Evidence map›Paper›PMID 30381393›Full record

ArticleThe Journal of biological chemistry2018

The aryl hydrocarbon receptor-cytochrome P450 1A1 pathway controls lipid accumulation and enhances the permissiveness for hepatitis C virus assembly.

Hirofumi Ohashi, Kazane Nishioka, Syo Nakajima, Sulyi Kim, Ryosuke Suzuki, Hideki Aizaki, Masayoshi Fukasawa, Shinji Kamisuki, Fumio Sugawara, Naoko Ohtani and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. The role of the AHR in host-pathogen interactions.Nature reviews. Immunology · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. Pharmaceuticals (Basel, Switzerland) · 2024
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Early-life exposure to cigarette smoke primes lung function and DNA methylation changes atAmerican journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  16. Article
  17. When AHR signaling pathways meet viral infections.Cell communication and signaling : CCS · 2023
    Review
  18. Article
  19. Article
  20. 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

13 authors at 3 institutions in 1 country.

Hirofumi OhashiFrom the Department of Virology II and.
Kazane NishiokaFrom the Department of Virology II and.
Syo NakajimaFrom the Department of Virology II and.
Sulyi KimFrom the Department of Virology II and.
Ryosuke SuzukiFrom the Department of Virology II and.
Hideki AizakiFrom the Department of Virology II and.
Masayoshi Fukasawathe Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Shinji Kamisukithe Tokyo University of Science Graduate School of Science and Technology, Noda 278-8510, Japan, and.
Fumio Sugawarathe Tokyo University of Science Graduate School of Science and Technology, Noda 278-8510, Japan, and.
Naoko Ohtanithe Tokyo University of Science Graduate School of Science and Technology, Noda 278-8510, Japan, and.
Masamichi MuramatsuFrom the Department of Virology II and.
Takaji WakitaFrom the Department of Virology II and.
Koichi WatashiFrom the Department of Virology II and kwatashi@nih.go.jp.
National Institute of Infectious Diseases · JPTokyo University of Science · JPJapan Science and Technology Agency · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Viruses hijack and modify host cell functions to maximize viral proliferation. Hepatitis C virus (HCV) reorganizes host cell metabolism to produce specialized membrane structures and to modify organelles such as double-membrane vesicles and enlarged lipid droplets (LDs), thereby enabling virus replication and assembly. However, the molecular bases of these host-HCV interactions are largely unknown. Here, using a chemical screen, we demonstrate that the benzamide derivative flutamide reduces the host capacity to produce infectious HCV. Flutamide disrupted the formation of enlarged LDs in HCV-infected cells, thereby abolishing HCV assembly. We also report that aryl hydrocarbon receptor (AhR), a known flutamide target, plays a key role in mediating LD accumulation and HCV production. This AhR function in lipid production was also observed in HCV-uninfected Huh-7 cells and primary human hepatocytes, suggesting that AhR signaling regulates lipid accumulation independently of HCV infection. We further observed that a downstream activity, that of cytochrome P450 1A1 (CYP1A1), was the primary regulator of AhR-mediated lipid production. Specifically, blockade of AhR-induced

Indexed as

Lipid MetabolismVirus AssemblyCell LineCytochrome P-450 CYP1A1FlutamideHepacivirusHumansLipid DropletsProtein BindingReceptors, Aryl HydrocarbonCytochrome P-450 CYP1A1FlutamideReceptors, Aryl Hydrocarbonaryl hydrocarbon receptor (AhR) (AHR)CYP1A1cytochrome P450fatty acid metabolismhepatitisHepatitis C virus (HCV)hepatocytelipid droplettriglyceridevirus assembly

Identifiers

PMID30381393
PMCPMC6314116
OpenAlexW2898766183

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.