Autophagy-Related Gene Expression Analysis of Wild-type and atg5 Gene Knockout Mouse Embryonic Fibroblast Cells Treated with Polyethylenimine

doi:10.1021/mp500111u

Chia Nan University of Pharmacy & Science Institutional Repository > 藥理學院 > 藥學系(所) > 期刊論文 > Item 310902800/28517

jsp.display-item.identifier=請使用永久網址來引用或連結此文件: https://ir.cnu.edu.tw/handle/310902800/28517

標題:	Autophagy-Related Gene Expression Analysis of Wild-type and atg5 Gene Knockout Mouse Embryonic Fibroblast Cells Treated with Polyethylenimine
作者:	Lin, Chia-Wei Jan, Ming-Shiou Kuo, Jung-Hua Steven
貢獻者:	藥學系
關鍵字:	polyethylenimine (PEI) autophagy apoptosis necrosis PCR array
日期:	2014-09
上傳時間:	2015-05-06 21:19:08 (UTC+8)
出版者:	Amer Chemical Soc
摘要:	The molecular mechanisms of autophagy in polyethylenimine (PEI)-treated cells are not well understood because of the use of nonspecific autophagy inhibitors Here, we applied autophagy-related gene expression analysis to pinpoint the molecular mechanisms of autophagy in PEI-treated wild type and atg5 gene knockout (atg5(-/-)) mouse embryonic fibroblast (MEF) cells It was demonstrated that the majority of induced genes are downregulated in wild type and atg5(-/-) MEF cells, indicating that autophagy exhibits a toward downregulation after treatment with PEI. In addition to regulating genes encoding autophagy machinery components, genes related to coregulation of autophagy and apoptosis were induced in wild-type and atg5(-/-) cells treated with PEI. These data indicate that autophagy and apoptosis are closely related in the PEI-induced mechanism of cell death. In the absence of autophagy, the regulation of apoptosis was enhanced in atg5(-/-) MEF cells treated with PEI, indicating that inhibition of autophagy may lead to higher levels of apoptosis. Our study may provide deeper insight into the molecular mechanisms of cell death caused by PEI.
關聯:	Molecular Pharmaceutics, v.11 n.9, pp.3002-3008
显示于类别:	[藥學系(所)] 期刊論文

文件中的档案:

档案	描述	大小	格式	浏览次数
index.html		0Kb	HTML	1743	检视/开启

在CNU IR中所有的数据项都受到原著作权保护.

TAIR相关文章

数据加载中.....