ArticleCellular microbiology2014
Phosphorylation and membrane association of the Rubella virus capsid protein is important for its anti-apoptotic function.
Article in Cellular microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Exogenous Rubella Virus Capsid Proteins Enhance Virus Genome Replication.Pathogens (Basel, Switzerland) · 2022Article
- Enhancement of Rubella Virus Infection in Immortalized Human First-Trimester Trophoblasts Under Low-Glucose Stress Conditions.Frontiers in microbiology · 2022Article
- Article
- The Epithelial-to-Mesenchymal Transition-Like Process Induced by TGF-β1 Enhances Rubella Virus Binding and Infection in A549 Cells via the Smad Pathway.Microorganisms · 2021Article
- Hantavirus inhibits apoptosis by preventing mitochondrial membrane potential loss through up-regulation of the pro-survival factor BCL-2.PLoS pathogens · 2020Article
- Altered mitochondrial dynamics as a consequence of Venezuelan Equine encephalitis virus infection.Virulence · 2017Article
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Rubella virus (RV), a member of Togaviridae, is an important human pathogen that can cause severe defects in the developing fetus. Compared to other togaviruses, RV replicates very slowly suggesting that it must employ effective mechanisms to delay the innate immune response. A recent study by our laboratory revealed that the capsid protein of RV is a potent inhibitor of apoptosis. A primary mechanism by which RV capsid interferes with programmed cell death appears to be through interaction with the pro-apoptotic Bcl-2 family member Bax. In the present study, we report that the capsid protein also blocks IRF3-dependent apoptosis induced by the double-strand RNA mimic polyinosinic-polycytidylic acid. In addition, analyses of cis-acting elements revealed that phosphorylation and membrane association are important for its anti-apoptotic function. Finally, the observation that hypo-phosphorylated capsid binds Bax just as well as wild-type capsid protein suggests that interaction with this pro-apoptotic host protein in and of itself is not sufficient to block programmed cell death. This provides additional evidence that this viral protein inhibits apoptosis through multiple mechanisms.
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Registered trials
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