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. 2018 Jul 30;8(15):4262–4278. doi: 10.7150/thno.26164

Figure 4.

Figure 4

JuA up-regulates HSP90β in an Axl/ERK-dependent manner. BV2 cells were treated with JuA (25 μM) for indicated periods of time (A), or treated with JuA at indicated concentrations for 0.5 h (B). (C) BV2 cells were pretreated with 0.1% DMSO (Ctrl), JuA (25 μM) or JuA (25 μM) + SCH772984 (10 μM) for 30 min, followed by administration of Aβ42 (5 μM) for 6 h. (D) BV2 cells were pretreated with 0.1% DMSO (Ctrl), JuA (25 μM) or JuA (25 μM) with the indicated antagonist of RTKs (Dovitinib at 1 μM, Gefinitib at 2.5 μM, Sunitinib at 2.5 μM and LDC1267 at 1 μM) for 30 min, followed by administration of Aβ42 (5 μM) for 12 h. (E) BV2 cells were pretreated with 0.1% DMSO (Ctrl), JuA (25 μM) or JuA (25 μM) with the indicated antagonist of TAM receptor (LDC1267 at 1 μM, UNC2250 at 5 μM, R428 at 5 μM) for 30 min, followed by administration of Aβ42 (5 μM) for 12 h. (F) BV2 cells were transiently transfected with non-target control siRNA or siAxl for 48 h. (G) BV2 cells were transfected with siAxl for 48 h, then pretreated with JuA (25 μM) followed by administration of Aβ42 (5 μM) for 12 h. The whole-cell proteins were subjected to western blot with the antibodies indicated. All experiments were repeated three times. *p < 0.05, **p < 0.01, ***p < 0.001.