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. 2015 May 26;106(7):875–882. doi: 10.1111/cas.12686

Fig 3.

Fig 3

Inhibitory effects of imatinib (Imt) in AXT and K562 cells. (a) Cell proliferation assay with AXT cells incubated for 2 days in the absence (left) or presence (right) of FBS and with or without platelet-derived growth factor-BB (PDGF-BB) or imatinib. Data are expressed relative to the control value. (b) Cell proliferation assay with K562 cells incubated in the presence of FBS and the indicated concentrations of imatinib. Data are expressed relative to the value for time 0. (c) Phosphorylation of PDGF receptor β (PDGFRβ) was evaluated by immunoprecipitation (IP) and immunoblot analysis. AXT cells were cultured without serum for 2 h in the absence or presence of imatinib. Then the medium was replaced with those containing PDGF-BB, imatinib, and/or FBS as indicated. Cells were cultured for 15 min prior to lysate collection. (d) Immunoblot analysis of whole cell lysates from AXT cells as in (c). (e) Immunoblot analysis of the indicated molecules in AXT and K562 cells deprived of serum for 2 h in the absence or presence of imatinib and then stimulated with FBS for 15 min (in the continued absence or presence of imatinib). The arrowhead shows the total form of protein kinase B (Akt). $P < 0.05; $$P < 0.005. GSK3β, glycogen synthase kinase 3β.