Evidence map›Paper›PMID 23832230›Full record

ArticleNucleic acids research2013

Deciphering the modulation of gene expression by type I and II interferons combining 4sU-tagging, translational arrest and in silico promoter analysis.

Mirko Trilling, Nicolás Bellora, Andrzej J Rutkowski, Miranda de Graaf, Paul Dickinson, Kevin Robertson, Olivia Prazeres da Costa, Peter Ghazal, Caroline C Friedel, M Mar Albà and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  5. Transcriptional control of interferon-stimulated genes.The Journal of biological chemistry · 2024
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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

11 authors at 5 institutions in 3 countries.

Mirko TrillingInstitute for Virology, University Hospital in Essen, University of Duisburg-Essen, Essen, D-45147, Germany, Computational Genomics Group, IMIM-UPF Research Programme on Biomedical Informatics, Barcelona Biomedical Research Park (PRBB), Barcelona 08003, Spain, Department of Medicine, University of Cambridge, Box 157, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK, Division of Pathway Medicine, University of Edinburgh Medical School, Edinburgh, EH16 4SB, Scotland, UK, SynthSys, University of Edinburgh, Edinburgh, EH9 3JU Scotland, UK, Institute of Medical Microbiology, Technical University Munich, Munich 81675, Germany, Institute for Informatics, Ludwig-Maximilians-University Munich, Munich 80333, Germany and Catalan Institution for Research and Advanced Studies (ICREA), Barcelona 08010, Spain.
Nicolás Bellora
Andrzej J Rutkowski
Miranda de Graaf
Paul Dickinson
Kevin Robertson
Olivia Prazeres da Costa
Peter Ghazal
Caroline C Friedel
M Mar Albà
Lars Dölken
Addenbrooke's Hospital · GBBarcelona Biomedical Research Park · ESUniversity of Edinburgh · GBLudwig-Maximilians-Universität München · DEUniversity of Duisburg-Essen · DE

Funding

Biotechnology and Biological Sciences Research Council BB/D019621/1Medical Research Council G1002523
6 · The paper itself

Abstract

Interferons (IFN) play a pivotal role in innate immunity, orchestrating a cell-intrinsic anti-pathogenic state and stimulating adaptive immune responses. The complex interplay between the primary response to IFNs and its modulation by positive and negative feedback loops is incompletely understood. Here, we implement the combination of high-resolution gene-expression profiling of nascent RNA with translational inhibition of secondary feedback by cycloheximide. Unexpectedly, this approach revealed a prominent role of negative feedback mechanisms during the immediate (≤60 min) IFNα response. In contrast, a more complex picture involving both negative and positive feedback loops was observed on IFNγ treatment. IFNγ-induced repression of genes associated with regulation of gene expression, cellular development, apoptosis and cell growth resulted from cycloheximide-resistant primary IFNγ signalling. In silico promoter analysis revealed significant overrepresentation of SP1/SP3-binding sites and/or GC-rich stretches. Although signal transducer and activator of transcription 1 (STAT1)-binding sites were not overrepresented, repression was lost in absence of STAT1. Interestingly, basal expression of the majority of these IFNγ-repressed genes was dependent on STAT1 in IFN-naïve fibroblasts. Finally, IFNγ-mediated repression was also found to be evident in primary murine macrophages. IFN-repressed genes include negative regulators of innate and stress response, and their decrease may thus aid the establishment of a signalling perceptive milieu.

Indexed as

Gene Expression RegulationPromoter Regions, GeneticTranscription, GeneticAnimalsCells, CulturedComputer SimulationCycloheximideFeedback, PhysiologicalGene Expression ProfilingInterferon-alphaInterferon-gammaMacrophagesMiceNIH 3T3 CellsProtein Synthesis InhibitorsResponse ElementsCycloheximideInterferon-alphaInterferon-gammaProtein Synthesis InhibitorsSTAT1 Transcription FactorThiouridine

Identifiers

PMID23832230
PMCPMC3783172
OpenAlexW2152427978

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.