ArticleCell reports2014
MOF phosphorylation by ATM regulates 53BP1-mediated double-strand break repair pathway choice.
Article in Cell reports, 2014. 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 63 papers.
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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
63 citing papers in PubMed, 96 citations in OpenAlex.
- Article
- Lactylation at lysine 145 fosters KAT8-TIP60 complex formation to promote p53 acetylation at lysine 120 and its pro-apoptotic function.Nature communications · 2026Article
- HP1β recruits RING1A to ubiquitinate histone H2A for BRCA1-mediated resection of double-stand breaks.iScience · 2026Article
- Lysine Acetyltransferase 8: A Target for Natural Compounds in Cancer Therapy.International journal of molecular sciences · 2025Review
- Article
- Phosphorylation of the DNA damage repair factor 53BP1 by ATM kinase controls neurodevelopmental programs in cortical brain organoids.PLoS biology · 2024Article
- Hotspot Cancer Mutation Impairs KAT8-mediated Nucleosomal Histone Acetylation.Journal of molecular biology · 2024Article
- FUS unveiled in mitochondrial DNA repair and targeted ligase-1 expression rescues repair-defects in FUS-linked motor neuron disease.Nature communications · 2024Article
- Nuclear DJ-1 Regulates DNA Damage Repair via the Regulation of PARP1 Activity.International journal of molecular sciences · 2023Article
- Live-cell tracking of γ-H2AX kinetics reveals the distinct modes of ATM and DNA-PK in the immediate response to DNA damage.Journal of cell science · 2023Article
- KAT8 acetylation-controlled lipolysis affects the invasive and migratory potential of colorectal cancer cells.Cell death & disease · 2023Article
- Functional Phosphoproteomics in Cancer Chemoresistance Using CRISPR-Mediated Base Editors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- The phosphorylation to acetylation/methylation cascade in transcriptional regulation: how kinases regulate transcriptional activities of DNA/histone-modifying enzymes.Cell & bioscience · 2022Review
- Role of the Histone Acetyl Transferase MOF and the Histone Deacetylase Sirtuins in Regulation of H4K16ac During DNA Damage Repair and Metabolic Programming: Implications in Cancer and Aging.Sub-cellular biochemistry · 2022Article
- Targeted Cancer Therapy Based on Acetylation and Deacetylation of Key Proteins Involved in Double-Strand Break Repair.Cancer management and research · 2022Review
- Autism-Associated Vigilin Depletion Impairs DNA Damage Repair.Molecular and cellular biology · 2021Article
- The Role of RNA in DNA Breaks, Repair and Chromosomal Rearrangements.Biomolecules · 2021Review
- Histone Acetyltransferase MOF Orchestrates Outcomes at the Crossroad of Oncogenesis, DNA Damage Response, Proliferation, and Stem Cell Development.Molecular and cellular biology · 2020Review
- TNF-α regulates diabetic macrophage function through the histone acetyltransferase MOF.JCI insight · 2020Article
- SIRT6 is a DNA double-strand break sensor.eLife · 2020Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 7 institutions in 1 country.
Funding
Abstract
Cell-cycle phase is a critical determinant of the choice between DNA damage repair by nonhomologous end-joining (NHEJ) or homologous recombination (HR). Here, we report that double-strand breaks (DSBs) induce ATM-dependent MOF (a histone H4 acetyl-transferase) phosphorylation (p-T392-MOF) and that phosphorylated MOF colocalizes with γ-H2AX, ATM, and 53BP1 foci. Mutation of the phosphorylation site (MOF-T392A) impedes DNA repair in S and G2 phase but not G1 phase cells. Expression of MOF-T392A also blocks the reduction in DSB-associated 53BP1 seen in wild-type S/G2 phase cells, resulting in enhanced 53BP1 and reduced BRCA1 association. Decreased BRCA1 levels at DSB sites correlates with defective repairosome formation, reduced HR repair, and decreased cell survival following irradiation. These data support a model whereby ATM-mediated MOF-T392 phosphorylation modulates 53BP1 function to facilitate the subsequent recruitment of HR repair proteins, uncovering a regulatory role for MOF in DSB repair pathway choice during S/G2 phase.
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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.