Evidence map›Paper›PMID 19380580›Full record

ArticleThe Journal of biological chemistry2009

Severe acute respiratory syndrome coronavirus M protein inhibits type I interferon production by impeding the formation of TRAF3.TANK.TBK1/IKKepsilon complex.

Kam-Leung Siu, Kin-Hang Kok, Ming-Him James Ng, Vincent K M Poon, Kwok-Yung Yuen, Bo-Jian Zheng, Dong-Yan Jin

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers.

0numbers the graph read from it
0cells of the map it votes in
203citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

203 citing papers in PubMed, 274 citations in OpenAlex.

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  7. Anti-interferon armamentarium of human coronaviruses.Cellular and molecular life sciences : CMLS · 2025
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143 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Kam-Leung SiuFrom the Departments of Biochemistry, 21 Sassoon Road, Pokfulam, Hong Kong.
Kin-Hang KokFrom the Departments of Biochemistry, 21 Sassoon Road, Pokfulam, Hong Kong.
Ming-Him James NgFrom the Departments of Biochemistry, 21 Sassoon Road, Pokfulam, Hong Kong.
Vincent K M PoonMicrobiology, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong.
Kwok-Yung YuenMicrobiology, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong.
Bo-Jian ZhengMicrobiology, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong.
Dong-Yan JinFrom the Departments of Biochemistry, 21 Sassoon Road, Pokfulam, Hong Kong. Electronic address: dyjin@hkucc.hku.hk.
University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome (SARS) coronavirus is highly pathogenic in humans and evades innate immunity at multiple levels. It has evolved various strategies to counteract the production and action of type I interferons, which mobilize the front-line defense against viral infection. In this study we demonstrate that SARS coronavirus M protein inhibits gene transcription of type I interferons. M protein potently antagonizes the activation of interferon-stimulated response element-dependent transcription by double-stranded RNA, RIG-I, MDA5, TBK1, IKKepsilon, and virus-induced signaling adaptor (VISA) but has no influence on the transcriptional activity of this element when IRF3 or IRF7 is overexpressed. M protein physically associates with RIG-I, TBK1, IKKepsilon, and TRAF3 and likely sequesters some of them in membrane-associated cytoplasmic compartments. Consequently, the expression of M protein prevents the formation of TRAF3.TANK.TBK1/IKKepsilon complex and thereby inhibits TBK1/IKKepsilon-dependent activation of IRF3/IRF7 transcription factors. Taken together, our findings reveal a new mechanism by which SARS coronavirus circumvents the production of type I interferons.

Indexed as

Adaptor Proteins, Signal TransducingCoronavirus M ProteinsGene Expression RegulationHeLa CellsHumansI-kappa B KinaseInterferon Regulatory Factor-3Interferon Type IKidneyPhosphorylationProtein Serine-Threonine KinasesSevere Acute Respiratory SyndromeSevere acute respiratory syndrome-related coronavirusSignal TransductionTNF Receptor-Associated Factor 3Viral Matrix ProteinsAdaptor Proteins, Signal TransducingCoronavirus M ProteinsI-kappa B KinaseInterferon Regulatory Factor-3Interferon Type IIRF3 protein, humanM protein, SARS-CoVProtein Serine-Threonine KinasesTANK protein, humanTBK1 protein, humanTNF Receptor-Associated Factor 3TRAF3 protein, humanViral Matrix Proteins

Identifiers

PMID19380580
PMCPMC2713514
OpenAlexW1560860164

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.