ReviewFrontiers in immunology2018
A Positive Feedback Amplifier Circuit That Regulates Interferon (IFN)-Stimulated Gene Expression and Controls Type I and Type II IFN Responses.
Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 205 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
205 citing papers in PubMed, 322 citations in OpenAlex.
- Altered increase in STAT1 expression and phosphorylation in severe COVID-19.European journal of immunology · 2022Trial
- [Pathophysiological aspects of primary Sjögren's disease : From epithelial activation to systemic autoimmunity].Zeitschrift fur Rheumatologie · 2026Review
- Spatial analysis reveals cellular microenvironments and mechanisms of inflammation and injury in acute interstitial nephritis.Nature communications · 2026Article
- Interferon Regulatory Factors as Potential Therapeutic Targets in Cardiovascular Disease: Focusing on Vascular Inflammation.International journal of molecular sciences · 2026Review
- Evolution ofInternational journal of molecular sciences · 2026Review
- Prolonged KRAS-MAPK Inhibition Induces Interferon Signaling That Promotes Cell State Transition and Confers Therapeutic Vulnerabilities.Cancer research · 2026Article
- Interferon Receptor Chain Deficiency in Murine Friend Erythroleukemia Cell Clone Resistant to Type I or Type I and II Interferons.International journal of molecular sciences · 2026Article
- The microbiota-gut-immunity axis in teleost fish: dual regulatory mechanisms of viral infections and prospects for microbiome-based antiviral strategies.Fish physiology and biochemistry · 2026Review
- Tripartite motif-containing 34 (TRIM34) protein interacts with the nucleocytoplasmic transport machinery and negatively modulates antiviral responses.PLoS pathogens · 2026Article
- CRISPR/Cas9-Mediated Knockout of CGNL1 Confers Resistance to Aflatoxin B1 in Porcine Intestinal Epithelial Cells via Suppressing ROS Generation.International journal of molecular sciences · 2026Article
- Reovirus resistance in tumors mediated by elevated ISG expression: overcoming therapeutic resistance via JAK/STAT pathway modulation.Virology journal · 2026Article
- Occludin modulates HIV and ischaemic stroke response via the mitochondrial antiviral signalling pathway.Brain : a journal of neurology · 2026Article
- Cell-Intrinsic Type I Interferon Signaling as a Pleiotropic Orchestrator of CD4 T Cell Immunity.Biomolecules · 2026Review
- EGFR activation disrupts immunotherapy response via SHP2-mediated suppression of tumor-intrinsic response to IFN-γ.The Journal of clinical investigation · 2026Article
- Dissection of innate-immune-ligand- and interferon-protein-mediated transcriptional responses in human THP1 cell states.Communications biology · 2026Article
- Long Non-Coding RNAs Can Govern the Antiviral Immune Response Through Interferon-Mediated Mechanisms in Respiratory Tract.Viruses · 2026Review
- Type I interferon signaling defines a novel disease signature in xeroderma pigmentosum C human keratinocytes.Scientific reports · 2026Article
- Beyond Viral Restriction: The Metabolic Dimensions of Interferon-Stimulated Genes in Antiviral Immunity.Viruses · 2026Review
- VPS34-IN1 potentiates STING-dependent activation in human CAL-1 cells.Cellular & molecular biology letters · 2026Article
- Immune profiling of anti-SSA-positive at-risk individuals reveals increased type I IFN activity preceding lymphocyte abnormalities in Sjögren's disease.Frontiers in immunology · 2026Article
145 more citing papers are in PubMed but not listed here.
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
Interferon (IFN)-I and IFN-II both induce IFN-stimulated gene (ISG) expression through Janus kinase (JAK)-dependent phosphorylation of signal transducer and activator of transcription (STAT) 1 and STAT2. STAT1 homodimers, known as γ-activated factor (GAF), activate transcription in response to all types of IFNs by direct binding to IFN-II activation site (γ-activated sequence)-containing genes. Association of interferon regulatory factor (IRF) 9 with STAT1-STAT2 heterodimers [known as interferon-stimulated gene factor 3 (ISGF3)] or with STAT2 homodimers (STAT2/IRF9) in response to IFN-I, redirects these complexes to a distinct group of target genes harboring the interferon-stimulated response element (ISRE). Similarly, IRF1 regulates expression of ISGs in response to IFN-I and IFN-II by directly binding the ISRE or IRF-responsive element. In addition, evidence is accumulating for an IFN-independent and -dependent role of unphosphorylated STAT1 and STAT2, with or without IRF9, and IRF1 in basal as well as long-term ISG expression. This review provides insight into the existence of an intracellular amplifier circuit regulating ISG expression and controlling long-term cellular responsiveness to IFN-I and IFN-II. The exact timely steps that take place during IFN-activated feedback regulation and the control of ISG transcription and long-term cellular responsiveness to IFN-I and IFN-II is currently not clear. Based on existing literature and our novel data, we predict the existence of a multifaceted intracellular amplifier circuit that depends on unphosphorylated and phosphorylated ISGF3 and GAF complexes and IRF1. In a combinatorial and timely fashion, these complexes mediate prolonged ISG expression and control cellular responsiveness to IFN-I and IFN-II. This proposed intracellular amplifier circuit also provides a molecular explanation for the existing overlap between IFN-I and IFN-II activated ISG expression.
Indexed as
Identifiers
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.