Activity Modulation of Beclin-1/class Ⅲ PI3 Complex and MTOR
發(fā)布時(shí)間: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...
【文章來源】:華中科技大學(xué)湖北省 211工程院校 985工程院校 教育部直屬院校
【文章頁數(shù)】:50 頁
【學(xué)位級(jí)別】:碩士
【文章目錄】:
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
自噬的分子基礎(chǔ),信號(hào)調(diào)控及自噬的功能
自噬的分子基礎(chǔ)
ULK 復(fù)合體
兩個(gè)泛素樣蛋白At912,和At98/LC-3 及其連接系統(tǒng)
Beclin-1/Class III P13K 復(fù)合體
At99 及其循環(huán)運(yùn)轉(zhuǎn)體系
自噬的生理性功能
自噬維持細(xì)胞的穩(wěn)衡
自噬在先天性免疫和獲得性免疫中的作用
自噬與細(xì)胞程序性死亡
自噬延緩衰老
自噬與疾病
自噬與腫瘤
自噬與神經(jīng)退行性病變
自噬與溶酶體蓄積癥
自噬與肌肉類疾病的發(fā)生
Reference
致謝
本文編號(hào):3428676
【文章來源】:華中科技大學(xué)湖北省 211工程院校 985工程院校 教育部直屬院校
【文章頁數(shù)】:50 頁
【學(xué)位級(jí)別】:碩士
【文章目錄】:
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
自噬的分子基礎(chǔ),信號(hào)調(diào)控及自噬的功能
自噬的分子基礎(chǔ)
ULK 復(fù)合體
兩個(gè)泛素樣蛋白At912,和At98/LC-3 及其連接系統(tǒng)
Beclin-1/Class III P13K 復(fù)合體
At99 及其循環(huán)運(yùn)轉(zhuǎn)體系
自噬的生理性功能
自噬維持細(xì)胞的穩(wěn)衡
自噬在先天性免疫和獲得性免疫中的作用
自噬與細(xì)胞程序性死亡
自噬延緩衰老
自噬與疾病
自噬與腫瘤
自噬與神經(jīng)退行性病變
自噬與溶酶體蓄積癥
自噬與肌肉類疾病的發(fā)生
Reference
致謝
本文編號(hào):3428676
本文鏈接:http://sikaile.net/xiyixuelunwen/3428676.html
最近更新
教材專著