ArticleBlood2010
Early mammalian erythropoiesis requires the Dot1L methyltransferase.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 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
93 citing papers in PubMed, 153 citations in OpenAlex.
- 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
- Histone modifications in the regulation of erythropoiesis.Annals of medicine · 2025Review
- 'Nomadic' Hematopoietic Stem Cells Navigate the Embryonic Landscape.Stem cell reviews and reports · 2025Review
- TET2 deficiency increases the competitive advantage of hematopoietic stem and progenitor cells through upregulation of thrombopoietin receptor signaling.Nature communications · 2025Article
- DOT1L Mediates Stem Cell Maintenance and Represents a Therapeutic Vulnerability in Cancer.Cancer research · 2025Review
- Erythropoiesis: insights from a genomic perspective.Experimental & molecular medicine · 2024Review
- The miR-144/Hmgn2 regulatory axis orchestrates chromatin organization during erythropoiesis.Nature communications · 2024Article
- Shared Genetic Features of Psoriasis and Myocardial Infarction: Insights From a Weighted Gene Coexpression Network Analysis.Journal of the American Heart Association · 2024Article
- An emerging maestro of immune regulation: how DOT1L orchestrates the harmonies of the immune system.Frontiers in immunology · 2024Review
- The histone methyltransferase DOT1B is dispensable for stage differentiation and macrophage infection ofFrontiers in cellular and infection microbiology · 2024Article
- DOT1L is a barrier to histone acetylation during reprogramming to pluripotency.Science advances · 2023Article
- The effect of ITLN1, XCL2 and DOT1L variants on knee osteoarthritis risk in the Han population.Archives of orthopaedic and trauma surgery · 2023Article
- The DOT1L-MLLT10 complex regulates male fertility and promotes histone removal during spermiogenesis.Development (Cambridge, England) · 2023Article
- Emerging Roles of Epigenetic Regulators in Maintaining Hematopoietic Stem Cell Homeostasis.Advances in experimental medicine and biology · 2023Article
- DOT-1.1 (DOT1L) deficiency inBBA advances · 2023Article
- Viewing AML through a New Lens: Technological Advances in the Study of Epigenetic Regulation.Cancers · 2022Review
- Histone methyltransferase DOT1L is essential for self-renewal of germline stem cells.Genes & development · 2022Article
- DOT1L Methyltransferase Regulates Calcium Influx in Erythroid Progenitor Cells in Response to Erythropoietin.International journal of molecular sciences · 2022Article
- DOT1L Is a Novel Cancer Stem Cell Target for Triple-Negative Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
33 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Histone methylation is an important regulator of gene expression; its coordinated activity is critical in complex developmental processes such as hematopoiesis. Disruptor of telomere silencing 1-like (DOT1L) is a unique histone methyltransferase that specifically methylates histone H3 at lysine 79. We analyzed Dot1L-mutant mice to determine influence of this enzyme on embryonic hematopoiesis. Mutant mice developed more slowly than wild-type embryos and died between embryonic days 10.5 and 13.5, displaying a striking anemia, especially apparent in small vessels of the yolk sac. Further, a severe, selective defect in erythroid, but not myeloid, differentiation was observed. Erythroid progenitors failed to develop normally, showing retarded progression through the cell cycle, accumulation during G₀/G₁ stage, and marked increase in apoptosis in response to erythroid growth factors. GATA2, a factor essential for early erythropoiesis, was significantly reduced in Dot1L-deficient cells, whereas expression of PU.1, a transcription factor that inhibits erythropoiesis and promotes myelopoiesis, was increased. These data suggest a model whereby DOT1L-dependent lysine 79 of histone H3 methylation serves as a critical regulator of a differentiation switch during early hematopoiesis, regulating steady-state levels of GATA2 and PU.1 transcription, thus controlling numbers of circulating erythroid and myeloid 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.