ArticleBMC biochemistry2012
The ORF2 glycoprotein of hepatitis E virus inhibits cellular NF-κB activity by blocking ubiquitination mediated proteasomal degradation of IκBα in human hepatoma cells.
Article in BMC biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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.
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.
Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
- Unraveling a mechanism underlying hepatitis E-associated kidney disease : Discovery of HEV ORF2 capsid protein-associated immune complex glomerulonephritis.Pathologie (Heidelberg, Germany) · 2026Article
- The hepatitis E virus capsid protein ORF2 counteracts cell-intrinsic antiviral responses to enable persistent replication in cell culture.PLoS pathogens · 2025Article
- Hepatitis E virus: from innate sensing to adaptive immune responses.Nature reviews. Gastroenterology & hepatology · 2024Review
- Pathogenesis and clinical features of severe hepatitis E virus infection.World journal of virology · 2024Review
- Review
- Hepatitis E Virus Protease Inhibits the Activity of Eukaryotic Initiation Factor 2-Alpha Kinase 4 and Promotes Virus Survival.Journal of virology · 2023Article
- Immunobiology and Host Response to HEV.Advances in experimental medicine and biology · 2023Article
- Characteristics and Functions of HEV Proteins.Advances in experimental medicine and biology · 2023Article
- Structural aspects of hepatitis E virus.Archives of virology · 2022Review
- Hepatitis E Virus Immunopathogenesis.Pathogens (Basel, Switzerland) · 2021Review
- Interplay between Hepatitis E Virus and Host Cell Pattern Recognition Receptors.International journal of molecular sciences · 2021Review
- Mechanism of Cross-Species Transmission, Adaptive Evolution and Pathogenesis of Hepatitis E Virus.Viruses · 2021Review
- Identification of the interferon-inducible GTPase GBP1 as major restriction factor for the Hepatitis E virus.Journal of virology · 2021Article
- Ectopic Expression of Genotype 1 Hepatitis E Virus ORF4 Increases Genotype 3 HEV Viral Replication in Cell Culture.Viruses · 2021Article
- Host Innate Immunity Against Hepatitis Viruses and Viral Immune Evasion.Frontiers in microbiology · 2021Review
- The Hepatitis E Virus Open Reading Frame 2 Protein: Beyond Viral Capsid.Frontiers in microbiology · 2021Review
- Hepatitis E virus infection during pregnancy.Virology journal · 2020Review
- Hepatitis E Virus ORF2 Inhibits RIG-I Mediated Interferon Response.Frontiers in microbiology · 2020Article
- The Capsid Protein of Hepatitis E Virus Inhibits Interferon Induction via Its N-terminal Arginine-Rich Motif.Viruses · 2019Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNuclear factor kappa B (NF-κB) is a key transcription factor that plays a crucial role in host survival during infection by pathogens. Therefore, it has been a priority of many pathogens to manipulate the cellular NF-κB activity in order to create a favorable environment for their survival inside the host.
resultsWe observed that heterologous expression of the open reading frame 2 (ORF2) protein in human hepatoma cells led to stabilization of the cellular I kappa B alpha (IκBα) pool, with a concomitant reduction in the nuclear localization of the p65 subunit of NF-κB and inhibition of NF-κB activity. Although basal or TPA induced phosphorylation of IκBα was not altered, its ubiquitination was markedly reduced in ORF2 expressing cells. Further analysis revealed that ORF2 protein could directly associate with the F-box protein, beta transducin repeat containing protein (βTRCP) and ORF2 over expression resulted in reduced association of IκBα with the SKP1 and CUL1 components of the SCFβTRCP complex. Chromatin immunoprecipitation (ChIP) assay of the proximal promoter regions of MHC-I heavy chain and IL-8 genes using p65 antibody and LPS stimulated ORF2 expressing cell extract revealed decreased association of p65 with the above regions, indicating that ORF2 inhibited p65 binding at endogenous promoters.
conclusionsIn this report we suggest a mechanism by which ORF2 protein of HEV may inhibit host cell NF-κB activity during the course of a viral infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.