Cited by 192interferon and immune responsesCytokine Signaling Pathways and InteractionsImmune Response and Inflammation

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Interferon Consensus sequence-Binding Protein, a Member of the Interferon Regulatory Factor Family, Suppresses Interferon-Induced Gene Transcription

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Nelson, Nancy, Marks, Michael S., Driggers, Paul H., Ozato, Keiko·1993·Molecular and Cellular Biology

DOI 10.1128/mcb.13.1.588-599.1993PMC PMC358938

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Abstract

We previously isolated a cDNA clone encoding interferon consensus sequence-binding protein (ICSBP), a member of the interferon regulatory factor (IRF) family, that binds to the interferon (IFN)-stimulated response element (ISRE) of many IFN-regulated genes. In this investigation, we studied the functional role of ICSBP by transient cotransfection of ICSBP cDNA with IFN-responsive reporter genes into the human embryonal carcinoma cell line N-Tera2. These cells were shown not to express ICSBP or IRF-2, thus allowing functional analysis of transfected cDNAs. Cotransfection of ICSBP into cells treated with retinoic acid or any of the IFNs (alpha, beta, or gamma) repressed expression of a chloramphenicol acetyltransferase reporter driven by the major histocompatibility complex class I gene promoter. Similarly, ICSBP repressed expression of chloramphenicol acetyltransferase reporters driven by the ISREs of the 2'-5' oligoadenylate synthetase, guanylate-binding protein, and ISG-15 genes in IFN-treated cells. The repression was dependent on the presence of the ISRE in the reporter. Deletion analysis showed that the putative N-terminal DNA binding domain of ICSBP by itself is capable of mediating the repression. Using the same cotransfection conditions as for ICSBP, a similar repression of these reporters was observed with IRF-2. Finally, ICSBP repressed the IRF-1-mediated induction of major histocompatibility complex class I and IFN-beta reporters in the absence of IFN or retinoic acid. Taken together, these results suggest that ICSBP is a negative regulatory factor capable of repressing transcription of target genes induced by IFN, retinoic acid, or IRF-1.

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Authors: Nelson, N., Marks, M. S., Driggers, P. H., & Ozato, K.
Affiliations: National Institutes of Health (US)
ORCID: Marks, Michael S.
Ozato, Keiko
Venue: Molecular and Cellular Biology
Publisher: Informa UK Limited
Published: 1993-01
Volume: 13
Issue: 1
Pages: 588-599
ISSN: 0270-7306 (ISSN-L)
1098-5549
DOI: 10.1128/mcb.13.1.588-599.1993
PMC: PMC358938
OpenAlex: W1857506864
Cited by: 192
References: 83
Citations by year: 2025: 2 · 2024: 4 · 2023: 1 · 2022: 5 · 2021: 2 · 2020: 2 · 2018: 2 · 2017: 2 · 2016: 3 · 2015: 1 · 2014: 2 · 2013: 4 · 2012: 2
FWCI: 6.94
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: journals.asm.org/non-commercial-tdm-license (tdm)
Locations: Molecular and Cellular Biology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords: IRF2, IRF1, interferon-stimulated response element, transcriptional repression, interferon-beta, retinoic acid, MHC class I, 2',5'-oligoadenylate synthetase, guanylate-binding proteins, DNA-binding domain, embryonal carcinoma cells
MeSH terms: Interferon Regulatory Factor-8, Base Sequence, Binding Sites, Carrier Proteins, Cells, Cultured, DNA-Binding Proteins, Enhancer Elements, Genetic, Gene Expression Regulation, Genes, MHC Class I, Humans, Interferons, Oligodeoxyribonucleotides, Phosphoproteins, Repressor Proteins, RNA, Messenger, Transcription Factors, Transcription, Genetic, Gene Expression, Polymerase Chain Reaction, Interferon-beta, Interferon Regulatory Factors, Interferon Regulatory Factor-2, Interferon Regulatory Factor-1, In Vitro Techniques

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Interferon Consensus sequence-Binding Protein, a Member of the Interferon Regulatory Factor Family, Suppresses Interferon-Induced Gene Transcription

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