ArticleOncogene2010
Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 55 citations in OpenAlex.
- The roles of the acetyltransferase domains of the chromatin regulators KAT6A and KAT6B in vivo.Development (Cambridge, England) · 2026Article
- KAT6A is essential for developmental control gene expression in neural stem and progenitor cells.PLoS genetics · 2026Article
- KMT2A-rearranged leukemia: from mechanism to drug development.Experimental hematology · 2025Review
- HMX3 is a critical vulnerability in MECOM-negative KMT2A::MLLT3 acute myelomonocytic leukemia.Leukemia · 2025Article
- The small inhibitor WM-1119 effectively targets KAT6A-rearranged AML, but not KMT2A-rearranged AML, despite shared KAT6 genetic dependency.Journal of hematology & oncology · 2024Article
- Protein arginine methyltransferase 2 controls inflammatory signaling in acute myeloid leukemia.Communications biology · 2024Article
- Identification of odontogenic ameloblast associated as a novel target gene of the Wnt/β-catenin signaling pathway.Cancer science · 2023Article
- Role of the MOZ/MLL-mediated transcriptional activation system for self-renewal in normal hematopoiesis and leukemogenesis.The FEBS journal · 2022Review
- MOZ is critical for the development of MOZ/MLL fusion-induced leukemia through regulation of Hoxa9/Meis1 expression.Blood advances · 2022Article
- MOZ and Menin-MLL Complexes Are Complementary Regulators of Chromatin Association and Transcriptional Output in Gastrointestinal Stromal Tumor.Cancer discovery · 2022Article
- A synthetic lethality screen reveals ING5 as a genetic dependency of catalytically dead Set1A/COMPASS in mouse embryonic stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The MOZ-BRPF1 acetyltransferase complex in epigenetic crosstalk linked to gene regulation, development, and human diseases.Frontiers in cell and developmental biology · 2022Review
- Impact of KMT2A Rearrangement and CSPG4 Expression in Pediatric Acute Myeloid Leukemia.Cancers · 2021Article
- The MLL/SET family and haematopoiesis.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020Review
- Why are so many MLL lysine methyltransferases required for normal mammalian development?Cellular and molecular life sciences : CMLS · 2019Review
- The non-specific lethal (NSL) complex at the crossroads of transcriptional control and cellular homeostasis.EMBO reports · 2019Review
- The many lives of KATs - detectors, integrators and modulators of the cellular environment.Nature reviews. Genetics · 2019Review
- Rewiring the Epigenetic Networks inFrontiers in cell and developmental biology · 2019Review
- The basic helix-loop-helix transcription factor SHARP1 is an oncogenic driver in MLL-AF6 acute myelogenous leukemia.Nature communications · 2018Article
- C-terminal BRE overexpression in 11q23-rearranged and t(8;16) acute myeloid leukemia is caused by intragenic transcription initiation.Leukemia · 2018Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MOZ and MLL, encoding a histone acetyltransferase (HAT) and a histone methyltransferase, respectively, are targets for recurrent chromosomal translocations found in acute myeloblastic or lymphoblastic leukemia. In MOZ (MOnocytic leukemia Zinc-finger protein)/CBP- or mixed lineage leukemia (MLL)-rearranged leukemias, abnormal levels of HOX transcription factors have been found to be critical for leukemogenesis. We show that MOZ and MLL cooperate to regulate these key genes in human cord blood CD34+ cells. These chromatin-modifying enzymes interact, colocalize and functionally cooperate, and both are recruited to multiple HOX promoters. We also found that WDR5, an adaptor protein essential for lysine 4 trimethylation of histone H3 (H3K4me3) by MLL, colocalizes and interacts with MOZ. We detected the binding of the HAT MOZ to H3K4me3, thus linking histone methylation to acetylation. In CD34+ cells, depletion of MLL causes release of MOZ from HOX promoters, which is correlated to defective histone activation marks, leading to repression of HOX gene expression and alteration of commitment of CD34+ cells into myeloid progenitors. Thus, our results unveil the role of the interaction between MOZ and MLL in CD34+ cells in which both proteins have a critical role in hematopoietic cell-fate decision, suggesting a new molecular mechanism by which MOZ or MLL deregulation leads to leukemogenesis.
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