ArticleThe EMBO journal2019
Conserved crosstalk between histone deacetylation and H3K79 methylation generates DOT1L-dose dependency in HDAC1-deficient thymic lymphoma.
Article in The EMBO journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Mesoscale proximity labeling at chromatin leads to identification of small molecule mechanism of action.Nature communications · 2026Article
- Histone methyltransferase DOT1L differentially affects the development of dendritic cell subsets.Life science alliance · 2026Article
- Trans-histone crosstalk establishes distinct H3K79 methylation zones with differential transcriptional functions.Nucleic acids research · 2026Article
- An emerging maestro of immune regulation: how DOT1L orchestrates the harmonies of the immune system.Frontiers in immunology · 2024Review
- Histone methylation in Epstein-Barr virus-associated diseases.Epigenomics · 2024Review
- DOT1L activity affects neural stem cell division mode and reduces differentiation and ASNS expression.EMBO reports · 2023Article
- Gain-of-function mutations in the catalytic domain ofScience advances · 2023Article
- Characterizing crosstalk in epigenetic signaling to understand disease physiology.The Biochemical journal · 2023Article
- Bioinformatic Analyses of Broad H3K79me2 Domains in Different Leukemia Cell Line Data Sets.Cells · 2022Article
- An Epigenetic Role of Mitochondria in Cancer.Cells · 2022Review
- SETD2: from chromatin modifier to multipronged regulator of the genome and beyond.Cellular and molecular life sciences : CMLS · 2022Review
- DOT1L inhibition does not modify the sensitivity of cutaneous T cell lymphoma to pan-HDAC inhibitorsFrontiers in genetics · 2022Article
- Signals for antigen-independent differentiation of memory CD8Cellular and molecular life sciences : CMLS · 2021Review
- Ready, SET, Go: Post-translational regulation of the histone lysine methylation network in budding yeast.The Journal of biological chemistry · 2021Review
- The language of chromatin modification in human cancers.Nature reviews. Cancer · 2021Review
- Current Methods of Post-Translational Modification Analysis and Their Applications in Blood Cancers.Cancers · 2021Review
- Histone methyltransferase DOT1L controls state-specific identity during B cell differentiation.EMBO reports · 2021Article
- Regulation of the Dot1 histone H3K79 methyltransferase by histone H4K16 acetylation.Science (New York, N.Y.) · 2021Article
- MCM5 Aggravates the HDAC1-Mediated Malignant Progression of Lung Cancer.Frontiers in cell and developmental biology · 2021Article
- The histone methyltransferase DOT1L prevents antigen-independent differentiation and safeguards epigenetic identity of CD8Proceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
DOT1L methylates histone H3K79 and is aberrantly regulated in MLL-rearranged leukemia. Inhibitors have been developed to target DOT1L activity in leukemia, but cellular mechanisms that regulate DOT1L are still poorly understood. We have identified the histone deacetylase Rpd3 as a negative regulator of budding yeast Dot1. At its target genes, the transcriptional repressor Rpd3 restricts H3K79 methylation, explaining the absence of H3K79me3 at a subset of genes in the yeast genome. Similar to the crosstalk in yeast, inactivation of the murine Rpd3 homolog HDAC1 in thymocytes led to an increase in H3K79 methylation. Thymic lymphomas that arise upon genetic deletion of Hdac1 retained the increased H3K79 methylation and were sensitive to reduced DOT1L dosage. Furthermore, cell lines derived from Hdac1
Indexed as
Identifiers
What OpenQuestion holds
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.