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. 2007 Aug 1;27(31):8314–8323. doi: 10.1523/JNEUROSCI.1972-07.2007

Figure 3.

Figure 3.

Overexpression of wild-type and mutant (T123A) G-substrate in BE(2)-M17 cells. Lentivirus containing the wild-type and T123A G-substrate gene were transduced to BE(2)-M17 cells with a multiplicity of infection of 15. a, b, Overexpression of the wild-type and T123A G-substrate was confirmed by Western blot (a) and immunocytochemistry (b). c–f, After exposing these cells to 6-OHDA (c, d) or MG-132 (e, f), cell viability was measured using MTS assay (c, e), and cytotoxicity was measured via LDH release (d, f). Overexpression of both the wild-type and T123A G-substrate was protective against 6-OHDA and MG-132 toxicity. There was significantly less protection in T123A G-substrate-expressing cells compared with the wild-type G-substrate-expressing cells. Data are shown as means ± SEM (n = 6–8) and are representatives of three or more experiments with the similar trends (§ p < 0.001, two-way ANOVA; *p < 0.001, not significant, one-way ANOVA, Tukey's test). g, h, Knockdown of the endogenous G-substrate using siRNA: cell viability was measured using the MTS assay, and results are expressed as a percentage of cells exposed to control siRNA without 6-OHDA treatment. The endogenous G-substrate knockdown increased vulnerability of the cells to 6-OHDA toxicity (g) and MG-132 toxicity (h). Data are shown as means ± SEM (n = 6–8) and are representatives of three or more experiments with the similar trends (**p < 0.001, not significant, one-way ANOVA, Tukey's test).