ArticleViruses2018
Newcastle Disease Virus V Protein Promotes Viral Replication in HeLa Cells through the Activation of MEK/ERK Signaling.
Article in Viruses, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Decoding the diversity: a comprehensive sequence analysis of accessory viral protein W of Newcastle disease virus.Journal of biosciences · 2026Article
- DNAJA2 inhibits Newcastle disease virus replication by targeting its V protein to modulate the MDA5-MAVS pathway.BMC microbiology · 2025Article
- Accessory viral protein, V, of Newcastle Disease Virus binds dsRNA to facilitate immune evasion.Virusdisease · 2025Article
- miRNA Expression Signatures Induced by Chicken Astrovirus Infection in Chickens.International journal of molecular sciences · 2023Article
- The Viral Knock: Ameliorating Cancer Treatment with Oncolytic Newcastle Disease Virus.Life (Basel, Switzerland) · 2023Review
- Molecular characterization suggests kinetic modulation of expression of accessory viral protein, W, in Newcastle disease virus infected DF1 cells.Virusdisease · 2023Article
- The V protein in oncolytic Newcastle disease virus promotes HepG2 hepatoma cell proliferation at the single-cell level.BMC cancer · 2023Article
- Upregulation of DUSP6 impairs infectious bronchitis virus replication by negatively regulating ERK pathway and promoting apoptosis.Veterinary research · 2021Article
- Advances in the Study of Antitumour Immunotherapy for Newcastle Disease Virus.International journal of medical sciences · 2021Review
- Newcastle Disease Virus Nonstructural V Protein Upregulates SOCS3 Expression to Facilitate Viral Replication Depending on the MEK/ERK Pathway.Frontiers in cellular and infection microbiology · 2019Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Newcastle disease virus (NDV) can infect a wide range of domestic and wild bird species. The non-structural V protein of NDV plays an important role in antagonizing innate host defenses to facilitate viral replication. However, there is a lack of knowledge related to the mechanisms through which the V protein regulates viral replication. The extracellular signal-regulated kinase (ERK) signaling pathway in the host is involved in a variety of functions and is activated by several stimuli, including viral replication. In this study, we show that both the lentogenic strain, La Sota, and the velogenic strain, F48E9, of NDV activate the mitogen-activated protein kinase (MEK)/ERK signaling pathway. The pharmacological inhibition of ERK1/2 phosphorylation using the highly selective inhibitors U0126 and SCH772984 resulted in the reduced levels of NDV RNA in cells and virus titers in the cell supernatant, which established an important role for the MEK/ERK signaling pathway in NDV replication. Moreover, the overexpression of the V protein in HeLa cells increased the phosphorylation of ERK1/2 and induced the transcriptional changes in the genes downstream of the MEK/ERK signaling pathway. Taken together, our results demonstrate that the V protein is involved in the ERK signaling pathway-mediated promotion of NDV replication and thus, can be investigated as a potential antiviral target.
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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 Socratic graph.