Tyrosine phosphorylated p91 binds to a single element in the ISGF2/IRF‐1 promoter to mediate induction by IFN alpha and IFN gamma, and is likely to autoregulate the p91 gene.
Open accessAbstract
ISGF2 was initially identified, purified and cloned as an interferon-alpha (IFN alpha) induced transcription factor that binds to the IFN-stimulated response element (ISRE) of IFN alpha/beta-stimulated genes (ISGs). It was reported to be transcriptionally regulated by several cytokines including IFN alpha and IFN gamma. IFN alpha and IFN gamma inducibility is mediated by a single element: a high affinity, nearly palindromic version of the IFN gamma activation site (GAS). The ISGF2 GAS is bound specifically by p91, which was previously identified as a subunit of the ISG activator ISGF3, and shown to mediate IFN gamma induction of the GBP gene via a GAS. Tyrosine phosphorylation and DNA binding activity of p91 parallel transcription of ISGF2 in response to IFN alpha and/or IFN gamma, consistent with induction mediated by only a GAS. Transcription of the genes that encode p91 and p113, another subunit of ISGF3, is activated only by IFN alpha. This result suggests induction mediated by an ISRE, and implies autoregulation, requiring the products of both genes. Specificity of the ISRE is the basis for the previous conclusion. In contrast, it appears likely that the ISGF2 GAS, and p91 or related factors, also mediate induction of ISGF2 by IL-6 and prolactin. Convergence of signalling pathways from at least four cytokines on this single site would thus be a key aspect of a general role for ISGF2 in cellular growth control.
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Interferon regulatory factor-1 is a likely candidate for sustaining Socs1 mRNA expression because it is induced by STAT1 and can associate with the Socs1 promoter to activate transcription of Socs1 mRNA.
“One likely candidate is interferon regulatory factor-1, because it is induced by STAT1 (32,42,43) and can associate with the Socs1 promoter to activate the transcription of Socs1 mRNA (18).”
From The Comparative Roles of Suppressor of Cytokine Signaling-1 and -3 in the Inhibition and Desensitization of Cytokine Signaling (2006) · cites this paper as [43]
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- Authors
- Pine, R., Canova, A., & Schindler, C.
- Venue
- The EMBO Journal
- Published
- 1994-01-01
- Volume
- 13
- Issue
- 1
- Pages
- 158-167
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC394789
- OpenAlex
- W1510347472
- Cited by
- 347
- References
- 1
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2022: 3 · 2021: 1 · 2020: 2 · 2019: 4 · 2018: 5 · 2016: 3 · 2015: 1 · 2014: 4 · 2013: 8 · 2012: 13
- FWCI
- 13.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The EMBO Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- James S. McDonnell Foundation (6-49556)
- Amgen
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- IRF1, tyrosine phosphorylation, interferon-stimulated response element, ISGF3, interferon-alpha, interferon-gamma, transcriptional regulation, autoregulation, cytokine signaling, interleukin-6, prolactin, interferon-stimulated genes, gene induction
- MeSH terms
- Base Sequence, DNA, DNA-Binding Proteins, Gene Expression Regulation, HeLa Cells, Humans, Interferon-gamma, Molecular Sequence Data, Phosphoproteins, Phosphorylation, Promoter Regions, Genetic, Protein Binding, Transcription Factors, Transcription, Genetic, Tyrosine, Blotting, Northern, Interferon-alpha, Alternative Splicing, Interferon Regulatory Factor-1
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