Evidence map›Paper›PMID 7678054›Full record

ArticleMolecular and cellular biology1993

Interferon consensus sequence-binding protein, a member of the interferon regulatory factor family, suppresses interferon-induced gene transcription.

N Nelson, M S Marks, P H Driggers, K Ozato

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Transcriptional control of interferon-stimulated genes.The Journal of biological chemistry · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Review
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  10. Article
  11. Article
  12. Article
  13. Article
  14. Relevance of Interferon Regulatory Factor-8 Expression in Myeloid-Tumor Interactions.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2016
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

N NelsonLaboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, Bethesda, Maryland 20892.
M S Marks
P H Driggers
K Ozato

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Transcription FactorsBase SequenceBinding SitesCarrier ProteinsCells, CulturedDNA-Binding ProteinsEnhancer Elements, GeneticGene ExpressionGene Expression RegulationGenes, MHC Class IHumansInterferon-betaInterferon Regulatory Factor-1Interferon Regulatory Factor-2Interferon Regulatory Factor-8Interferon Regulatory FactorsCarrier ProteinsDNA-Binding ProteinsInterferon-betaInterferon Regulatory Factor-1Interferon Regulatory Factor-2Interferon Regulatory Factor-8Interferon Regulatory FactorsInterferonsIRF1 protein, humanIRF2 protein, humanOligodeoxyribonucleotidesPhosphoproteinsRepressor ProteinsRNA, MessengerTranscription Factors

Identifiers

PMID7678054
PMCPMC358938
OpenAlexW1857506864

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.