ArticleJournal of hematology & oncology2018
The chromatin remodeling subunit Baf200 promotes normal hematopoiesis and inhibits leukemogenesis.
Article in Journal of hematology & oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 35 citations in OpenAlex.
- In-depth functional analysis of BRD9 in fetal hematopoiesis reveals context-dependent roles.iScience · 2025Article
- Actin-Like Protein 6A as an Oncogene and Therapeutic Target in Cancer.International journal of medical sciences · 2025Review
- Chromatin remodeling in lymphocytic function and fate: the multifaceted roles of SWI/SNF complex.Frontiers in immunology · 2025Review
- Chromatin remodeling in tissue stem cell fate determination.Cell regeneration (London, England) · 2024Review
- Baf155 controls hematopoietic differentiation and regeneration through chromatin priming.Cell reports · 2024Article
- The ncBAF Complex Regulates Transcription in AML Through H3K27ac Sensing by BRD9.Cancer research communications · 2024Article
- Dysregulation of epigenetic modifications in inborn errors of immunity.Epigenomics · 2024Review
- BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state.Nature communications · 2023Article
- Bidirectional interplay between metabolism and epigenetics in hematopoietic stem cells and leukemia.The EMBO journal · 2023Review
- Dissecting the role of SWI/SNF component ARID1B in steady-state hematopoiesis.Blood advances · 2023Article
- Epigenetic Regulation of Fibroblasts and Crosstalk between Cardiomyocytes and Non-Myocyte Cells in Cardiac Fibrosis.Biomolecules · 2023Review
- SWI/SNF complexes in hematological malignancies: biological implications and therapeutic opportunities.Molecular cancer · 2023Review
- Targeting Chromatin-Remodeling Factors in Cancer Cells: Promising Molecules in Cancer Therapy.International journal of molecular sciences · 2022Review
- PBAF chromatin remodeler complexes that mediate meiotic transitions in mouse.Development (Cambridge, England) · 2022Article
- Arid2 regulates hematopoietic stem cell differentiation in normal hematopoiesis.Experimental hematology · 2021Article
- Deficiency of eIF4B Increases Mouse Mortality and Impairs Antiviral Immunity.Frontiers in immunology · 2021Article
- Review
- Single‑cell RNA sequencing of t(8;21) acute myeloid leukemia for risk prediction.Oncology reports · 2020Article
- Intrinsic Disorder of the BAF Complex: Roles in Chromatin Remodeling and Disease Development.International journal of molecular sciences · 2019Article
- Article
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Authors and funding
17 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAdenosine triphosphate (ATP)-dependent chromatin remodeling SWI/SNF-like BAF and PBAF complexes have been implicated in the regulation of stem cell function and cancers. Several subunits of BAF or PBAF, including BRG1, BAF53a, BAF45a, BAF180, and BAF250a, are known to be involved in hematopoiesis. Baf200, a subunit of PBAF complex, plays a pivotal role in heart morphogenesis and coronary artery angiogenesis. However, little is known on the importance of Baf200 in normal and malignant hematopoiesis.
methodsUtilizing Tie2-Cre-, Vav-iCre-, and Mx1-Cre-mediated Baf200 gene deletion combined with fetal liver/bone marrow transplantation, we investigated the function of Baf200 in fetal and adult hematopoiesis. In addition, a mouse model of MLL-AF9-driven leukemogenesis was used to study the role of Baf200 in malignant hematopoiesis. We also explored the potential mechanism by using RNA-seq, RT-qPCR, cell cycle, and apoptosis assays.
resultsTie2-Cre-mediated loss of Baf200 causes perinatal death due to defective erythropoiesis and impaired hematopoietic stem cell expansion in the fetal liver. Vav-iCre-mediated loss of Baf200 causes only mild anemia and enhanced extramedullary hematopoiesis. Fetal liver hematopoietic stem cells from Tie2-Cre
conclusionOur current studies uncover critical roles of Baf200 in both normal and malignant hematopoiesis and provide a potential therapeutic target for suppressing the progression of leukemia without interfering with normal hematopoiesis.
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