ArticleDNA repair2013
Slow accumulation of mutations in Xpc-/- mice upon induction of oxidative stress.
Article in DNA repair, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Cigarette smoke and decreased DNA repair by Xeroderma Pigmentosum Group C use a double hit mechanism for epithelial cell lung carcinogenesis.Oncotarget · 2025Article
- UVA-light-induced mutagenesis in the exome of human nucleotide excision repair-deficient cells.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025Article
- Article
- Can accelerated ageing models inform us on age-related tauopathies?Aging cell · 2023Review
- Xeroderma Pigmentosum Complementation Group C (XPC): Emerging Roles in Non-Dermatologic Malignancies.Frontiers in oncology · 2022Review
- Association between polymorphisms rs2228001 and rs2228000 in XPC and genetic susceptibility to preeclampsia: a case control study.BMC pregnancy and childbirth · 2021Article
- The impact of oxidative stress damage induced by the environmental stressors on COVID-19.Life sciences · 2021Review
- XPC deficiency increases risk of hematologic malignancies through mutator phenotype and characteristic mutational signature.Nature communications · 2020Article
- Genomic alterations and abnormal expression of APE2 in multiple cancers.Scientific reports · 2020Article
- Xeroderma Pigmentosum C (XPC) Mutations in Primary Fibroblasts Impair Base Excision Repair Pathway and Increase Oxidative DNA Damage.Frontiers in genetics · 2020Article
- Environmentally relevant exposure to dibutyl phthalate disrupts DNA damage repair gene expression in the mouse ovary†.Biology of reproduction · 2019Article
- XPC protects against smoking- and carcinogen-induced lung adenocarcinoma.Carcinogenesis · 2019Article
- The impact of oxidative DNA damage and stress on telomere homeostasis.Mechanisms of ageing and development · 2019Review
- Xeroderma Pigmentosum Group C Deficiency Alters Cigarette Smoke DNA Damage Cell Fate and Accelerates Emphysema Development.American journal of respiratory cell and molecular biology · 2018Article
- Nucleotide Excision Repair Factor XPC Ameliorates Prognosis by Increasing the Susceptibility of Human Colorectal Cancer to Chemotherapy and Ionizing Radiation.Frontiers in oncology · 2018Article
- Ultra-flexible nanocarriers for enhanced topical delivery of a highly lipophilic antioxidative molecule for skin cancer chemoprevention.Colloids and surfaces. B, Biointerfaces · 2016Article
- XPC: Going where no DNA damage sensor has gone before.DNA repair · 2015Review
- Engrailed Homeoprotein Protects Mesencephalic Dopaminergic Neurons from Oxidative Stress.Cell reports · 2015Article
- Premature skin aging features rescued by inhibition of NADPH oxidase activity in XPC-deficient mice.The Journal of investigative dermatology · 2015Article
- A closer look at papillary thyroid carcinoma.Endocrinology and metabolism (Seoul, Korea) · 2015Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
XPC is one of the key DNA damage recognition proteins in the global genome repair route of the nucleotide excision repair (NER) pathway. Previously, we demonstrated that NER-deficient mouse models Xpa(-/-) and Xpc(-/-) exhibit a divergent spontaneous tumor spectrum and proposed that XPC might be functionally involved in the defense against oxidative DNA damage. Others have mechanistically dissected several functionalities of XPC to oxidative DNA damage sensitivity using in vitro studies. XPC has been linked to regulation of base excision repair (BER) activity, redox homeostasis and recruitment of ATM and ATR to damage sites, thereby possibly regulating cell cycle checkpoints and apoptosis. XPC has additionally been implicated in recognition of bulky (e.g. cyclopurines) and non-bulky DNA damage (8-oxodG). However, the ultimate contribution of the XPC functionality in vivo in the oxidative DNA damage response and subsequent mutagenesis process remains unclear. Our study indicates that Xpc(-/-) mice, in contrary to Xpa(-/-) and wild type mice, have an increased mutational load upon induction of oxidative stress and that mutations arise in a slowly accumulative fashion. The effect of non-functional XPC in vivo upon oxidative stress exposure appears to have implications in mutagenesis, which can contribute to the carcinogenesis process. The levels and rate of mutagenesis upon oxidative stress correlate with previous findings that lung tumors in Xpc(-/-) mice overall arise late in the lifespan and that the incidence of internal tumors in XP-C patients is relatively low in comparison to skin cancer incidence.
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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.