Journal
BLOOD
Volume 125, Issue 13, Pages 2075-2078Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2014-08-596734
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Funding
- Kay Kendall Leukaemia Fund
- Merton College Oxford
- EMBO
- Danish Medical Research Council
- Leukaemia and Lymphoma Research
- Cancer Research UK
- Cancer Research UK [12796] Funding Source: researchfish
- Great Ormond Street Hospital Childrens Charity [W1062] Funding Source: researchfish
- Medical Research Council [MC_U137973817, MR/M009033/1] Funding Source: researchfish
- MRC [MR/M009033/1, MC_U137973817] Funding Source: UKRI
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Jarid1b/KDM5bis a histone demethylase that regulates self-renewal and differentiation in stem cells and cancer; however, its function in hematopoiesis is unclear. Here, we find that Jarid1b is highly expressed in primitive hematopoietic compartments and is over-expressed in acute myeloid leukemias. Constitutive genetic deletion of Jarid1b did not impact steady-state hematopoiesis. In contrast, acute deletion of Jarid1b from bone marrow increased peripheral blood T cells and, following secondary transplantation, resulted in loss of bone marrow reconstitution. Our results reveal that deletion of Jarid1b compromises hematopoietic stem cell (HSC) self-renewal capacity and suggest that Jarid1b is a positive regulator of HSC potential.
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