Evidence map›Paper›PMID 26927796›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

POU2AF1 Functions in the Human Airway Epithelium To Regulate Expression of Host Defense Genes.

Haixia Zhou, Angelika Brekman, Wu-Lin Zuo, Xuemei Ou, Renat Shaykhiev, Francisco J Agosto-Perez, Rui Wang, Matthew S Walters, Jacqueline Salit, Yael Strulovici-Barel and 5 more

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
–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

35 citing papers in PubMed.

  1. Article
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  4. Genes Co-Expressed withInternational journal of molecular sciences · 2024
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  9. A comparative study ofbioRxiv : the preprint server for biology · 2023
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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

15 authors.

Haixia ZhouDepartment of Respiratory Medicine, West China Hospital, Sichuan University, Sichuan 610041, China; Department of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065;
Angelika BrekmanDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065;
Wu-Lin ZuoDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065;
Xuemei OuDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065;
Renat ShaykhievDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065;
Francisco J Agosto-PerezDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065;
Rui WangDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065;
Matthew S WaltersDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065;
Jacqueline SalitDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065;
Yael Strulovici-BarelDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065;
Michelle R StaudtDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065;
Robert J KanerDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065; Division of Pulmonary and Critical Care Medicine, Department of Medicine, Weill Cornell Medical College, New York, NY 10065; and.
Jason G MezeyDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065; Department of Biological Statistics and Computational Biology, Cornell University, Ithaca, New York, NY 14853.
Ronald G CrystalDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065; Division of Pulmonary and Critical Care Medicine, Department of Medicine, Weill Cornell Medical College, New York, NY 10065; and geneticmedicine@med.cornell.edu.
Guoqing WangDepartment of Genetic Medicine, Weill Cornell Medical College, New York, NY 10065;

Funding

Clinical and Translational Science CenterUL1TR000457 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IMPERATO-MCGINLEY, JULIANNE L · 2012 to 2016
$46.0M
Overlapping Airway Basal Cell Transcriptome Reprogramming in COPD and Lung CancerR01HL107882 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CRYSTAL, RONALD G · 2011 to 2014
$5.8M
COPD Metabolome, Smoking Oxidants and Aberrant Ciliated Cell FunctionP20HL113443 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CRYSTAL, RONALD G · 2012 to 2016
$5.3M
Pulmonary Genetic Medicine Training ProgramT32HL094284 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CRYSTAL, RONALD G · 2009 to 2019
$3.0M
NCATS NIH HHS UL1 TR000457NCRR NIH HHS UL1 RR0204143NHLBI NIH HHS P20 HL113443NHLBI NIH HHS R01 HL107882NHLBI NIH HHS T32 HL094284
6 · The paper itself

Abstract

In the process of seeking novel lung host defense regulators by analyzing genome-wide RNA sequence data from normal human airway epithelium, we detected expression of POU domain class 2-associating factor 1 (POU2AF1), a known transcription cofactor previously thought to be expressed only in lymphocytes. Lymphocyte contamination of human airway epithelial samples obtained by bronchoscopy and brushing was excluded by immunohistochemistry staining, the observation of upregulation of POU2AF1 in purified airway basal stem/progenitor cells undergoing differentiation, and analysis of differentiating single basal cell clones. Lentivirus-mediated upregulation of POU2AF1 in airway basal cells induced upregulation of host defense genes, including MX1, IFIT3, IFITM, and known POU2AF1 downstream genes HLA-DRA, ID2, ID3, IL6, and BCL6. Interestingly, expression of these genes paralleled changes of POU2AF1 expression during airway epithelium differentiation in vitro, suggesting POU2AF1 helps to maintain a host defense tone even in pathogen-free condition. Cigarette smoke, a known risk factor for airway infection, suppressed POU2AF1 expression both in vivo in humans and in vitro in human airway epithelial cultures, accompanied by deregulation of POU2AF1 downstream genes. Finally, enhancing POU2AF1 expression in human airway epithelium attenuated the suppression of host defense genes by smoking. Together, these findings suggest a novel function of POU2AF1 as a potential regulator of host defense genes in the human airway epithelium.

Indexed as

Gene Expression RegulationCell DifferentiationCluster AnalysisEpithelial CellsGene Expression ProfilingHumansImmunityRespiratory MucosaSmokingTrans-ActivatorsPOU2AF1 protein, humanTrans-Activators

Identifiers

PMID26927796
PMCPMC4799774

What OpenQuestion holds

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Registered trials

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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.