ArticleScientific reports2016
The matrix protein of rabies virus binds to RelAp43 to modulate NF-κB-dependent gene expression related to innate immunity.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 49 citations in OpenAlex.
- Biological barriers underlying the extremely high fatality of symptomatic rabies: neuroinvasion, immune evasion, and blood-brain barrier restriction.Frontiers in immunology · 2026Review
- Human brain cell types shape host-rabies virus transcriptional interactions revealing a preexisting pro-viral astrocyte subpopulation.Cell reports · 2025Article
- Immunological findings of West Caucasian bat virus in an accidental host.Journal of virology · 2025Article
- Reverse genetic approaches allowing the characterization of the rabies virus street strain belonging to the SEA4 subclade.Scientific reports · 2024Article
- Lyssavirus M protein degrades neuronal microtubules by reprogramming mitochondrial metabolism.mBio · 2024Article
- TRIM72 restricts lyssavirus infection by inducing K48-linked ubiquitination and proteasome degradation of the matrix protein.PLoS pathogens · 2024Article
- Article
- Susceptibilities of CNS Cells towards Rabies Virus Infection Is Linked to Cellular Innate Immune Responses.Viruses · 2022Article
- Establishment of a reverse genetics system for rabies virus strain Komatsugawa.The Journal of veterinary medical science · 2022Article
- Looking at the Pathogenesis of the Rabies Lyssavirus Strain Pasteur Vaccins through a Prism of the Disorder-Based Bioinformatics.Biomolecules · 2022Article
- Optimization of BRET saturation assays for robust and sensitive cytosolic protein-protein interaction studies.Scientific reports · 2022Article
- Deactivation of the antiviral state by rabies virus through targeting and accumulation of persistently phosphorylated STAT1.PLoS pathogens · 2022Article
- Review
- Toll-like Receptors in Viral Encephalitis.Viruses · 2021Review
- Expression Profiling and Bioinformatics Analysis of CircRNA in Mice Brain Infected with Rabies Virus.International journal of molecular sciences · 2021Article
- Early Transcriptional Changes in Rabies Virus-Infected Neurons and Their Impact on Neuronal Functions.Frontiers in microbiology · 2021Article
- Street RABV Induces the Cholinergic Anti-inflammatory Pathway in Human Monocyte-Derived Macrophages by Binding to nAChr α7.Frontiers in immunology · 2021Article
- Naturally occurring substitution in one amino acid in VHSV phosphoprotein enhances viral virulence in flounder.PLoS pathogens · 2021Article
- Article
- Structure of the prefusion-locking broadly neutralizing antibody RVC20 bound to the rabies virus glycoprotein.Nature communications · 2020Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The matrix (M) protein of wild isolates of rabies virus such as Tha (M-Tha) was previously shown to be able to interact with RelAp43, a protein of the NF-κB family, and to efficiently suppress NF-κB-dependent reporter gene expression, in contrast with the vaccine strain SAD. Here, we analyze the mechanisms involved in RelAp43-M protein interaction. We demonstrate that the central part of M-Tha, and the specific C-terminal region of RelAp43 are required for this interaction. Four differences in the corresponding amino acid sequences of the M-Tha and M-SAD are shown to be crucial for RelAp43 interaction and subsequent modulation of innate immune response. Furthermore, the capacity of M-Tha to interact with RelAp43 was shown to be crucial for the control of the expression of four genes (IFN, TNF, IL8 and CXCL2) during viral infection. These findings reveal that RelAp43 is a potent regulator of transcription of genes involved in innate immune response during rabies virus infection and that the M protein of wild isolates of rabies virus is a viral immune-modulatory factor playing an important role in this RelAp43-mediated host innate immunity response in contrast to M protein of vaccine strains, which have lost this property.
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