Evidence map›Paper›PMID 23994473›Full record

ArticleCell reports2013

Extensive cooperation of immune master regulators IRF3 and NFκB in RNA Pol II recruitment and pause release in human innate antiviral transcription.

Jonathan E Freaney, Rebecca Kim, Roli Mandhana, Curt M Horvath

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

58 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. IRF3 inhibits nuclear translocation of NF-κB to prevent viral inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Epigenetic and transcriptional control of interferon-β.The Journal of experimental medicine · 2021
    Article
  18. Review
  19. Article
  20. Article
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 at 1 institution in 1 country.

Jonathan E FreaneyDepartment of Molecular Biosciences, Northwestern University, Evanston, IL 60208, USA.
Rebecca Kim
Roli Mandhana
Curt M Horvath
Northwestern University · US

Funding

New Paradigms in Gene Regulation During Influenza Virus InfectionsU01AI082984 · NIAID · NORTHWESTERN UNIVERSITY · PI HORVATH, CURT M · 2009 to 2013
$3.6M
Helicase Regulation of dsRNA Signaling and Innate Antiviral Immune ResponsesR01AI073919 · NIAID · NORTHWESTERN UNIVERSITY · PI HORVATH, CURT M · 2008 to 2012
$1.8M
Analysis of Novel Virus-Induced RNAsR01GM111652 · NIGMS · NORTHWESTERN UNIVERSITY · PI HORVATH, CURT M · 2015 to 2018
$1.2M
NIAID NIH HHS R01 AI073919NIAID NIH HHS U01 AI082984NIAID NIH HHS U01AI082984NIGMS NIH HHS R01 GM111652PHS HHS R01A1073919
6 · The paper itself

Abstract

Transcription factors interferon regulatory factor 3 (IRF3) and nuclear factor κB (NFκB) are activated by external stimuli, including virus infection, to translocate to the nucleus and bind genomic targets important for immunity and inflammation. To investigate RNA polymerase II (Pol II) recruitment and elongation in the human antiviral gene regulatory network, a comprehensive genome-wide analysis was conducted during the initial phase of virus infection. Results reveal extensive integration of IRF3 and NFκB with Pol II and associated machinery and implicate partners for antiviral transcription. Analysis indicates that both de novo polymerase recruitment and stimulated release of paused polymerase work together to control virus-induced gene activation. In addition to known messenger-RNA-encoding loci, IRF3 and NFκB stimulate transcription at regions not previously associated with antiviral transcription, including abundant unannotated loci that encode novel virus-inducible RNAs (nviRNAs). These nviRNAs are widely induced by virus infections in diverse cell types and represent a previously overlooked cellular response to virus infection.

Indexed as

Transcription, GeneticGene ExpressionGenome-Wide Association StudyHeLa CellsHumansInterferon Regulatory Factor-3NF-kappa BRespirovirus InfectionsRNA Polymerase IISendai virusTranscription Factor RelAInterferon Regulatory Factor-3IRF3 protein, humanNF-kappa BRNA Polymerase IITranscription Factor RelA

Identifiers

PMID23994473
PMCPMC3792498
OpenAlexW1996934443

What OpenQuestion holds

Textmetadata
LicenceTDM
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.