期刊
CELL REPORTS
卷 19, 期 8, 页码 1503-1511出版社
CELL PRESS
DOI: 10.1016/j.celrep.2017.04.074
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资金
- BBSRC [BB/K010867/1]
- Wellcome Trust [095645/Z/11/Z, 104710/Z/14/Z]
- EU BLUEPRINT
- EpiGeneSys
- Bloodwise [13003]
- Medical Research Council
- Kay Kendall Leukaemia Fund
- Cambridge NIHR Biomedical Research Center
- Cambridge Experimental Cancer Medicine Centre
- Leukemia and Lymphoma Society of America [07037]
- MRC
- Wellcome Trust ISSF Fellowship [105641/Z/14/Z]
- Chancellor's Fellowship at the University
- Biotechnology and Biological Sciences Research Council [BBS/E/T/000PR9819, BBS/E/B/000C0425] Funding Source: researchfish
- Cancer Research UK [21762] Funding Source: researchfish
- Medical Research Council [MC_PC_12009] Funding Source: researchfish
- Wellcome Trust [104710/Z/14/Z] Funding Source: researchfish
- BBSRC [BBS/E/T/000PR9819, BBS/E/B/000C0425] Funding Source: UKRI
- Wellcome Trust [104710/Z/14/Z] Funding Source: Wellcome Trust
Aging of the hematopoietic stem cell (HSC) compartment is characterized by lineage bias and reduced stem cell function, the molecular basis of which is largely unknown. Using single-cell transcriptomics, we identified a distinct subpopulation of old HSCs carrying a p53 signature indicative of stem cell decline alongside pro-proliferative JAK/STAT signaling. To investigate the relationship between JAK/ STAT and p53 signaling, we challenged HSCs with a constitutively active form of JAK2 (V617F) and observed an expansion of the p53-positive subpopulation in old mice. Our results reveal cellular heterogeneity in the onset of HSC aging and implicate a role for JAK2V617F-driven proliferation in the p53-mediated functional decline of old HSCs.
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