Data for: Seipin deletion in mice enhances phosphorylation and aggregation of tau protein through reduced neuronal PPARγ and insulin resistance

We attached the independent replicates of Western blot analyses in the supplementary section that were used in various quantifications. The regions of line rectangles in these blots/gels, as representative images, were used in Figures of the main Text.
In the Fig. 1e: the levels of hippocampal NF-H protein in seipin-sKO mice (sKO) and seipin-nKO mice (nKO) were lower than those of WT mice.
In the Fig. 2a: the levels of tau protein in hippocampus of seipin-sKO mice, seipin-nKO mice and seipin-aKO mice (aKO) were not altered.
In the Fig. 2b: the levels of oligomer tau protein were increased in seipin-sKO mice and seipin-nKO mice.
In the Fig. 2c: the levels of hippocampal tau phosphorylation at Thr212/Ser214 and Ser202/Thr205 were increased in seipin-sKO mice and seipin-nKO mic.
In the Fig. 3a: the levels of PPARγ protein were decreased in hippocampus of seipin-sKO mice and seipin-nKO mice.
In the Fig. 3b: the administration of PPARγ agonist rosiglitazone (rosi) for 7 days could correct the increased tau phosphorylation at Thr212/Ser214 and Ser202/Thr205 in seipin-sKO mice and seipin-nKO mice.
In the Fig. 4a: seipin-sKO mice and seipin-nKO mice showed an increase in the GSK3β phosphorylation at Tyr21 and a decrease at Ser9, which were corrected by rosi.
In the Fig. 4b: the treatment with AR-A014418 (AR) corrected the increased tau phosphorylation at Thr212/Ser214 and Ser202/Thr205 in seipin-nKO mice.
In the Fig. 5a&5b: the phosphorylation of Akt and mTOR was elevated in seipin-sKO mice and seipin-nKO mice, which were corrected by rosi.
In the Fig. 5c&5d: seipin-sKO mice and seipin-nKO mice showed a decrease in the ratio of LC3II/I and an elevation of p62 protein, which was rescued by the PI3K inhibitor LY294002 (LY) and mTOR inhibitor rapamycin (Rap), but not AR.
In the Fig. 5e&5f: the administration of LY and Rap reduced the levels of oligomer tau protein and tau phosphorylation at Thr212/Ser214 and Ser202/Thr205 in seipin-nKO mice.
In the Fig. 6c: the increased phosphorylation of JNK in seipin-sKO mice were corrected by treatment with rosi for 30 days.
In the Fig. 6d: the P38 phosphorylation in seipin-sKO mice was not altered.
In the Fig. 6e: the increased phosphorylation of tau at Ser396 in seipin-sKO mice was prevented by treatment with rosi for 30 days and the JNK inhibitor SP600125 (SP).

本研究将用于各项定量分析的免疫印迹（Western blot）独立重复实验结果附于补充材料中。上述印迹/凝胶电泳图中的矩形框选区域作为代表性图像，被用于正文章节的各图中。
在图1e中，seipin-sKO小鼠（简称sKO）与seipin-nKO小鼠（简称nKO）的海马体神经丝重链蛋白（NF-H）水平均低于野生型（WT）小鼠。
在图2a中，seipin-sKO、seipin-nKO与seipin-aKO小鼠（aKO）的海马体tau蛋白水平无显著变化。
在图2b中，seipin-sKO与seipin-nKO小鼠的tau寡聚体蛋白水平升高。
在图2c中，seipin-sKO与seipin-nKO小鼠的海马体tau蛋白在Thr212/Ser214及Ser202/Thr205位点的磷酸化水平升高。
在图3a中，seipin-sKO与seipin-nKO小鼠的海马体过氧化物酶体增殖物激活受体γ（PPARγ）蛋白水平降低。
在图3b中，给予PPARγ激动剂罗格列酮（rosiglitazone，简称rosi）干预7天，可纠正seipin-sKO与seipin-nKO小鼠中升高的tau蛋白Thr212/Ser214及Ser202/Thr205位点磷酸化水平。
在图4a中，seipin-sKO与seipin-nKO小鼠的糖原合成激酶3β（GSK3β）在Tyr21位点的磷酸化水平升高，而Ser9位点的磷酸化水平降低，上述异常可被rosi逆转。
在图4b中，AR-A014418（简称AR）干预可纠正seipin-nKO小鼠中升高的tau蛋白Thr212/Ser214及Ser202/Thr205位点磷酸化水平。
在图5a与5b中，seipin-sKO与seipin-nKO小鼠的蛋白激酶B（Akt）与雷帕霉素靶蛋白（mTOR）的磷酸化水平升高，该异常可被rosi纠正。
在图5c与5d中，seipin-sKO与seipin-nKO小鼠的LC3II/I比值降低，p62蛋白水平升高，上述表型可被PI3K抑制剂LY294002（简称LY）与mTOR抑制剂雷帕霉素（rapamycin，简称Rap）挽救，但AR无此效果。
在图5e与5f中，给予LY与Rap干预可降低seipin-nKO小鼠的tau寡聚体蛋白水平，以及tau蛋白Thr212/Ser214与Ser202/Thr205位点的磷酸化水平。
在图6c中，经rosi干预30天可纠正seipin-sKO小鼠中升高的c-Jun氨基末端激酶（JNK）磷酸化水平。
在图6d中，seipin-sKO小鼠的P38磷酸化水平无显著变化。
在图6e中，经rosi干预30天或JNK抑制剂SP600125（SP）处理，可阻止seipin-sKO小鼠中tau蛋白Ser396位点的磷酸化水平升高。