ArticleJournal of virology2009
Rift valley fever virus L protein forms a biologically active oligomer.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed.
- Genetic investigation of glycosylphosphatidylinositol (GPI) anchored Bd37 orthologs in Babesia divergens group and potential use of recombinant protein for ecological survey in deer.The Journal of veterinary medical science · 2024Article
- CK1 and PP1 regulate Rift Valley fever virus genome replication through L protein phosphorylation.Antiviral research · 2024Article
- Host entry factors of Rift Valley Fever Virus infection.Advances in virus research · 2023Article
- Modeling the Tertiary Structure of the Rift Valley Fever Virus L Protein.Molecules (Basel, Switzerland) · 2019Article
- Supramolecular arrangement of the full-length Zika virus NS5.PLoS pathogens · 2019Article
- A single-cycle replicable Rift Valley fever phlebovirus vaccine carrying a mutated NSs confers full protection from lethal challenge in mice.Scientific reports · 2018Article
- Polycipiviridae: a proposed new family of polycistronic picorna-like RNA viruses.The Journal of general virology · 2017Article
- RNA-Dependent RNA Polymerases of Picornaviruses: From the Structure to Regulatory Mechanisms.Viruses · 2015Review
- Identification of virulence determinants within the L genomic segment of the pichinde arenavirus.Journal of virology · 2013Article
- Toscana virus NSs protein promotes degradation of double-stranded RNA-dependent protein kinase.Journal of virology · 2013Article
- Molecular biology and genetic diversity of Rift Valley fever virus.Antiviral research · 2012Review
- Disulfide linkages mediating nucleocapsid protein dimerization are not required for porcine arterivirus infectivity.Journal of virology · 2012Article
- Article
- p53 Activation following Rift Valley fever virus infection contributes to cell death and viral production.PloS one · 2012Article
- Characterization of wild-type and alternate transcription termination signals in the Rift Valley fever virus genome.Journal of virology · 2011Article
- Recombinant Rift Valley fever vaccines induce protective levels of antibody in baboons and resistance to lethal challenge in mice.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Mutational analysis of the SDD sequence motif of a PRRSV RNA-dependent RNA polymerase.Science China. Life sciences · 2011Article
- Minigenomes, transcription and replication competent virus-like particles and beyond: reverse genetics systems for filoviruses and other negative stranded hemorrhagic fever viruses.Antiviral research · 2011Review
- NSs protein of rift valley fever virus promotes posttranslational downregulation of the TFIIH subunit p62.Journal of virology · 2011Article
- Rift valley fever: recent insights into pathogenesis and prevention.Journal of virology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Rift Valley fever virus (RVFV) (genus Phlebovirus, family Bunyaviridae) causes mosquito-borne epidemic diseases in humans and livestock. The virus carries three RNA segments, L, M, and S, of negative or ambisense polarity. L protein, an RNA-dependent RNA polymerase, encoded in the L segment, and N protein, encoded in the S segment, exert viral RNA replication and transcription. Coexpression of N, hemagglutinin (HA)-tagged L, and viral minigenome resulted in minigenome replication and transcription, a finding that demonstrated HA-tagged L was biologically active. Likewise L tagged with green fluorescent protein (GFP) was biologically competent. Coimmunoprecipitation analysis using extracts from cells coexpressing HA-tagged L and GFP-tagged L showed the formation of an L oligomer. Bimolecular fluorescence complementation analysis and coimmunoprecipitation studies demonstrated the formation of an intermolecular L-L interaction through its N-terminal and C-terminal regions and also suggested an intramolecular association between the N-terminal and C-terminal regions of L protein. A biologically inactive L mutant, in which the conserved signature SDD motif was replaced by the amino acid residues GNN, exhibited a dominant negative phenotype when coexpressed with wild-type L in the minigenome assay system. Expression of this mutant L also inhibited viral gene expression in virus-infected cells. These data provided compelling evidence for the importance of oligomerization of RVFV L protein for its polymerase activity.
Indexed as
Identifiers
What OpenQuestion holds
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.