ArticleCommunications biology2021
IKKε isoform switching governs the immune response against EV71 infection.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Voxtalisib inhibits enterovirus 71 replication by downregulating host RAN and restoring IFN-STAT signaling.Journal of advanced research · 2026Article
- Phorbol Myristate Acetate Inhibits Senecavirus A Replication by Activating IKBKE-Mediated IFN Pathway and NF-κB Signal.Transboundary and emerging diseases · 2026Article
- Sse1, Hsp110 chaperone of yeast, controls the cellular fate during endoplasmic reticulum stress.G3 (Bethesda, Md.) · 2024Article
- Role of protein Post-translational modifications in enterovirus infection.Frontiers in microbiology · 2024Review
- Anti-Inflammatory Functions of Methanol Extract fromPlants (Basel, Switzerland) · 2022Article
- Alternative pre-mRNA splicing as a mechanism for terminating Toll-like Receptor signaling.Frontiers in immunology · 2022Review
- Role of IKKε in the Metabolic Diseases: Physiology, Pathophysiology, and Pharmacology.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The reciprocal interactions between pathogens and hosts are complicated and profound. A comprehensive understanding of these interactions is essential for developing effective therapies against infectious diseases. Interferon responses induced upon virus infection are critical for establishing host antiviral innate immunity. Here, we provide a molecular mechanism wherein isoform switching of the host IKKε gene, an interferon-associated molecule, leads to alterations in IFN production during EV71 infection. We found that IKKε isoform 2 (IKKε v2) is upregulated while IKKε v1 is downregulated in EV71 infection. IKKε v2 interacts with IRF7 and promotes IRF7 activation through phosphorylation and translocation of IRF7 in the presence of ubiquitin, by which the expression of IFNβ and ISGs is elicited and virus propagation is attenuated. We also identified that IKKε v2 is activated via K63-linked ubiquitination. Our results suggest that host cells induce IKKε isoform switching and result in IFN production against EV71 infection. This finding highlights a gene regulatory mechanism in pathogen-host interactions and provides a potential strategy for establishing host first-line defense against pathogens.
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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.