Evidence map›Paper›PMID 30626683›Full record

ArticleJournal of virology2019

USP15 Participates in Hepatitis C Virus Propagation through Regulation of Viral RNA Translation and Lipid Droplet Formation.

Shinji Kusakabe, Tatsuya Suzuki, Yukari Sugiyama, Saori Haga, Kanako Horike, Makoto Tokunaga, Junki Hirano, He Zhang, David Virya Chen, Hanako Ishiga and 16 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

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  14. Sar1 Affects the Localization of Perilipin 2 to Lipid Droplets.International journal of molecular sciences · 2022
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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

26 authors at 5 institutions in 1 country.

Shinji KusakabeDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Tatsuya SuzukiDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Yukari SugiyamaDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Saori HagaDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Kanako HorikeDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Makoto TokunagaDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Junki HiranoDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
He ZhangDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
David Virya ChenDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Hanako IshigaDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Yasumasa KomodaDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Chikako OnoDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Takasuke FukuharaDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Masahiro YamamotoDepartment of Immunoparasitology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Masahito IkawaDepartment of Experimental Genome Research, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Takashi SatohDepartment of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Shizuo AkiraDepartment of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Tomohisa TanakaDepartment of Microbiology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan.
Kohji MoriishiDepartment of Microbiology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan.ORCID 0000-0002-9542-5188
Moto FukaiDepartment of Gastroenterological Surgery I, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Akinobu TaketomiDepartment of Gastroenterological Surgery I, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Sachiyo YoshioResearch Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Ichikawa, Japan.
Tatsuya KantoResearch Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Ichikawa, Japan.
Tetsuro SuzukiDepartment of Virology and Parasitology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Toru OkamotoDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan toru@biken.osaka-u.ac.jp matsuura@biken.osaka-u.ac.jp.
Yoshiharu MatsuuraDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan toru@biken.osaka-u.ac.jp matsuura@biken.osaka-u.ac.jp.
The University of Osaka · JPHamamatsu University School of Medicine · JPHokkaido University · JPNational Center for Global Health and Medicine · JPUniversity of Yamanashi · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) utilizes cellular factors for efficient propagation. Ubiquitin is covalently conjugated to the substrate to alter its stability or to modulate signal transduction. In this study, we examined the importance of ubiquitination for HCV propagation. We found that inhibition of deubiquitinating enzymes (DUBs) or overexpression of nonspecific DUBs impaired HCV replication, suggesting that ubiquitination regulates HCV replication. To identify specific DUBs involved in HCV propagation, we set up RNA interference (RNAi) screening against DUBs and successfully identified ubiquitin-specific protease 15 (USP15) as a novel host factor for HCV propagation. Our studies showed that USP15 is involved in translation of HCV RNA and production of infectious HCV particles. In addition, deficiency of USP15 in human hepatic cell lines (Huh7 and Hep3B/miR-122 cells) but not in a nonhepatic cell line (293T cells) impaired HCV propagation, suggesting that USP15 participates in HCV propagation through the regulation of hepatocyte-specific functions. Moreover, we showed that loss of USP15 had no effect on innate immune responses

Indexed as

AnimalsCell LineCell Line, TumorChlorocebus aethiopsGene Expression RegulationHEK293 CellsHepacivirusHepatitis CHepatocytesHumansLipid DropletsLipid MetabolismLiverRNA InterferenceRNA, ViralSignal TransductionRNA, ViralUbiquitin-Specific ProteasesUSP15 protein, humandeubiquitinationHCVinnate immunitylipidtranslation

Identifiers

PMID30626683
PMCPMC6401473
OpenAlexW2919024775

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.