ArticleThe Journal of biological chemistry
The ATPase ATP6V1A facilitates rabies virus replication by promoting virion uncoating and interacting with the viral matrix protein.
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- TRIM7 Inhibits Rabies Virus Replication by Promoting K48-Linked Ubiquitination and Degradation of RABV-M.Emerging microbes & infections · 2026Article
- Article
- Identification of clade-defining single nucleotide polymorphisms for improved rabies virus surveillance.New microbes and new infections · 2024Article
- AP3B1 facilitates PDIA3/ERP57 function to regulate rabies virus glycoprotein selective degradation and viral entry.Autophagy · 2024Article
- The matrix protein of lyssavirus hijacks autophagosome for efficient egress by recruiting NEDD4 through its PPxY motif.Autophagy · 2024Article
- Defective Lamtor5 Leads to Autoimmunity by Deregulating v-ATPase and Lysosomal Acidification.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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
- Mining Autoimmune-Disorder-Linked Molecular-Mimicry Candidates inMicroorganisms · 2023Article
- Molecular Mimicry Mapping inPathogens (Basel, Switzerland) · 2023Article
- Article
- Lipid Droplets Are Beneficial for Rabies Virus Replication by Facilitating Viral Budding.Journal of virology · 2022Article
- A genome-wide CRISPR/Cas9 gene knockout screen identifies immunoglobulin superfamily DCC subclass member 4 as a key host factor that promotes influenza virus endocytosis.PLoS pathogens · 2021Article
- Article
- Rabies Infection: An Overview of Lyssavirus-Host Protein Interactions.Iranian biomedical journal · 2021Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rabies virus (RABV) matrix protein (M) plays crucial roles in viral transcription, replication, assembly, and budding; however, its function during the early stage of virus replication remains unknown. Here, we mapped the protein interactome between RABV M and human host factors using a proteomic approach, finding a link to the V-type proton ATPase catalytic subunit A (ATP6V1A), which is located in the endosomes where RABV first enters. By downregulating or upregulating ATP6V1A expression in HEK293T cells, we found that ATP6V1A facilitated RABV replication. We further found that ATP6V1A was involved in the dissociation of incoming viral M proteins during viral uncoating. Coimmunoprecipitation demonstrated that M interacted with the full length or middle domain of ATP6V1A, which was dependent on the lysine residue at position 256 and the glutamic acid residue at position 279. RABV growth and uncoating in ATP6V1A-depleted cells was restored by trans-complementation with the full length or interaction domain of ATP6V1A. Moreover, stably overexpressed ATP6V1A enhanced RABV growth in Vero cells, which are used for the production of rabies vaccine. Our findings identify a new partner for RABV M proteins and establish a new role of ATP6V1A by promoting virion uncoating during RABV replication.
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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.