ArticleStem cell reports2026
Comparison with Ezh2 reveals the PRC2-dependent functions of Jarid2 in hematopoietic stem Cell lineage commitment.
Article in Stem cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- JARID2 inhibition reprograms human hematopoietic progenitor cells to enhance bone marrow transplantation.Blood advances · 2026Article
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11 authors.
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Abstract
Previous studies showed the polycomb repressive complex 2 (PRC2) co-factor Jarid2 represses self-renewal transcriptional networks in mouse multipotent progenitor cells (MPPs). But only a fraction of de-repressed HSC-specific genes were associated with loss of H3K27me3, implying Jarid2 may have non-canonical (PRC2-independent) functions in hematopoiesis. We sought to delineate these potential PRC2-independent functions by comparing stem and progenitor cells genetically deficient for either Jarid2 or Ezh2 (enzymatic component of PRC2). Loss of Ezh2 increased myeloid differentiation but with a defect in lymphopoiesis. In contrast, loss of Jarid2 enhanced multi-lineage differentiation proportionally. Single-cell transcriptomics showed loss of Jarid2 had minimal impact across progenitor populations, but loss of Ezh2 led to accumulation of lymphoid-biased MPP4 cells and B cell progenitors in the bone marrow. Functional assays confirmed a differentiation block at the pre-pro-B cell stage. These data suggest the major PRC2-dependent function of Jarid2 in hematopoietic progenitors is restriction of myeloid differentiation potential.
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