Evidence map›Paper›PMID 28380049›Full record

ArticlePLoS pathogens2017

miR-144 attenuates the host response to influenza virus by targeting the TRAF6-IRF7 signaling axis.

Carrie M Rosenberger, Rebecca L Podyminogin, Alan H Diercks, Piper M Treuting, Jacques J Peschon, David Rodriguez, Madhumati Gundapuneni, Mitchell J Weiss, Alan Aderem

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

61 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. The Role ofChronic obstructive pulmonary diseases (Miami, Fla.) · 2025
    Article
  6. Article
  7. Article
  8. The Role of miR-144 in Inflammatory Diseases: A Review.Immunity, inflammation and disease · 2025
    Review
  9. miR-144/451: A Regulatory Role in Inflammation.Current molecular medicine · 2025
    Review
  10. Review
  11. Review
  12. Article
  13. Roles of p53-Mediated Host-Virus Interaction in Coronavirus Infection.International journal of molecular sciences · 2023
    Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

1 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

9 authors at 5 institutions in 1 country.

Carrie M RosenbergerCenter for Infectious Disease Research, Seattle, WA United States of America.
Rebecca L PodyminoginCenter for Infectious Disease Research, Seattle, WA United States of America.
Alan H DiercksCenter for Infectious Disease Research, Seattle, WA United States of America.
Piper M TreutingDepartment of Comparative Medicine, School of Medicine, University of Washington, Seattle, WA, United States of America.
Jacques J PeschonCenter for Infectious Disease Research, Seattle, WA United States of America.
David RodriguezCenter for Infectious Disease Research, Seattle, WA United States of America.
Madhumati GundapuneniInstitute for Systems Biology, Seattle, WA, United States of America.
Mitchell J WeissHematology, St. Jude Children's Research Hospital, Memphis, TN United States of America.
Alan AderemCenter for Infectious Disease Research, Seattle, WA United States of America.
Center for Infectious Disease Research · USInfectious Disease Research Institute · USInstitute for Systems Biology · USSt. Jude Children's Research Hospital · USUniversity of Washington · US

Funding

Systems Biology CoreU19AI100627 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI ULEVITCH, RICHARD J · 2012 to 2021
$49.1M
LPS Signaling in Macrophages: The Roll of TollR01AI032972 · NIAID · UNIVERSITY OF WASHINGTON · PI ADEREM, ALAN A · 1992 to 2020
$14.6M
LPS REGULATION OF MACROPHAGE FUNCTIONR01AI025032 · NIAID · SEATTLE BIOMEDICAL RESEARCH INSTITUTE · PI ADEREM, ALAN A · 1987 to 2016
$6.7M
Regulation of erythropoiesis by the miR-144/451 microRNA locusR01DK092318 · NIDDK · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI WEISS, MITCHELL J · 2012 to 2016
$1.8M
NIAID NIH HHS R01 AI025032NIAID NIH HHS R01 AI032972NIAID NIH HHS U19 AI100627NIDDK NIH HHS R01 DK092318
6 · The paper itself

Abstract

Antiviral responses must rapidly defend against infection while minimizing inflammatory damage, but the mechanisms that regulate the magnitude of response within an infected cell are not well understood. miRNAs are small non-coding RNAs that suppress protein levels by binding target sequences on their cognate mRNA. Here, we identify miR-144 as a negative regulator of the host antiviral response. Ectopic expression of miR-144 resulted in increased replication of three RNA viruses in primary mouse lung epithelial cells: influenza virus, EMCV, and VSV. We identified the transcriptional network regulated by miR-144 and demonstrate that miR-144 post-transcriptionally suppresses TRAF6 levels. In vivo ablation of miR-144 reduced influenza virus replication in the lung and disease severity. These data suggest that miR-144 reduces the antiviral response by attenuating the TRAF6-IRF7 pathway to alter the cellular antiviral transcriptional landscape.

Indexed as

Signal TransductionAnimalsCell LineEpithelial CellsGene Expression ProfilingGenes, ReporterHumansInfluenza, HumanLungMiceMice, Inbred C57BLMicroRNAsOrthomyxoviridaeRNA, MessengerRNA Processing, Post-TranscriptionalTNF Receptor-Associated Factor 6MicroRNAsMIRN144 microRNA, mouseRNA, MessengerTNF Receptor-Associated Factor 6Traf7 protein, mouseTumor Necrosis Factor Receptor-Associated Peptides and Proteins

Identifiers

PMID28380049
PMCPMC5393898
OpenAlexW2604434684

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.