ArticleNucleic acids research2014
Novel method for site-specific induction of oxidative DNA damage reveals differences in recruitment of repair proteins to heterochromatin and euchromatin.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 99 citations in OpenAlex.
- Interplay Between Epigenetics and Reactive Oxygen Species in Tumor Radioresistance: Mechanisms and Therapeutic Strategies for Radiotherapy.Cancer medicine · 2026Review
- Suppression of transcription-replication conflicts by sequence-coordinated actions of TRDMT1 and MutLα.Nature communications · 2026Article
- cGAS restricts PARP1-mediated microhomology-mediated end joining by suppressing poly-ADP-ribosylation.Cell death and differentiation · 2026Article
- Oxidative DNA lesions destabilize centromeres and drive chromosome instability.bioRxiv : the preprint server for biology · 2026Article
- Ubiquitylation of DNA polymerase β via atypical K27 chains signals a DNA damage response.Nucleic acids research · 2026Article
- Genetic approaches for targeted oxidative stress.NAR cancer · 2025Review
- ABL1-mediated tyrosine phosphorylation of SYCP2 contributes to transcription-coupled homologous recombination and platinum resistance in ovarian cancer.NAR cancer · 2025Article
- TRIP12's role in the governance of DNA polymerase β involvement in DNA damage response and repair.Nucleic acids research · 2025Article
- CHD6 has poly(ADP-ribose)- and DNA-binding domains and regulates PARP1/2-trapping inhibitor sensitivity via abasic site repair.Nature communications · 2025Article
- Transcription-coupled DNA repair protects genome stability upon oxidative stress-derived DNA strand breaks.FEBS letters · 2025Review
- Chromophore-Assisted Light Inactivation for Protein Degradation and Its Application in Biomedicine.Bioengineering (Basel, Switzerland) · 2024Review
- SIRT2 promotes base excision repair by transcriptionally activating OGG1 in an ATM/ATR-dependent manner.Nucleic acids research · 2024Article
- CDK-independent role of D-type cyclins in regulating DNA mismatch repair.Molecular cell · 2024Article
- The FANCI/FANCD2 complex links DNA damage response to R-loop regulation through SRSF1-mediated mRNA export.Cell reports · 2024Article
- D-type cyclins regulate DNA mismatch repair in the G1 and S phases of the cell cycle, maintaining genome stability.bioRxiv : the preprint server for biology · 2024Article
- Chemical biology approaches to uncovering nuclear ROS control.Current opinion in chemical biology · 2023Review
- The RNA m5C modification in R-loops as an off switch of Alt-NHEJ.Nature communications · 2023Article
- FMRP promotes transcription-coupled homologous recombination via facilitating TET1-mediated m5C RNA modification demethylation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Immunostaining and Protein Pull-Down of Methyl-5-Cytosine-Marked RNA:DNA Hybrids.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Advances in the Genetically Engineered KillerRed for Photodynamic Therapy Applications.International journal of molecular sciences · 2021Review
6 more citing papers are in PubMed but not listed here.
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
Reactive oxygen species (ROS)-induced DNA damage is repaired by the base excision repair pathway. However, the effect of chromatin structure on BER protein recruitment to DNA damage sites in living cells is poorly understood. To address this problem, we developed a method to specifically produce ROS-induced DNA damage by fusing KillerRed (KR), a light-stimulated ROS-inducer, to a tet-repressor (tetR-KR) or a transcription activator (TA-KR). TetR-KR or TA-KR, bound to a TRE cassette (∼ 90 kb) integrated at a defined genomic locus in U2OS cells, was used to induce ROS damage in hetero- or euchromatin, respectively. We found that DNA glycosylases were efficiently recruited to DNA damage in heterochromatin, as well as in euchromatin. PARP1 was recruited to DNA damage within condensed chromatin more efficiently than in active chromatin. In contrast, recruitment of FEN1 was highly enriched at sites of DNA damage within active chromatin in a PCNA- and transcription activation-dependent manner. These results indicate that oxidative DNA damage is differentially processed within hetero or euchromatin.
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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.