ArticleeLife2021
HBO1-MLL interaction promotes AF4/ENL/P-TEFb-mediated leukemogenesis.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Distinct roles of the JADE and BRPF scaffolding subunits of the acetyltransferase HBO1 complex.Nature communications · 2026Article
- Histone acetyltransferase HBO1 in cancer biology: Essential mechanisms and implications for targeted therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Outer membrane vesicles fromFrontiers in microbiology · 2026Article
- Research Advances in the Endometriotic Microenvironment: Synergistic Immune-Inflammatory-Angiogenic Interactions and their Therapeutic Translation.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- KMT2A-rearranged leukemia: from mechanism to drug development.Experimental hematology · 2025Review
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- Role of Histone H3 Lysine 4 Methylation in Chromatin Biology.Molecules (Basel, Switzerland) · 2025Review
- Catalytic Inhibition of KAT6/KAT7 Enhances the Efficacy and Overcomes Primary and Acquired Resistance to Menin Inhibitors in MLL Leukemia.Cancer discovery · 2025Article
- The phenylalanine-and-glycine repeats of NUP98 oncofusions form condensates that selectively partition transcriptional coactivators.Molecular cell · 2025Article
- Uncoupling histone modification crosstalk by engineering lysine demethylase LSD1.Nature chemical biology · 2025Article
- Targeting KAT7 inhibits the progression of colorectal cancer.Theranostics · 2025Article
- HBO1, a MYSTerious KAT and its links to cancer.Biochimica et biophysica acta. Gene regulatory mechanisms · 2024Review
- Guiding the HBO1 complex function through the JADE subunit.Nature structural & molecular biology · 2024Article
- Article
- The YEATS domain epigenetic reader proteins ENL and AF9 and their therapeutic value in leukemia.Experimental hematology · 2023Review
- MOZ/ENL complex is a recruiting factor of leukemic AF10 fusion proteins.Nature communications · 2023Article
- Chromatin complex dependencies reveal targeting opportunities in leukemia.Nature communications · 2023Article
- RNA-binding proteins of KHDRBS and IGF2BP families control the oncogenic activity of MLL-AF4.Nature communications · 2022Article
- MiR-27a downregulates 14-3-3θ, RUNX1, AF4, and MLL-AF4, crucial drivers of blast transformation in t(4;11) leukemia cells.Cell biochemistry and function · 2022Article
- Molecular Characteristics and Therapeutic Vulnerabilities of Claudin-low Breast Cancers Derived from Cell Line Models.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leukemic oncoproteins cause uncontrolled self-renewal of hematopoietic progenitors by aberrant gene activation, eventually causing leukemia. However, the molecular mechanism underlying aberrant gene activation remains elusive. Here, we showed that leukemic MLL fusion proteins associate with the HBO1 histone acetyltransferase (HAT) complex through their trithorax homology domain 2 (THD2) in various human cell lines. MLL proteins associated with the HBO1 complex through multiple contacts mediated mainly by the ING4/5 and PHF16 subunits in a chromatin-bound context where histone H3 lysine 4 tri-methylation marks were present. Of the many MLL fusions, MLL-ELL particularly depended on the THD2-mediated association with the HBO1 complex for leukemic transformation. The C-terminal portion of ELL provided a binding platform for multiple factors including AF4, EAF1, and p53. MLL-ELL activated gene expression in murine hematopoietic progenitors by loading an AF4/ENL/P-TEFb (AEP) complex onto the target promoters wherein the HBO1 complex promoted the association with AEP complex over EAF1 and p53. Moreover, the NUP98-HBO1 fusion protein exerted its oncogenic properties via interaction with MLL but not its intrinsic HAT activity. Thus, the interaction between the HBO1 complex and MLL is an important nexus in leukemic transformation, which may serve as a therapeutic target for drug development.
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