ArticleThe EMBO journal2012
Bat3 facilitates H3K79 dimethylation by DOT1L and promotes DNA damage-induced 53BP1 foci at G1/G2 cell-cycle phases.
Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 112 citations in OpenAlex.
- DOT1L Drives Endothelial-to-Mesenchymal Transition and Fibrotic Vascular Remodeling via H3K79 Methylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- DOT1L inhibition exerts the anti-tumor effect by activating interferon signaling in breast cancer cells.Clinical epigenetics · 2025Article
- Review
- Circular SNX25 encoded radioresistance augmenter facilitates DNA damage repair in hepatocellular carcinoma by targeting BAG6-GET4 interaction.Cell death & disease · 2025Article
- Discovery of the first-in-class DOT1L PROTAC degrader.European journal of medicinal chemistry · 2025Article
- Loss of DOT1L disrupts neuronal transcription, behavior, and leads to a neurodevelopmental disorder.medRxiv : the preprint server for health sciences · 2025Article
- DOT1L-mediated RAP80 methylation promotes BRCA1 recruitment to elicit DNA repair.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- PARP1-DOT1L transcription axis drives acquired resistance to PARP inhibitor in ovarian cancer.Molecular cancer · 2024Article
- An emerging maestro of immune regulation: how DOT1L orchestrates the harmonies of the immune system.Frontiers in immunology · 2024Review
- Rare de novo gain-of-function missense variants in DOT1L are associated with developmental delay and congenital anomalies.American journal of human genetics · 2023Article
- The chromatin network helps prevent cancer-associated mutagenesis at transcription-replication conflicts.Nature communications · 2023Article
- Genome maintenance in retinoblastoma: Implications for therapeutic vulnerabilities.Oncology letters · 2022Review
- Targeting the histone H3 lysine 79 methyltransferase DOT1L in MLL-rearranged leukemias.Journal of hematology & oncology · 2022Review
- Chromatin Ubiquitination Guides DNA Double Strand Break Signaling and Repair.Frontiers in cell and developmental biology · 2022Review
- The Chromatin Landscape Channels DNA Double-Strand Breaks to Distinct Repair Pathways.Frontiers in cell and developmental biology · 2022Review
- Article
- Targeting of histone methyltransferase DOT1L plays a dual role in chemosensitization of retinoblastoma cells and enhances the efficacy of chemotherapy.Cell death & disease · 2021Article
- DOT1L modulates the senescence-associated secretory phenotype through epigenetic regulation of IL1A.The Journal of cell biology · 2021Article
- Review
- Primitive Erythropoiesis in the Mouse is Independent of DOT1L Methyltransferase Activity.Frontiers in cell and developmental biology · 2021Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The methyltransferase DOT1L methylates histone H3 at K79 to facilitate specific biological events. H3K79 dimethylation (H3K79-2Me) by DOT1L influences the DNA damage response by promoting 53BP1 recruitment to DNA damage sites; however, it is unclear if this methylation is required as 53BP1 interacts with dimethylated H4 (H4K20-2Me) with a much higher affinity. We demonstrate that H3K79-2Me, while negligible during S-phase, is required for ionizing radiation (IR)-induced 53BP1 foci formation during G1/G2-phases when H4K20-2Me levels are low. Further, we describe an essential role for HLA-B-associated transcript 3 (Bat3) in regulating this process in U2OS cells. Bat3 co-localizes with DOT1L at histone H3, and Bat3 knockdown results in decreased DOT1L-H3 interaction and H3K79-2Me, leading to a reduction in IR-induced 53BP1 foci formation, defects in DNA repair and increased sensitivity to IR. We demonstrate that a conserved Bat3 ubiquitin-like motif and a conserved DOT1L ubiquitin-interacting motif promote DOT1L-Bat3 interaction to facilitate efficient H3K79-2Me and IR-induced 53BP1 foci formation during G1/G2-phases. Taken together, our findings identify a novel role for Bat3 in regulating DOT1L function, which plays a critical role in 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.