excision repair.DNA repair · 2022Article
- Article
- Differences in peripheral neuropathy in xeroderma pigmentosum complementation groups A and D as evaluated by nerve conduction studies.BMC neurology · 2021Article
- Review
- Xeroderma Pigmentosum: A Model for Human Premature Aging.The Journal of investigative dermatology · 2021Review
- Article
- DNA damage-how and why we age?eLife · 2021Review
- The Influence of Single, Tandem, and Clustered DNA Damage on the Electronic Properties of the Double Helix: A Theoretical Study.Molecules (Basel, Switzerland) · 2020Article
- Role of Base Excision Repair Pathway in the Processing of Complex DNA Damage Generated by Oxidative Stress and Anticancer Drugs.Frontiers in cell and developmental biology · 2020Review
- The DNA damage response to transcription stress.Nature reviews. Molecular cell biology · 2019Review
- Xeroderma pigmentosum: overview of pharmacology and novel therapeutic strategies for neurological symptoms.British journal of pharmacology · 2019Review
- The Influence of (5'Cells · 2019Article
- Measurement of Oxidatively Induced DNA Damage inAnalytical chemistry · 2019Article
- 5',8-Cyclopurine Lesions in DNA Damage: Chemical, Analytical, Biological, and Diagnostic Significance.Cells · 2019Review
- Nucleotide Excision Repair and Impact of Site-Specific 5',8-Cyclopurine and Bulky DNA Lesions on the Physical Properties of Nucleosomes.Biochemistry · 2019Article
10 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
1 author at 1 institution in 1 country.
Funding
Abstract
It is a commonly held view that oxidatively induced DNA lesions are repaired by the base excision repair (BER) pathway, whereas DNA lesions induced by UV light and other "bulky" chemical adducts are repaired by the nucleotide excision repair (NER) pathway. While this distinction is generally accurate, the 8,5'-cyclopurine deoxynucleosides represent an important exception, in that they are formed in DNA by the hydroxyl radical, but are specifically repaired by NER, not by BER. They are also strong blocks to nucleases and polymerases, including RNA polymerase II in human cells. In this review, I will discuss the evidence that these lesions are in part responsible for the neurodegeneration that occurs in some XP patients, and what additional evidence would be necessary to prove such a role. I will also consider other DNA lesions that might be involved in XP neurologic disease. Finally, I will also discuss how our recent studies of these lesions have generated novel insights into the process of transcriptional mutagenesis in human cells, as well as the value of studying these lesions not only for a better understanding of NER but also for other aspects of human health and disease.
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.