BI1激活自噬介导TDP43抑制SOD1G93A诱导NSC-34细胞凋亡.pdf,BI1 激活自噬介导TDP43 抑制SOD1G93A 诱导NSC-34 细胞凋亡 中文摘要 肌萎缩性侧索硬化症 (Amyotrophic lateral sclerosis ,ALS )是一类非常致命 的神经退行性疾病,其主要特征是上下运动神经元功能异常和变性,
GCLM蛋白水平在SOD1-G93A-D组明显降低(P<0.05)。结论抑制芳香化酶通过降低抗氧化应激能力影 响稳转hSODl-G93A的NSC-34细胞活力。【关键词】肌萎缩侧索硬化；hSODl-G93A;Cy P19al;芳香化酶；氧化应激 中图分类号：R742.5文献标识码：A文章编号：1006-351X(2022)04-0210-05 Cypl9al knockdown by ShRNA...
hSOD1G93ANSC34细胞肌萎缩侧索硬化凋亡目的探讨稳定转染hSOD1G93A对NSC34细胞凋亡的影响.方法常规体外培养稳定转染空质粒,hSOD1WT或hSOD1G93A质粒的NSC34细胞系,分为3组:空转组,野生组和突变组.应用CCK-8试剂盒和LDH试剂盒来测定各组细胞活力,应用透射电镜观察细胞线粒体形态,通过TUNEL染色来检测细胞凋亡情况,...
自噬目的观察羟丙基-β-环糊精(HpβCD)对稳转hSOD1G93A的NSC34细胞活力的影响并探讨可能的机制.方法应用HpBCD分别干预对照组(稳转空质粒的NSC34细胞)和实验组(稳转hSOD1G93A的NSC34细胞),通过CCK-8试剂盒检测各组细胞活力,通过透射电镜观察细胞自噬结构,应用Western blotting检测human SOD1,LC3Ⅱ/Ⅰ,P62...
Here, NSC-34 cells stably expressing hSOD1-G93A (hSOD1-G93A cells) were transiently transfected with Cyp19a1 mouse open reading frame (ORF) cDNA or a short hairpin RNA (ShRNA) plasmid. Overexpression of aromatase resulting from Cyp19a1 mouse ORF cDNA plasmid transfection enhanced cell ...
Analysis of TIF of NSC-34 cells expressing WT and G93A hSOD1, treated or not with MG132, L-NAME or both.Manuela, BassoGiuseppina, SamengoGiovanni, NardoTania, MassignanGiuseppina, D'AlessandroSilvia, TartariLavinia, CantoniMarianna, Marino...
The effect of G93A SOD1 mutation on NSC34 cell viability.Katie RichardsonScott P. AllenHeather MortiboysAndrew J. GriersonStephen B. WhartonPaul G. IncePamela J. ShawPaul R. Heath
AK106-001616 (1 - 10 渭M) protected NSC34 cells (mouse motor neuron like cells) against SOD1G93A-induced motor neuron cell death. Furthermore, aspirin, an inhibitor of COX1/2, reduced the SOD1G93A-induced motor neuron cell death at a concentration that inhibited COX2. Celecoxib, a ...
we transfected the Cu/Zn superoxide dismutase 1 G93A mutant protein into the motor neuron-like cell line NSC34 cultured in vitro.Western blotting and co-immunoprecipitation showed that the Cu/Zn superoxide dismutase 1 G93A mutant enhanced the turnover of autophagic marker microtub...
The aim of our study was to investigate the protective effects and mechanisms of MF in the hSOD1-G93A ALS cell model. Our result revealed that MF treatment reduced the generation of reactive oxygen species (ROS) and malondialdehyde (MDA), decreased oxidative damage, and reduced apoptosis. ...