ArticleBlood2015
MOZ regulates B-cell progenitors and, consequently, Moz haploinsufficiency dramatically retards MYC-induced lymphoma development.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 54 citations in OpenAlex.
- The roles of the acetyltransferase domains of the chromatin regulators KAT6A and KAT6B in vivo.Development (Cambridge, England) · 2026Article
- Lysine Acetyltransferase 6A Drives M1 Macrophage Polarization Through Metabolic Reprogramming in Sepsis-Induced Acute Lung Injury.Biomolecules · 2026Article
- Biological Activity and Structural Biology of Current KAT6A Inhibitor Chemotypes.Journal of medicinal chemistry · 2026Article
- IgG Idiotype Diversity Shapes Cytokine Profiles and Autoantibody Targets in HTLV-1 Clinical Outcomes.International journal of molecular sciences · 2025Article
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- KAT6B overexpression rescues embryonic lethality in homozygous null KAT6A mice restoring vitality and normal lifespan.Nature communications · 2025Article
- The histone acetyltransferase KAT6B is required for hematopoietic stem cell development and function.Stem cell reports · 2024Article
- In Silico Study on the Interactions, Molecular Docking, Dynamics and Simulation of Potential Compounds fromMolecules (Basel, Switzerland) · 2023Article
- The chromatin reader protein ING5 is required for normal hematopoietic cell numbers in the fetal liver.Frontiers in immunology · 2023Article
- Review
- Article
- MOZ is critical for the development of MOZ/MLL fusion-induced leukemia through regulation of Hoxa9/Meis1 expression.Blood advances · 2022Article
- BRPF1-KAT6A/KAT6B Complex: Molecular Structure, Biological Function and Human Disease.Cancers · 2022Review
- The MOZ-BRPF1 acetyltransferase complex in epigenetic crosstalk linked to gene regulation, development, and human diseases.Frontiers in cell and developmental biology · 2022Review
- Histone Modifications and Their Targeting in Lymphoid Malignancies.International journal of molecular sciences · 2021Review
- Article
- Chromatin-Remodeled State in Lymphoma.Current hematologic malignancy reports · 2019Review
- Heart failure drug proscillaridin A targets MYC overexpressing leukemia through global loss of lysine acetylation.Journal of experimental & clinical cancer research : CR · 2019Article
- Epigenomic drivers of immune dysfunction in aging.Aging cell · 2019Review
- The many lives of KATs - detectors, integrators and modulators of the cellular environment.Nature reviews. Genetics · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The histone acetyltransferase MOZ (MYST3, KAT6A) is the target of recurrent chromosomal translocations fusing the MOZ gene to CBP, p300, NCOA3, or TIF2 in particularly aggressive cases of acute myeloid leukemia. In this study, we report the role of wild-type MOZ in regulating B-cell progenitor proliferation and hematopoietic malignancy. In the Eμ-Myc model of aggressive pre-B/B-cell lymphoma, the loss of just one allele of Moz increased the median survival of mice by 3.9-fold. MOZ was required to maintain the proliferative capacity of B-cell progenitors, even in the presence of c-MYC overexpression, by directly maintaining the transcriptional activity of genes required for normal B-cell development. Hence, B-cell progenitor numbers were significantly reduced in Moz haploinsufficient animals. Interestingly, we find a significant overlap in genes regulated by MOZ, mixed lineage leukemia 1, and mixed lineage leukemia 1 cofactor menin. This includes Meis1, a TALE class homeobox transcription factor required for B-cell development, characteristically upregulated as a result of MLL1 translocations in leukemia. We demonstrate that MOZ localizes to the Meis1 locus in pre-B-cells and maintains Meis1 expression. Our results suggest that even partial inhibition of MOZ may reduce the proliferative capacity of MEIS1, and HOX-driven lymphoma and leukemia cells.
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.