ArticleJournal of immunology (Baltimore, Md. : 1950)2012
The Akt1 isoform is required for optimal IFN-β transcription through direct phosphorylation of β-catenin.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Genome-wide RNAi screen reveals a new role of a WNT/CTNNB1 signaling pathway as negative regulator of virus-induced innate immune responses.PLoS pathogens · 2013Trial
- Immune and Stem Cell Interactions in Periodontal Disease: The Regulatory Role of Toll-Like Receptor 3.Advances in experimental medicine and biology · 2026Review
- Pregabalin Mediates Retinal Ganglion Cell Survival From Retinal Ischemia/Reperfusion Injury Via the Akt/GSK3β/β-Catenin Signaling Pathway.Investigative ophthalmology & visual science · 2022Article
- Akt isoforms in the immune system.Frontiers in immunology · 2022Review
- Article
- Phosphor-IWS1-dependent U2AF2 splicing regulates trafficking of CAR-E-positive intronless gene mRNAs and sensitivity to viral infection.Communications biology · 2021Article
- Transformation of SOX9Scientific reports · 2021Article
- PER2-mediated ameloblast differentiation via PPARγ/AKT1/β-catenin axis.International journal of oral science · 2021Article
- Disruption of innate defense responses by endoglycosidase HPSE promotes cell survival.JCI insight · 2021Article
- Phosphorylation of Shrimp Tcf by a Viral Protein Kinase WSV083 Suppresses Its Antiviral Effect.Frontiers in immunology · 2021Article
- Review
- β-Catenin Is Required for the cGAS/STING Signaling Pathway but Antagonized by the Herpes Simplex Virus 1 US3 Protein.Journal of virology · 2020Article
- The critical role of EGF-β-catenin signaling in the epithelial-mesenchymal transition in human glioblastoma.OncoTargets and therapy · 2017Article
- Regulation of Wnt/β-catenin signaling by herpesviruses.World journal of virology · 2016Review
- Modulation of Inflammatory Responses by Wnt/β-Catenin Signaling in Dendritic Cells: A Novel Immunotherapy Target for Autoimmunity and Cancer.Frontiers in immunology · 2016Review
- β-Catenin Upregulates the Constitutive and Virus-Induced Transcriptional Capacity of the Interferon Beta Promoter through T-Cell Factor Binding Sites.Molecular and cellular biology · 2016Article
- Akt isoforms in vascular disease.Vascular pharmacology · 2015Review
- Wnt signaling in dendritic cells: its role in regulation of immunity and tolerance.Discovery medicine · 2015Review
- Article
- Retinoid X receptor α attenuates host antiviral response by suppressing type I interferon.Nature communications · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
IFN-β is a critical antiviral cytokine that is capable of modulating the systemic immune response. The transcriptional induction of IFN-β is a highly regulated process, involving the activation of pattern recognition receptors and their downstream signaling pathways. The Akt family of serine/threonine kinases includes three isoforms. The specific role for the individual Akt isoforms in pattern recognition and signaling remains unclear. In this article, we report that the TLR3-mediated expression of IFN-β is blunted in cells that lack Akt1. The expression of IFN-β-inducible genes such as CCL5 and CXCL10 was also reduced in Akt1-deficient cells; the induction of TNF-α and CXCL2, whose expression does not rely on IFN-β, was not reduced in the absence of Akt1. Macrophages from Akt1(-/-) mice displayed deficient clearance of HSV-1 along with reduced IFN-β expression. Our results demonstrate that Akt1 signals through β-catenin by phosphorylation on Ser(552), a site that differs from the glycogen synthase kinase 3 β phosphorylation site. Stimulation of a chemically activated version of Akt1, in the absence of other TLR3-dependent signaling, was sufficient for accumulation and phosphorylation of β-catenin at Ser(552). Taken together, these results demonstrate that the Akt1 isoform is required for β-catenin-mediated promotion of IFN-β transcription downstream of TLR3 activation.
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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.