期刊
AUTOPHAGY
卷 10, 期 4, 页码 708-709出版社
LANDES BIOSCIENCE
DOI: 10.4161/auto.28103
关键词
COPII; macroautophagy; TRAPPIII; Ypt1; Atg1
类别
资金
- Howard Hughes Medical Institute Funding Source: Medline
- NIGMS NIH HHS [GM0622580, R01 GM080616, GM080616] Funding Source: Medline
A major unanswered question in the field of autophagy is how the double-membrane phagophore is formed. As this membrane expands, it engulfs proteins and organelles that are destined for degradation and then seals to form an autophagosome. A growing consensus in the field is that a subdomain of the ER initiates formation of the phagophore. We show that ER-derived COPII-coated vesicles, which bud from a specialized domain of the ER called the ER exit site (ERES), are a source of this membrane. This finding will now pave the way for a biochemical description of the early steps of phagophore initiation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据