Fig. 7

Stx17 ameliorates Meth-induced autophagic dysfunction by facilitating CCZ1 activation of Rab7. (A) CoIP analysis of interactions among Flag-Stx17, endogenous LC3-II/I, and CCZ1 in HEK293T cells under Meth treatment and starvation conditions. (B) Data indicate the means ± SEMs of the ratio between Flag-Stx17 expressed in IP and Flag-Stx17 level in inputs. Data are shown as the means ± SEMs (n = 3). ^****p < 0.0001 compared with the Meth group. (C) Data are presented as the means ± SEMs between the LC3-II/I ratio in Flag-Stx17 IP relative (normalized) to the LC3-II/I ratio in inputs. Data are shown as the means ± SEMs (n = 3). ^*p < 0.05 compared with the Meth group; (D) Statistical diagram of interactions between endogenous CCZ1 and Flag-Stx17. ^****p < 0.0001 compared with the Meth group. (E-F) Colocalization of EGFP-LC3, Rab7, and CCZ1 in primary hippocampal neurons and N2a cells after Meth treatment and Stx17 overexpression. Scale bar = 5 μm. (G) The interaction between Rab7 (late endosomes) and CCZ1/Stx17 was determined by IP. Data are shown as the means ± SEMs (n = 3). ^*p < 0.05 and ^****p < 0.0001 compared with the control group; ^###p < 0.001 and ^####p < 0.0001 compared to the Meth group