ReviewProceedings of the Japan Academy. Series B, Physical and biological sciences2026
BRD9 at the crossroads of splicing, chromatin remodeling, and hematopoiesis.
Review in Proceedings of the Japan Academy. Series B, Physical and biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Abstract
BAF complexes are ATP-dependent chromatin remodelers that govern gene expression and cellular identity. The non-canonical BAF (ncBAF) complex, with BRD9 as its signature component, orchestrates chromatin remodeling essential for balanced hematopoiesis. BRD9 loss disrupts enhancer-promoter interactions and CTCF-mediated chromatin architecture, causing myeloid skewing, impaired lymphoid differentiation, and diminished hematopoietic stem cell (HSC) fitness-phenotypes recapitulating physiological aging. This mechanism underlies aging-related pathologies such as myelodysplastic syndromes (MDS), in which spliceosomal mutations in SF3B1 trigger aberrant BRD9 splicing and destabilize its mRNA. Remarkably, BRD9 exhibits context-dependent functions: its depletion consistently promotes differentiation and apoptosis in myeloid leukemias, contrasting its differential roles in myeloid differentiation in adult versus fetal hematopoiesis. Thus, BRD9 mechanistically links spliceosomal dysfunction to chromatin dysregulation, bridging aging-associated disease and malignant transformation through context-dependent roles. Among the diverse assemblies of BAF family, these findings position the BRD9-ncBAF axis as both a critical determinant of hematopoietic fate decisions and a promising therapeutic target in hematologic malignancies.
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