Evidence map›Paper›PMID 28768874›Full record

ArticleJournal of virology2017

PGC1α Transcriptional Adaptor Function Governs Hepatitis B Virus Replication by Controlling HBcAg/p21 Protein-Mediated Capsid Formation.

Rasha E Shalaby, Saira Iram, Bülent Çakal, Claudia E Oropeza, Alan McLachlan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Review
  3. Illuminating HBV with multi-scale modeling.Frontiers in systems biology · 2023
    Article
  4. Article
  5. β-Catenin Signaling Regulates theJournal of virology · 2021
    Article
  6. Article
  7. Article
  8. Article
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 2 countries.

Rasha E ShalabyDepartment of Microbiology and Immunology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA.
Saira IramDepartment of Microbiology and Immunology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA.
Bülent ÇakalDepartment of Microbiology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Claudia E OropezaDepartment of Microbiology and Immunology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA.
Alan McLachlanDepartment of Microbiology and Immunology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA mclach@uic.edu.
University of Illinois Chicago · USIstanbul University · TR

Funding

Developmental regulation of HBV biosynthesis by FoxA and DNA methylationR01AI125401 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MCLACHLAN, ALAN · 2016 to 2020
$2.0M
Liver lobule zonation, hepatocellular carcinoma (HCC) and β-catenin mediated hepatitis B virus (HBV) biosynthesisR01CA238328 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MCLACHLAN, ALAN · 2020 to 2024
$1.8M
NCI NIH HHS R01 CA238328NIAID NIH HHS R01 AI125401
6 · The paper itself

Abstract

In the human hepatoma cell line Huh7, the coexpression of the coactivators peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α), cyclic AMP-responsive element binding protein binding protein (CBP), steroid receptor coactivator 1 (SRC1), and protein arginine methyltransferase 1 (PRMT1) only modestly increase hepatitis B virus (HBV) biosynthesis. However, by utilizing the human embryonic kidney cell line HEK293T, it was possible to demonstrate that PGC1α alone can support viral biosynthesis independently of the expression of additional coactivators or transcription factors. In contrast, additional coactivators failed to support robust HBV replication in the absence of PGC1α. These observations indicate that PGC1α represents a novel adaptor molecule capable of recruiting the necessary transcriptional machinery to the HBV nucleocapsid promoter to modestly enhance viral pregenomic 3.5-kb RNA synthesis. Although this change in transcription is associated with a similar modest change in hepatitis B virus core antigen polypeptide (HBcAg/p21) synthesis, it mediates a dramatic increase in viral capsid production and robust viral replication. Therefore, it is apparent that the synthesis of cytoplasmic HBcAg/p21 above a critical threshold level is required for the efficient assembly of HBV replication-competent viral capsids.

Indexed as

Host-Pathogen InteractionsVirus ReplicationCapsidCapsid ProteinsCell Line, TumorDNA ReplicationHEK293 CellsHepatitis B Core AntigensHepatitis B virusHepatocytesHumansPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRNA, ViralTranscription, GeneticVirus AssemblyCapsid ProteinsHepatitis B Core AntigensPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanRNA, Viralcapsid assemblyhepatitis B virusPGC1αtranscriptional coactivators

Identifiers

PMID28768874
PMCPMC5625508
OpenAlexW2740023756

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.