ArticleOncogene1999
The proapoptotic effect of hepatitis B virus HBx protein correlates with its transactivation activity in stably transfected cell lines.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 80 citations in OpenAlex.
- Intermolecular Electrostatic Interactions in CytochromeInternational journal of molecular sciences · 2024Article
- Hepatitis B Virus X and Regulation of Viral Gene Expression.Cold Spring Harbor perspectives in medicine · 2016Review
- Hepatitis B virus molecular biology and pathogenesis.Hepatoma research · 2016Article
- Molecular mechanism of hepatitis B virus-induced hepatocarcinogenesis.World journal of gastroenterology · 2014Review
- MicroRNAs as therapeutic strategy for hepatitis B virus-associated hepatocellular carcinoma: current status and future prospects.World journal of gastroenterology · 2014Review
- Review
- Hepatitis B virus X gene and hepatocarcinogenesis.Journal of gastroenterology · 2011Review
- Hepatoma cell line HepG2.2.15 demonstrates distinct biological features compared with parental HepG2.World journal of gastroenterology · 2011Article
- Hepatitis B virus X protein impedes the DNA repair via its association with transcription factor, TFIIH.BMC microbiology · 2011Article
- Stimulation of inducible nitric oxide by hepatitis B virus transactivator protein HBx requires MTA1 coregulator.The Journal of biological chemistry · 2010Article
- NF-kappaB signaling mediates the induction of MTA1 by hepatitis B virus transactivator protein HBx.Oncogene · 2010Article
- Hepatitis B virus X protein modulates apoptosis in primary rat hepatocytes by regulating both NF-kappaB and the mitochondrial permeability transition pore.Journal of virology · 2009Article
- Differential effects on apoptosis induction in hepatocyte lines by stable expression of hepatitis B virus X protein.World journal of gastroenterology · 2006Article
- Hepatitis B virus-related hepatocellular carcinoma: paradigms for viral-related human carcinogenesis.Oncogene · 2006Review
- Biological impacts of "hot-spot" mutations of hepatitis B virus X proteins are genotype B and C differentiated.World journal of gastroenterology · 2005Article
- The enigmatic X gene of hepatitis B virus.Journal of virology · 2004Review
- Transfection and expression of hepatitis B virus x gene and its effect on apoptosis in HL-7702 cells.World journal of gastroenterology · 2004Article
- Tumor necrosis factor alpha inhibition of hepatitis B virus replication involves disruption of capsid Integrity through activation of NF-kappaB.Journal of virology · 2003Article
- Conserved transactivating and pro-apoptotic functions of hepadnaviral X protein in ortho- and avihepadnaviruses.Oncogene · 2002Article
- Turnover of hepatitis B virus X protein is regulated by damaged DNA-binding complex.Journal of virology · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of hepatitis B virus HBx protein in the carcinogenesis associated with chronic viral infection remains ill-defined. Indeed, pleiotropic effects have been ascribed to HBx: in addition to its well-documented ability to indirectly stimulate transcription, the protein has been reported to affect cell growth, signal transduction, DNA repair and apoptosis. In this work, we generated Chang (CCL-13)-derived cell lines constitutively expressing wild type or mutant HBx, as a model of HBx-host cell interaction closer to the chronic infection setting, than the classically used transient expression systems. We document the potentiation by HBx of the apoptotic cell death pathway in the recipient cells. This effect is unlikely to rely on p53 activity since the protein is functionally inactivated in CCL-13. In addition, antioxidants and cyclosporin A failed to reduce the apoptotic response back to the normal level, suggesting that production of reactive oxygen species and calcineurin activation are not directly involved in the proapoptotic effect of HBx. In contrast, our data show that transactivation and stimulation of apoptosis are tightly linked HBx activities. Finally, expression of transactivation-active protein did not result in detectable change in the pattern of MAP kinases phosphorylation nor did it affect the ability of the host cell to repair in vitro irradiated plasmid DNA.
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.