ArticleOncogene2002
Mitochondrial repair of 8-oxoguanine is deficient in Cockayne syndrome group B.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 105 citations in OpenAlex.
- Anti-Aging Potential of Avocado Oil via Its Antioxidant Effects.Pharmaceuticals (Basel, Switzerland) · 2025Review
- DNA repair-related genes and adipogenesis: Lessons from congenital lipodystrophies.Genetics and molecular biology · 2022Article
- Mammalian Resilience Revealed by a Comparison of Human Diseases and Mouse Models Associated With DNA Helicase Deficiencies.Frontiers in molecular biosciences · 2022Review
- DNA Damage-Induced Neurodegeneration in Accelerated Ageing and Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Current and emerging roles of Cockayne syndrome group B (CSB) protein.Nucleic acids research · 2021Review
- Cockayne syndrome proteins CSA and CSB maintain mitochondrial homeostasis through NADAging cell · 2020Article
- Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase.Nucleic acids research · 2020Article
- DNA Repair and the Stability of the Plant Mitochondrial Genome.International journal of molecular sciences · 2020Review
- Mechanistic and biological considerations of oxidatively damaged DNA for helicase-dependent pathways of nucleic acid metabolism.Free radical biology & medicine · 2017Review
- Lack of XPC leads to a shift between respiratory complexes I and II but sensitizes cells to mitochondrial stress.Scientific reports · 2017Article
- Cockayne syndrome: Clinical features, model systems and pathways.Ageing research reviews · 2017Review
- Photosensitive human syndromes.Mutation research · 2015Review
- Xeroderma Pigmentosum Group A Suppresses Mutagenesis Caused by Clustered Oxidative DNA Adducts in the Human Genome.PloS one · 2015Article
- DNA repair diseases: What do they tell us about cancer and aging?Genetics and molecular biology · 2014Review
- Damaged mitochondria in Fanconi anemia - an isolated event or a general phenomenon?Oncoscience · 2014Article
- Cockayne Syndrome group B protein stimulates NEIL2 DNA glycosylase activity.Mechanisms of ageing and development · 2014Article
- Autophagy and genomic integrity.Cell death and differentiation · 2013Review
- Article
- Repair of hydantoin lesions and their amine adducts in DNA by base and nucleotide excision repair.Journal of the American Chemical Society · 2013Article
- UVSSA and USP7, a new couple in transcription-coupled DNA repair.Chromosoma · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Reactive oxygen species, which are prevalent in mitochondria, cause oxidative DNA damage including the mutagenic DNA lesion 7,8-dihydroxyguanine (8-oxoG). Oxidative damage to mitochondrial DNA has been implicated as a causative factor in a wide variety of degenerative diseases, and in cancer and aging. 8-oxoG is repaired efficiently in mammalian mitochondrial DNA by enzymes in the base excision repair pathway, including the 8-oxoguanine glycosylase (OGG1), which incizes the lesion in the first step of repair. Cockayne syndrome (CS) is a segmental premature aging syndrome in humans that has two complementation groups, CSA and CSB. Previous studies showed that CSB-deficient cells have reduced capacity to repair 8-oxoG. This study examines the role of the CSB gene in regulating repair of 8-oxoG in mitochondrial DNA in human and mouse cells. 8-oxoG repair was measured in liver cells from CSB deficient mice and in human CS-B cells carrying expression vectors for wild type or mutant forms of the human CSB gene. For the first time we report that CSB stimulates repair of 8-oxoG in mammalian mitochondrial DNA. Furthermore, evidence is presented to support the hypothesis that wild type CSB regulates expression of OGG1.
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.