Evidence map›Paper›PMID 31363036›Full record

ArticlemBio2019

Hepatitis C Virus Infection Induces Hepatic Expression of NF-κB-Inducing Kinase and Lipogenesis by Downregulating miR-122.

Brianna Lowey, Laura Hertz, Stephan Chiu, Kristin Valdez, Qisheng Li, T Jake Liang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in mBio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% 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, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Emerging roles of stress granules in liver diseases: a comprehensive review.Frontiers in cell and developmental biology · 2025
    Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Noncanonical NF-κB Signaling Pathway in Liver Diseases.Journal of clinical and translational hepatology · 2021
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Brianna Lowey *Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Laura Hertz *Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Stephan ChiuLiver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Kristin ValdezLiver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Qisheng LiLiver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA liqisheng@niddk.nih.gov jakel@bdg10.niddk.nih.gov.
T Jake LiangLiver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA liqisheng@niddk.nih.gov jakel@bdg10.niddk.nih.gov.ORCID 0000-0003-3828-702X
National Institutes of Health · US

Funding

NLM NIH HHS HHSN276201200017C
6 · The paper itself

Abstract

Hepatitis C virus (HCV) harnesses host dependencies to infect human hepatocytes. We previously identified a pivotal role of IκB kinase α (IKK-α) in regulating cellular lipogenesis and HCV assembly. In this study, we defined and characterized NF-κB-inducing kinase (NIK) as an IKK-α upstream serine/threonine kinase in IKK-α-mediated proviral effects and the mechanism whereby HCV exploits this innate pathway to its advantage. We manipulated NIK expression in Huh7.5.1 cells through loss- and gain-of-function approaches and examined the effects on IKK-α activation, cellular lipid metabolism, and viral assembly. We demonstrated that NIK interacts with IKK-α to form a kinase complex in association with the stress granules, in which IKK-α is phosphorylated upon HCV infection. Depletion of NIK significantly diminished cytosolic lipid droplet content and impaired HCV particle production. NIK overexpression enhanced HCV assembly, and this process was abrogated in cells deprived of IKK-α, suggesting that NIK acts upstream of IKK-α. NIK abundance was increased in HCV-infected hepatocytes, liver tissues from

Indexed as

Cell LineHepacivirusHepatitis CHumansLipogenesisLiverMicroRNAsNF-kappaB-Inducing KinaseProtein Serine-Threonine KinasesSignal TransductionMicroRNAsNF-kappaB-Inducing KinaseProtein Serine-Threonine Kinasescell signalinghepatic inflammationlipid synthesismicroRNAviral pathogenesis

Identifiers

PMID31363036
PMCPMC6667626
OpenAlexW2966081670

What Socratic 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 Socratic graph.