Skip to main content
. 2020 Nov 23;17(10):2891–2904. doi: 10.1080/15548627.2020.1847798

Figure 2.

Figure 2.

GLIPR2 knockout cells respond to Tat-BECN1 peptide. (A) Quantification of GFP-LC3 puncta in indicated HeLa cell lines treated for 2 h with either 10 µM autophagy-inducing peptide (Tat-BECN1) or an inactive, control mutant peptide (Tat-BECN1F270S). Bars represent mean ± SEM of triplicate samples (30–70 cells analyzed per sample). Similar results were observed in three independent experiments. n.s., not significant, *p < 0.05, **p < 0.01, ***p < 0.001; one-way ANOVA with Tukey’s test for multiple comparisons. (B and C) Representative western blots (B) of endogenous LC3 in indicated cell lines treated with indicated concentration of Tat-BECN1 or control Tat-BECN1F270S peptides for 2 h. Similar results were observed in six independent experiments and the relative quantification (C) of LC3-II to LC3-I. Bars represent mean ± SEM. n.s., not significant, *p < 0.05, ***p < 0.001; one-way ANOVA with Dunnett’s test for multiple comparisons. (D) Relative quantification of LC3-II to LC3-I in indicated cells without peptide treatments (B and C). Bars represent mean ± SEM (n = 12). **p < 0.01; unpaired, two-tailed t-test