ArticleNucleic acids research2008
XRCC1 protects against the lethality of induced oxidative DNA damage in nondividing neural cells.
Article in Nucleic acids research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Proteins Associated with Neurodegenerative Diseases: Link to DNA Repair.Biomedicines · 2024Review
- TiOInternational journal of nanomedicine · 2020Article
- The Emerging Role of GLP-1 Receptors in DNA Repair: Implications in Neurological Disorders.International journal of molecular sciences · 2017Review
- Coordination of DNA single strand break repair.Free radical biology & medicine · 2017Review
- Oxidative stress-induced CREB upregulation promotes DNA damage repair prior to neuronal cell death protection.Molecular and cellular biochemistry · 2017Article
- The Response to Oxidative DNA Damage in Neurons: Mechanisms and Disease.Neural plasticity · 2016Review
- Activation of GLP-1 Receptor Enhances Neuronal Base Excision Repair via PI3K-AKT-Induced Expression of Apurinic/Apyrimidinic Endonuclease 1.Theranostics · 2016Article
- Partial loss of the DNA repair scaffolding protein, Xrcc1, results in increased brain damage and reduced recovery from ischemic stroke in mice.Neurobiology of aging · 2015Article
- CSB interacts with SNM1A and promotes DNA interstrand crosslink processing.Nucleic acids research · 2015Article
- BDNF and exercise enhance neuronal DNA repair by stimulating CREB-mediated production of apurinic/apyrimidinic endonuclease 1.Neuromolecular medicine · 2014Article
- Modulation of DNA base excision repair during neuronal differentiation.Neurobiology of aging · 2013Article
- Base excision repair in physiology and pathology of the central nervous system.International journal of molecular sciences · 2012Review
- XRCC1 and base excision repair balance in response to nitric oxide.DNA repair · 2011Article
- XRCC1 haploinsufficiency in mice has little effect on aging, but adversely modifies exposure-dependent susceptibility.Nucleic acids research · 2011Article
- Aprataxin localizes to mitochondria and preserves mitochondrial function.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Evidence that OGG1 glycosylase protects neurons against oxidative DNA damage and cell death under ischemic conditions.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2011Article
- Neurons efficiently repair glutamate-induced oxidative DNA damage by a process involving CREB-mediated up-regulation of apurinic endonuclease 1.The Journal of biological chemistry · 2010Article
- Functional capacity of XRCC1 protein variants identified in DNA repair-deficient Chinese hamster ovary cell lines and the human population.Nucleic acids research · 2010Article
- Article
- The genesis of cerebellar interneurons and the prevention of neural DNA damage require XRCC1.Nature neuroscience · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
XRCC1 is a critical scaffold protein that orchestrates efficient single-strand break repair (SSBR). Recent data has found an association of XRCC1 with proteins causally linked to human spinocerebellar ataxias-aprataxin and tyrosyl-DNA phosphodiesterase 1-implicating SSBR in protection against neuronal cell loss and neurodegenerative disease. We demonstrate herein that shRNA lentiviral-mediated XRCC1 knockdown in human SH-SY5Y neuroblastoma cells results in a largely selective increase in sensitivity of the nondividing (i.e. terminally differentiated) cell population to the redox-cycling agents, menadione and paraquat; this reduced survival was accompanied by an accumulation of DNA strand breaks. Using hypoxanthine-xanthine oxidase as the oxidizing method, XRCC1 deficiency affected both dividing and nondividing SH-SY5Y cells, with a greater effect on survival seen in the former case, suggesting that the spectrum of oxidative DNA damage created dictates the specific contribution of XRCC1 to cellular resistance. Primary XRCC1 heterozygous mouse cerebellar granule cells exhibit increased strand break accumulation and reduced survival due to increased apoptosis following menadione treatment. Moreover, knockdown of XRCC1 in primary human fetal brain neurons leads to enhanced sensitivity to menadione, as indicated by increased levels of DNA strand breaks relative to control cells. The cumulative results implicate XRCC1, and more broadly SSBR, in the protection of nondividing neuronal cells from the genotoxic consequences of oxidative stress.
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