ArticleProceedings of the National Academy of Sciences of the United States of America2010
Human cytomegalovirus UL69 protein facilitates translation by associating with the mRNA cap-binding complex and excluding 4EBP1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 43 citations in OpenAlex.
- Viral interference of nucleocytoplasmic transport.The Journal of biological chemistry · 2025Review
- A autophagy related gene signature to predict the prognosis of pancreatic carcinoma and tumor immune microenvironment evaluation.Scientific reports · 2025Article
- RNA-targeted proteomics identifies YBX1 as critical for efficient HCMV mRNA translation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Proximity-dependent mapping of the HCMV US28 interactome identifies RhoGEF signaling as a requirement for efficient viral reactivation.PLoS pathogens · 2023Article
- Review
- When Poly(A) Binding Proteins Meet Viral Infections, Including SARS-CoV-2.Journal of virology · 2022Review
- Identification of UL69 Gene and Protein in Cytomegalovirus-Transformed Human Mammary Epithelial Cells.Frontiers in oncology · 2021Article
- Newcastle Disease virus infection activates PI3K/Akt/mTOR and p38 MAPK/Mnk1 pathways to benefit viral mRNA translation via interaction of the viral NP protein and host eIF4E.PLoS pathogens · 2020Article
- Human Cytomegalovirus Primary Infection and Reactivation: Insights From Virion-Carried Molecules.Frontiers in microbiology · 2020Review
- Human cytomegalovirus induces and exploits Roquin to counteract the IRF1-mediated antiviral state.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Eukaryotic initiation factor 4A (eIF4A) during viral infections.Virus genes · 2019Review
- Interferon-Independent Innate Responses to Cytomegalovirus.Frontiers in immunology · 2019Review
- Article
- Dengue Virus Selectively Annexes Endoplasmic Reticulum-Associated Translation Machinery as a Strategy for Co-opting Host Cell Protein Synthesis.Journal of virology · 2018Article
- Epstein-Barr Virus Protein EB2 Stimulates Translation Initiation of mRNAs through Direct Interactions with both Poly(A)-Binding Protein and Eukaryotic Initiation Factor 4G.Journal of virology · 2018Article
- HIV-1 Gag Blocks Selenite-Induced Stress Granule Assembly by Altering the mRNA Cap-Binding Complex.mBio · 2016Article
- Modulation of the Translational Landscape During Herpesvirus Infection.Annual review of virology · 2015Review
- An unbiased proteomics approach to identify human cytomegalovirus RNA-associated proteins.Virology · 2015Article
- EIF4EBP1 overexpression is associated with poor survival and disease progression in patients with hepatocellular carcinoma.PloS one · 2015Article
- Differential role for host translation factors in host and viral protein synthesis during human cytomegalovirus infection.Journal of virology · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
4EBP1 is phosphorylated by the mTORC1 kinase. When mTORC1 activity is inhibited, hypophosphorylated 4EBP1 binds and sequesters eIF4E, a component of the mRNA cap-binding complex, and blocks translation. As a consequence, mTORC1 activity is needed to maintain active translation. The human cytomegalovirus pUL38 protein preserves mTORC1 activity, keeping most of the E4BP1 in the infected cell in a hyperphosphorylated, inactive state. Here we report that a second viral protein, pUL69, also antagonizes the activity of 4EBP1, but by a separate mechanism. pUL69 interacts directly with eIF4A1, an element of the cap-binding complex, and the poly(A)-binding protein, which binds to the complex. When pUL69 accumulates during infection with wild-type virus, 4EBP1 is excluded from the complex. However, 4EBP1 is present in the cap-binding complex after infection with a pUL69-deficient virus, coincident with reduced accumulation of several late virus-coded proteins. We propose that pUL69 supports translation in human cytomegalovirus-infected cells by excluding hypophosphorylated 4EBP1 from the cap-binding complex.
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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.