ArticleThe Journal of biological chemistry2012
Dephosphorylation of HuR protein during alphavirus infection is associated with HuR relocalization to the cytoplasm.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 61 citations in OpenAlex.
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- Cellular Protein HuR Regulates the Switching of Genomic RNA Templates for Differential Functions during the Coxsackievirus B3 Life Cycle.Journal of virology · 2021Article
- De-Coding the Contributions of the Viral RNAs to Alphaviral Pathogenesis.Pathogens (Basel, Switzerland) · 2021Review
- Heat stress induced arginylation of HuR promotes alternative polyadenylation of Hsp70.3 by regulating HuR stability and RNA binding.Cell death and differentiation · 2021Article
- Discovery of Widespread Host Protein Interactions with the Pre-replicated Genome of CHIKV Using VIR-CLASP.Molecular cell · 2020Article
- RNA regulatory processes in RNA virus biology.Wiley interdisciplinary reviews. RNA · 2019Review
- Viral modulation of cellular RNA alternative splicing: A new key player in virus-host interactions?Wiley interdisciplinary reviews. RNA · 2019Review
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- Zika Virus Subverts Stress Granules To Promote and Restrict Viral Gene Expression.Journal of virology · 2019Article
- Regulation of Kv11.1 potassium channel C-terminal isoform expression by the RNA-binding proteins HuR and HuD.The Journal of biological chemistry · 2018Article
- Rotavirus Induces Formation of Remodeled Stress Granules and P Bodies and Their Sequestration in Viroplasms To Promote Progeny Virus Production.Journal of virology · 2018Article
- Long-read sequencing uncovers a complex transcriptome topology in varicella zoster virus.BMC genomics · 2018Article
- Cytoplasmic Relocalization and Colocalization with Viroplasms of Host Cell Proteins, and Their Role in Rotavirus Infection.Journal of virology · 2018Article
- Viral manipulation of host mRNA decay.Future virology · 2018Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
We have demonstrated previously that the cellular HuR protein binds U-rich elements in the 3' untranslated region (UTR) of Sindbis virus RNA and relocalizes from the nucleus to the cytoplasm upon Sindbis virus infection in 293T cells. In this study, we show that two alphaviruses, Ross River virus and Chikungunya virus, lack the conserved high-affinity U-rich HuR binding element in their 3' UTRs but still maintain the ability to interact with HuR with nanomolar affinities through alternative binding elements. The relocalization of HuR protein occurs during Sindbis infection of multiple mammalian cell types as well as during infections with three other alphaviruses. Interestingly, the relocalization of HuR is not a general cellular reaction to viral infection, as HuR protein remained largely nuclear during infections with dengue and measles virus. Relocalization of HuR in a Sindbis infection required viral gene expression, was independent of the presence of a high-affinity U-rich HuR binding site in the 3' UTR of the virus, and was associated with an alteration in the phosphorylation state of HuR. Sindbis virus-induced HuR relocalization was mechanistically distinct from the movement of HuR observed during a cellular stress response, as there was no accumulation of caspase-mediated HuR cleavage products. Collectively, these data indicate that virus-induced HuR relocalization to the cytoplasm is specific to alphavirus infections and is associated with distinct posttranslational modifications of this RNA-binding protein.
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