ArticleProceedings of the National Academy of Sciences of the United States of America2014
PARP1-dependent recruitment of KDM4D histone demethylase to DNA damage sites promotes double-strand break repair.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.
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Who cites it
95 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.
- Meta-analysis of DNA double-strand break response kinetics.Nucleic acids research · 2017Pooled it
- Kdm2a histone demethylase ablation restores anti-tumor immunogenicity in liver cancer.British journal of cancer · 2026Article
- Therapeutic implications of epigenetic alterations in burns: a new frontier in burn medicine.Clinical science (London, England : 1979) · 2026Review
- Review
- KDM4A promotes NEPC progression through regulation of MYC expression.Cancer letters · 2026Article
- KDM4D enhances radiosensitivity in esophageal squamous cell carcinoma through the SRBD1/RPL11/c-Myc/WIP1/CHK1 axis.American journal of translational research · 2026Article
- XPC Deficiency Activate Cisplatin-Mediated Autophagy in Bladder Cancer by Limiting Novel PHRF1-Mediated Ubiquitination of the p53 Protein.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- C8orf33 dictates DNA double-strand break repair choice by modulating KAT8-mediated H4K16 acetylation.Cell death & disease · 2025Article
- Hepatocyte reporter cells and integrated metabolomic and transcriptomic analyses reveal insights into hepatocyte changes in offspring of pregnancies with obesity.Scientific reports · 2025Article
- Histone demethylase JMJD2D emerges as a novel prognostic biomarker and exhibits correlation with immune infiltration in lung adenocarcinoma.Discover oncology · 2025Article
- Review
- DNA damage causes ATM-dependent heterochromatin loss leading to nuclear softening, blebbing, and rupture.Molecular biology of the cell · 2025Article
- RECQL4 requires PARP1 for recruitment to DNA damage, and PARG dePARylation facilitates its associated role in end joining.Experimental & molecular medicine · 2025Article
- Tricarboxylic Acid Cycle Relationships with Non-Metabolic Processes: A Short Story with DNA Repair and Its Consequences on Cancer Therapy Resistance.International journal of molecular sciences · 2024Review
- Harnessing DNA replication stress to target RBM10 deficiency in lung adenocarcinoma.Nature communications · 2024Article
- Triple Combinations of Histone Lysine Demethylase Inhibitors with PARP1 Inhibitor-Olaparib and Cisplatin Lead to Enhanced Cytotoxic Effects in Head and Neck Cancer Cells.Biomedicines · 2024Article
- DNA damage causes ATM-dependent heterochromatin loss leading to nuclear softening, blebbing, and rupture.bioRxiv : the preprint server for biology · 2024Article
- Article
- A dual role of RBM42 in modulating splicing and translation of CDKN1A/p21 during DNA damage response.Nature communications · 2023Article
- Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Members of the lysine (K)-specific demethylase 4 (KDM4) A-D family of histone demethylases are dysregulated in several types of cancer. Here, we reveal a previously unrecognized role of KDM4D in the DNA damage response (DDR). We show that the C-terminal region of KDM4D mediates its rapid recruitment to DNA damage sites. Interestingly, this recruitment is independent of the DDR sensor ataxia telangiectasia mutated (ATM), but dependent on poly (ADP-ribose) polymerase 1 (PARP1), which ADP ribosylates KDM4D after damage. We demonstrate that KDM4D is required for efficient phosphorylation of a subset of ATM substrates. We note that KDM4D depletion impairs the DNA damage-induced association of ATM with chromatin, explaining its effect on ATM substrate phosphorylation. Consistent with an upstream role in DDR, KDM4D knockdown disrupts the damage-induced recombinase Rad51 and tumor protein P53 binding protein foci formation. Consequently, the integrity of homology-directed repair and nonhomologous end joining of DNA breaks is impaired in KDM4D-deficient cells. Altogether, our findings implicate KDM4D in DDR, furthering the links between the cancer-relevant networks of epigenetic regulation and genome stability.
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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.