PINK1 Antibody - #DF7742

Figure 9 TRPM2-mediated Ca2+ influx is involved in the inhibition of the AKT-mTOR pathway in response to cisplatin. Intracellular Ca2+ signals indicated by the fluorescence of Fluo-4 AM in cisplatin (CP, 20 μM) or normal saline (NS) treated Trpm2-/- and WT MEFs (A, B) and mRTECs (C, D) (n = 7). Scale bars, 20 μm and 10μm, respectively. (E) Immunoblotting analysis and quantification of LC3B II in WT MEFs after incubation with clotrimazole (CLT, 10 μM) or vehicle (Veh) for 1 h followed by treatment with CP at the indicated concentration for 24 h. (F) Immunoblotting analysis and quantification of LC3B II in WT MEFs after incubation with 5 μM BAPTA-AM for 1 h followed by treatment with 20 μM CP for 24 h. (G) Immunoblotting analysis and quantification of p-AKT, AKT and p-p70S6K in WT MEFs after incubation with 5 μM BAPTA-AM or 10 μM clotrimazole for 1 h followed by treatment with 20 μM CP for 24 h. (H, I) Mitochondrial Ca2+ signals indicated by the fluorescence of Rhod-2 in mRTECs treated by CP or NS (n = 7). Scale bars, 10 μm. (J) Immunoblotting analysis and quantification of BNIP3 and PINK1 in mRTECs treated by CP or NS. Data are presented as mean±SEM. Statistical analysis was performed using one-way ANOVA with Tukey post-hoc test. ns, not significant; *p < 0.05, **p < 0.01, ***p < 0.001.

Fig. 2.| Effects of PS-MPS on mitochondrial membrane protein and membrane potential in control group and PS-MPS group after 24 h. (A) Relative transcription of mRNA of PINK1; (B) Relative protein expression of PINK1