ArticleMolecular and cellular biology2007
Rbm15 modulates Notch-induced transcriptional activation and affects myeloid differentiation.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 100 citations in OpenAlex.
- RBM15 in leukemogenesis: an emerging regulator at the interface of RNA biology and hematopoiesis.Trends in cancer · 2026Review
- m6A and NuRD complexes regulate monocytic differentiation and resistance to BCL2/BCL2L1 inhibitors in acute myeloid leukemia.Haematologica · 2026Article
- RBM15 in diseases: Molecular mechanisms and clinical opportunities from RNA mGenes & diseases · 2026Review
- Spen and Nito prevent dedifferentiation of intermediate progenitors by maintaining Notch target expression in stem cells at low levels.Cell reports · 2026Article
- Revealing RELL1 signaling relying on the phosphoregulatory network analysis.Frontiers in bioinformatics · 2026Article
- IncreasedInternational journal of molecular sciences · 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
- N6-methyladenosine RNA modifications: a potential therapeutic target for AML.Annals of hematology · 2024Review
- Exploring the role of mFrontiers in oncology · 2024Review
- Characterization of the long noncoding RNA transcriptome in human preimplantation embryo development.Journal of assisted reproduction and genetics · 2023Article
- 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
- NAdvances in experimental medicine and biology · 2023Article
- Physio-pathological effects of N6-methyladenosine and its therapeutic implications in leukemia.Biomarker research · 2022Review
- RBM22, a Key Player of Pre-mRNA Splicing and Gene Expression Regulation, Is Altered in Cancer.Cancers · 2022Review
- The Role of NCancers · 2022Review
- RNA mFrontiers in immunology · 2022Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
RBM15 is the fusion partner with MKL in the t(1;22) translocation of acute megakaryoblastic leukemia. To understand the role of the RBM15-MKL1 fusion protein in leukemia, we must understand the normal functions of RBM15 and MKL. Here, we show a role for Rbm15 in myelopoiesis. Rbm15 is expressed at highest levels in hematopoietic stem cells and at more moderate levels during myelopoiesis of murine cell lines and primary murine cells. Decreasing Rbm15 levels with RNA interference enhances differentiation of the 32DWT18 myeloid precursor cell line. Conversely, enforced expression of Rbm15 inhibits 32DWT18 differentiation. We show that Rbm15 alters Notch-induced HES1 promoter activity in a cell type-specific manner. Rbm15 inhibits Notch-induced HES1 transcription in nonhematopoietic cells but stimulates this activity in hematopoietic cell lines, including 32DWT18 and human erythroleukemia cells. Moreover, the N terminus of Rbm15 coimmunoprecipitates with RBPJkappa, a critical factor in Notch signaling, and the Rbm15 N terminus has a dominant negative effect, impairing activation of HES1 promoter activity by full-length-Rbm15. Thus, Rbm15 is differentially expressed during hematopoiesis and may act to inhibit myeloid differentiation in hematopoietic cells via a mechanism that is mediated by stimulation of Notch signaling via RBPJkappa.
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.