Evidence map›Paper›PMID 24251647›Full record

ArticleAmerican journal of respiratory and critical care medicine2014

Regulation of IL-4 receptor signaling by STUB1 in lung inflammation.

Qin Wei, Youbao Sha, Abhisek Bhattacharya, Elmoataz Abdel Fattah, Diana Bonilla, Soma S S K Jyothula, Lavannya Pandit, Gurjit K Khurana Hershey, N Tony Eissa

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In one paragraph

Article in American journal of respiratory and critical care medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

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  16. Spinocerebellar ataxia type 48: last but not least.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020
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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.

Qin Wei1 Department of Medicine, Baylor College of Medicine, Houston, Texas; and.
Youbao Sha
Abhisek Bhattacharya
Elmoataz Abdel Fattah
Diana Bonilla
Soma S S K Jyothula
Lavannya Pandit
Gurjit K Khurana Hershey
N Tony Eissa
Baylor College of Medicine · USCincinnati Children's Hospital Medical Center · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
Virology CoreP30AI036211 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BUTEL, JANET S · 1994 to 2015
$21.7M
TRAINING PROGRAM FOR CLINICAL RESEARCH ON AIDST32AI007456 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI SHEARER, WILLIAM THOMAS · 1992 to 2012
$2.8M
BD Biosciences Special Order LSRIIS10RR024574 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI LUMPKIN, ELLEN A · 2009 to 2009
$430k
NCI NIH HHS P30 CA125123NCI NIH HHS P30CA125123NCRR NIH HHS S10 RR024574NCRR NIH HHS S10RR024574NIAID NIH HHS P30 AI036211NIAID NIH HHS P30AI036211NIAID NIH HHS T32-5T32AI007456NIAID NIH HHS T32 AI007456
6 · The paper itself

Abstract

rationaleIL-4Rα, the common receptor component for IL-4 and IL-13, plays a critical role in IL-4- and IL-13-mediated signaling pathways that regulate airway inflammation and remodeling. However, the regulatory mechanisms underlying IL-4Rα turnover and its signal termination remain elusive.

objectivesTo evaluate the role of STUB1 (STIP1 homology and U-Box containing protein 1) in regulating IL-4R signaling in airway inflammation.

methodsThe roles of STUB1 in IL-4Rα degradation and its signaling were investigated by immunoblot, immunoprecipitation, and flow cytometry. The involvement of STUB1 in airway inflammation was determined in vivo by measuring lung inflammatory cells infiltration, mucus production, serum lgE levels, and alveolar macrophage M2 activation in STUB1(-/-) mice. STUB1 expression was evaluated in airway epithelium of patients with asthma and lung tissues of subjects with chronic obstructive pulmonary disease. MEASUREMENTS AND MAIN

resultsSTUB1 interacted with IL-4Rα and targeted it for ubiquitination-mediated proteasomal degradation, terminating IL-4 or IL-13 signaling. STUB1 knockout cells showed increased levels of IL-4Rα and sustained STAT6 activation, whereas STUB1 overexpression reduced IL-4Rα levels. Mice deficient in STUB1 had spontaneous airway inflammation, alternative M2 activation of alveolar macrophage, and increased serum IgE. STUB1 levels were increased in airways of subjects with asthma or chronic obstructive pulmonary disease, suggesting that up-regulation of STUB1 might be an important feedback mechanism to dampen IL-4R signaling in airway inflammation.

conclusionsOur study identified a previously uncharacterized role for STUB1 in regulating IL-4R signaling, which might provide a new strategy for attenuating airway inflammation.

Indexed as

AdultAnimalsAsthmaChildDown-RegulationFemaleFlow CytometryHumansImmunoblottingImmunoprecipitationInterleukin-4 Receptor alpha SubunitMacrophage ActivationMaleMiceMice, KnockoutPneumoniaIl4ra protein, mouseInterleukin-4 Receptor alpha SubunitProteasome Endopeptidase ComplexReceptors, Cell SurfaceReceptors, Interleukin-4Stat6 protein, mouseSTAT6 Transcription FactorStub1 protein, mouseUbiquitinUbiquitin-Protein Ligases

Identifiers

PMID24251647
PMCPMC3919125
OpenAlexW2115110969

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.