ArticleJournal of virology2000
Structural and functional dissection of human cytomegalovirus US3 in binding major histocompatibility complex class I molecules.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
The trial behind it
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
20 citing papers in PubMed, 50 citations in OpenAlex.
- Viral manipulation of the HLA class I antigen processing and presentation pathway.Frontiers in immunology · 2025Review
- The nonclassical immune surveillance for ERAAP function.Current opinion in immunology · 2021Review
- Battle between Host Immune Cellular Responses and HCMV Immune Evasion.International journal of molecular sciences · 2019Review
- Human cytomegalovirus-encoded US9 targets MAVS and STING signaling to evade type I interferon immune responses.Nature communications · 2018Article
- How does cytomegalovirus factor into diseases of aging and vaccine responses, and by what mechanisms?GeroScience · 2017Article
- Classical and non-classical MHC I molecule manipulation by human cytomegalovirus: so many targets—but how many arrows in the quiver?Cellular & molecular immunology · 2015Review
- The cytoplasmic domain of rhesus cytomegalovirus Rh178 interrupts translation of major histocompatibility class I leader peptide-containing proteins prior to translocation.Journal of virology · 2011Article
- MHC class I antigen presentation: learning from viral evasion strategies.Nature reviews. Immunology · 2009Review
- Human cytomegalovirus-encoded immune modulators partner to downregulate major histocompatibility complex class I molecules.Journal of virology · 2009Article
- Feeling manipulated: cytomegalovirus immune manipulation.Virology journal · 2009Article
- Pathogen evasion strategies for the major histocompatibility complex class I assembly pathway.Immunology · 2008Review
- A short isoform of human cytomegalovirus US3 functions as a dominant negative inhibitor of the full-length form.Journal of virology · 2006Article
- Viral evasion of the MHC class I antigen-processing machinery.Pflugers Archiv : European journal of physiology · 2005Review
- Rhesus cytomegalovirus contains functional homologues of US2, US3, US6, and US11.Journal of virology · 2005Article
- Virus subversion of protective immunity.Current allergy and asthma reports · 2004Review
- Structural and functional analysis of human cytomegalovirus US3 protein.Journal of virology · 2004Article
- Review
- Determinant for endoplasmic reticulum retention in the luminal domain of the human cytomegalovirus US3 glycoprotein.Journal of virology · 2003Article
- The human cytomegalovirus US10 gene product delays trafficking of major histocompatibility complex class I molecules.Journal of virology · 2002Article
- Human cytomegalovirus US2 endoplasmic reticulum-lumenal domain dictates association with major histocompatibility complex class I in a locus-specific manner.Journal of virology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human cytomegalovirus US3, an endoplasmic reticulum (ER)-resident transmembrane glycoprotein, forms a complex with major histocompatibility complex (MHC) class I molecules and retains them in the ER, thereby preventing cytolysis by cytotoxic T lymphocytes. To identify which parts of US3 confine the protein to the ER and which parts are responsible for the association with MHC class I molecules, we constructed truncated mutant and chimeric forms in which US3 domains were exchanged with corresponding domains of CD4 and analyzed them for their intracellular localization and the ability to associate with MHC class I molecules. All of the truncated mutant and chimeric proteins containing the luminal domain of US3 were retained in the ER, while replacement of the US3 luminal domain with that of CD4 led to cell surface expression of the chimera. Thus, the luminal domain of US3 was sufficient for ER retention. Immunolocalization of the US3 glycoprotein after nocodazole treatment and the observation that the carbohydrate moiety of the US3 glycoprotein was not modified by Golgi enzymes indicated that the ER localization of US3 involved true retention, without recycling through the Golgi. Unlike the ER retention signal, the ability to associate with MHC class I molecules required the transmembrane domain in addition to the luminal domain of US3. Direct interaction between US3 and MHC class I molecules could be demonstrated after in vitro translation by coimmunoprecipitation. Together, the present data indicate that the properties that allow US3 to be localized in the ER and bind MHC class I molecules are located in different parts of the molecule.
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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.