Evidence map›Paper›PMID 27183919›Full record

ArticleOncotarget2016

HCV core protein binds to gC1qR to induce A20 expression and inhibit cytokine production through MAPKs and NF-κB signaling pathways.

Xiaotian Song, Zhiyan Yao, Jianling Yang, Zhengzheng Zhang, Yuqing Deng, Miao Li, Cuiqing Ma, Lijuan Yang, Xue Gao, Wenjian Li and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

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  8. SLE: Novel Postulates for Therapeutic Options.Frontiers in immunology · 2020
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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

12 authors at 2 institutions in 2 countries.

Xiaotian SongDepartment of Immunology, Hebei Medical University, Shijiazhuang, China.
Zhiyan YaoDepartment of Immunology, Hebei Medical University, Shijiazhuang, China.
Jianling YangDepartment of Immunology, Hebei Medical University, Shijiazhuang, China.
Zhengzheng ZhangDepartment of Immunology, Hebei Medical University, Shijiazhuang, China.
Yuqing DengDepartment of Immunology, Hebei Medical University, Shijiazhuang, China.
Miao LiDepartment of Immunology, Hebei Medical University, Shijiazhuang, China.
Cuiqing MaDepartment of Immunology, Hebei Medical University, Shijiazhuang, China.
Lijuan YangDepartment of Immunology, Hebei Medical University, Shijiazhuang, China.
Xue GaoDepartment of Immunology, Hebei Medical University, Shijiazhuang, China.
Wenjian LiDepartment of Immunology, Hebei Medical University, Shijiazhuang, China.
Jianguo LiuDivision of Infectious Diseases, Allergy and Immunology, Departments of Internal Medicine and Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Lin WeiDepartment of Immunology, Hebei Medical University, Shijiazhuang, China.
Hebei Medical University · CNSaint Louis University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) infection is characterized by a strong propensity toward chronicity. During chronic HCV infection, HCV core protein is implicated in deregulating cytokine expression that associates with chronic inflammation. A20 is known as a powerful suppressor in cytokine signaling, in this study, we explored the A20 expression in macrophages induced by HCV core protein and the involved signaling pathways. Results demonstrated that HCV core protein induced A20 expression in macrophages. Silencing A20 significantly enhanced the secretion of IL-6, IL-1β and TGF-β1, but not IL-8 and TNF. Additionally, HCV core protein interacted with gC1qR, but not TLR2, TLR3 and TLR4 in pull-down assay. Silencing gC1qR abrogated core-induced A20 expression. Furthermore, HCV core protein activated MAPK, NF-κB and PI3K/AKT pathways in macrophages. Inhibition of P38, JNK and NF-κB but not ERK and AKT activities greatly reduced the A20 expression. In conclusion, the study suggests that HCV core protein ligates gC1qR to induce A20 expression in macrophages via P38, JNK and NF-κB signaling pathways, which leads to a low-grade chronic inflammation during HCV infection. It represents a novel mechanism by which HCV usurps the host for persistence.

Indexed as

AnimalsCarrier ProteinsCell Line, TumorCytokinesHepacivirusHepatitis C, ChronicHost-Pathogen InteractionsHumansMacrophagesMiceMitochondrial ProteinsMitogen-Activated Protein KinasesNF-kappa BPhosphatidylinositol 3-KinasePhosphorylationProtein BindingC1QBP protein, humanC1qbp protein, mouseCarrier ProteinsCytokinesMitochondrial ProteinsMitogen-Activated Protein KinasesNF-kappa BPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktTNFAIP3 protein, humanTnfaip3 protein, mouseTumor Necrosis Factor alpha-Induced Protein 3Viral Core Proteinscore proteingC1qRhepatitis C virusImmune responseImmunityImmunology and Microbiology Sectionmacrophagenegative regulator A20

Identifiers

PMID27183919
PMCPMC5085119
OpenAlexW2385669458

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.