Human interferon consensus sequence binding protein is a negative regulator of enhancer elements common to interferon-inducible genes.

Weisz, A; Marx, P; Sharf, R; Appella, E; Driggers, P.H.; Ozato, K; Levi, B.Z.

doi:10.1016/s0021-9258(19)74081-2

Cited by 152interferon and immune responsesGenomics and Chromatin DynamicsCytokine Signaling Pathways and Interactions

Human interferon consensus sequence binding protein is a negative regulator of enhancer elements common to interferon-inducible genes.

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Weisz, A, Marx, P, Sharf, R, Appella, E, Driggers, P.H., Ozato, K, Levi, B.Z.·1992·Journal of Biological Chemistry

DOI 10.1016/s0021-9258(19)74081-2

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Abstract

The promoter regions of many interferon-inducible genes share a short DNA sequence motif, termed the interferon consensus sequence (ICS) to which several regulatory proteins bind. A murine cDNA which encodes an ICS binding protein has been reported (M-ICSBP). The cloning of the human homologue of ICSBP (H-ICSBP) is described. H-ICSBP shares high sequence homology with its murine cognate. The derived sequence of H-ICSBP reveals restricted homology within the first 120 amino acids to three other interferon regulatory factors, IRF-1, IRF-2, and ISGF3 gamma. Truncated ICSBP lacking the first 33 amino-terminal amino acids fails to bind to the ICS, indicating that at least part of the DNA binding domain is located within the well conserved amino terminus. H-ICSBP is expressed exclusively in cell lines of hematopoietic origin. The results of transient transfection assays carried out either in hematopoietic or nonhematopoietic cells suggest that ICSBP acts as a negative regulatory factor on ICS-containing promoters. Furthermore, either interferon-gamma (IFN-gamma) or IFN-beta can alleviate the repression mediated by ICSBP. Therefore, ICSBP may be involved in maintaining submaximal transcriptional activity of IFN-inducible genes in hematopoietic cells. IFN treatment would then alleviate repression allowing maximal transcriptional activity of these genes.

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Previous reporter analysis indicated that ICSBP is a repressor of ISRE-dependent transcription.
“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 [57]
Transfection of ICSBP alone reduced ISRE reporter activity by ∼40% irrespective of IFNγ treatment.
“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 [57]
ICSBP/IRF-8 is an IFN-γ-inducible transcription factor of the IRF family that regulates transcription through multiple target DNA elements, including ISRE, EICE, and GAS.
“Interferon (IFN) consensus sequence binding protein (ICSBP)/IFN regulatory factor (IRF)-8 is an IFN g -inducible transcription factor of the IRF family and regulates transcription through multiple target DNA elements, such as IFN-stimulated response element (ISRE), Ets/IRF composite element, and IFNg activation site (GAS).”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [6]
ICSBP is expressed in hematopoietic cells, including monocyte/macrophage lineage, B lymphocytes, and activated T lymphocytes, and is inducible by IFN-γ in these cells.
“ICSBP is expressed in the hematopoietic cells, including cells of the monocyte/macrophage lineage, B lymphocytes, and activated T lymphocytes, and is inducible by IFNg in these cells, suggesting its role in immune cells. (6,9-13)”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [6]
ICSBP is a transcriptional repressor acting through the IFN-stimulated response element (ISRE).
“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 [6]

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Authors: Weisz, A., Marx, P., Sharf, R., Appella, E., Driggers, P. H., Ozato, K., & Levi, B. Z.
Affiliations: Technion – Israel Institute of Technology (IL)
ORCID: Weisz, A
Appella, E
Ozato, K
Levi, B.Z.
Venue: Journal of Biological Chemistry
Publisher: Elsevier BV
Published: 1992-12
Volume: 267
Issue: 35
Pages: 25589-25596
ISSN: 0021-9258 (ISSN-L)
DOI: 10.1016/s0021-9258(19)74081-2
OpenAlex: W1528284784
Cited by: 152
References: 39
Citations by year: 2026: 1 · 2025: 3 · 2024: 2 · 2023: 1 · 2022: 5 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 2 · 2016: 2 · 2014: 3 · 2013: 4 · 2012: 2
FWCI: 2.86
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by/4.0/ (vor, 10174 d)
Locations: Journal of Biological Chemistry (publishedVersion, cc-by)
PubMed (publishedVersion)
Topics: Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
Keywords: IRF8, interferon-stimulated genes, enhancer repression, negative transcriptional regulation, interferon regulatory factors, IRF1, IRF2, DNA-binding domain, hematopoietic cells, interferon-gamma, interferon-beta, transcriptional regulation
MeSH terms: Interferon Regulatory Factor-8, Amino Acid Sequence, Base Sequence, beta-Galactosidase, Carrier Proteins, Cell Line, Cycloheximide, DNA, DNA-Binding Proteins, Enhancer Elements, Genetic, HeLa Cells, Humans, Interferon-gamma, Lung, Molecular Sequence Data, Plasmids, Promoter Regions, Genetic, Recombinant Proteins, Repressor Proteins, RNA, Messenger, Transfection, Tumor Cells, Cultured, Blotting, Northern, Chloramphenicol O-Acetyltransferase, Gene Library, Gene Expression Regulation, Neoplastic, Interferon-beta, Sequence Homology, Amino Acid, Interferon Regulatory Factors

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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Human interferon consensus sequence binding protein is a negative regulator of enhancer elements common to interferon-inducible genes.

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