ArticleMolecular and cellular biology2003
The inv(16) fusion protein associates with corepressors via a smooth muscle myosin heavy-chain domain.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 158 citations in OpenAlex.
- Disrupting the CBFβ-SMMHC-RUNX1 oncogenic protein-protein interaction in inv(16) AML: from fusion biology to targeted therapy.Discover oncology · 2026Review
- CBFβ-SMMHC-driven leukemogenesis requires enhanced RUNX1-DNA binding affinity in mice.The Journal of clinical investigation · 2025Article
- Hypoxia-induced conversion of sensory Schwann cells into repair cells is regulated by HDAC8.Nature communications · 2025Article
- Discovery of a Highly Potent and Selective HDAC8 Degrader: Advancing the Functional Understanding and Therapeutic Potential of HDAC8.Journal of medicinal chemistry · 2024Article
- Inhibition of HDAC8 Reduces the Proliferation of Adult Neural Stem Cells in the Subventricular Zone.International journal of molecular sciences · 2024Article
- Proteogenomic analysis reveals cytoplasmic sequestration of RUNX1 by the acute myeloid leukemia-initiating CBFB::MYH11 oncofusion protein.The Journal of clinical investigation · 2023Article
- A Therapeutic Perspective of HDAC8 in Different Diseases: An Overview of Selective Inhibitors.International journal of molecular sciences · 2022Review
- Emerging therapies for inv(16) AML.Blood · 2021Review
- Protein Acetylation at the Interface of Genetics, Epigenetics and Environment in Cancer.Metabolites · 2021Review
- Article
- An updated account on molecular heterogeneity of acute leukemia.American journal of blood research · 2021Review
- CBFB-MYH11 Fusion Sequesters RUNX1 in Cytoplasm to Prevent DNMT3A Recruitment to Target Genes in AML.Frontiers in cell and developmental biology · 2021Article
- Article
- Switching the Switch: Ligand Induced Disulfide Formation in HDAC8.Chemistry (Weinheim an der Bergstrasse, Germany) · 2020Article
- Natural HDAC-1/8 inhibitor baicalein exerts therapeutic effect in CBF-AML.Clinical and translational medicine · 2020Article
- Histone deacetylase 3 preferentially binds and collaborates with the transcription factor RUNX1 to repress AML1-ETO-dependent transcription in t(8;21) AML.The Journal of biological chemistry · 2020Article
- HDAC8: A Promising Therapeutic Target for Acute Myeloid Leukemia.Frontiers in cell and developmental biology · 2020Article
- Core Binding Factor Leukemia: Chromatin Remodeling Moves Towards Oncogenic Transcription.Cancers · 2019Review
- Dysregulation of histone deacetylases in carcinogenesis and tumor progression: a possible link to apoptosis and autophagy.Cellular and molecular life sciences : CMLS · 2019Review
- HDAC1 Is a Required Cofactor of CBFβ-SMMHC and a Potential Therapeutic Target in Inversion 16 Acute Myeloid Leukemia.Molecular cancer research : MCR · 2019Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Inversion(16) is one of the most frequent chromosomal translocations found in acute myeloid leukemia (AML), occurring in over 8% of AML cases. This translocation results in a protein product that fuses the first 165 amino acids of core binding factor beta to the coiled-coil region of a smooth muscle myosin heavy chain (CBFbeta/SMMHC). CBFbeta interacts with AML1 to form a heterodimer that binds DNA; this interaction increases the affinity of AML1 for DNA. The CBFbeta/SMMHC fusion protein cooperates with AML1 to repress the transcription of AML1-regulated genes. We show that CBFbeta/SMMHC contains a repression domain in the C-terminal 163 amino acids of the SMMHC region that is required for inv(16)-mediated transcriptional repression. This minimal repression domain is sufficient for the association of CBFbeta/SMMHC with the mSin3A corepressor. In addition, the inv(16) fusion protein specifically associates with histone deacetylase 8 (HDAC8). inv(16)-mediated repression is sensitive to HDAC inhibitors. We propose a model whereby the inv(16) fusion protein associates with AML1 to convert AML1 into a constitutive transcriptional repressor.
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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.