The DOI matches its Crossref record; 81 of the 83 references it cites were found in a registry or an index.
Interferon Consensus sequence-Binding Protein, a Member of the Interferon Regulatory Factor Family, Suppresses Interferon-Induced Gene Transcription
Open accessAbstract
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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In the citing paper
“ICSBP/IRF8 is expressed exclusively in myeloid and B-cells (10)”
In the citing paper
“Likewise, previous reporter analysis indicated that ICSBP is a repressor of ISRE-dependent transcription (36, 57).”
From Gamma Interferon Triggers Interaction between ICSBP (IRF-8) and TEL, Recruiting the Histone Deacetylase HDAC3 to the Interferon-Responsive Element (2002) · cites this paper as [36]
In the citing paper
“transfection of ICSBP alone reduced ISRE reporter activity by ∼ 40% irrespective of IFN𝛄 treatment, consistent with the previous finding that ICSBP represses ISRE-dependent transcription (36, 57).”
From Gamma Interferon Triggers Interaction between ICSBP (IRF-8) and TEL, Recruiting the Histone Deacetylase HDAC3 to the Interferon-Responsive Element (2002) · cites this paper as [36]
In the citing paper
“Subsequent studies have shown that ICSBP is a transcriptional repressor acting through the IFN-stimulated response element (ISRE). (6,20,21)”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [20]
Citations
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- Weisz A. P. Marx R. Sharf E. Appella P. H. Driggers K. Ozato and B. Levi. The cloning and characterization of the human homologue of ICSBP that binds enhancer element common to interferon inducible genes. J. Biol. Chem. in press.
Cited by
Sorted by citations
HOW CELLS RESPOND TO INTERFERONS
Stark, G. R., Kerr, I. M., Williams, B. R. G., Silverman, R. H., & Schreiber, R. D. (1998) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.67.1.227 · Cited by 3,932
CELLULAR RESPONSES TO INTERFERON-γ
Boehm, U., Klamp, T., Groot, M., & Howard, J. C. (1997) · Annual Review of Immunology · doi:10.1146/annurev.immunol.15.1.749 · Cited by 2,890
IRF Family of Transcription Factors as Regulators of Host Defense
Taniguchi, T., Ogasawara, K., Takaoka, A., & Tanaka, N. (2001) · Annual Review of Immunology · doi:10.1146/annurev.immunol.19.1.623 · Cited by 1,658
Interferons: cell signalling, immune modulation, antiviral response and virus countermeasures
Goodbourn, S., Didcock, L., & Randall, R. E. (2000) · Journal of General Virology · doi:10.1099/0022-1317-81-10-2341 · Cited by 977
“, 1989) and the IFN-consensus sequence-binding protein (ICSBP, also called IRF-8 ; Nelson et al., 1993), are known to bind ISREs and negatively regulate expression, and may help to prevent expression in the absence of IFN or down-regulate the induced response.”
BackgroundMethodHoltschke, T., Löhler, J., Kanno, Y., Fehr, T., Giese, N., Rosenbauer, F., Lou, J., Knobeloch, K.-P., Gabriele, L., Waring, J. F., et al. (1996) · Cell · doi:10.1016/s0092-8674(00)81348-3 · Cited by 644
Self-citation
Metadata
- Authors
- Nelson, N., Marks, M. S., Driggers, P. H., & Ozato, K.
- Affiliations
- National Institutes of Health (US)
- 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
- 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
- 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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