Evidence map›Paper›PMID 29559679›Full record

ArticleNature communications2018

ZFR coordinates crosstalk between RNA decay and transcription in innate immunity.

Nazmul Haque, Ryota Ouda, Chao Chen, Keiko Ozato, J Robert Hogg

Abstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

28 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Unveiling the prevalence and impact of silent rhinovirus infection in chronic rhinosinusitis with nasal polyps.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

5 authors.

Nazmul HaqueBiochemistry and Biophysics Center, National Heart, Lung, and Blood Institute, National Institutes of Health, 50 South Drive, Room 2341, Bethesda, MD, 20892, USA. nazmul.haque@nih.gov.
Ryota OudaDivision of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, 6 Center Drive, Room 2A01, Bethesda, MD, 20892, USA.
Chao ChenDivision of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, 6 Center Drive, Room 2A01, Bethesda, MD, 20892, USA.
Keiko OzatoDivision of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health, 6 Center Drive, Room 2A01, Bethesda, MD, 20892, USA.
J Robert HoggBiochemistry and Biophysics Center, National Heart, Lung, and Blood Institute, National Institutes of Health, 50 South Drive, Room 2341, Bethesda, MD, 20892, USA. j.hogg@nih.gov.ORCID http://orcid.org/0000-0001-5729-5135

Funding

Gene Regulation In The Immune SystemZIAHD001310 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI OZATO, KEIKO · 2009 to 2025
$15.0M
mRNP assembly in response to translational repressionZIAHL006169 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI HOGG, J ROBERT · 2013 to 2025
$5.4M
6 · The paper itself

Abstract

Control of type I interferon production is crucial to combat infection while preventing deleterious inflammatory responses, but the extent of the contribution of post-transcriptional mechanisms to innate immune regulation is unclear. Here, we show that human zinc finger RNA-binding protein (ZFR) represses the interferon response by regulating alternative pre-mRNA splicing. ZFR expression is tightly controlled during macrophage development; monocytes express truncated ZFR isoforms, while macrophages induce full-length ZFR to modulate macrophage-specific alternative splicing. Interferon-stimulated genes are constitutively activated by ZFR depletion, and immunostimulation results in hyper-induction of interferon β (IFNβ/IFNB1). Through whole-genome analyses, we show that ZFR controls interferon signaling by preventing aberrant splicing and nonsense-mediated decay of histone variant macroH2A1/H2AFY mRNAs. Together, our data suggest that regulation of ZFR in macrophage differentiation guards against aberrant interferon responses and reveal a network of mRNA processing and decay that shapes the transcriptional response to infection.

Indexed as

Immunity, InnateAlternative SplicingCell DifferentiationCell LineHistonesHumansInterferon-betaMacrophagesNonsense Mediated mRNA DecayRNA-Binding ProteinsRNA InterferenceRNA, MessengerRNA StabilityHistonesInterferon-betaRNA-Binding ProteinsRNA, MessengerZFR protein, human

Identifiers

PMID29559679
PMCPMC5861047

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.