ArticleThe EMBO journal1993
Complementation of a mutant cell line: central role of the 91 kDa polypeptide of ISGF3 in the interferon-alpha and -gamma signal transduction pathways.
Article in The EMBO journal, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers.
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Who cites it
166 citing papers in PubMed, 415 citations in OpenAlex.
- 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 expression patterns of Interleukin-26, Interleukin-35, and signal transducer and activator of transcription 1 in Type1 diabetes patients with diabetic nephropathy.Molecular biology reports · 2026Article
- IFNγ shapes macrophage inflammatory responses by STAT1 isoform-specific epigenetic and transcriptional mechanisms.BMC genomics · 2026Article
- Glycolytic flux sustains human Th1 identity and effector function via STAT1 glycosylation.Life science alliance · 2026Article
- Hepatitis C virus-associated B-cell non-Hodgkin lymphomas: immune evasion, multistep lymphomagenesis, and candidate biomarkers for risk stratification and disease monitoring.Frontiers in immunology · 2026Review
- Characterization of a pathogenic gain-of-function mutation in the N-terminal domain of STAT1 which is reported to be associated with eosinophilic esophagitis.Cell communication and signaling : CCS · 2025Article
- Review
- Decidual macrophage subsets and polarization puzzle during the human early pregnancy.Frontiers in immunology · 2025Review
- Regulation of versican expression in macrophages is mediated by canonical type I interferon signaling via ISGF3.American journal of physiology. Cell physiology · 2024Article
- Regulation of Versican Expression in Macrophages is Mediated by Canonical Type I Interferon Signaling via ISGF3.bioRxiv : the preprint server for biology · 2024Article
- Suppression of Innate Immunity by the Hepatitis C Virus (HCV): Revisiting the Specificity of Host-Virus Interactive Pathways.International journal of molecular sciences · 2023Review
- Alternative Splicing of RIOK3 Engages the Noncanonical NFκB Pathway during Rift Valley Fever Virus Infection.Viruses · 2023Article
- Article
- Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor.BMC molecular and cell biology · 2022Article
- An inhibitory effect on the nuclear accumulation of phospho-STAT1 by its unphosphorylated form.Cell communication and signaling : CCS · 2022Article
- The Role of IFITM Proteins in Tick-Borne Encephalitis Virus Infection.Journal of virology · 2022Article
- Decorin promotes decidual M1-like macrophage polarization via mitochondrial dysfunction resulting in recurrent pregnancy loss.Theranostics · 2022Article
- Mechanisms of Viral Degradation of Cellular Signal Transducer and Activator of Transcription 2.International journal of molecular sciences · 2022Review
- The JAK/STAT signaling pathway: from bench to clinic.Signal transduction and targeted therapy · 2021Review
- Genetic Lesions of Type I Interferon Signalling in Human Antiviral Immunity.Trends in genetics : TIG · 2021Review
106 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutants in complementation group U3, completely defective in the response of all genes tested to interferons (IFNs) alpha and gamma, do not express the 91 and 84 kDa polypeptide components of interferon-stimulated gene factor 3 (ISGF3), a transcription factor known to play a primary role in the IFN-alpha response pathway. The 91 and 84 kDa polypeptides are products of a single gene. They result from differential splicing and differ only in a 38 amino acid extension at the C-terminus of the 91 kDa polypeptide. Complementation of U3 mutants with cDNA constructs expressing the 91 kDa product at levels comparable to those observed in induced wild-type cells completely restored the response to both IFN-alpha and -gamma and the ability to form ISGF3. Complementation with the 84 kDa component similarly restored the ability to form ISGF3 and, albeit to a lower level, the IFN-alpha response of all genes tested so far. It failed, however, to restore the IFN-gamma response of any gene analysed. The precise nature of the DNA motifs and combination of factors required for the transcriptional response of all genes inducible by IFN-alpha and -gamma remains to be established. The results presented here, however, emphasize the apparent general requirement of the 91 kDa polypeptide in the primary transcriptional response to both types of IFN.
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