ReviewThe Journal of biological chemistry2017
The molecular basis for differential type I interferon signaling.
Review 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 135 papers.
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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
135 citing papers in PubMed, 243 citations in OpenAlex.
- Article
- Flavonoid-modulated JAK-STAT signaling mitigates malignant transformation and drug resistance in breast tumors: A clinically relevant 3PM-guided innovation.Journal of advanced research · 2026Review
- 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
- Single-cell analysis of signalling and transcriptional responses to type I interferons.EMBO reports · 2026Article
- CDK6 inactivation counteracts CALR-mutant-induced MPN evolution and sensitizes MPN stem cells to interferon-α treatment.HemaSphere · 2026Article
- Subverting Host Defense from Within: Innate Immune Modulation byPathogens (Basel, Switzerland) · 2026Review
- Interferon-β Modulates Early Viral Replication Kinetics and Innate Responses to Non-Fatal Alphavirus Encephalomyelitis.Pathogens (Basel, Switzerland) · 2026Article
- Type I interferons in tuberculosis pathogenesis and prevention.Trends in microbiology · 2026Review
- Type I-interferon β induces a strong anti-tumour response in bladder cancer cells.Journal of cancer research and clinical oncology · 2026Article
- SAVI: molecular mechanisms, clinical spectrum and precision medicine approaches beyond type-I IFN.Frontiers in immunology · 2026Review
- Unraveling the Biology of Interferon-Stimulated Genes: Mechanisms, Functions, and Clinical Implications.Infection and drug resistance · 2026Review
- MERS-CoV and SARS-CoV-1 proteins inhibit the IFN-α JAK/STAT pathway of epithelial cells, via IFN-λ-induced USP18.Frontiers in immunology · 2026Article
- The mitochondrial logic of inflammaging: how energy imbalance drives fibroblast SASP and tissue-specific aging.Frontiers in immunology · 2026Review
- Differential host responses by the type I and III interferons in primary differentiated human nasal epithelial cells are a determinant of antiviral activity.Frontiers in pharmacology · 2026Article
- Interferon-induced immune signatures are associated with suppression of HEV infection in porcine cell culture models.Emerging microbes & infections · 2025Article
- The Concise Guide to PHARMACOLOGY 2025/26: Catalytic receptors.British journal of pharmacology · 2025Review
- Geometric Tuning of Cytokine Receptor Association Modulates Synthetic Agonist Signaling.bioRxiv : the preprint server for biology · 2025Article
- Type I IFNs enhance human dorsal root ganglion nociceptor excitability and induce TRPV1 sensitization.JCI insight · 2025Article
- MAPL regulates gasdermin-mediated release of mtDNA from lysosomes to drive pyroptotic cell death.Nature cell biology · 2025Article
- Tumor cells upregulate CCL22 in a STING-dependent manner in response to paracrine factors released by STING-activated myeloid cells and type I interferons.ImmunoHorizons · 2025Article
75 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I interferons (IFN-1) are cytokines that affect the expression of thousands of genes, resulting in profound cellular changes. IFN-1 activates the cell by dimerizing its two-receptor chains, IFNAR1 and IFNAR2, which are expressed on all nucleated cells. Despite a similar mode of binding, the different IFN-1s activate a spectrum of activities. The causes for differential activation may stem from differences in IFN-1-binding affinity, duration of binding, number of surface receptors, induction of feedbacks, and cell type-specific variations. All together these will alter the signal that is transmitted from the extracellular domain inward. The intracellular domain binds, directly or indirectly, different effector proteins that transmit signals. The composition of effector molecules deviates between different cell types and tissues, inserting an additional level of complexity to the system. Moreover, IFN-1s do not act on their own, and clearly there is much cross-talk between the activated effector molecules by IFN-1 and other cytokines. The outcome generated by all of these factors (processing step) is an observed phenotype, which can be the transformation of the cell to an antiviral state, differentiation of the cell to a specific immune cell, senescence, apoptosis, and many more. IFN-1 activities can be divided into robust and tunable. Antiviral activity, which is stimulated by minute amounts of IFN-1 and is common to all cells, is termed robust. The other activities, which we term tunable, are cell type-specific and often require more stringent modes of activation. In this review, I summarize the current knowledge on the mode of activation and processing that is initiated by IFN-1, in perspective of the resulting phenotypes.
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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.