ArticleNature communications2019
The CHD6 chromatin remodeler is an oxidative DNA damage response factor.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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Who cites it
47 citing papers in PubMed.
- Assessment and detection of nucleotide excision repair capability in human cells: a critical review of current functional methods.Molecular biology reports · 2026Review
- Molecular basis of nick ligation in the nucleosome by DNA Ligase IIIα.Nature communications · 2026Article
- Fluorescent reporter assay reveals ribonucleotides promote mismatch correction in vivo.Nucleic acids research · 2026Article
- Navigating the base excision repair pathway in chromatin-focus on oxidative DNA damage.Nucleic acids research · 2026Review
- CHD6 promotes triple-negative breast cancer progression and is associated with PI3K/AKT and MAPK pathways.International journal of clinical oncology · 2026Article
- 8oxoG:A Is Structurally Accommodated in the Nucleosome Core Particle, Yet Inaccessible to MUTYH-Initiated DNA Repair.Biomolecules · 2026Article
- Molecular Acrobats: How CHD Remodelers Shape the Genetic Playground to License Cell Identity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Beyond KEAP1: The Context-Specific NRF2 Partner Code in Disease and Therapy.Antioxidants (Basel, Switzerland) · 2026Review
- Role of CHD chromatin remodelers in heart development.World journal of pediatrics : WJP · 2026Review
- Urbanisation Drives Microevolution in the Egyptian Fruit Bat (Evolutionary applications · 2026Article
- Chromodomain helicase DNA-binding proteins and orofacial cleft.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2026Review
- How histone modifications influence cellular radiosensitivity: Pharmaceutically targeting epigenetic regulators as a promising avenue to overcome radioresistance.Acta pharmaceutica Sinica. B · 2025Review
- Comprehensive Measurement of Inter-Individual Variation in DNA Repair Capacity in Healthy Individuals.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Base excision repair in chromatin: A tug-of-war for DNA damage.DNA repair · 2025Review
- CHD6 has poly(ADP-ribose)- and DNA-binding domains and regulates PARP1/2-trapping inhibitor sensitivity via abasic site repair.Nature communications · 2025Article
- CHD6 eviction of promoter nucleosomes maintains housekeeping transcriptional program in prostate cancer.Molecular therapy. Nucleic acids · 2024Article
- Loss-of-function of the Zinc Finger Homeobox 4 (medRxiv : the preprint server for health sciences · 2024Article
- Multiomic profiling of medulloblastoma reveals subtype-specific targetable alterations at the proteome and N-glycan level.Nature communications · 2024Article
- PARP trapping is governed by the PARP inhibitor dissociation rate constant.Cell chemical biology · 2024Article
- Deep learning with a small dataset predicts chromatin remodelling contribution to winter dormancy of apple axillary buds.Tree physiology · 2024Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell survival after oxidative DNA damage requires signaling, repair and transcriptional events often enabled by nucleosome displacement, exchange or removal by chromatin remodeling enzymes. Here, we show that Chromodomain Helicase DNA-binding protein 6 (CHD6), distinct to other CHD enzymes, is stabilized during oxidative stress via reduced degradation. CHD6 relocates rapidly to DNA damage in a manner dependent upon oxidative lesions and a conserved N-terminal poly(ADP-ribose)-dependent recruitment motif, with later retention requiring the double chromodomain and central core. CHD6 ablation increases reactive oxygen species persistence and impairs anti-oxidant transcriptional responses, leading to elevated DNA breakage and poly(ADP-ribose) induction that cannot be rescued by catalytic or double chromodomain mutants. Despite no overt epigenetic or DNA repair abnormalities, CHD6 loss leads to impaired cell survival after chronic oxidative stress, abnormal chromatin relaxation, amplified DNA damage signaling and checkpoint hypersensitivity. We suggest that CHD6 is a key regulator of the oxidative DNA damage response.
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