Evidence map›Paper›PMID 25911105›Full record

ArticleThe Journal of biological chemistry2015

Aryl Hydrocarbon Receptor Interacting Protein Targets IRF7 to Suppress Antiviral Signaling and the Induction of Type I Interferon.

Qinjie Zhou, Alfonso Lavorgna, Melissa Bowman, John Hiscott, Edward W Harhaj

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

28 citing papers in PubMed, 40 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Qinjie ZhouFrom the Department of Microbiology and Immunology, The University of Miami, Miller School of Medicine, Miami, Florida 33136.
Alfonso Lavorgnathe Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, Maryland 21287.
Melissa Bowmanthe Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, Maryland 21287, the Graduate Program in Cellular and Molecular Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, and.
John Hiscottthe Division of Infectious Diseases, Vaccine & Gene Therapy Institute of Florida, Port Saint Lucie, Florida 34987.
Edward W Harhajthe Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, Maryland 21287, eharhaj1@jhmi.edu.
Johns Hopkins University · USUniversity of Miami · USVaccine & Gene Therapy Institute of Florida · US

Funding

Training Program in Cellular and Molecular MedicineT32GM008752 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI RAO, RAJINI · 2000 to 2019
$11.7M
Tissue/Pathology CoreP01CA128115 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI GUETTOUCHE, TOUMY · 2009 to 2013
$5.6M
Mechanisms of HTLV-I Tax-mediated NF-kB activationR01CA135362 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARHAJ, EDWARD W · 2009 to 2018
$2.7M
NCI NIH HHS P01 CA128115NCI NIH HHS P01CA128115NCI NIH HHS R01 CA135362NCI NIH HHS R01CA135362NIGMS NIH HHS T32 GM008752
6 · The paper itself

Abstract

The transcription factor IRF7 (interferon regulatory factor 7) is a key regulator of type I interferon and plays essential roles in restricting virus infection and spread. IRF7 activation is tightly regulated to prevent excessive inflammation and autoimmunity; however, how IRF7 is suppressed by negative regulators remains poorly understood. Here, we have identified AIP (aryl hydrocarbon receptor interacting protein) as a new binding partner of IRF7. The interaction between AIP and IRF7 is enhanced upon virus infection, and AIP potently inhibits IRF7-induced type I IFN (IFNα/β) production. Overexpression of AIP blocks virus-induced activation of IFN, whereas knockdown of AIP by siRNA potentiates virally activated IFN production. Consistently, AIP-deficient murine embryonic fibroblasts are highly resistant to virus infection because of increased production of IFNα/β. AIP inhibits IRF7 function by antagonizing the nuclear localization of IRF7. Together, our study identifies AIP as a novel inhibitor of IRF7 and a negative regulator of innate antiviral signaling.

Indexed as

AnimalsCell LineHumansInterferon-alphaInterferon-betaInterferon Regulatory Factor-7Intracellular Signaling Peptides and ProteinsMiceRNA InterferenceRNA, Small InterferingUp-RegulationVirus Diseasesaryl hydrocarbon receptor-interacting proteinInterferon-alphaInterferon-betaInterferon Regulatory Factor-7Intracellular Signaling Peptides and ProteinsIRF7 protein, humanRNA, Small InterferingAIPantiviral signalingIRF7type I interferon

Identifiers

PMID25911105
PMCPMC4505538
OpenAlexW2027539039

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.