Activity Modulation of Beclin-1/class Ⅲ PI3 Complex and MTOR
发布时间：2021-10-10 15:48
Multiple cell signaling pathways and biological processes are involved in cerebral ischemia/reperfusion （I/R） injury, among which, autophagy is a most confusing one. Studies suggest that autophagy is activated during ischemia and reperfusion （I/R）, however there’s no data to dynamically mimic autophagy level during the whole process of I/R, and it’s still not known whether autophagy functions as a guardian or plays a detrimental role in I/R injury.Here we employed simulated I/R of N2a cells （mou...
【文章来源】：华中科技大学湖北省 211工程院校 985工程院校 教育部直属院校
【文章页数】：50 页
【学位级别】：硕士
【文章目录】：
Abstract
Introduction
1 Material and methods
1.1 agents
1.2 Cell Line and Culture Conditions
1.3 I/R Model of N2a cells and Experimental Groups
1.4 Transfection of N2a cells with EGFP-LC3 plasmid and observation of punctare EGFP-LC3.
1.5 MCAO model of rat
1.6 Immunofluorescence staining of LC-3 and At95
1.7 Immunoblot Analysis
1.8 Analysis of mitochondria function by relative cell viability among I /R model groups and 3MA-treated groups
1.9 Statistical Analysis
2 Results
2.1 Autophagy was gradually activated within N2a cells as oxygen-glucose- serum deprivation went on, and highly elevated especially after reperfusion.
2.2 Autophagsome was found more in cortex and hippocampus of MCAO side of brain tissue after reperfusion than the untreated side
2.3 Cytosolic Beclin-1 shared the same change pattern with LC-311 in IR model groups,and class Ⅲ P13K/beclin-1 was indispensable for activation of autopahagy in the process of reperfusion.
2.4 Reperfusion induced delayed inactivation of mTORC1, while Rapamycin treatment weakened the autophagy activation during the process of reperfusion.
2.5 Analysis of mitochondria function by relative cell viability among I /R model groups and 3MA-treated groups
Discussion
Reference
自噬的分子基础，信号调控及自噬的功能
自噬的分子基础
ULK 复合体
两个泛素样蛋白At912,和At98/LC-3 及其连接系统
Beclin-1/Class III P13K 复合体
At99 及其循环运转体系
自噬的生理性功能
自噬维持细胞的稳衡
自噬在先天性免疫和获得性免疫中的作用
自噬与细胞程序性死亡
自噬延缓衰老
自噬与疾病
自噬与肿瘤
自噬与神经退行性病变
自噬与溶酶体蓄积症
自噬与肌肉类疾病的发生
Reference
致谢
本文编号：3428676
【文章来源】：华中科技大学湖北省 211工程院校 985工程院校 教育部直属院校
【文章页数】：50 页
【学位级别】：硕士
【文章目录】：
Abstract
Introduction
1 Material and methods
1.1 agents
1.2 Cell Line and Culture Conditions
1.3 I/R Model of N2a cells and Experimental Groups
1.4 Transfection of N2a cells with EGFP-LC3 plasmid and observation of punctare EGFP-LC3.
1.5 MCAO model of rat
1.6 Immunofluorescence staining of LC-3 and At95
1.7 Immunoblot Analysis
1.8 Analysis of mitochondria function by relative cell viability among I /R model groups and 3MA-treated groups
1.9 Statistical Analysis
2 Results
2.1 Autophagy was gradually activated within N2a cells as oxygen-glucose- serum deprivation went on, and highly elevated especially after reperfusion.
2.2 Autophagsome was found more in cortex and hippocampus of MCAO side of brain tissue after reperfusion than the untreated side
2.3 Cytosolic Beclin-1 shared the same change pattern with LC-311 in IR model groups,and class Ⅲ P13K/beclin-1 was indispensable for activation of autopahagy in the process of reperfusion.
2.4 Reperfusion induced delayed inactivation of mTORC1, while Rapamycin treatment weakened the autophagy activation during the process of reperfusion.
2.5 Analysis of mitochondria function by relative cell viability among I /R model groups and 3MA-treated groups
Discussion
Reference
自噬的分子基础，信号调控及自噬的功能
自噬的分子基础
ULK 复合体
两个泛素样蛋白At912,和At98/LC-3 及其连接系统
Beclin-1/Class III P13K 复合体
At99 及其循环运转体系
自噬的生理性功能
自噬维持细胞的稳衡
自噬在先天性免疫和获得性免疫中的作用
自噬与细胞程序性死亡
自噬延缓衰老
自噬与疾病
自噬与肿瘤
自噬与神经退行性病变
自噬与溶酶体蓄积症
自噬与肌肉类疾病的发生
Reference
致谢
本文编号：3428676
本文链接：https://www.wllwen.com/xiyixuelunwen/3428676.html
最近更新
教材专著
