Evidence map›Paper›PMID 24470589›Full record

ArticleBlood2014

ATF3 is a novel regulator of mouse neutrophil migration.

Nicholas D Boespflug, Sachin Kumar, Jaclyn W McAlees, James D Phelan, H Leighton Grimes, Kasper Hoebe, Tsonwin Hai, Marie-Dominique Filippi, Christopher L Karp

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Nicholas D BoespflugDivision of Cellular and Molecular Immunology, and.
Sachin Kumar
Jaclyn W McAlees
James D Phelan
H Leighton Grimes
Kasper Hoebe
Tsonwin Hai
Marie-Dominique Filippi
Christopher L Karp
Cincinnati Children's Hospital Medical Center · USThe Ohio State University · US

Funding

Cincinnati Center for Clinical and Translational Sciences and TrainingUL1TR000077 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., TSEVAT, JOEL · 2012 to 2014
$9.9M
ROLE OF ANGPTL4, AN ANGIOGENIC MEDIATOR, IN ARTHRITISP30AR047363 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI WAGNER, MICHAEL · 2001 to 2015
$9.2M
Medical Scientist Training ProgramT32GM063483 · NIGMS · UNIVERSITY OF CINCINNATI · PI KHURANA HERSHEY, GURJIT K. · 2002 to 2022
$6.7M
Training Program in Cancer TherapeuticsT32CA117846 · NCI · UNIVERSITY OF CINCINNATI · PI PRICE, CAROLYN M, TAKIAR, VINITA · 2006 to 2022
$6.5M
Regulation of Neutrophil Migration and PolarityR01HL090676 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI FILIPPI, MARIE-DOMINIQUE · 2010 to 2014
$1.9M
Immunobiology of IFRD1, a gene modifying CF lung diseaseR01HL094576 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI HOEBE, KASPER · 2009 to 2012
$1.5M
NCATS NIH HHS UL1 TR000077NCI NIH HHS T32 CA117846NHLBI NIH HHS R01 HL090676NHLBI NIH HHS R01 HL094576NIAMS NIH HHS P30 AR047363NIGMS NIH HHS T-32 GM063483NIGMS NIH HHS T32 GM063483
6 · The paper itself

Abstract

Expression of the activating transcription factor 3 (ATF3) gene is induced by Toll-like receptor (TLR) signaling. In turn, ATF3 protein inhibits the expression of various TLR-driven proinflammatory genes. Given its counter-regulatory role in diverse innate immune responses, we defined the effects of ATF3 on neutrophilic airway inflammation in mice. ATF3 deletion was associated with increased lipopolysaccharide (LPS)-driven airway epithelia production of CXCL1, but not CXCL2, findings concordant with a consensus ATF3-binding site identified solely in the Cxcl1 promoter. Unexpectedly, ATF3-deficient mice did not exhibit increased airway neutrophilia after LPS challenge. Bone marrow chimeras revealed a specific reduction in ATF3(-/-) neutrophil recruitment to wild-type lungs. In vitro, ATF3(-/-) neutrophils exhibited a profound chemotaxis defect. Global gene expression analysis identified ablated Tiam2 expression in ATF3(-/-) neutrophils. TIAM2 regulates cellular motility by activating Rac1-mediated focal adhesion disassembly. Notably, ATF3(-/-) and ATF3-sufficient TIAM2 knockdown neutrophils, both lacking TIAM2, exhibited increased focal complex area, along with excessive CD11b-mediated F-actin polymerization. Together, our data describe a dichotomous role for ATF3-mediated regulation of neutrophilic responses: inhibition of neutrophil chemokine production but promotion of neutrophil chemotaxis.

Indexed as

Activating Transcription Factor 3AnimalsCells, CulturedChemokine CXCL1Immune System DiseasesLeukocyte DisordersLipopolysaccharidesLungMiceMice, Inbred C57BLMice, KnockoutNeutrophil InfiltrationRespiratory MucosaActivating Transcription Factor 3Atf3 protein, mouseChemokine CXCL1Lipopolysaccharides

Identifiers

PMID24470589
PMCPMC3968391
OpenAlexW2064573089

What OpenQuestion holds

Textmetadata
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.