ReviewInternational journal of molecular sciences2021
Nucleotide Excision Repair: From Molecular Defects to Neurological Abnormalities.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
- XPA lactylation is required for UV-induced DNA damage repair.Nucleic acids research · 2026Article
- UV damage mapping reveals different impacts of yeast XPD mutations on global genomic and transcription-coupled DNA repair.The Journal of biological chemistry · 2026Article
- Nucleotide excision repair and poly(ADP-ribose) polymerase 1 cooperate in HBV cccDNA synthesis: A potential viral therapeutic target.JHEP reports : innovation in hepatology · 2026Article
- Transcription-coupled nucleotide excision repair protects against genomic instability and cell death induced by the liver toxin methyleugenol.Cell death & disease · 2026Article
- Interactions between rare variants in DNA repair genes and cardiometabolic risk explain more variability in cognitive function.GeroScience · 2026Article
- Integrating Structural, Biochemical, and Cellular Perspectives on the TFIIH Helicases XPB and XPD.Biomolecules · 2026Review
- DNA Damage and Repair in Thyroid Physiology and Disease.Endocrine reviews · 2026Review
- Oxidative Stress in DNA Damage and Neurodegenerative Diseases: Unveiling The Mechanisms and Therapeutic Opportunities.Cell biochemistry and biophysics · 2025Review
- DNA Damage and Repair in Pancreatic Cancer-The Latest Findings.International journal of molecular sciences · 2025Review
- Antibacterial Efficacy of Ethanol Extracts from EdibleFoods (Basel, Switzerland) · 2025Article
- USP7 at the Crossroads of Ubiquitin Signaling, Cell Cycle, and Tumorigenesis.Molecules (Basel, Switzerland) · 2025Review
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- Biological Models of Oxidative Purine DNA Damage in Neurodegenerative Disorders.Antioxidants (Basel, Switzerland) · 2025Review
- Association of XRCC1 (rs1799782) and XPD (rs13181) gene polymorphisms with renal failure risk in a sample of Iraqi population: a case-control study.Molecular biology reports · 2025Article
- Proteins Associated with Neurodegenerative Diseases: Link to DNA Repair.Biomedicines · 2024Review
- Molecular mechanisms of cisplatin resistance in ovarian cancer.Genes & diseases · 2024Review
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- DoUBLing up: ubiquitin and ubiquitin-like proteases in genome stability.The Biochemical journal · 2024Review
- The role of Transcription Factor IIH complex in nucleotide excision repair.Environmental and molecular mutagenesis · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Nucleotide excision repair (NER) is the most versatile DNA repair pathway, which can remove diverse bulky DNA lesions destabilizing a DNA duplex. NER defects cause several autosomal recessive genetic disorders. Xeroderma pigmentosum (XP) is one of the NER-associated syndromes characterized by low efficiency of the removal of bulky DNA adducts generated by ultraviolet radiation. XP patients have extremely high ultraviolet-light sensitivity of sun-exposed tissues, often resulting in multiple skin and eye cancers. Some XP patients develop characteristic neurodegeneration that is believed to derive from their inability to repair neuronal DNA damaged by endogenous metabolites. A specific class of oxidatively induced DNA lesions, 8,5'-cyclopurine-2'-deoxynucleosides, is considered endogenous DNA lesions mainly responsible for neurological problems in XP. Growing evidence suggests that XP is accompanied by defective mitophagy, as in primary mitochondrial disorders. Moreover, NER pathway is absent in mitochondria, implying that the mitochondrial dysfunction is secondary to nuclear NER defects. In this review, we discuss the current understanding of the NER molecular mechanism and focuses on the NER linkage with the neurological degeneration in patients with XP. We also present recent research advances regarding NER involvement in oxidative DNA lesion repair. Finally, we highlight how mitochondrial dysfunction may be associated with XP.
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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.