Abstract
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, pepfide-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.
Original language | English (US) |
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Pages (from-to) | 841-851 |
Number of pages | 11 |
Journal | Immunity |
Volume | 13 |
Issue number | 6 |
DOIs | |
State | Published - Jan 1 2000 |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Infectious Diseases