Evidence map›Paper›PMID 26868272›Full record

ArticleNature communications2016

Interferon-inducible protein SCOTIN interferes with HCV replication through the autolysosomal degradation of NS5A.

Nari Kim, Min-Jung Kim, Pil Soo Sung, Yong Chul Bae, Eui-Cheol Shin, Joo-Yeon Yoo

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Regulation of Innate Immune Signaling by Autophagy.International journal of molecular sciences · 2026
    Review
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  20. Viruses and autophagy: bend, but don't break.Nature reviews. Microbiology · 2024
    Review

5 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

6 authors at 3 institutions in 1 country.

Nari KimDivision of Molecular and Life Sciences, Department of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Min-Jung KimDivision of Molecular and Life Sciences, Department of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Pil Soo SungLaboratory of Immunology and Infectious Diseases, Graduate School of Medical Science and Engineering, KAIST, Daejeon 305-701, Republic of Korea.
Yong Chul BaeDepartment of Anatomy and Neurobiology, School of Dentistry, Kyungpook National University, Daegu 41940, Republic of Korea.
Eui-Cheol ShinLaboratory of Immunology and Infectious Diseases, Graduate School of Medical Science and Engineering, KAIST, Daejeon 305-701, Republic of Korea.
Joo-Yeon YooDivision of Molecular and Life Sciences, Department of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.
Pohang University of Science and Technology · KRKorea Advanced Institute of Science and Technology · KRKyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) utilizes autophagy to promote its propagation. Here we show the autophagy-mediated suppression of HCV replication via the endoplasmic reticulum (ER) protein SCOTIN. SCOTIN overexpression inhibits HCV replication and infectious virion production in cells infected with cell culture-derived HCV. HCV nonstructural 5A (NS5A) protein, which is a critical factor for HCV RNA replication, interacts with the IFN-β-inducible protein SCOTIN, which transports NS5A to autophagosomes for degradation. Furthermore, the suppressive effect of SCOTIN on HCV replication is impaired in both ATG7-silenced cells and cells treated with autophagy or lysosomal inhibitors. SCOTIN does not affect the overall flow of autophagy; however, it is a substrate for autophagic degradation. The physical association between the transmembrane/proline-rich domain (TMPRD) of SCOTIN and Domain-II of NS5A is essential for autophagosomal trafficking and NS5A degradation. Altogether, our findings suggest that IFN-β-induced SCOTIN recruits the HCV NS5A protein to autophagosomes for degradation, thereby restricting HCV replication.

Indexed as

HepatocytesApoptosis Regulatory ProteinsAutophagyCell Line, TumorFluorescent Antibody TechniqueHepacivirusHumansImmunoblottingImmunoprecipitationInterferon-betaMembrane ProteinsPhagosomesReverse Transcriptase Polymerase Chain ReactionRNA-Dependent RNA PolymeraseRNA, ViralViral Nonstructural ProteinsApoptosis Regulatory ProteinsInterferon-betaMembrane ProteinsNS-5 protein, hepatitis C virusRNA-Dependent RNA PolymeraseRNA, ViralSHISA5 protein, humanViral Nonstructural Proteins

Identifiers

PMID26868272
PMCPMC4754343
OpenAlexW2298200762

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.