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. 2017 Oct 4;36(21):3139–3155. doi: 10.15252/embj.201797994

Figure 7. Suppression of Prmt1 abolishes β‐catenin‐ or Hoxa9‐independent transformation in HSC‐derived MLL‐CSCs.

Figure 7

  1. The relative number of colonies from Hoxa9 −/− LSK‐MLL‐ENL leukemic cells with empty vector or shPRMT1 (n = 3, t‐test).
  2. The % of CD45.2+ donor cells in the bone marrow of recipient mice at the indicated time points post‐transplantation of Hoxa9 −/− LSK‐MLL‐ENL leukemic cells with empty vector or shPrmt1 (n = 4, t‐test).
  3. Kaplan–Meier survival curve of secondary recipient mice transplanted with Hoxa9 −/− LSK‐MLL‐ENL leukemic cells with vector control or shPrmt1 (n = 5/cohort, log‐rank test).
  4. The relative number of colonies from Ctnnb1 −/− LSK‐MLL‐ENL leukemic cells with empty vector or shPRMT1 (n = 3, t‐test).
  5. The % of CD45.2+ donor cells in the bone marrow of recipient mice at the indicated time points post‐transplantation of Ctnnb1 −/− LSK‐MLL‐ENL leukemic cells with empty vector or shPrmt1 (n = 4, t‐test).
  6. Kaplan–Meier survival curve of secondary recipient mice transplanted with Ctnnb1 −/− LSK‐MLL‐ENL leukemic cells with vector control or shPrmt1 (n = 4/cohort, log‐rank test).
Data information: Data are represented as mean ± SD. See also Appendix Fig S6.