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Additional file 4 of p38-TFEB pathways promote microglia activation through inhibiting CMA-mediated NLRP3 degradation in Parkinson's disease

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posted on 2021-12-21, 04:42 authored by Jialong Chen, Kanmin Mao, Honglin Yu, Yue Wen, Hua She, He Zhang, Linhua Liu, Mingque Li, Wenjun Li, Fei Zou
Additional file 4: Fig S4. (A, B) BV2 cells were labeled with Lysosome tracker and visualized lysosome biogenesis under a microscope demonstrating si-p38 increased the levels of lysosome biogenesis and shown in B. Mean ± SEM, n = 10, *p < 0.05. (C, D) Cell lysates from BV2 cells were immunoblotted demonstrating si-p38 decreased the levels of NLRP3, cleaved CASP1 and shown in D. Mean ± SEM, n = 6, *p < 0.05. (E, F) Cell lysates from BV2 cells were immunoblotted demonstrating TFEB decreased the levels of NLRP3, cleaved CASP1 and shown in F. Mean ± SEM, n = 6, *p < 0.05. (G, H) Cell lysates from BV2 cells were immunoblotted and shown in H. Mean ± SEM, n = 6, *p < 0.05. (I, J) Levels of IL-1β and IL-18 in conditional mediate of BV2were assessed by ELISA assay. Data were performed in F. (K, L) Cell lysates from BV2 cells were immunoblotted demonstrating autophagy inhibitor CQ eliminate the effect of decreased NLRP3 from SB20350 and shown in L. Mean ± SEM, n = 6, *p < 0.05.

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National Natural Science Foundation of China national natural science foundation of china discipline construction project of guangdong medical university

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