The Endoplasmic Reticulum Stress Sensor, ATF6α, Protects against Neurotoxin-induced Dopaminergic Neuronal Death

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  • Supplemental Figures S1-3 and Table 1 (.pdf, 12.4 MB) - Figure S1. (A) ER stress sensors, IRE1���, sXBP1 and p-PERK are not different in various brain regions of ATF6��� KO mice under physiological conditions in vivo.(B) Comparative analysis of levels of protein involved in synaptic secretion and vesicular transport between ATF6��� WT (+/+) and KO (-/-) mice.(C-E) ATF6��� is not essential for the development and the survival of dopaminergic neurons. Figure S2. (A) Hydrogen peroxide (H2O2)���induced oxidative stress induced phosphorylation of p38MAPK and cleavage of pATF6��� (P) to produce pATF6���(N).(B) There was no aggregate stained with 1% Thioflavin T and no accumulated material immunostained with anti-���-synuclein antibody or anti-phosphorylated ���-synuclein antibody.(C) Representative images of primary co-cultured dopaminergic neurons derived from the midbrain and the striatum of the embryonic day 15 ATF6��� WT/KO mice. Figure S3. (A-C) MPP+ induces release of N-terminal ATF6��� fragment with subsequent translocation into the nucleus and colocalization with phosphorylated p38MAPK. (D-G) Hydrogen peroxide (H2O2) induces release of N-terminal ATF6��� fragment with subsequent translocation into the nucleus and colocalization with phosphorylated p38MAPK.(H) H2O2 treatment enhances the binding of N-terminal fragment of ATF6��� with p-p38MAPK.(I and J) p38MAPK phosphorylation enhances the transcriptional activity of ATF6���. Table S1. The Lists of the primers and the sequences