ArticleNature communications2019
DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation.
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 92 papers.
What it found
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Who cites it
92 citing papers in PubMed, 165 citations in OpenAlex.
- Transcription initiation drives dosage compensation establishment and maintenance in maleScience advances · 2026Article
- Histone methyltransferase DOT1L differentially affects the development of dendritic cell subsets.Life science alliance · 2026Article
- Inhibition of Dot1L Histone Methyltransferase Expands Bone Injury-Responsive CXCL12bioRxiv : the preprint server for biology · 2026Article
- Dot1L licenses DNA demethylation to establish regulatory T cell identity.bioRxiv : the preprint server for biology · 2026Article
- A sub-set of guanine- and cytosine-rich genes are actively transcribed at the nuclear lamin B1 region.Cellular and molecular life sciences : CMLS · 2026Article
- 5'-Methylthioadenosine Metabolic Reprogramming Drives H3K79 Monomethylation-Mediated PAK2 Upregulation to Promote Cadmium-Induced Breast Cancer Progression by Impairing Autophagic Flux.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Enhancer heterogeneity in acute lymphoblastic leukemia drives differential gene expression in patients.Blood · 2025Article
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- The histone-methyltransferase DOT1L cooperates with LSD1 to control cell division in blast-phase MPN.Leukemia · 2025Article
- PROM1/CD133 marks a proliferative stem cell-like population of blasts in KMT2A rearranged infant ALL.Blood advances · 2025Article
- Mammalian conservation of endogenous G-quadruplex reveals their associations with complex traits.Genome biology · 2025Article
- H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells.Science advances · 2025Article
- Is Enhancer Function Driven by Protein-Protein Interactions? From Bacteria to Leukemia.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Article
- Loss of DOT1L disrupts neuronal transcription, behavior, and leads to a neurodevelopmental disorder.medRxiv : the preprint server for health sciences · 2025Article
- DOT1L Mediates Stem Cell Maintenance and Represents a Therapeutic Vulnerability in Cancer.Cancer research · 2025Review
- Life cycle and morphogenetic differentiation in heteromorphic cell types of a cosmopolitan marine microalga.The New phytologist · 2025Article
- Fusion-specific chromatin profiles mediate transcriptional heterogeneity in MLL-rearranged acute lymphoblastic leukemia.Blood advances · 2025Article
- Article
- Chromatin environment-dependent effects of DOT1L on gene expression in male germ cells.Communications biology · 2025Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Enhancer elements are a key regulatory feature of many important genes. Several general features including the presence of specific histone modifications are used to demarcate potentially active enhancers. Here we reveal that putative enhancers marked with H3 lysine 79 (H3K79) di or trimethylation (me2/3) (which we name H3K79me2/3 enhancer elements or KEEs) can be found in multiple cell types. Mixed lineage leukemia gene (MLL) rearrangements (MLL-r) such as MLL-AF4 are a major cause of incurable acute lymphoblastic leukemias (ALL). Using the DOT1L inhibitor EPZ-5676 in MLL-AF4 leukemia cells, we show that H3K79me2/3 is required for maintaining chromatin accessibility, histone acetylation and transcription factor binding specifically at KEEs but not non-KEE enhancers. We go on to show that H3K79me2/3 is essential for maintaining enhancer-promoter interactions at a subset of KEEs. Together, these data implicate H3K79me2/3 as having a functional role at a subset of active enhancers in MLL-AF4 leukemia cells.
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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.