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. Author manuscript; available in PMC: 2014 Mar 15.
Published in final edited form as: Cancer Res. 2013 Jul 25;73(18):5775–5786. doi: 10.1158/0008-5472.CAN-13-1318

Figure 1. BCR-ABL1 and KIT inhibitor profile.

Figure 1

(A) Mo7ep210BCR-ABL1 or Mo7e cells stimulated with SCF were treated overnight with 2 μM imatinib (IM), 50 nM dasatinib (das), 1 μM BAW667, 1 μM PPY-A or 200 ng/mL SCF blocking antibody (SCF-block). Lysates were immunoblotted for phosphotyrosine or pKITY721 respectively. Total BCR-ABL1 and total KIT are shown as loading controls. Mean relative signal intensity in the presence of inhibiting agents, determined by densitometric quantitation of band intensity, is shown for n=3 replicates. Error bars represent SEM; *p<0.05; **p<0.01; ***p<0.001 (Student’s t-test). (B) CD34+ cells from newly diagnosed chronic phase CML patients (n=3) were treated for 4 hours with 2 μM IM, 1 μM BAW667, 1 μM PPY-A, or 200 ng/mL SCF-block ± SCF stimulation as indicated. Lysates were immunoblotted for pCRKL or pKITY721. Total CRKL and total KIT are shown as loading controls. One representative experiment is shown. Dasatinib was not tested due to cell number limitations.