Supplementary Figure 9: SHP-1-CAMK1 rescues the lair1-null AML phenotype.

(a) Retrovirally-expressed SHP-1 increased CFU numbers of lair1-null AML cells in secondary plating. Data from one experiment with n = 3 technical replicate samples are shown. The experiment was repeated 3 times with similar results. (b) The expression of endogenous shp-1 was inhibited by Cre virus infection, as determined by Q-PCR at 48 h after infection. Data are from a single experiment, representative of 3 independent experiments. (c,d) SHP-1 inhibitors have little effect on (c) CFU activity of MLL-AF9 AML cells or (d) cell growth capacity of human AML leukemia cell line (MV4-11). Data from one experiment with n = 3 technical replicate samples are shown. The experiment was repeated 3 times with similar results. (e) Retrovirally-expressed SHP-1 WT, C₄₅₃S, and 4YF(278, 303, 538, 566), but not SHP-1 PTPc, increased CFU numbers of lair1-null AML cells in secondary plating. Data from one experiment with n = 3 technical replicate samples are shown. The experiment was repeated 3 times with similar results. (f) Retrovirally-expressed CAMK1 increased CFU numbers of lair1-null AML cells in secondary plating. Data from one experiment with n = 3 technical replicate samples are shown. The experiment was repeated 3 times with similar results. (g) IP-western assay of MLL-AF9 BM cells of wide-type mouse by precipitating SHP-1, followed by detection of CAMK1 or LAIR1. (h) Additional 4 times of western-blot analyses as in Fig. 4a, showing SHP-1 protein levels in both primarily and secondarily transplanted WT and LAIR1 null leukemic mice.