ArticleThe Journal of experimental medicine1991
Retention of adenovirus E19 glycoprotein in the endoplasmic reticulum is essential to its ability to block antigen presentation.
Article in The Journal of experimental medicine, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
50 citing papers in PubMed, 104 citations in OpenAlex.
- Viral manipulation of the HLA class I antigen processing and presentation pathway.Frontiers in immunology · 2025Review
- An oncolytic HAdV-5 with reduced surface charge combines diminished toxicity and improved tumor targeting.Molecular therapy. Oncology · 2024Article
- A Renaissance for Oncolytic Adenoviruses?Viruses · 2023Review
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- Article
- Immune evasion by adenoviruses: a window into host-virus adaptation.FEBS letters · 2019Review
- Adenoviromics: Mining the Human Adenovirus Species D Genome.Frontiers in microbiology · 2018Review
- Structure of the Adenovirus Type 4 (Species E) E3-19K/HLA-A2 Complex Reveals Species-Specific Features in MHC Class I Recognition.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Porcine reproductive and respiratory syndrome (PRRS): an immune dysregulatory pandemic.Immunologic research · 2014Review
- Homologous recombination in E3 genes of human adenovirus species D.Journal of virology · 2013Article
- The transmembrane domain of the adenovirus E3/19K protein acts as an endoplasmic reticulum retention signal and contributes to intracellular sequestration of major histocompatibility complex class I molecules.Journal of virology · 2013Article
- Crystal structure of adenovirus E3-19K bound to HLA-A2 reveals mechanism for immunomodulation.Nature structural & molecular biology · 2012Article
- The human herpesvirus-7 (HHV-7) U21 immunoevasin subverts NK-mediated cytoxicity through modulation of MICA and MICB.PLoS pathogens · 2011Article
- Adenovirus E3-19K proteins of different serotypes and subgroups have similar, yet distinct, immunomodulatory functions toward major histocompatibility class I molecules.The Journal of biological chemistry · 2011Article
- Determinants of the endoplasmic reticulum (ER) lumenal-domain of the adenovirus serotype 2 E3-19K protein for association with and ER-retention of major histocompatibility complex class I molecules.Molecular immunology · 2011Article
- Verapamil enhances the antitumoral efficacy of oncolytic adenoviruses.Molecular therapy : the journal of the American Society of Gene Therapy · 2010Article
- MHC class I antigen presentation: learning from viral evasion strategies.Nature reviews. Immunology · 2009Review
- Specificity of amyloid precursor-like protein 2 interactions with MHC class I molecules.Immunogenetics · 2008Article
- Adenovirus E3/19K promotes evasion of NK cell recognition by intracellular sequestration of the NKG2D ligands major histocompatibility complex class I chain-related proteins A and B.Journal of virology · 2008Article
- Pathogen evasion strategies for the major histocompatibility complex class I assembly pathway.Immunology · 2008Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The E3/19K glycoprotein of adenovirus functions to diminish recognition of adenovirus-infected cells by major histocompatibility complex class I-restricted cytotoxic T lymphocytes (CTLs) by binding intracellular class I molecules and preventing them from reaching the plasma membrane. In the present study we have characterized the nature of the interaction between E3/19K and the H-2Kd (Kd) molecule. An E3/19K molecule genetically engineered to terminate six residues from its normal COOH terminus (delta E19), was found to associate with Kd in a manner indistinguishable from wild-type E3/19K. Unlike E3/19K, however, delta E19 was transported through the Golgi complex to the plasma membrane, where it could be detected biochemically and immunocytochemically using a monoclonal antibody specific for the lumenal domain of E3/19K. Importantly, delta E19 also differed from E3/19K in being unable to prevent the presentation of Kd-restricted viral proteins to CTLs. This is unlikely to be due to delta E19 having a lower avidity for Kd than E3/19K, since delta E19 was able to compete with E3/19K for Kd binding, both physically, and functionally in nullifying the E3/19K blockade of antigen presentation. These findings indicate that the ability of E3/19K to block antigen presentation is due solely to its ability to retain newly synthesized class I molecules in the endoplasmic reticulum.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.