ArticleOncogene2016
ATM-mediated KDM2A phosphorylation is required for the DNA damage repair.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 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
32 citing papers in PubMed, 71 citations in OpenAlex.
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- SMYD3 promotes endometrial cancer through epigenetic regulation of LIG4/XRCC4/XLF complex in non-homologous end joining repair.Oncogenesis · 2024Article
- A novel STAT3/ NFκB p50 axis regulates stromal-KDM2A to promote M2 macrophage-mediated chemoresistance in breast cancer.Cancer cell international · 2023Article
- MLL methyltransferases regulate H3K4 methylation to ensure CENP-A assembly at human centromeres.PLoS biology · 2023Article
- Oocyte-Specific Knockout of Histone Lysine Demethylase KDM2a Compromises Fertility by Blocking the Development of Follicles and Oocytes.International journal of molecular sciences · 2022Article
- Genome Maintenance Mechanisms at the Chromatin Level.International journal of molecular sciences · 2021Review
- SETD2-mediated H3K14 trimethylation promotes ATR activation and stalled replication fork restart in response to DNA replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Role of Histone Lysine Methylation in the Response of Mammalian Cells to Ionizing Radiation.Frontiers in genetics · 2021Review
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- H3K36 dimethylation by MMSET promotes classical non-homologous end-joining at unprotected telomeres.Oncogene · 2020Article
- GLP-catalyzed H4K16me1 promotes 53BP1 recruitment to permit DNA damage repair and cell survival.Nucleic acids research · 2019Article
- The RNA demethylase FTO is required for maintenance of bone mass and functions to protect osteoblasts from genotoxic damage.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The roles of the human SETMAR (Metnase) protein in illegitimate DNA recombination and non-homologous end joining repair.DNA repair · 2019Article
- Loss of Msh2 and a single-radiation hit induce common, genome-wide, and persistent epigenetic changes in the intestine.Clinical epigenetics · 2019Article
- Lysine-specific demethylase 2A enhances binding of various nuclear factors to CpG-rich genomic DNAs by action of its CXXC-PHD domain.Scientific reports · 2019Article
- Radiation biology and oncology in the genomic era.The British journal of radiology · 2018Review
- Jumonji Inhibitors Overcome Radioresistance in Cancer through Changes in H3K4 Methylation at Double-Strand Breaks.Cell reports · 2018Article
- Histone H1 acetylation at lysine 85 regulates chromatin condensation and genome stability upon DNA damage.Nucleic acids research · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ataxia-telangiectasia mutated (ATM) protein is a key signaling molecule that modulates the DNA damage response. However, the exact mechanism by which ATM regulates DNA damage repair has not yet been elucidated. Here, we report that ATM regulates the DNA damage response by phosphorylating lysine-specific demethylase 2A (KDM2A), a histone demethylase that acts at sites of H3K36 dimethylation. ATM interacts with KDM2A, and their interaction significantly increases in response to DNA double-stranded, but not single-stranded, breaks. ATM specifically phosphorylates KDM2A at threonine 632 (T632) following DNA damage, as demonstrated by a mutagenesis assay and mass spectrometric analysis. Although KDM2A phosphorylation does not alter its own demethylase activity, T632 phosphorylation of KDM2A largely abrogates its chromatin-binding capacity, and H3K36 dimethylation near DNA damage sites is significantly increased. Consequently, enriched H3K36 dimethylation serves as a platform to recruit the MRE11 complex to DNA damage sites by directly interacting with the BRCT2 domain of NBS1, which results in efficient DNA damage repair and enhanced cell survival. Collectively, our study reveals a novel mechanism for ATM in connecting histone modifications with the DNA damage response.
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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.