Evidence map›Paper›PMID 26434584›Full record

ArticleOncogene2016

Hepatitis C virus upregulates B-cell receptor signaling: a novel mechanism for HCV-associated B-cell lymphoproliferative disorders.

B Dai, A Y Chen, C P Corkum, R J Peroutka, A Landon, S Houng, P A Muniandy, Y Zhang, E Lehrmann, K Mazan-Mamczarz and 8 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2016. 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
2.1field-weighted citation impact, top 13% 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, 50 citations in OpenAlex.

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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

18 authors at 5 institutions in 2 countries.

B DaiDepartment of Medicine, Marlene and Stewart Greenebaum Cancer Center, University of Maryland, Baltimore, MD, USA.
A Y ChenMolecular Virology and Hepatology Research Group, Division of BioMedical Sciences, Faculty of Medicine, Memorial University, St John's, Newfoundland and Labrador, Canada.
C P CorkumMolecular Virology and Hepatology Research Group, Division of BioMedical Sciences, Faculty of Medicine, Memorial University, St John's, Newfoundland and Labrador, Canada.
R J PeroutkaDepartment of Medicine, Marlene and Stewart Greenebaum Cancer Center, University of Maryland, Baltimore, MD, USA.
A LandonDepartment of Medicine, Marlene and Stewart Greenebaum Cancer Center, University of Maryland, Baltimore, MD, USA.
S HoungDepartment of Medicine, Marlene and Stewart Greenebaum Cancer Center, University of Maryland, Baltimore, MD, USA.
P A MuniandyDepartment of Medicine, Marlene and Stewart Greenebaum Cancer Center, University of Maryland, Baltimore, MD, USA.
Y ZhangGene Expression and Genomics Unit, Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
E LehrmannGene Expression and Genomics Unit, Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
K Mazan-MamczarzDepartment of Medicine, Marlene and Stewart Greenebaum Cancer Center, University of Maryland, Baltimore, MD, USA.
J SteinhardtDepartment of Medicine, Marlene and Stewart Greenebaum Cancer Center, University of Maryland, Baltimore, MD, USA.
M ShlyakDepartment of Infectious Diseases, Institute of Human Virology, University of Maryland School of Medicine, Baltimore, MD, USA.
Q C ChenDepartment of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA.
K G BeckerGene Expression and Genomics Unit, Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
F LivakDepartment of Medicine, Marlene and Stewart Greenebaum Cancer Center, University of Maryland, Baltimore, MD, USA.
T I MichalakMolecular Virology and Hepatology Research Group, Division of BioMedical Sciences, Faculty of Medicine, Memorial University, St John's, Newfoundland and Labrador, Canada.
R TalwaniDepartment of Infectious Diseases, Institute of Human Virology, University of Maryland School of Medicine, Baltimore, MD, USA.
R B GartenhausDepartment of Medicine, Marlene and Stewart Greenebaum Cancer Center, University of Maryland, Baltimore, MD, USA.
University of Maryland, Baltimore · USMemorial University of Newfoundland · CAInstitute on Aging · USNational Institute on Aging · USNational Institutes of Health · US

Funding

Alcohol Consumption and Risk of NHL: Role of MTOR DysfunctionR01AA017972 · NIAAA · UNIVERSITY OF MARYLAND BALTIMORE · PI GARTENHAUS, RONALD B · 2009 to 2013
$1.7M
MAP Kinase Signaling in Lymphoma: A Novel Therapeutic ParadigmR01CA164311 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI EVENS, ANDREW M, GARTENHAUS, RONALD B · 2012 to 2015
$1.4M
MEK/ERK pathways and MCT-1 in Diffuse Large B-cell LymphomaI01BX001219 · VA · BALTIMORE VA MEDICAL CENTER · PI GARTENHAUS, RONALD B · 2011 to 2014
–
Lymphoma development in the elderly: Perturbed posttranscriptional regulationI01BX002990 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI GARTENHAUS, RONALD B · 2016 to 2019
–
BLRD VA I01 BX001219BLRD VA I01 BX002990CIHR MOP-126056NCI NIH HHS R01 CA164311NIAAA NIH HHS R01 AA017972
6 · The paper itself

Abstract

B-cell receptor (BCR) signaling is essential for the development of B cells and has a critical role in B-cell neoplasia. Increasing evidence indicates an association between chronic hepatitis C virus (HCV) infection and B-cell lymphoma, however, the mechanisms by which HCV causes B-cell lymphoproliferative disorder are still unclear. Herein, we demonstrate the expression of HCV viral proteins in B cells of HCV-infected patients and show that HCV upregulates BCR signaling in human primary B cells. HCV nonstructural protein NS3/4A interacts with CHK2 and downregulates its activity, modulating HuR posttranscriptional regulation of a network of target mRNAs associated with B-cell lymphoproliferative disorders. Interestingly, the BCR signaling pathway was found to have the largest number of transcripts with increased association with HuR and was upregulated by NS3/4A. Our study reveals a previously unidentified role of NS3/4A in regulation of host BCR signaling during HCV infection, contributing to a better understanding of the molecular mechanisms underlying HCV-associated B-cell lymphoproliferative disorders.

Indexed as

B-LymphocytesCheckpoint Kinase 2Down-RegulationHeLa CellsHepacivirusHepatitis C, ChronicHumansLymphoma, Large B-Cell, DiffuseLymphoproliferative DisordersReceptors, Antigen, B-CellRNA, MessengerSerine ProteasesSignal TransductionUp-RegulationViral Nonstructural ProteinsCheckpoint Kinase 2CHEK2 protein, humanNS3-4A serine protease, Hepatitis C virusReceptors, Antigen, B-CellRNA, MessengerSerine ProteasesViral Nonstructural Proteins

Identifiers

PMID26434584
PMCPMC4821826
OpenAlexW2231798535

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.