ArticleMolecular and cellular biology2004
Different effects of CSA and CSB deficiency on sensitivity to oxidative DNA damage.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 100 citations in OpenAlex.
- The Converging Roles of Nucleases and Helicases in Genome Maintenance and the Aging Process.Life (Basel, Switzerland) · 2025Review
- Review
- Contributing factors to the oxidation-induced mutational landscape in human cells.Nature communications · 2024Article
- A novel role for CSA in the regulation of nuclear envelope integrity: uncovering a non-canonical function.Life science alliance · 2024Article
- Article
- Functional interplay between the oxidative stress response and DNA damage checkpoint signaling for genome maintenance in aerobic organisms.Journal of microbiology (Seoul, Korea) · 2020Review
- Cockayne Syndrome: The many challenges and approaches to understand a multifaceted disease.Genetics and molecular biology · 2020Article
- Comparative study of cytotoxic effects induced by environmental genotoxins using XPC- and CSB-deficient human lymphoblastoid TK6 cells.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2019Article
- Function and Interactions of ERCC1-XPF in DNA Damage Response.Molecules (Basel, Switzerland) · 2018Review
- BERing the burden of damage: Pathway crosstalk and posttranslational modification of base excision repair proteins regulate DNA damage management.DNA repair · 2017Review
- Elements That Regulate the DNA Damage Response of Proteins Defective in Cockayne Syndrome.Journal of molecular biology · 2016Article
- Combination of Aβ Secretion and Oxidative Stress in an Alzheimer-Like Cell Line Leads to the Over-Expression of the Nucleotide Excision Repair Proteins DDB2 and XPC.International journal of molecular sciences · 2015Article
- Oxidative and energy metabolism as potential clues for clinical heterogeneity in nucleotide excision repair disorders.The Journal of investigative dermatology · 2015Review
- Oxidative stress, bone marrow failure, and genome instability in hematopoietic stem cells.International journal of molecular sciences · 2015Review
- Cell-autonomous progeroid changes in conditional mouse models for repair endonuclease XPG deficiency.PLoS genetics · 2014Article
- Understanding nucleotide excision repair and its roles in cancer and ageing.Nature reviews. Molecular cell biology · 2014Review
- Cockayne Syndrome group B protein stimulates NEIL2 DNA glycosylase activity.Mechanisms of ageing and development · 2014Article
- UVSSA and USP7, a new couple in transcription-coupled DNA repair.Chromosoma · 2013Review
- Article
- Oxidative DNA damage and nucleotide excision repair.Antioxidants & redox signaling · 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
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in the CSA and CSB genes cause Cockayne syndrome, a rare inherited disorder characterized by UV sensitivity, severe neurological abnormalities, and progeriod symptoms. Both gene products function in the transcription-coupled repair (TCR) subpathway of nucleotide excision repair (NER), providing the cell with a mechanism to remove transcription-blocking lesions from the transcribed strands of actively transcribed genes. Besides a function in TCR of NER lesions, a role of CSB in (transcription-coupled) repair of oxidative DNA damage has been suggested. In this study we used mouse models to compare the effect of a CSA or a CSB defect on oxidative DNA damage sensitivity at the levels of the cell and the intact organism. In contrast to CSB(-/-) mouse embryonic fibroblasts (MEFs), CSA(-/-) MEFs are not hypersensitive to gamma-ray or paraquat treatment. Similar results were obtained for keratinocytes. In contrast, both CSB(-/-) and CSA(-/-) embryonic stem cells show slight gamma-ray sensitivity. Finally, CSB(-/-) but not CSA(-/-) mice fed with food containing di(2-ethylhexyl)phthalate (causing elevated levels of oxidative DNA damage in the liver) show weight reduction. These findings not only uncover a clear difference in oxidative DNA damage sensitivity between CSA- and CSB-deficient cell lines and mice but also show that sensitivity to oxidative DNA damage is not a uniform characteristic of Cockayne syndrome. This difference in the DNA damage response between CSA- and CSB-deficient cells is unexpected, since until now no consistent differences between CSA and CSB patients have been reported. We suggest that the CSA and CSB proteins in part perform separate roles in different DNA damage response pathways.
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.