The E5 oncoprotein of BPV-4 does not interfere with the biosynthetic pathway of non-classical MHC class I
Virology, ISSN: 0042-6822, Vol: 353, Issue: 1, Page: 174-183
2006
- 16Citations
- 26Captures
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Metrics Details
- Citations16
- Citation Indexes16
- 16
- CrossRef15
- Captures26
- Readers26
- 26
Article Description
The major histocompatibility complex (MHC) class I region in mammals contains both classical and non-classical MHC class I genes. Classical MHC class I molecules present antigenic peptides to cytotoxic T lymphocytes, whereas non-classical MHC class I molecules have a variety of functions. Both classical and non-classical MHC molecules interact with natural killer cell receptors and may under some circumstances prevent cell death by natural killer cytotoxicity. The E5 oncoprotein of BPV-4 down-regulates the expression of classical MHC class I on the cell surface and retains the complex in the Golgi apparatus. The inhibition of classical MHC class I to the cell surface results from both the impaired acidification of the Golgi, due to the interaction of E5 with subunit c of the H + V-ATPase, and to the physical binding of E5 to the heavy chain of MHC class I. Despite the profound effect of E5 on classical MHC class I, E5 does not retain a non-classical MHC class I in the Golgi, does not inhibit its transport to the cell surface and does not bind its heavy chain. We conclude that, as is the case for HPV-16 E5, BPV-4 E5 does not down-regulate certain non-classical MHC class I, potentially providing a mechanism for the escape of the infected cell from attack by both cytotoxic T lymphocytes and NK cells.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S004268220600362X; http://dx.doi.org/10.1016/j.virol.2006.05.031; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33747874274&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/16806386; https://linkinghub.elsevier.com/retrieve/pii/S004268220600362X; https://dx.doi.org/10.1016/j.virol.2006.05.031
Elsevier BV
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