ArticleCell stress & chaperones2017
Participation of dengue virus NS4B protein in the modulation of immune effectors dependent on ER stress in insect cells.
Article in Cell stress & chaperones, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Spring viraemia of carp virus modulates the time-dependent unfolded protein response to facilitate viral replication.Frontiers in immunology · 2025Article
- Dengue virus NS4B protein as a target for developing antivirals.Frontiers in cellular and infection microbiology · 2022Review
- Flavivirus infections induce a Golgi stress response in vertebrate and mosquito cells.Scientific reports · 2021Article
- Review
- ER stress-related molecules induced by Hantaan virus infection in differentiated THP-1 cells.Cell stress & chaperones · 2021Article
- Japanese Encephalitis Virus Induces Apoptosis and Encephalitis by Activating the PERK Pathway.Journal of virology · 2019Article
- Article
- A small molecule inhibitor of ER-to-cytosol protein dislocation exhibits anti-dengue and anti-Zika virus activity.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Organisms' reactions to adverse events result in the generation of immune effectors, which, in the case of insects, may be produced from the direct activation of pathways such as Toll, Jak-STAT, Imd, or RNAi or may be derived from the crosstalk of different intracellular pathways. One such pathway, the unfolded protein response (UPR), has the primary objective of restoring homeostasis in the endoplasmic reticulum. In addition, the UPR participates in signaling crosstalk with the immune pathways, generating protection against pathogenic organisms. Dengue virus is a plus-strand RNA virus belonging to the Flavivirus genus that uses the ER as a replication site; during the infection, there are indicators of the activation of the UPR, which in turn, induces the synthesis of internal membranes and preferential translation of viral proteins enhancing the replication. One of the dengue virus proteins, the NS4B can block the pathway of α/β interferon in mammals. However, what happen in insects is interesting because the lack of the main antiviral pathway, the interferon and the role of the NS4B protein in the UPR-immunity relationship can be better understood. Thus, in this study, we demonstrated that the DENV2/16681 NS4B protein is capable of modulating the immune effectors that result from the activation of the UPR in insect cells.
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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.