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• W2045298605 startingPage "2796" @default.
• W2045298605 abstract "To persist in the presence of an active immune system, viruses encode proteins that decrease expression of major histocompatibility complex class I molecules by using a variety of mechanisms. For example, murine gamma-2 herpesvirus 68 expresses the K3 protein, which causes the rapid turnover of nascent class I molecules. In this report we show that certain mouse class I alleles are more susceptible than others to K3-mediated down regulation. Prior to their rapid degradation, class I molecules in K3-expressing cells exhibit impaired assembly with beta(2)-microglobulin. Furthermore, K3 is detected predominantly in association with class I molecules lacking assembly with high-affinity peptides, including class I molecules associated with the peptide loading complex TAP/tapasin/calreticulin. The detection of K3 with class I assembly intermediates raises the possibility that molecular chaperones involved in class I assembly are involved in K3-mediated class I regulation." @default.
• W2045298605 created "2016-06-24" @default.
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• W2045298605 date "2002-03-15" @default.
• W2045298605 modified "2023-09-27" @default.
• W2045298605 title "Physical Association of the K3 Protein of Gamma-2 Herpesvirus 68 with Major Histocompatibility Complex Class I Molecules with Impaired Peptide and β₂-Microglobulin Assembly" @default.
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• W2045298605 doi "https://doi.org/10.1128/jvi.76.6.2796-2803.2002" @default.
• W2045298605 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/135993" @default.
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