ArticleProceedings of the National Academy of Sciences of the United States of America2007
Ott1(Rbm15) has pleiotropic roles in hematopoietic development.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 92 citations in OpenAlex.
- RBM15 in leukemogenesis: an emerging regulator at the interface of RNA biology and hematopoiesis.Trends in cancer · 2026Review
- mCells · 2025Review
- Role of N6-methyladenosine methyltransferase component RBM15 in cancer progression and its therapeutic potential.Discover oncology · 2025Review
- Dynamics and regulatory roles of RNA meLife · 2025Article
- RBM15-mediated mFrontiers in cell and developmental biology · 2025Review
- RNA Binding Motif Protein 15 (RBM15): Structure, Function and Its Research Progress in Tumors.International journal of general medicine · 2025Review
- NMolecular medicine (Cambridge, Mass.) · 2024Review
- RBM15 Protects From Myocardial Infarction by Stabilizing NAE1.JACC. Basic to translational science · 2024Article
- Exploring the role of mFrontiers in oncology · 2024Review
- mEpigenetics · 2023Article
- SPOC domain proteins in health and disease.Genes & development · 2023Review
- The Role of mInternational journal of molecular sciences · 2023Review
- NAdvances in experimental medicine and biology · 2023Article
- AZGP1P2/UBA1/RBM15 Cascade Mediates the Fate Determinations of Prostate Cancer Stem Cells and Promotes Therapeutic Effect of Docetaxel in Castration-Resistant Prostate Cancer via TPM1 m6A Modification.Research (Washington, D.C.) · 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
- The Role of NCancers · 2022Review
- RBM15 condensates modulate mComputational and structural biotechnology journal · 2022Article
- RNA mFrontiers in immunology · 2022Review
- Review
- The functions and prognostic values of m6A RNA methylation regulators in thyroid carcinoma.Cancer cell international · 2021Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
OTT1(RBM15) was originally described as a 5' translocation partner of the MAL(MKL1) gene in t(1,22)(p13;q13) infant acute mega karyocytic leukemia. OTT1 has no established physiological function, but it shares homology with the spen/Mint/SHARP family of proteins defined by three amino-terminal RNA recognition motifs and a carboxyl-terminal SPOC (Spen paralog and ortholog carboxyl-terminal) domain believed to act as a transcriptional repressor. To define the role of OTT1 in hematopoiesis and help elucidate the mechanism of t(1,22) acute megakaryocytic leukemia pathogenesis, a conditional allele of Ott1 was generated in mice. Deletion of Ott1 in adult mice caused a loss of peripheral B cells due to a block in pro/pre-B differentiation. There is myeloid and megakaryocytic expansion in spleen and bone marrow, an increase in the Lin(-)Sca-1(+)c-Kit(+) compartment that includes hematopoietic stem cells, and a shift in progenitor fate toward granulocyte differentiation. These data show a requirement for Ott1 in B lymphopoiesis, and inhibitory roles in the myeloid, megakaryocytic, and progenitor compartments. The ability of Ott1 to affect hematopoietic cell fate and expansion in multiple lineages is a novel attribute for a spen family member and delineates Ott1 from other known effectors of hematopoietic development. It is plausible that dysregulation of Ott1-dependent hematopoietic developmental pathways, in particular those affecting the megakaryocyte lineage, may contribute to OTT1-MAL-mediated leukemogenesis.
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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.