Evidence map›Paper›PMID 26860204›Full record

ArticleScientific reports2016

Ankyrin Repeat Domain 1 is Up-regulated During Hepatitis C Virus Infection and Regulates Hepatitis C Virus Entry.

Thoa T Than, Giao V Q Tran, Kidong Son, Eun-Mee Park, Seungtaek Kim, Yun-Sook Lim, Soon B Hwang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

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  9. The ORMDL3 Asthma Gene Regulates ICAM1 and Has Multiple Effects on Cellular Inflammation.American journal of respiratory and critical care medicine · 2019
    Article
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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

7 authors at 2 institutions in 1 country.

Thoa T ThanNational Research Laboratory of Hepatitis C Virus, Ilsong Institute of Life Science, Hallym University, Anyang, South Korea.
Giao V Q TranNational Research Laboratory of Hepatitis C Virus, Ilsong Institute of Life Science, Hallym University, Anyang, South Korea.
Kidong SonNational Research Laboratory of Hepatitis C Virus, Ilsong Institute of Life Science, Hallym University, Anyang, South Korea.
Eun-Mee ParkNational Research Laboratory of Hepatitis C Virus, Ilsong Institute of Life Science, Hallym University, Anyang, South Korea.
Seungtaek KimInstitute of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea.
Yun-Sook LimNational Research Laboratory of Hepatitis C Virus, Ilsong Institute of Life Science, Hallym University, Anyang, South Korea.
Soon B HwangNational Research Laboratory of Hepatitis C Virus, Ilsong Institute of Life Science, Hallym University, Anyang, South Korea.
Hallym University · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) is highly dependent on host proteins for its own propagation. By transcriptome sequencing (RNA-Seq) analysis, we identified 30 host genes that were significantly differentially expressed in cell culture-grown HCV (HCVcc)-infected cells. Of these candidate genes, we selected and characterized ankyrin repeat domain 1 (ANKRD1). Here, we showed that protein expression of ANKRD1 was up-regulated in HCVcc-infected cells. We further showed that protein expression level of ANKRD1 was increased by nonstructural 5A (NS5A) protein. ANKRD1 specifically interacted with NS5A both in vitro and coimmunoprecipitation assays. Protein interaction was mediated through the domain II of NS5A and the C-terminal region of ANKRD1. Promoter activity of ANKRD1 was also increased by NS5A protein. Moreover, up-regulation of ANKRD1 expression was mediated through alteration in intracellular calcium homeostasis and ER stress in HCVcc-infected cells. We showed that silencing of ANKRD1 impaired HCV propagation without affecting HCV replication. By using HCV-like infectious particle (HCV-LP), we demonstrated that HCV single-cycle infection was drastically impaired in ANKRD1 knockdown cells. Finally, we verified that ANKRD1 was required for HCV entry. These data suggest that HCV coopts ANKRD1 for its own propagation and up-regulation of ANKRD1 may contribute to HCV-mediated liver pathogenesis.

Indexed as

Host-Pathogen InteractionsVirus InternalizationCell LineGene Expression ProfilingHepacivirusHepatitis CHepatocytesHumansMuscle ProteinsNuclear ProteinsProtein Interaction MappingRepressor ProteinsRNA-Dependent RNA PolymeraseUp-RegulationViral Nonstructural ProteinsANKRD1 protein, humanMuscle ProteinsNS-5 protein, hepatitis C virusNuclear ProteinsRepressor ProteinsRNA-Dependent RNA PolymeraseViral Nonstructural Proteins

Identifiers

PMID26860204
PMCPMC4748412
OpenAlexW2266688119

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.