ArticlePloS one2012
Rbm15-Mkl1 interacts with the Setd1b histone H3-Lys4 methyltransferase via a SPOC domain that is required for cytokine-independent proliferation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- RBM15 in leukemogenesis: an emerging regulator at the interface of RNA biology and hematopoiesis.Trends in cancer · 2026Review
- RBM15 in diseases: Molecular mechanisms and clinical opportunities from RNA mGenes & diseases · 2026Review
- NNature reviews. Cancer · 2026Review
- RBM15-MKL1 fusion protein promotes leukemia via m6A methylation and Wnt pathway activation.Blood · 2025Article
- Regulation of H3K4me3 breadth and MYC expression by the SETD1B catalytic domain in MLL-rearranged leukemia.Leukemia · 2025Article
- Role of N6-methyladenosine methyltransferase component RBM15 in cancer progression and its therapeutic potential.Discover oncology · 2025Review
- RNA Binding Motif Protein 15 (RBM15): Structure, Function and Its Research Progress in Tumors.International journal of general medicine · 2025Review
- Structures and mechanisms of the RNA mActa biochimica et biophysica Sinica · 2024Review
- Exploring the role of mFrontiers in oncology · 2024Review
- SPOC domain proteins in health and disease.Genes & development · 2023Review
- The SPOC domain is a phosphoserine binding module that bridges transcription machinery with co- and post-transcriptional regulators.Nature communications · 2023Article
- Advances in molecular characterization of pediatric acute megakaryoblastic leukemia not associated with Down syndrome; impact on therapy development.Frontiers in cell and developmental biology · 2023Review
- Acute depletion of METTL3 implicatesGenome research · 2021Article
- Setd1a Plays Pivotal Roles for the Survival and Proliferation of Retinal Progenitors via Histone Modifications of Uhrf1.Investigative ophthalmology & visual science · 2021Article
- Interrogation of the cell wall integrity pathway inGene: X · 2020Article
- Progress toward understanding chromosome silencing by Xist RNA.Genes & development · 2020Review
- RNA-Binding Proteins in Acute Leukemias.International journal of molecular sciences · 2020Review
- RNA Regulators in Leukemia and Lymphoma.Cold Spring Harbor perspectives in medicine · 2020Review
- NMolecular therapy. Nucleic acids · 2020Review
- The role of the Xist 5' m6A region and RBM15 in X chromosome inactivation.Wellcome open research · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Rbm15-Mkl1 fusion protein is associated with acute megakaryoblastic leukemia (AMKL), although little is known regarding the molecular mechanism(s) whereby this fusion protein contributes to leukemogenesis. Here, we show that both Rbm15 and the leukemogenic Rbm15-Mkl1 fusion protein interact with the Setd1b histone H3-Lys4 methyltransferase (also known as KMT2G). This interaction is direct and requires the Rbm15 SPOC domain and the Setd1b LSD motif. Over-expression of Rbm15-Mkl1 in the 6133 megakaryoblastic leukemia cell line, previously established by expression of the Rbm15-Mkl1 fusion protein in mice (Mercher et al., [2009] J. Clin. Invest. 119, 852-864), leads to decreased levels of endogenous Rbm15 and increased levels of endogenous Mkl1. These cells exhibit enhanced proliferation and cytokine-independent cell growth, which requires an intact Rbm15 SPOC domain that mediates interaction between the Rbm15-Mkl1 fusion protein and the Setd1b methyltransferase. These results reveal altered Setd1b complex function and consequent altered epigenetic regulation as a possible molecular mechanism that mediates the leukemogenic activity of the Rbm15-Mkl1 fusion protein in AMKL.
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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.