Evidence map›Paper›PMID 25414701›Full record

ArticleFrontiers in immunology2014

Type I Interferon Regulates the Expression of Long Non-Coding RNAs.

Elena Carnero, Marina Barriocanal, Victor Segura, Elizabeth Guruceaga, Celia Prior, Kathleen Börner, Dirk Grimm, Puri Fortes

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

48 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
  2. Non-coding RNA · 2025
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  20. Roles of lncRNAs in influenza virus infection.Emerging microbes & infections · 2020
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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

8 authors at 2 institutions in 2 countries.

Elena CarneroDepartment of Gene therapy and Hepatology, Center for Applied Medical Research (CIMA), University of Navarra , Pamplona , Spain.
Marina BarriocanalDepartment of Gene therapy and Hepatology, Center for Applied Medical Research (CIMA), University of Navarra , Pamplona , Spain.
Victor SeguraBioinformatics Unit, Center for Applied Medical Research (CIMA), University of Navarra , Pamplona , Spain.
Elizabeth GuruceagaBioinformatics Unit, Center for Applied Medical Research (CIMA), University of Navarra , Pamplona , Spain.
Celia PriorDepartment of Gene therapy and Hepatology, Center for Applied Medical Research (CIMA), University of Navarra , Pamplona , Spain.
Kathleen BörnerCentre for Infectious Diseases/Virology, Heidelberg University Hospital, Cluster of Excellence CellNetworks , Heidelberg , Germany ; German Center for Infection Research (DZIF) , Heidelberg , Germany.
Dirk GrimmCentre for Infectious Diseases/Virology, Heidelberg University Hospital, Cluster of Excellence CellNetworks , Heidelberg , Germany.
Puri FortesDepartment of Gene therapy and Hepatology, Center for Applied Medical Research (CIMA), University of Navarra , Pamplona , Spain.
Universidad de Navarra · ESHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferons (IFNs) are key players in the antiviral response. IFN sensing by the cell activates transcription of IFN-stimulated genes (ISGs) able to induce an antiviral state by affecting viral replication and release. IFN also induces the expression of ISGs that function as negative regulators to limit the strength and duration of IFN response. The ISGs identified so far belong to coding genes. However, only a small proportion of the transcriptome corresponds to coding transcripts and it has been estimated that there could be as many coding as long non-coding RNAs (lncRNAs). To address whether IFN can also regulate the expression of lncRNAs, we analyzed the transcriptome of HuH7 cells treated or not with IFNα2 by expression arrays. Analysis of the arrays showed increased levels of several well-characterized coding genes that respond to IFN both at early or late times. Furthermore, we identified several IFN-stimulated or -downregulated lncRNAs (ISRs and IDRs). Further validation showed that ISR2, 8, and 12 expression mimics that of their neighboring genes GBP1, IRF1, and IL6, respectively, all related to the IFN response. These genes are induced in response to different doses of IFNα2 in different cell lines at early (ISR2 or 8) or later (ISR12) time points. IFNβ also induced the expression of these lncRNAs. ISR2 and 8 were also induced by an influenza virus unable to block the IFN response but not by other wild-type lytic viruses tested. Surprisingly, both ISR2 and 8 were significantly upregulated in cultured cells and livers from patients infected with HCV. Increased levels of ISR2 were also detected in patients chronically infected with HIV. This is relevant as genome-wide guilt-by-association studies predict that ISR2, 8, and 12 may function in viral processes, in the IFN pathway and the antiviral response. Therefore, we propose that these lncRNAs could be induced by IFN to function as positive or negative regulators of the antiviral response.

Indexed as

GBP1HCVHIVIFNIRF1lncRNAsviral infection

Identifiers

PMID25414701
PMCPMC4222131
OpenAlexW1992808569

What OpenQuestion holds

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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.