ArticleProceedings of the National Academy of Sciences of the United States of America2014
Mitochondrial reactive oxygen species are scavenged by Cockayne syndrome B protein in human fibroblasts without nuclear DNA damage.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 64 citations in OpenAlex.
- The Cellular Response to Oxidatively Induced DNA Damage and Polymorphism of Some DNA Repair Genes Associated with Clinicopathological Features of Bladder Cancer.Oxidative medicine and cellular longevity · 2016Trial
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- Lovastatin-Induced Mitochondrial Oxidative Stress Leads to the Release of mtDNA to Promote Apoptosis by Activating cGAS-STING Pathway in Human Colorectal Cancer Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Mitochondrial HNature communications · 2024Article
- The Mitochondrial Connection: The Nek Kinases' New Functional Axis in Mitochondrial Homeostasis.Cells · 2024Review
- Genetic variability of oxidative stress and DNA repair genes associated with pre-treatment cancer-related fatigue in women with breast cancer.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2023Article
- Targeting Mitochondrial Function with Chemoptogenetics.Biomedicines · 2022Review
- The UVSSA protein is part of a genome integrity homeostasis network with links to transcription-coupled DNA repair and ATM signaling.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Cockayne syndrome group A and ferrochelatase finely tune ribosomal gene transcription and its response to UV irradiation.Nucleic acids research · 2021Article
- DRP1 Inhibition Rescues Mitochondrial Integrity and Excessive Apoptosis in CS-A Disease Cell Models.International journal of molecular sciences · 2021Article
- LEO1 is a partner for Cockayne syndrome protein B (CSB) in response to transcription-blocking DNA damage.Nucleic acids research · 2021Article
- Review
- Xeroderma Pigmentosum: A Model for Human Premature Aging.The Journal of investigative dermatology · 2021Review
- DNA damage and mitochondria in cancer and aging.Carcinogenesis · 2020Review
- Tumour predisposition and cancer syndromes as models to study gene-environment interactions.Nature reviews. Cancer · 2020Review
- Atypical features and de novo heterozygous mutations in two siblings with Cockayne syndrome.Molecular genetics & genomic medicine · 2020Article
- Cockayne Syndrome: The many challenges and approaches to understand a multifaceted disease.Genetics and molecular biology · 2020Article
- Xeroderma pigmentosum: overview of pharmacology and novel therapeutic strategies for neurological symptoms.British journal of pharmacology · 2019Review
- CSB affected on the sensitivity of lung cancer cells to platinum-based drugs through the global decrease of let-7 and miR-29.BMC cancer · 2019Article
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Cockayne syndrome (CS) is a human DNA repair-deficient disease that involves transcription coupled repair (TCR), in which three gene products, Cockayne syndrome A (CSA), Cockayne syndrome B (CSB), and ultraviolet stimulated scaffold protein A (UVSSA) cooperate in relieving RNA polymerase II arrest at damaged sites to permit repair of the template strand. Mutation of any of these three genes results in cells with increased sensitivity to UV light and defective TCR. Mutations in CSA or CSB are associated with severe neurological disease but mutations in UVSSA are for the most part only associated with increased photosensitivity. This difference raises questions about the relevance of TCR to neurological disease in CS. We find that CSB-mutated cells, but not UVSSA-deficient cells, have increased levels of intramitochondrial reactive oxygen species (ROS), especially when mitochondrial complex I is inhibited by rotenone. Increased ROS would result in oxidative damage to mitochondrial proteins, lipids, and DNA. CSB appears to behave as an electron scavenger in the mitochondria whose absence leads to increased oxidative stress. Mitochondrial ROS, however, did not cause detectable nuclear DNA damage even when base excision repair was blocked by an inhibitor of polyADP ribose polymerase. Neurodegeneration in Cockayne syndrome may therefore be associated with ROS-induced damage in the mitochondria, independent of nuclear TCR. An implication of our present results is that mitochondrial dysfunction involving ROS has a major impact on CS-B pathology, whereas nuclear TCR may have a minimal role.
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