Evidence map›Paper›PMID 34471099›Full record

ArticleSignal transduction and targeted therapy2021

A dual-role of SARS-CoV-2 nucleocapsid protein in regulating innate immune response.

Yinghua Zhao, Liyan Sui, Ping Wu, Wenfang Wang, Zedong Wang, Yang Yu, Zhijun Hou, Guangyun Tan, Quan Liu, Guoqing Wang

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

75 citing papers in PubMed, 113 citations in OpenAlex.

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  18. Anti-interferon armamentarium of human coronaviruses.Cellular and molecular life sciences : CMLS · 2025
    Review
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  20. Article

15 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

10 authors at 3 institutions in 1 country.

Yinghua ZhaoCenter for Pathogen Biology and Infectious Diseases, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, The First Hospital of Jilin University, State Key Laboratory of Human-Animal Zoonotic infectious Diseases, Changchun, China.
Liyan SuiCenter for Pathogen Biology and Infectious Diseases, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, The First Hospital of Jilin University, State Key Laboratory of Human-Animal Zoonotic infectious Diseases, Changchun, China.
Ping WuCollege of Wildlife and Protected Area, Northeast Forestry University, Harbin, China.
Wenfang WangDepartment of Pathogenbiology, The Key Laboratory of Zoonosis, Chinese Ministry of Education, College of Basic Medicine, Jilin University, Changchun, China.
Zedong WangCenter for Pathogen Biology and Infectious Diseases, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, The First Hospital of Jilin University, State Key Laboratory of Human-Animal Zoonotic infectious Diseases, Changchun, China.
Yang YuHospital of Stomatology, Jilin University, Changchun, China.
Zhijun HouCollege of Wildlife and Protected Area, Northeast Forestry University, Harbin, China.
Guangyun TanCenter for Pathogen Biology and Infectious Diseases, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, The First Hospital of Jilin University, State Key Laboratory of Human-Animal Zoonotic infectious Diseases, Changchun, China. tgy0425@jlu.edu.cn.
Quan LiuCenter for Pathogen Biology and Infectious Diseases, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, The First Hospital of Jilin University, State Key Laboratory of Human-Animal Zoonotic infectious Diseases, Changchun, China. liuquan1973@hotmail.com.ORCID 0000-0003-3411-3196
Guoqing WangDepartment of Pathogenbiology, The Key Laboratory of Zoonosis, Chinese Ministry of Education, College of Basic Medicine, Jilin University, Changchun, China. qing@jlu.edu.cn.ORCID 0000-0001-9326-3755
Jilin University · CNNortheast Forestry University · CNFoshan University · CN

Funding

Department of Science and Technology of Jilin Province (Jilin Province Science and Technology Department) 172408GH010234983Department of Science and Technology of Jilin Province (Jilin Province Science and Technology Department) 20200301001RQNational Natural Science Foundation of China (National Science Foundation of China) 81871699National Natural Science Foundation of China (National Science Foundation of China) 81972873National Natural Science Foundation of China (National Science Foundation of China) 82072330
6 · The paper itself

Abstract

The recently emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is the causative agent of ongoing global pandemic of COVID-19, may trigger immunosuppression in the early stage and overactive immune response in the late stage of infection; However, the underlying mechanisms are not well understood. Here we demonstrated that the SARS-CoV-2 nucleocapsid (N) protein dually regulated innate immune responses, i.e., the low-dose N protein suppressed type I interferon (IFN-I) signaling and inflammatory cytokines, whereas high-dose N protein promoted IFN-I signaling and inflammatory cytokines. Mechanistically, the SARS-CoV-2 N protein dually regulated the phosphorylation and nuclear translocation of IRF3, STAT1, and STAT2. Additionally, low-dose N protein combined with TRIM25 could suppress the ubiquitination and activation of retinoic acid-inducible gene I (RIG-I). Our findings revealed a regulatory mechanism of innate immune responses by the SARS-CoV-2 N protein, which would contribute to understanding the pathogenesis of SARS-CoV-2 and other SARS-like coronaviruses, and development of more effective strategies for controlling COVID-19.

Indexed as

Immunity, InnateA549 CellsCaco-2 CellsCoronavirus Nucleocapsid ProteinsCOVID-19HEK293 CellsHep G2 CellsHumansInterferon Type IPhosphoproteinsSARS-CoV-2Signal TransductionCoronavirus Nucleocapsid ProteinsInterferon Type Inucleocapsid phosphoprotein, SARS-CoV-2Phosphoproteins

Identifiers

PMID34471099
PMCPMC8409078
OpenAlexW3196427335

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.