ReviewFrontiers in cell and developmental biology2022
The Role of DOT1L in Normal and Malignant Hematopoiesis.
Review in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Histone modifications: mechanisms, metabolic regulation, and therapeutic targeting in cancer.Precision clinical medicine · 2026Review
- Combined inhibition of DOT1L and BCL-2 induces synergistic anti-leukemic effects in MLL-rearranged acute myeloid leukemia via suppression of the PI3K/AKT pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Histone methyltransferase DOT1L differentially affects the development of dendritic cell subsets.Life science alliance · 2026Article
- Efficient Generation of Functional TCRαβbioRxiv : the preprint server for biology · 2026Article
- PICALM::MLLT10 translocated leukemia.FEBS letters · 2026Review
- Review
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- Discovery of the first-in-class DOT1L PROTAC degrader.European journal of medicinal chemistry · 2025Article
- Review
- Rational design of small-sized peptidomimetic inhibitors disrupting protein-protein interaction.RSC medicinal chemistry · 2024Review
- Beyond the tail: the consequence of context in histone post-translational modification and chromatin research.The Biochemical journal · 2024Article
- DOT-1.1 (DOT1L) deficiency inBBA advances · 2023Article
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 3 institutions in 1 country.
Funding
Abstract
Disruptor of telomeric silencing 1 (DOT1) was first identified in yeast (DOT1p) and is the sole methyltransferase responsible for histone three lysine 79 (H3K79) mono-, di-, and tri-methylation. Mammalian DOT1 (DOT1-like protein or DOT1L) has been implicated in many cellular processes, such as cell cycle progression, DNA damage response, and development. A notable developmental process reliant on DOT1L function is normal hematopoiesis, as DOT1L knockout leads to impairment in blood lineage formation. Aberrant activity of DOT1L has been implicated in hematopoietic malignancies as well, especially those with high expression of the homeobox (HOX) genes, as genetic or pharmacological DOT1L inhibition causes defects in leukemic transformation and maintenance. Recent studies have uncovered methyltransferase-independent functions and a novel mechanism of DOT1L function. Here, we summarize the roles of DOT1L in normal and malignant hematopoiesis and the potential mechanism behind DOT1L function in hematopoiesis, in light of recent discoveries.
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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.