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. 2019 Jun 23;16(3):531–547. doi: 10.1080/15548627.2019.1630224

Figure 8.

Figure 8.

Activation of autophagy or inhibition of UPR rescues abnormal protein processing and increased cell death in WDR45-deficient cells. (a and b) Western blot analysis of endogenous HSPA5 and CASP3 levels after rapamycin (100 nM, 24 h) or TUDCA (100 μM, 24 h) treatment in HeLa cells with or without ER stress. (c and d) Flow cytometry analysis of apoptosis (ANXA5+ 7ADD− and ANXA5+ 7ADD+) in WDR45-deficient HeLa cells after inducing ER stress (2 μg/ml Tm, 36 h). (e and f) Effects of rapamycin or TUDCA on HSPA5 accumulation (2 μg/ml Tm, for 8 h), CASP3 cleavage (2 μg/ml Tm, 24 h), and LC3-II production, in mouse neurons after inducing ER stress. Data were expressed as mean ± SEM (n = 3). *P < 0.05, **P < 0.01, *** P < 0.001. n.s., not significant.w.