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. 2018 Mar 12;28(4):476–490. doi: 10.1038/s41422-018-0015-9

Fig. 2.

Fig. 2

Setd2 deficiency abolishes HSC self-renewal capacity. a Long-term follow-up of donor-derived cell (CD45.2) proportion in PB of competitive BM transplanted (cBMT) mice. n = 16. b Proportion analysis of donor-derived cells in different BM subsets of cBMT mice. n = 7. c Long-term follow-up of donor-derived cell proportion in PB of primary (WT, n = 19; KO, n = 18) and secondary (n = 14) noncompetitive BM transplanted (ncBMT) mice. d Proportion analysis of donor-derived cells in different BM subsets of primary ncBMT mice. WT, n = 5, KO, n = 4. e Absolute cell count of donor-derived HSPC subsets in BM of primary ncBMT mice. WT, n = 5; KO, n = 4. f Proportion analysis of donor-derived cells in different BM subsets of secondary ncBMT mice. n = 4. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001