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. Author manuscript; available in PMC: 2020 Feb 1.
Published in final edited form as: Mol Cancer Ther. 2018 Nov 9;18(2):267–277. doi: 10.1158/1535-7163.MCT-18-0478

Figure 6. BTK knockdown model confers resistance to BGB-3111.

Figure 6.

A, Immunoblotting of BTK in parental Jeko cells and two BTK knockdown Jeko BTK-KD1 and BTK-KD2 clones. B, Drug sensitivity of Jeko, BTK-KD1, and BTK-KD2 to BGB-3111. Cell survival was measured following 72-hour treatment with serial concentrations of BGB-3111. Note: the Jeko mock treatment control is identical to that of Fig. 1C because both experiments were carried out in the same set of triplicate 96-wells. C, Steady-state phosphokinase activation in Jeko, BTK-KD1, and BTK-KD2 as determined by quantitative phosphokinase array. D, RPPA profiling of BGB-3111 treatment in Jeko, BTK-KD1, and BTK-KD2 in triplicate following plating for 0, 6, and 24 hr. Heat maps of differential protein expression in these cells were shown. Each data point consists of three technical replicates. E, Validation of differential protein expression in Jeko, Jeko R, and BTK knockdown cells by immunoblotting. F, Immunoblotting of differential protein expression in Jeko, Jeko R, BTK knockdown mutant, Mino and Maver cell lines exposed to BGB-3111 for three hours.