ArticleThe Journal of experimental medicine1990
E3/19K from adenovirus 2 is an immunosubversive protein that binds to a structural motif regulating the intracellular transport of major histocompatibility complex class I proteins.
Article in The Journal of experimental medicine, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 46 citations in OpenAlex.
- Adenoviromics: Mining the Human Adenovirus Species D Genome.Frontiers in microbiology · 2018Review
- Cytomegalovirus immune evasion by perturbation of endosomal trafficking.Cellular & molecular immunology · 2015Review
- Article
- Homologous recombination in E3 genes of human adenovirus species D.Journal of virology · 2013Article
- Review
- Murine cytomegalovirus perturbs endosomal trafficking of major histocompatibility complex class I molecules in the early phase of infection.Journal of virology · 2010Article
- Article
- The adenovirus E3-6.7K protein adopts diverse membrane topologies following posttranslational translocation.Journal of virology · 2004Article
- Expression of gp19K increases the persistence of transgene expression from an adenovirus vector in the mouse lung and liver.Journal of virology · 1997Article
- Herpes simplex virus type 2 inhibition of Fas ligand expression.Journal of virology · 1996Article
- LMP-associated proteolytic activities and TAP-dependent peptide transport for class 1 MHC molecules are suppressed in cell lines transformed by the highly oncogenic adenovirus 12.The Journal of experimental medicine · 1996Article
- Identification of the mouse cytomegalovirus genomic region affecting major histocompatibility complex class I molecule transport.Journal of virology · 1995Article
- Conserved cysteine residues within the E3/19K protein of adenovirus type 2 are essential for binding to major histocompatibility complex antigens.Journal of virology · 1994Article
- Adenovirus infection enhances in vitro adherence of Streptococcus pneumoniae.Infection and immunity · 1994Article
- Article
- Hierarchy in the assembly of HLA-B27 and HLA-Cw3 molecules in transgenic mice.Immunogenetics · 1994Article
- Article
- Different rates of HLA class I molecule assembly which are determined by amino acid sequence in the alpha 2 domain.Immunogenetics · 1993Article
- Retention of adenovirus E19 glycoprotein in the endoplasmic reticulum is essential to its ability to block antigen presentation.The Journal of experimental medicine · 1991Article
- Adenovirus infection inhibits the phosphorylation of major histocompatibility complex class I proteins.The Journal of experimental medicine · 1991Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously expressed in transgenic mice a chimeric H-2Kd/Kk protein called C31, which contains the extracellular alpha 1 domain of Kd, whereas the rest of the molecule is of Kk origin. This molecule functions as a restriction element for alloreactive and influenza A-specific cytotoxic T lymphocytes (CTL) but is only weakly expressed at the cell surface of splenocytes. Here, we show that the low cell surface expression is the result of slow intracellular transport and processing of the C31 protein. A set of hybrid molecules between Kd and Kk were used to localize the regions in major histocompatibility complex (MHC) molecules that are important for their intracellular transport and to further localize the structures responsible for binding to the adenovirus 2 E3/19K protein. This protein appears to be an important mediator of adenovirus persistence. It acts by binding to the immaturely glycosylated forms of MHC class I proteins in the endoplasmic reticulum (ER), preventing their passage to the cell surface and thereby reducing the recognition of infected cells by virus-specific T cells. We find the surprising result that intracellular transport and E3/19K binding are controlled primarily by the first half of the second domain of Kd, thus localizing these phenomena to the five polymorphic residues in this region of the Kd protein. This result implies that the E3/19K protein may act by inhibiting peptide binding or by disrupting the oligomerization of MHC class I molecules required for transport out of the ER. Alternatively, the E3/19K protein may inhibit the function of a positively acting transport molecule necessary for cell surface expression of MHC class I molecules.
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