期刊
IMMUNITY
卷 13, 期 6, 页码 841-851出版社
CELL PRESS
DOI: 10.1016/S1074-7613(00)00081-9
关键词
-
类别
资金
- NIAID NIH HHS [AI14584] Funding Source: Medline
It has been assumed that upon dissociation from TAP, MHC class I molecules exit the ER by nonselective bulk flow. We now show that exit must occur by association with cargo receptors. Inconsistent with exit by bulk flow, loading of MHC class I molecules with high-affinity peptides triggers dissociation from TAP but has no effect on rates of ER-to-Golgi transport. Moreover, peptide-loaded MHC class I molecules accumulate at ER exit sites from which TAP molecules are excluded. Consistent with receptor-mediated exit, ER-to-Golgi transport of MHC class I molecules is independent of their cytoplasmic tails, which themselves lack ER export motifs. In addition, we show that MHC class I molecules associate with the putative cargo receptor BAP31.
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