ArticleBlood2011
The ability of MLL to bind RUNX1 and methylate H3K4 at PU.1 regulatory regions is impaired by MDS/AML-associated RUNX1/AML1 mutations.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 76 citations in OpenAlex.
- Review
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- Epigenetic Modulation and Brain Function in Parkinson's Disease: The Role of Exercise Alone or Combined With Polyphenols.Food science & nutrition · 2025Review
- Epigenetic mechanism of SET7/9-mediated histone methylation modification in high glucose-induced ferroptosis in retinal pigment epithelial cells.Journal of bioenergetics and biomembranes · 2024Article
- Review
- RUNX1 colludes with NOTCH1 to reprogram chromatin in T cell acute lymphoblastic leukemia.iScience · 2023Article
- A critical role of RUNX1 in governing megakaryocyte-primed hematopoietic stem cell differentiation.Blood advances · 2023Article
- Review
- Pan-cancer Landscape of the RUNX Protein Family Reveals their Potential as Carcinogenic Biomarkers and the Mechanisms Underlying their Action.Journal of translational internal medicine · 2022Article
- Effects of the Lysine Methyltransferase Inhibitor AZ505 on Bone Metabolism.Journal of bone metabolism · 2021Article
- Mutational synergy during leukemia induction remodels chromatin accessibility, histone modifications and three-dimensional DNA topology to alter gene expression.Nature genetics · 2021Article
- The role of epigenetic mechanisms in the regulation of gene expression in the cyclical endometrium.Clinical epigenetics · 2021Review
- Interplay between cofactors and transcription factors in hematopoiesis and hematological malignancies.Signal transduction and targeted therapy · 2021Review
- Runx Transcription Factors in T Cells-What Is Beyond Thymic Development?Frontiers in immunology · 2021Review
- Accurate germline RUNX1 variant interpretation and its clinical significance.Blood advances · 2020Article
- Hematopoietic Stem Cell Transcription Factors in Cardiovascular Pathology.Frontiers in genetics · 2020Review
- Super-enhancers: critical roles and therapeutic targets in hematologic malignancies.Journal of hematology & oncology · 2019Review
- Identification of the Regulatory Elements and Target Genes of Megakaryopoietic Transcription Factor MEF2C.Thrombosis and haemostasis · 2019Article
- Expression and Prognosis Analyses of Runt-Related Transcription Factor Family in Human Leukemia.Molecular therapy oncolytics · 2019Article
- The histone demethylase Jmjd3 regulates zebrafish myeloid development by promoting spi1 expression.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 6 institutions in 2 countries.
Funding
Abstract
The mixed-lineage leukemia (MLL) H3K4 methyltransferase protein, and the heterodimeric RUNX1/CBFβ transcription factor complex, are critical for definitive and adult hematopoiesis, and both are frequently targeted in human acute leukemia. We identified a physical and functional interaction between RUNX1 (AML1) and MLL and show that both are required to maintain the histone lysine 4 trimethyl mark (H3K4me3) at 2 critical regulatory regions of the AML1 target gene PU.1. Similar to CBFβ, we show that MLL binds to AML1 abrogating its proteasome-dependent degradation. Furthermore, a subset of previously uncharacterized frame-shift and missense mutations at the N terminus of AML1, found in MDS and AML patients, impairs its interaction with MLL, resulting in loss of the H3K4me3 mark within PU.1 regulatory regions, and decreased PU.1 expression. The interaction between MLL and AML1 provides a mechanism for the sequence-specific binding of MLL to DNA, and identifies RUNX1 target genes as potential effectors of MLL function.
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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.