ArticleThe Journal of biological chemistry2017
SOCS1 is an inducible negative regulator of interferon λ (IFN-λ)-induced gene expression
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 68 citations in OpenAlex.
- Trial
- Mechanisms of Differential Signal Transduction by Interferon Lambda Receptor 1 Variants.Journal of innate immunity · 2026Article
- Mechanisms of Differential Signal Transduction by IFNLR1 Variants.bioRxiv : the preprint server for biology · 2025Article
- Article
- Function of Interferon Lambda Receptor 1 Variants in Stem Cell-Derived Hepatocytes with Abrogated EndogenousJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2025Article
- Expression and function of interferon lambda receptor 1 variants.FEBS letters · 2025Review
- Multiomics uncovers the epigenomic and transcriptomic response to viral and bacterial stimulation in turbot.GigaScience · 2025Article
- Review
- Inflammatory Skin Diseases: Focus on the Role of Suppressors of Cytokine Signaling (SOCS) Proteins.Cells · 2024Review
- Genetic retargeting of E3 ligases to enhance CAR T cell therapy.Cell chemical biology · 2024Article
- The cGAS-STING pathway: a therapeutic target in diabetes and its complications.Burns & trauma · 2024Review
- Interferon lambda receptor-1 isoforms differentially influence gene expression and HBV replication in stem cell-derived hepatocytes.Antiviral research · 2024Article
- SOCS1 is a critical checkpoint in immune homeostasis, inflammation and tumor immunity.Frontiers in immunology · 2024Review
- Interferon lambda in respiratory viral infection: immunomodulatory functions and antiviral effects in epithelium.Frontiers in immunology · 2024Review
- ZIKV Strains Elicit Different Inflammatory and Anti-Viral Responses in Microglia Cells.Viruses · 2023Article
- A stimulus-contingent positive feedback loop enables IFN-β dose-dependent activation of pro-inflammatory genes.Molecular systems biology · 2023Article
- Influence of Canonical and Non-Canonical IFNLR1 Isoform Expression on Interferon Lambda Signaling.Viruses · 2023Article
- Excessive negative regulation of type I interferon disrupts viral control in individuals with Down syndrome.Immunity · 2022Article
- Interferon Signaling-Dependent Contribution of Glycolysis to Rubella Virus Infection.Pathogens (Basel, Switzerland) · 2022Article
- The Suppressor of Cytokine Signalling family of proteins and their potential impact on COVID-19 disease progression.Reviews in medical virology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I (α and β) and type III (λ) IFNs are induced upon viral infection through host sensory pathways that activate IFN regulatory factors (IRFs) and nuclear factor κB. Secreted IFNs induce autocrine and paracrine signaling through the JAK-STAT pathway, leading to the transcriptional induction of hundreds of IFN-stimulated genes, among them sensory pathway components such as cGAS, STING, RIG-I, MDA5, and the transcription factor IRF7, which enhance the induction of IFN-αs and IFN-λs. This positive feedback loop enables a very rapid and strong host response that, at some point, has to be controlled by negative regulators to maintain tissue homeostasis. Type I IFN signaling is controlled by the inducible negative regulators suppressor of cytokine signaling 1 (SOCS1), SOCS3, and ubiquitin-specific peptidase 18 (USP18). The physiological role of these proteins in IFN-γ signaling has not been clarified. Here we used knockout cell lines and mice to show that IFN-λ signaling is regulated by SOCS1 but not by SOCS3 or USP18. These differences were the basis for the distinct kinetic properties of type I and III IFNs. We found that IFN-α signaling is transient and becomes refractory after hours, whereas IFN-λ provides a long-lasting IFN-stimulated gene induction.
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What OpenQuestion holds
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.