ArticlemSphere2020
Interactions of the Nipah Virus P, V, and W Proteins across the STAT Family of Transcription Factors.
Article in mSphere, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Ephrin B2 and Ephrin B3 are receptors for a novel putative henipavirus with zoonotic potential.PLoS neglected tropical diseases · 2026Article
- Hendra virus genotypes 1 and 2 differ in V protein-mediated immune evasion.The Journal of general virology · 2026Article
- Current knowledge on the host-pathogen interactions of henipaviruses and novel platforms to enable further characterisation.EBioMedicine · 2026Review
- The intracellular virus-host interface of henipaviruses.Journal of virology · 2025Review
- Nipah virus: a summary for clinicians.International journal of emergency medicine · 2025Review
- A conserved motif in Henipavirus P/V/W proteins drives the fibrillation of the W protein from Hendra virus.Protein science : a publication of the Protein Society · 2025Article
- Dissecting Henipavirus W proteins conformational and fibrillation properties: contribution of their N- and C-terminal constituent domains.The FEBS journal · 2025Article
- Uncovering human kinase substrates in nipah proteome.Frontiers in bioinformatics · 2025Article
- Recent Advances in Immunological Landscape and Immunotherapeutic Agent of Nipah Virus Infection.Cell biochemistry and biophysics · 2024Review
- Recent Advances of Nipah Virus Disease: Pathobiology to Treatment and Vaccine Advancement.Journal of microbiology (Seoul, Korea) · 2024Review
- Molecular determinants of cross-species transmission in emerging viral infections.Microbiology and molecular biology reviews : MMBR · 2024Review
- Pathogenicity and virulence of henipaviruses.Virulence · 2023Review
- Single-dose mucosal replicon-particle vaccine protects against lethal Nipah virus infection up to 3 days after vaccination.Science advances · 2023Article
- Host-Pathogen Interactions Influencing Zoonotic Spillover Potential and Transmission in Humans.Viruses · 2023Review
- Nipah Virus Impairs Autocrine IFN Signaling by Sequestering STAT1 and STAT2 into Inclusion Bodies.Viruses · 2023Article
- Reprogramming viral immune evasion for a rational design of next-generation vaccines for RNA viruses.Frontiers in immunology · 2023Review
- The Immunobiology of Nipah Virus.Microorganisms · 2022Review
- Poxviruses and paramyxoviruses use a conserved mechanism of STAT1 antagonism to inhibit interferon signaling.Cell host & microbe · 2022Article
- Experimental Evidence of Intrinsic Disorder and Amyloid Formation by theInternational journal of molecular sciences · 2022Article
- Mechanisms of Viral Degradation of Cellular Signal Transducer and Activator of Transcription 2.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The Nipah virus (NiV) phosphoprotein (P) gene encodes four proteins. Three of these-P, V, and W-possess a common N-terminal domain but distinct C termini. These proteins interact with immune modulators. Previous studies demonstrated that P, V, and W bind STAT1 and STAT4 and that V also interacts with STAT2 but not with STAT3. The STAT1 and STAT2 interactions block interferon (IFN)-induced STAT tyrosine phosphorylation. To more fully characterize the interactions of P, V, and W with the STATs, we screened for interaction of each viral protein with STATs 1 to 6 by coimmunoprecipitation. We demonstrate that NiV P, V, and W interact with STAT4 through their common N-terminal domain and block STAT4 activity, based on a STAT4 response element reporter assay. Although none of the NiV proteins interact with STAT3 or STAT6, NiV V, but not P or W, interacts with STAT5 through its unique C terminus. Furthermore, the interaction of NiV V with STAT5 was not disrupted by overexpression of the N-terminal binding STAT1 or the C-terminal binding MDA5. NiV V also inhibits a STAT5 response element reporter assay. Residues 114 to 140 of the common N-terminal domain of the NiV P gene products were found to be sufficient to bind STAT1 and STAT4. Analysis of STAT1-STAT3 chimeras suggests that the P gene products target the STAT1 SH2 domain. When fused to GST, the 114-140 peptide is sufficient to decrease STAT1 phosphorylation in IFN-β-stimulated cells, suggesting that this peptide could potentially be fused to heterologous proteins to confer inhibition of STAT1- and STAT4-dependent responses.
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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.