ReviewExperimental & molecular medicine2022
Transcriptional regulation and chromatin dynamics at DNA double-strand breaks.
Review in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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Who cites it
22 citing papers in PubMed.
- From cell to disease: Regulatory networks and mechanisms of super‑enhancers in aging (Review).Molecular medicine reports · 2026Review
- RSF1-Dependent PAR Turnover Promotes 53BP1 Liquid Condensate Formation at DNA Damage Sites.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Epigenetic remodeling during UV exposure: high resolution analysis of histone post-translational modifications in a DNA binding protein 2 mutant model.Histochemistry and cell biology · 2026Article
- ZNF689 loss impairs homologous recombination sensitizing triple-negative breast cancer to combined PARP and PD-L1 inhibition.Nature communications · 2026Article
- Histone modifications across cancers: mechanisms, therapy and clinical translation.Molecular cancer · 2026Review
- ATRX loss couples genome instability at a G-rich repeat to dysregulation of human alpha-globin expression.Nature communications · 2026Article
- Superenhancers shape the landscape and repair dynamics of transcription-associated DNA breaks in cancer.Science advances · 2026Article
- How ATP-Dependent Chromatin Remodeling Complexes Regulate Vertebrate Embryonic Development.International journal of molecular sciences · 2026Review
- The breakome of BRCA1 and BRCA2 pathway mutation carriers reveals early processes in breast oncogenesis.Cell death & disease · 2025Article
- Epigenotoxicity: Decoding the epigenetic imprints of genotoxic agents and their implications for regulatory genetic toxicology.Environmental and molecular mutagenesis · 2025Review
- Nuclear poly(A)-binding protein and nucleolin utilize their RNA recognition motifs to read PAR chains.Nucleic acids research · 2025Article
- Article
- The WWP1-JARID1B axis sustains acute myeloid leukemia chemoresistance.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- CITK modulates BRCA1 recruitment at DNA double strand breaks sites through HDAC6.Cell death & disease · 2025Article
- Interplay and Dynamics of Chromatin Architecture and DNA Damage Response: An Overview.Cancers · 2025Review
- DNA contamination within recombinant adeno-associated virus preparations correlates with decreased CD34Molecular therapy. Methods & clinical development · 2024Article
- EZH1/2 plays critical roles in oocyte meiosis prophase I in mice.Biological research · 2024Article
- Base excision repair and double strand break repair cooperate to modulate the formation of unrepaired double strand breaks in mouse brain.Nature communications · 2024Article
- CDK12 controls transcription at damaged genes and prevents MYC-induced transcription-replication conflicts.Nature communications · 2024Article
- HJURP is recruited to double-strand break sites and facilitates DNA repair by promoting chromatin reorganization.Oncogene · 2024Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In eukaryotic cells, DNA damage can occur at any time and at any chromatin locus, including loci at which active transcription is taking place. DNA double-strand breaks affect chromatin integrity and elicit a DNA damage response to facilitate repair of the DNA lesion. Actively transcribed genes near DNA lesions are transiently suppressed by crosstalk between DNA damage response factors and polycomb repressive complexes. Epigenetic modulation of the chromatin environment also contributes to efficient DNA damage response signaling and transcriptional repression. On the other hand, RNA transcripts produced in the G1 phase, as well as the active chromatin context of the lesion, appear to drive homologous recombination repair. Here, we discuss how the ISWI family of chromatin remodeling factors coordinates the DNA damage response and transcriptional repression, especially in transcriptionally active regions, highlighting the direct modulation of the epigenetic environment.
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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.