ArticleJournal of virology2011
Parainfluenza virus 5 m protein interaction with host protein 14-3-3 negatively affects virus particle formation.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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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
17 citing papers in PubMed, 27 citations in OpenAlex.
- Mumps Virus: Replication, Immune Response, and the Changing Landscape of Vaccine Effectiveness.Pathogens (Basel, Switzerland) · 2026Review
- YWHAG inhibits influenza a virus replication by suppressing the release of viral M2 protein.Frontiers in microbiology · 2022Article
- Evaluation of the relationship between the 14-3-3ε protein and LvRab11 in the shrimp Litopenaeus vannamei during WSSV infection.Scientific reports · 2021Article
- The tail domain of PRRSV NSP2 plays a key role in aggrephagy by interacting with 14-3-3ε.Veterinary research · 2020Article
- Review
- The 14-3-3η chaperone protein promotes antiviral innate immunity via facilitating MDA5 oligomerization and intracellular redistribution.PLoS pathogens · 2019Article
- Article
- Host-Driven Phosphorylation Appears to Regulate the Budding Activity of the Lassa Virus Matrix Protein.Pathogens (Basel, Switzerland) · 2018Article
- Comparative proteomic analysis reveals different responses in porcine lymph nodes to virulent and attenuated homologous African swine fever virus strains.Veterinary research · 2018Article
- Differential abundance and transcription of 14-3-3 proteins during vegetative growth and sexual reproduction in budding yeast.Scientific reports · 2018Article
- The Lymphocytic Choriomeningitis Virus Matrix Protein PPXY Late Domain Drives the Production of Defective Interfering Particles.PLoS pathogens · 2016Article
- Proteomic analysis by iTRAQ in red claw crayfish, Cherax quadricarinatus, hematopoietic tissue cells post white spot syndrome virus infection.Fish & shellfish immunology · 2016Article
- Matrix proteins of Nipah and Hendra viruses interact with beta subunits of AP-3 complexes.Journal of virology · 2014Article
- Viral and Cellular Components of AAV2 Replication Compartments.The open virology journal · 2013Article
- Identification and expression analysis of two splice variants of the 14-3-3 epsilon from Litopenaeus Vannamei during WSSV infections.Molecular biology reports · 2012Article
- Abortive replication of influenza virus in mouse dendritic cells.Journal of virology · 2012Article
- Role of ubiquitin in parainfluenza virus 5 particle formation.Journal of virology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Paramyxovirus matrix (M) proteins organize virus assembly, linking viral glycoproteins and viral ribonucleoproteins together at virus assembly sites on cellular membranes. Using a yeast two-hybrid screening approach, we identified 14-3-3 as a binding partner for the M protein of parainfluenza virus 5 (PIV5). Binding in both transfected and PIV5-infected cells was confirmed by coimmunoprecipitation and was mapped to a C-terminal region within the M protein, namely, 366-KTKSLP-371. This sequence resembles known 14-3-3 binding sites, in which the key residue for binding is a phosphorylated serine residue. Mutation of S369 within the PIV5 M protein disrupted 14-3-3 binding and improved the budding of both virus-like particles (VLPs) and recombinant viruses, suggesting that 14-3-3 binding impairs virus budding. 14-3-3 protein overexpression reduced the budding of VLPs. Using (33)P labeling, phosphorylated M protein was detected in PIV5-infected cells, and this phosphorylation was nearly absent in cells infected with a recombinant virus harboring an S369A mutation within the M protein. Assembly of the M protein into clusters and filaments at infected cell surfaces was enhanced in cells infected with a recombinant virus defective in 14-3-3 binding. These findings support a model in which a portion of M protein within PIV5-infected cells is phosphorylated at residue S369, binds the 14-3-3 protein, and is held away from sites of virus budding.
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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.