Evidence map›Paper›PMID 28090674›Full record

ArticleHepatology (Baltimore, Md.)2017

Nonstructural protein 5B promotes degradation of the NORE1A tumor suppressor to facilitate hepatitis C virus replication.

Payal Arora, Amartya Basu, M Lee Schmidt, Geoffrey J Clark, Howard Donninger, Daniel B Nichols, Diego F Calvisi, Neerja Kaushik-Basu

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. NORE1A loss promotes MASLD/MASH.Transgenic research · 2024
    Article
  2. Article
  3. Viral hepatitis and liver cancer.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    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

8 authors at 4 institutions in 2 countries.

Payal AroraDepartment of Biochemistry and Molecular Biology, UMDNJ-New Jersey Medical School, Newark, NJ.
Amartya BasuDepartment of Biochemistry and Molecular Biology, UMDNJ-New Jersey Medical School, Newark, NJ.
M Lee SchmidtDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, KY.
Geoffrey J ClarkDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, KY.
Howard DonningerDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, KY.
Daniel B NicholsDepartment of Biochemistry and Molecular Biology, UMDNJ-New Jersey Medical School, Newark, NJ.
Diego F CalvisiDepartment of Clinical and Experimental Medicine, University of Sassari, Sassari, Italy.
Neerja Kaushik-BasuDepartment of Biochemistry and Molecular Biology, UMDNJ-New Jersey Medical School, Newark, NJ.
University of Louisville · USRutgers New Jersey Medical SchoolRutgers, The State University of New Jersey · USUniversity of Sassari · IT

Funding

The role of the Ras effector Nore1a in tumor suppressionR01CA133171 · NCI · UNIVERSITY OF LOUISVILLE · PI CLARK, GEOFFREY J. · 2010 to 2014
$1.3M
Role of Autotaxin in HCV-associated Hepatocellular CarcinomaR21CA153147 · NCI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI KAUSHIK-BASU, NEERJA · 2010 to 2011
$367k
NCI NIH HHS R01 CA133171NCI NIH HHS R21 CA153147
6 · The paper itself

Abstract

Hepatitis C virus (HCV) infection is a common risk factor for the development of liver cancer. The molecular mechanisms underlying this effect are only partially understood. Here, we show that the HCV protein, nonstructural protein (NS) 5B, directly binds to the tumor suppressor, NORE1A (RASSF5), and promotes its proteosomal degradation. In addition, we show that NORE1A colocalizes to sites of HCV viral replication and suppresses the replication process. Thus, NORE1A has antiviral activity, which is specifically antagonized by NS5B. Moreover, the suppression of NORE1A protein levels correlated almost perfectly with elevation of Ras activity in primary human samples. Therefore, NORE1A inactivation by NS5B may be essential for maximal HCV replication and may make a major contribution to HCV-induced liver cancer by shifting Ras signaling away from prosenescent/proapoptotic signaling pathways.

conclusionHCV uses NS5B to specifically suppress NORE1A, facilitating viral replication and elevated Ras signaling. (Hepatology 2017;65:1462-1477).

Indexed as

Virus ReplicationAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCarcinoma, HepatocellularDown-RegulationHEK293 CellsHepacivirusHumansLiverLiver NeoplasmsMonomeric GTP-Binding ProteinsProteasome Endopeptidase ComplexRNA-Dependent RNA PolymeraseViral Nonstructural ProteinsAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsMonomeric GTP-Binding ProteinsNS-5 protein, hepatitis C virusProteasome Endopeptidase ComplexRASSF5 protein, humanRNA-Dependent RNA PolymeraseViral Nonstructural Proteins

Identifiers

PMID28090674
PMCPMC5397368
OpenAlexW2572787603

What OpenQuestion holds

Textmetadata
LicenceTDM
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.