Evidence map›Paper›PMID 25463603›Full record

ArticleVirology2015

NS5B induces up-regulation of the BH3-only protein, BIK, essential for the hepatitis C virus RNA replication and viral release.

Jude Juventus Aweya, Ching Wooen Sze, Anthony Bayega, Nur Khairiah Mohd-Ismail, Lin Deng, Hak Hotta, Yee-Joo Tan

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
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 3 institutions in 2 countries.

Jude Juventus AweyaDepartment of Microbiology, Yong Loo Lin School of Medicine, National University Health System (NUHS), National University of Singapore, Singapore.
Ching Wooen SzeDepartment of Microbiology, Yong Loo Lin School of Medicine, National University Health System (NUHS), National University of Singapore, Singapore.
Anthony BayegaDepartment of Microbiology, Yong Loo Lin School of Medicine, National University Health System (NUHS), National University of Singapore, Singapore; Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A⁎STAR), Singapore 138673, Singapore.
Nur Khairiah Mohd-IsmailInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research (A⁎STAR), Singapore 138673, Singapore.
Lin DengDivision of Microbiology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, Hyogo 650-0017, Japan.
Hak HottaDivision of Microbiology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, Hyogo 650-0017, Japan.
Yee-Joo TanDepartment of Microbiology, Yong Loo Lin School of Medicine, National University Health System (NUHS), National University of Singapore, Singapore; Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A⁎STAR), Singapore 138673, Singapore. Electronic address: yee_joo_tan@nuhs.edu.sg.
Agency for Science, Technology and Research · SGKobe University · JPNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) induces cytopathic effects in the form of hepatocytes apoptosis thought to be resulted from the interaction between viral proteins and host factors. Using pathway specific PCR array, we identified 9 apoptosis-related genes that are dysregulated during HCV infection, of which the BH3-only pro-apoptotic Bcl-2 family protein, BIK, was consistently up-regulated at the mRNA and protein levels. Depletion of BIK protected host cells from HCV-induced caspase-3/7 activation but not the inhibitory effect of HCV on cell viability. Furthermore, viral RNA replication and release were significantly suppressed in BIK-depleted cells and over-expression of the RNA-dependent RNA polymerase, NS5B, was able to induce BIK expression. Immunofluorescence and co-immunoprecipitation assays showed co-localization and interaction of BIK and NS5B, suggesting that BIK may be interacting with the HCV replication complex through NS5B. These results imply that BIK is essential for HCV replication and that NS5B is able to induce BIK expression.

Indexed as

ApoptosisApoptosis Regulatory ProteinsCell LineCell SurvivalGene Knockdown TechniquesHEK293 CellsHepacivirusHost-Pathogen InteractionsHumansMembrane ProteinsMitochondrial ProteinsRNA-Dependent RNA PolymeraseRNA, Small InterferingRNA, ViralUp-RegulationViral Nonstructural ProteinsApoptosis Regulatory ProteinsBIK protein, humanMembrane ProteinsMitochondrial ProteinsNS-5 protein, hepatitis C virusRNA-Dependent RNA PolymeraseRNA, Small InterferingRNA, ViralViral Nonstructural ProteinsBIKHepatitis C virus (HCV)NS5B

Identifiers

PMID25463603
PMCPMC7127593
OpenAlexW2016979442

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.