ArticleJournal of virology1999
Hepatitis B virus X protein is both a substrate and a potential inhibitor of the proteasome complex.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
What it found
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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.
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Who cites it
89 citing papers in PubMed, 235 citations in OpenAlex.
- [The E3 ubiquitin ligase KLHL8 degrades HBx protein via the ubiquitin-proteasome pathway and inhibits HBV cccDNA transcription].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Article
- Ubiquitination dynamics in human tumour viruses: Viral infection, oncogenesis and antiviral therapy.The FEBS journal · 2026Review
- Identification of novel HLA class I-restricted hepatitis B virus peptides and their modulation by peptide editor TAPBPR.Frontiers in immunology · 2026Article
- The Dual Role of Nrf2 Signaling in Virus Infections: Antiviral Guardian or Proviral Accomplice?Pathogens (Basel, Switzerland) · 2025Review
- Molecular regulation by ubiquitin-specific proteases (USPs) in HCC: cell cycle, oncogenic signaling, and beyond.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- HBV Infection Drives PSMB5-Dependent Proteasomal Activation in Humanized Mice and HBV-Associated HCC.Viruses · 2025Article
- The LUBAC subunit HOIL-1 promotes the progression of HBV-associated hepatocellular carcinoma independently of linear ubiquitination.Experimental & molecular medicine · 2025Article
- Hepatitis B virus genotypes A1 and A2 have distinct replication phenotypes due to polymorphisms in the HBx gene.PLoS pathogens · 2025Article
- Viral manipulation of the HLA class I antigen processing and presentation pathway.Frontiers in immunology · 2025Review
- The role of proteasomes in tumorigenesis.Genes & diseases · 2024Review
- PreS1BP mediates inhibition of Hepatitis B virus replication by promoting HBx protein degradation.Virus research · 2024Article
- The Role of the NRF2 Pathway in the Pathogenesis of Viral Respiratory Infections.Pathogens (Basel, Switzerland) · 2023Review
- PROTACs in gastrointestinal cancers.Molecular therapy oncolytics · 2022Review
- Pathogenicity and virulence of Hepatitis B virus.Virulence · 2022Review
- Article
- Identification of STAU1 as a regulator of HBV replication by TurboID-based proximity labeling.iScience · 2022Article
- NS5-independent Ablation of STAT2 by Zika virus to antagonize interferon signalling.Emerging microbes & infections · 2021Article
- Silencing hepatitis B virus covalently closed circular DNA: The potential of an epigenetic therapy approach.World journal of gastroenterology · 2021Review
- EBV miRNAs are potent effectors of tumor cell transcriptome remodeling in promoting immune escape.PLoS pathogens · 2021Article
- Role of Virally-Encoded Deubiquitinating Enzymes in Regulation of the Virus Life Cycle.International journal of molecular sciences · 2021Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The hepatitis B virus X protein (HBX) is essential for the establishment of HBV infection in vivo and exerts a pleiotropic effect on diverse cellular functions. The yeast two-hybrid system had indicated that HBX could interact with two subunits of the 26S proteasome. Here we demonstrate an association in vivo of HBX with the 26S proteasome complex by coimmunoprecipitation and colocalization upon sucrose gradient centrifugation. Expression of HBX in HepG2 cells caused a modest decrease in the proteasome's chymotrypsin- and trypsin-like activities and in hydrolysis of ubiquitinated lysozyme, suggesting that HBX functions as an inhibitor of proteasome. In these cells, HBX is degraded with a half-life of 30 min. Proteasome inhibitors retarded this rapid degradation and caused a marked increase in the level of HBX and an accumulation of HBX in polyubiquitinated form. Thus, the low intracellular level of HBX is due to rapid proteolysis by the ubiquitin-proteasome pathway. Surprisingly, the proteasome inhibitors blocked the transactivation by HBX, and this effect was not a result of a squelching phenomenon due to HBX accumulation. Therefore, proteasome function is possibly required for the transactivation function of HBX. The inhibition of protein breakdown by proteasomes may account for the multiple actions of HBX and may be an important feature of HBV infection, possibly in helping stabilize viral gene products and suppressing antigen presentation.
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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.