ArticleMutagenesis2010
XPA impacts formation but not proteasome-sensitive repair of DNA-protein cross-links induced by chromate.
Article in Mutagenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Monoubiquitinated H2B, a Main Chromatin Target of Formaldehyde, Is Important for S-Phase Checkpoint Signaling and Genome Stability.Molecular carcinogenesis · 2024Article
- Ubx5-Cdc48 assists the protease Wss1 at DNA-protein crosslink sites in yeast.The EMBO journal · 2023Article
- Chemical mechanisms of DNA damage by carcinogenic chromium(VI).Advances in pharmacology (San Diego, Calif.) · 2023Article
- DNA-protein crosslinks from environmental exposure: Mechanisms of formation and repair.Environmental and molecular mutagenesis · 2020Review
- XPA: DNA Repair Protein of Significant Clinical Importance.International journal of molecular sciences · 2020Review
- DNA-Histone Cross-Links: Formation and Repair.Frontiers in cell and developmental biology · 2020Review
- Roles ofJournal of bacteriology · 2019Article
- Replication-Coupled DNA-Protein Crosslink Repair by SPRTN and the Proteasome in Xenopus Egg Extracts.Molecular cell · 2019Article
- Formation and repair of DNA-protein crosslink damage.Science China. Life sciences · 2017Review
- Differential sensitivities of cellular XPA and PARP-1 to arsenite inhibition and zinc rescue.Toxicology and applied pharmacology · 2017Article
- Carcinogenicity of chromium and chemoprevention: a brief update.OncoTargets and therapy · 2017Review
- Article
- Proteasome activity is important for replication recovery, CHK1 phosphorylation and prevention of G2 arrest after low-dose formaldehyde.Toxicology and applied pharmacology · 2015Article
- Article
- Detection of DNA-protein crosslinks (DPCs) by novel direct fluorescence labeling methods: distinct stabilities of aldehyde and radiation-induced DPCs.Nucleic acids research · 2012Article
- S-phase sensing of DNA-protein crosslinks triggers TopBP1-independent ATR activation and p53-mediated cell death by formaldehyde.Cell cycle (Georgetown, Tex.) · 2012Article
- Involvement of the nuclear proteasome activator PA28γ in the cellular response to DNA double-strand breaks.Cell cycle (Georgetown, Tex.) · 2011Article
- Chromium in drinking water: sources, metabolism, and cancer risks.Chemical research in toxicology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
DNA-protein cross-links (DPCs) are caused by a large number of human carcinogens and anti-cancer drugs. However, cellular processes involved in decreasing a burden of these genotoxic lesions remain poorly understood. Here, we examined the impact of nucleotide excision repair (NER), which is a principal repair pathway for bulky DNA adducts, and the main cellular reducers on removal of chromium(VI)-induced DPC. We found that standard and ascorbate-restored cultures of isogenic XPA-null (NER deficient) and XPA-complemented human fibroblasts had very similar repair of Cr-DPC (60-65% average DPC removal after 24 h). However, XPA absence caused depletion of G1 and accumulation of G2 cells at low Cr(VI) doses, suggesting that Cr-DPC were not a significant cause of cell cycle perturbations. Interestingly, although pro-oxidant metabolism of Cr(VI) in glutathione-depleted cells generated significantly fewer DPC, they were repair resistant irrespective of the NER status of cells. Inhibition of proteasome activity by MG132 abolished DPC repair in both XPA-null and XPA-complemented cells. XPA loss caused two to three times higher initial DPC formation, demonstrating the importance of NER in removal of the precursor lesions. Our results indicate that human NER is not involved in removal of Cr-DPC containing non-histone proteins but it acts as a defence mechanism against these large lesions by preventing their formation. Therefore, individual differences in NER activity are expected to alter sensitivity but not persistence of DPC as a biomarker of hexavalent Cr.
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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.