羊瘙痒因子139A感染的小鼠脑组织中AMPK-ULK1自噬调节通路的研究
To investigate the AMPK-ULK1 signal transduction pathway in the scrapie 139A infected mice brain tissues
摘要目的 研究感染羊瘙痒因子139A的小鼠脑组织中自噬的活化及其机制.方法 采用Western Blot方法检测感染羊瘙痒因子139A的小鼠终末期脑组织匀浆中的AMPK、ULK1及其磷酸化水平和LC3 Ⅱ的表达,并对其进行定量分析.结果 感染139A毒株的小鼠脑组织终末期脑组织中AMPK、ULK1及其磷酸化水平均表达升高.同时发现LC3 Ⅱ水平增加.结论 AMPK-ULK1通路在139A感染的小鼠脑组织中活化并且有可能对自噬的激活起到了重要的作用.
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abstractsObjective To investigate the activation of the autophagy and the signal transduction pathway in the scrapie 139A infected mice brain tissues.Methods The Western Blot was used to evaluate the expression level of AMPK,ULK1,p-AMPK,P-ULKI and LC3 Ⅱ in the normal and scrapie 139A infected mice brain tissues.Results The expression levels of AMPK,ULK1 and their phosphorylated form p-AMPK (Thr172),p-ULK1 (Ser555) are markedly up-regulated in the brains of the mice infected with scrapie agent 139A.Furthermore,the expression of LC3 Ⅱ was also found increased in the brains of 139A infected mice,but not in normal mice.Conclusion AMPK-ULK1 pathway activated and contributed to autophagy in 139A infected mice brain.
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