Evidence map›Paper›PMID 19264780›Full record

ArticleJournal of virology2009

Involvement of creatine kinase B in hepatitis C virus genome replication through interaction with the viral NS4A protein.

Hiromichi Hara, Hideki Aizaki, Mami Matsuda, Fumiko Shinkai-Ouchi, Yasushi Inoue, Kyoko Murakami, Ikuo Shoji, Hayato Kawakami, Yoshiharu Matsuura, Michael M C Lai and 3 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Chaperones in hepatitis C virus infection.World journal of hepatology · 2016
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Update on the Development of Anti-Viral Agents Against Hepatitis C.Journal of clinical and translational hepatology · 2013
    Review
  18. Review
  19. Article
  20. 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

13 authors at 7 institutions in 2 countries.

Hiromichi HaraDepartment of Virology II, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8640, Japan.
Hideki Aizaki
Mami Matsuda
Fumiko Shinkai-Ouchi
Yasushi Inoue
Kyoko Murakami
Ikuo Shoji
Hayato Kawakami
Yoshiharu Matsuura
Michael M C Lai
Tatsuo Miyamura
Takaji Wakita
Tetsuro Suzuki
International University of Health and Welfare · JPJikei University School of Medicine · JPKobe University · JPKyorin University · JPNational Institute of Infectious Diseases · JPOsaka University · JPUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent infection with hepatitis C virus (HCV) is a major cause of chronic liver diseases. The aim of this study was to identify host cell factor(s) participating in the HCV replication complex (RC) and to clarify the regulatory mechanisms of viral genome replication dependent on the host-derived factor(s) identified. By comparative proteome analysis of RC-rich membrane fractions and subsequent gene silencing mediated by RNA interference, we identified several candidates for RC components involved in HCV replication. We found that one of these candidates, creatine kinase B (CKB), a key ATP-generating enzyme that regulates ATP in subcellular compartments of nonmuscle cells, is important for efficient replication of the HCV genome and propagation of infectious virus. CKB interacts with HCV NS4A protein and forms a complex with NS3-4A, which possesses multiple enzyme activities. CKB upregulates both NS3-4A-mediated unwinding of RNA and DNA in vitro and replicase activity in permeabilized HCV replicating cells. Our results support a model in which recruitment of CKB to the HCV RC compartment, which has high and fluctuating energy demands, through its interaction with NS4A is important for efficient replication of the viral genome. The CKB-NS4A association is a potential target for the development of a new type of antiviral therapeutic strategy.

Indexed as

Virus ReplicationAdenosine TriphosphateCarrier ProteinsCell Line, TumorCreatine Kinase, BB FormGene Expression Regulation, ViralGenome, ViralHepacivirusHepatitis CHumansIntracellular Signaling Peptides and ProteinsProteomicsRNA InterferenceRNA, ViralViral Nonstructural ProteinsViral ProteinsAdenosine TriphosphateCarrier ProteinsCreatine Kinase, BB FormIntracellular Signaling Peptides and ProteinsNS4A cofactor peptide, Hepatitis C virusRNA, ViralViral Nonstructural ProteinsViral Proteins

Identifiers

PMID19264780
PMCPMC2682066
OpenAlexW2132732495

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.