Skip to main content
. 2013 Sep 3;123(10):4144–4157. doi: 10.1172/JCI68951

Figure 4. JAK2 activity requires BCR-ABL1 expression and is essential for CML HSCs survival.

Figure 4

(A) Left: BCR-ABL1 and JAK2 protein activity and expression in MIGR1–empty vector, WT BCR-ABL1–expressing, and K1172R BCR-ABL1–expressing LSK cells (n = 10). GRB2 levels were detected as loading control. Middle: PP2A phosphatase activity assay (mean ± SD) of MIGR1–empty vector (EV), WT BCR-ABL1–expressing, and K1172R BCR-ABL1–expressing LSK cells. Right: Flow cytometric analysis of active JAK2 (pJAK2) levels in MIGR1–empty vector, BCR-ABL1–, and K1172R BCR-ABL1–expressing LSK cells (n = 10). (B) Active JAK2 levels and BCR-ABL1 (pABLY245) in untreated, BCR-ABL1 shRNA–expressing, and FTY720-treated CFSEmaxCD34+ and CD34+CD38– cells from NBM and/or CML samples. Representative flow cytometry histogram overlays are shown. Inset: BCR-ABL1 levels in CML CD34+ cells transduced with a shRNA specific for the b3a2 BCR-ABL1 junction. Levels of BCR-ABL1 expression normalized to that of GRB2 are expressed as arbitrary densitometric units. (C) Effect of JAK2 inhibitors on (left) CFSEmax/CD34+ frequency, (middle) LTC-IC (6 weeks), and (right) replating efficiency of CML cells. *P < 0.05, **P < 0.01, ***P < 0.001, Student’s t test.