作者: Nobuko Hosokawa , Zhipeng You , Linda O. Tremblay , Kazuhiro Nagata , Annette Herscovics
DOI: 10.1016/J.BBRC.2007.08.057
关键词: Endoplasmic reticulum 、 Cell biology 、 Mannose 、 Cytoplasm 、 Mannosidase 、 Mannosidases 、 Biology 、 Protein degradation 、 Golgi apparatus 、 Biochemistry 、 Endoplasmic-reticulum-associated protein degradation
摘要: Terminally misfolded or unassembled proteins are degraded by the cytoplasmic ubiquitin-proteasome pathway in a process known as ERAD (endoplasmic reticulum-associated protein degradation). Overexpression of ER alpha1,2-mannosidase I and EDEMs target glycoproteins for ERAD, most likely due to trimming N-glycans. Here we demonstrate that overexpression Golgi IA, IB, IC also accelerates terminally human alpha1-antitrypsin variant null (Hong Kong) (NHK), mannose from N-glycans on NHK 293 cells. Although transfected is primarily localized ER, some co-localizes with markers, suggesting alpha1,2-mannosidases can contribute degradation.