ArticlePLoS pathogens2010
Ubiquitin-regulated nuclear-cytoplasmic trafficking of the Nipah virus matrix protein is important for viral budding.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 147 citations in OpenAlex.
- Reduced expression of human metapneumovirus matrix protein impacts virus assembly and ribonucleoprotein localization.Journal of virology · 2026Article
- NSUN2‑mediated epitranscriptomic and ubiquitin modulation of Nipah virus matrix protein reveals a dual-targeting antiviral strategy.Protein & cell · 2026Article
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- Regulation of HPV-16 infection by ubiquitination of the L1 major capsid protein.Journal of virology · 2026Article
- Cell-cell fusion limits activation of the unfolded protein response induced by the Nipah virus glycoproteins.Journal of virology · 2026Article
- The E3 ligase RAD18-mediated ubiquitination of henipavirus matrix protein promotes its nuclear-cytoplasmic trafficking and viral egress.Emerging microbes & infections · 2025Article
- Paramyxovirus matrix protein redirects METTL3 for dual regulation of viral replication and immune evasion.PLoS pathogens · 2025Article
- Nipah virus matrix protein uses cortical actin to stabilize the virus assembly sites and promote budding.Science advances · 2025Article
- The intracellular virus-host interface of henipaviruses.Journal of virology · 2025Review
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- Identification of conserved CD8+ T cell epitopes in Nipah virus towards vaccine development using an immunoinformatics approach.Clinical and experimental vaccine research · 2025Article
- Sub-Nucleolar Trafficking of Hendra Virus Matrix Protein Is Regulated by Ubiquitination.Viruses · 2025Article
- Multidimensional Regulatory Mechanisms and Targeting Strategies of the eEF1 Family in RNA Virus Infection.Viruses · 2025Review
- Henipaviruses: epidemiology, ecology, disease, and the development of vaccines and therapeutics.Clinical microbiology reviews · 2025Review
- The nanoscale organization of the Nipah virus fusion protein informs new membrane fusion mechanisms.eLife · 2025Article
- Pathogenicity and virulence of human respiratory syncytial virus: Multifunctional nonstructural proteins NS1 and NS2.Virulence · 2024Review
- Nipah virus: epidemiology, pathogenesis, treatment, and prevention.Frontiers of medicine · 2024Review
- Tetracistronic minigenomes elucidate a functional promoter for Ghana virus and unveils Cedar virus replicase promiscuity for all henipaviruses.Journal of virology · 2024Article
- The role of ubiquitination in health and disease.MedComm · 2024Review
37 more citing papers are in PubMed but not listed here.
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Paramyxoviruses are known to replicate in the cytoplasm and bud from the plasma membrane. Matrix is the major structural protein in paramyxoviruses that mediates viral assembly and budding. Curiously, the matrix proteins of a few paramyxoviruses have been found in the nucleus, although the biological function associated with this nuclear localization remains obscure. We report here that the nuclear-cytoplasmic trafficking of the Nipah virus matrix (NiV-M) protein and associated post-translational modification play a critical role in matrix-mediated virus budding. Nipah virus (NiV) is a highly pathogenic emerging paramyxovirus that causes fatal encephalitis in humans, and is classified as a Biosafety Level 4 (BSL4) pathogen. During live NiV infection, NiV-M was first detected in the nucleus at early stages of infection before subsequent localization to the cytoplasm and the plasma membrane. Mutations in the putative bipartite nuclear localization signal (NLS) and the leucine-rich nuclear export signal (NES) found in NiV-M impaired its nuclear-cytoplasmic trafficking and also abolished NiV-M budding. A highly conserved lysine residue in the NLS served dual functions: its positive charge was important for mediating nuclear import, and it was also a potential site for monoubiquitination which regulates nuclear export of the protein. Concordantly, overexpression of ubiquitin enhanced NiV-M budding whereas depletion of free ubiquitin in the cell (via proteasome inhibitors) resulted in nuclear retention of NiV-M and blocked viral budding. Live Nipah virus budding was exquisitely sensitive to proteasome inhibitors: bortezomib, an FDA-approved proteasome inhibitor for treating multiple myeloma, reduced viral titers with an IC(50) of 2.7 nM, which is 100-fold less than the peak plasma concentration that can be achieved in humans. This opens up the possibility of using an "off-the-shelf" therapeutic against acute NiV infection.
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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.