Fig. 1

Camk transduction enhances PirBTM MLL-AF9 AML development. a Phosphorylation of CAMKI, CAMKII, and CAMKIV was decreased in the PirBTM MLL-AF9 AML BM cells compared to WT cells. b, c Colonies formed from WT or PirB TM AML cells upon CAMK or CAMKK inhibitor treatment. Numbers of colonies formed by WT AML cells are decreased by addition of STO609 (STO) or KN93 (KN) (n = 3). d, e, h Retrovirally expressed Camk1 and Camk4, but not Camk1 mutant (K49E) or Camk4 mutant (K75M), rescued PIRB TM phenotype upon secondary transplantation. Retrovirally expressed Camk1 and Camk4 had similar levels as endogenous proteins in WT controls (Additional file 1: Figure S1). d Survival curves of mice transplanted with 3000 of these ectopically Camk1-expressing, Camk4-expressing, Camk1 K49E-expressing, Camk4 K75M-expressing, or control cells (n = 15 mice). e Percentages of retrovirus-infected (GFP⁺) AML cells in PB of secondary recipient mice after 28 days of transplantation. (n = 5 mice). h CFU numbers of retrovirus-infected (GFP⁺) AML cells in colony-forming assays. The experiment was repeated three times with similar results. f, g, i Retrovirally expressed Camk1 and Camk4 cannot change WT AML phenotype upon second transplantation. f Survival curves of mice transplanted with 3000 WT AML cells of these ectopically Camk1-expressing, Camk4-expressing, Camk1 K49E-expressing, Camk4 K75M-expressing, or control cells (n = 15 mice). g Percentages of retrovirus-infected (GFP⁺) AML cells in PB of secondary recipient mice after 28 days of transplantation. (n = 5 mice). i CFU numbers of retrovirus-infected (GFP⁺) AML cells in colony-forming assays. The experiment was repeated three times with similar results; *p < 0.05