ArticleOncogene1999
HBV transcription repression in response to genotoxic stress is p53-dependent and abrogated by pX.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- The role of the hepatitis B virus genome and its integration in the hepatocellular carcinoma.Frontiers in microbiology · 2024Review
- Interaction of mutant hepatitis B X protein with p53 tumor suppressor protein affects both transcription and cell survival.Molecular carcinogenesis · 2011Article
- Occult hepatitis B in blood donors: a description of two cases.Blood transfusion = Trasfusione del sangue · 2010Article
- High-level expression and large-scale preparation of soluble HBx antigen from Escherichia coli.Biotechnology and applied biochemistry · 2009Article
- Molecular functions and biological roles of hepatitis B virus x protein.Cancer science · 2006Review
- 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 X protein stimulates viral genome replication via a DDB1-dependent pathway distinct from that leading to cell death.Journal of virology · 2005Article
- Enhancer I predominance in hepatitis B virus gene expression.Molecular and cellular biology · 2004Article
- p73beta inhibits transcriptional activities of enhancer I and X promoter in hepatitis B virus more efficiently than p73alpha.World journal of gastroenterology · 2002Article
- p73 overexpression and nuclear accumulation in hepatitis C virus-associated hepatocellular carcinoma.Digestive diseases and sciences · 2002Article
- Article
- Hepatitis B virus X mutants derived from human hepatocellular carcinoma retain the ability to abrogate p53-induced apoptosis.Oncogene · 2001Article
- Chemotherapeutic drug, adriamycin, restores the function of p53 protein in hepatitis B virus X (HBx) protein-expressing liver cells.Oncogene · 2000Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription of hepatitis B Virus (HBV), an important risk factor of hepatocellular carcinoma (HCC), is controlled by cellular transcription activators including some of the cellular signaling targets. Consequently, HBV transcription rate changes in response to the cellular physiological conditions. In this report we investigated HBV gene expression and the role of physiological levels of the viral X protein (pX) under cisplatin induced genotoxic stress. We show that under these conditions the RNA level of an HBV mutant which does not express pX is sharply reduced. Studies revealed that transcription repression is responsible for the observed reduction in HBV RNA level. Repression of HBV transcription was obtained only in the p53 proficient cells. Furthermore, HBV transcription rate is recovered by the cotransfected p53 dominant negative plasmid, indicating that p53 is directly responsible for HBV transcription repression. Unexpectedly, p73, the recent p53 homologue, does not repress but rather activates HBV transcription. Interestingly, pX produced either by the HBV genome or by a cotransfected plasmid, relieves the p53 mediated repression. Collectively, these results attribute a physiological role to p53-inactivation by pX, and explain how pX may support HCC development.
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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.