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Fig. 7 | Journal of Biomedical Science

Fig. 7

From: N-terminal functional domain of Gasdermin A3 regulates mitochondrial homeostasis via mitochondrial targeting

Fig. 7

Inhibition of ROS and the mitochondrial permeability transition alleviates cell death induced by Gsdma3 mutants. (a, b) Quantification results for MitoSox Red staining. Bar graphs depict the mitochondrial ROS levels (mean + s.d., n = 3 in duplicates) in NAC-treated transfected cells relative to vehicle-treated transfected cells. (c, d) Quantification results for 7AAD and DiIC1(5) staining. Bar graphs depict the fractions of dead (7AAD+) cells and mitochondrial membrane potential depolarization (DiIC1(5)low) cells (mean + s.d., n = 3 in duplicates) in NAC-treated transfected cells relative to vehicle-treated transfected cells. (e) Immunoblot analysis of cytochrome c release in the cytosolic fraction of transfected HEK293T cells. GAPDH was used as a loading control. Relative densitometry levels normalized to GAPDH expressions are indicated. (f) Quantification of 7-AAD staining in bar graphs representing the fraction of dead (7AAD+) cells (mean + s.d., n = 3) in inhibitor-treated N-Gsdma3 transfected cells relative to vehicle-treated N-Gsdma3 transfected cells. n.s., not significant, P = 0.29. (g) Quantification results of 7AAD staining. Bar graphs depict the fraction of dead (7AAD+) cells (mean + s.d., n = 5 in duplicates) in CsA-treated N-Gsdma3 transfected cells relative to vehicle-treated 2N-Gsdma3 transfected cells. pIRES vector-transfected cells were used as the staining baseline. *, P < 0.05; **, P < 0.01; ***, P < 0.001

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