Evidence map›Paper›PMID 31383738›Full record

ArticleThe Journal of biological chemistry2019

Hepatitis C virus infection increases autophagosome stability by suppressing lysosomal fusion through an Arl8b-dependent mechanism.

Kellyann N Jones-Jamtgaard, Ann L Wozniak, Hiroshi Koga, Robert Ralston, Steven A Weinman

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. 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
1.9field-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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Viruses and autophagy: bend, but don't break.Nature reviews. Microbiology · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Autophagy in HCV Replication and Protein Trafficking.International journal of molecular sciences · 2021
    Review
  15. Review
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

5 authors at 2 institutions in 1 country.

Kellyann N Jones-JamtgaardDepartment of Microbiology, Immunology, and Molecular Genetics, University of Kansas Medical Center, Kansas City, Kansas 66160.
Ann L WozniakDepartment of Internal Medicine and Liver Center, University of Kansas Medical Center, Kansas City, Kansas 66160.
Hiroshi KogaDepartment of Developmental and Molecular Biology and Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, New York 10461.
Robert RalstonDepartment of Pharmacology and Toxicology, University of Kansas Medical Center, Kansas City, Kansas 66160.
Steven A WeinmanDepartment of Microbiology, Immunology, and Molecular Genetics, University of Kansas Medical Center, Kansas City, Kansas 66160 sweinman@kumc.edu.
University of Kansas Medical Center · USAlbert Einstein College of Medicine · US

Funding

Molecular Regulation of Cell Development and Differentiation Phase III COBREP30GM122731 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LITTLE, CHARLES D. · 2017 to 2021
$5.6M
Pilot Grants ProgramP30GM118247 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI WEINMAN, STEVEN A · 2016 to 2020
$5.5M
Novel Approaches for the Control of Microbial PathogensP30GM103326 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI YANKEE, THOMAS M. · 2012 to 2016
$5.3M
NIGMS NIH HHS P30 GM103326NIGMS NIH HHS P30 GM118247NIGMS NIH HHS P30 GM122731
6 · The paper itself

Abstract

Autophagy is a conserved cellular process involving intracellular membrane trafficking and degradation. Pathogens, including hepatitis C virus (HCV), often exploit this process to promote their own survival. The aim of this study was to determine the mechanism by which HCV increases steady-state autophagosome numbers while simultaneously inhibiting flux through the autophagic pathway. Using the lysosomal inhibitor bafilomycin A1, we showed that HCV-induced alterations in autophagy result from a blockage of autophagosome degradation rather than an increase in autophagosome generation. In HCV-infected cells, lysosome function was normal, but a tandem RFP-GFP-LC3 failed to reach the lysosome even under conditions that activate autophagy. Autophagosomes and lysosomes isolated from HCV-infected cells were able to fuse with each other normally

Indexed as

ADP-Ribosylation FactorsAutophagosomesCell Line, TumorHepatitis CHumansLysosomesProtein TransportADP-Ribosylation FactorsARL8B protein, humanArl8bautophagyGTPaseHepatitis C virus (HCV)intracellular traffickinglysosome

Identifiers

PMID31383738
PMCPMC6768644
OpenAlexW2965034294

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.