自噬
细胞生物学
糖蛋白
生物
内质网
病毒包膜
溶酶体
病毒
袋3
自噬体
病毒学
分子生物学
细胞凋亡
生物化学
酶
作者
Qiang Fu,Huijun Shi,Mengting Shi,Luping Meng,Haiyang Bao,Guoqi Zhang,Yan Ren,Hui Zhang,Fei Guo,Jun Qiao,Bin Jia,Pengyan Wang,Wei Ni,Jinliang Sheng,Chuangfu Chen
标识
DOI:10.1016/j.micpath.2014.09.011
摘要
Macroautophagy (autophagy) is an evolutionarily conserved control process that maintains cellular homeostasis in eukaryotic cells. Autophagy principally serves an adaptive role to degrade dysfunctional proteins and to clean damaged organelles in response to pathogenic, viral, or microbial infection, nutrient deprivation and endoplasmic reticulum (ER) stress. In previous study, we showed bovine viral diarrhea virus (BVDV) NADL infection induced autophagy and significantly elevated the expression levels of autophagy-related genes, Beclin1 and ATG14, at 12 h post-infection in MDBK cells. However, the specific mechanisms involved in controlling autophagic activity remain unclear. Here, we investigate the effects of BVDV NADL envelope glycoproteins overexpression on inducing autophagy. The results show that viral envelope glycoproteins E(rns) and E2 overexpression mediated by lentivirus increase the formation of autophagosome, the percentage of GFP-LC3 puncta-positive cells and the expression levels of Beclin1 and ATG14. Whereas E1 overexpression doesn't affect autophagic activity. Collectively, these findings suggest that the viral envelope glycoproteins E(rns) and E2 are involved in inducing autophagy, and provide a mechanistic insight into the regulation of autophagy in viral infected cells.
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