ArticleProceedings of the National Academy of Sciences of the United States of America1997
Hepatitis B virus HBx protein sensitizes cells to apoptotic killing by tumor necrosis factor alpha.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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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.
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Who cites it
108 citing papers in PubMed, 299 citations in OpenAlex.
- Hepatitis B virus protein X promotes survival and loss of hepatocyte identity in a differentiated human liver organoid system.Cell death and differentiation · 2026Article
- Hepatocyte-Derived Apoptotic Bodies as Pathological Intercellular Messengers in the Liver.Biomolecules · 2026Review
- Cooperation Between Aflatoxin-Induced p53 Aberrations and Hepatitis B Virus in Hepatocellular Carcinoma.Journal of xenobiotics · 2025Review
- The Crosstalk between Mesenchymal Stromal/Stem Cells and Hepatocytes in Homeostasis and under Stress.International journal of molecular sciences · 2023Review
- Transcriptome wide functional analysis of HBx expressing human hepatocytes stimulated with endothelial cell cross-talk.Genomics · 2023Article
- TNF in the liver: targeting a central player in inflammation.Seminars in immunopathology · 2022Review
- Interaction between the Hepatitis B Virus and Cellular FLIP Variants in Viral Replication and the Innate Immune System.Viruses · 2022Review
- Hepatic RACK1 deficiency protects against fulminant hepatitis through myeloid-derived suppressor cells.Theranostics · 2022Article
- The mechanism of TiaoGanYiPi formula for treating chronic hepatitis B by network pharmacology and molecular docking verification.Scientific reports · 2021Article
- Withaferin A alleviates fulminant hepatitis by targeting macrophage and NLRP3.Cell death & disease · 2021Article
- Hepatocellular carcinoma (HCC): Epidemiology, etiology and molecular classification.Advances in cancer research · 2021Review
- AnFrontiers in genetics · 2021Article
- Cell Death and Liver Disease.Gut and liver · 2020Review
- HBV-related hepatocarcinogenesis: the role of signalling pathways and innovative ex vivo research models.BMC cancer · 2019Review
- Hepatitis B Spliced Protein (HBSP) Suppresses Fas-Mediated Hepatocyte Apoptosis via Activation of PI3K/Akt Signaling.Journal of virology · 2018Article
- Distinctiveness in virological features and pathogenic potentials of subgenotypes D1, D2, D3 and D5 of Hepatitis B virus.Scientific reports · 2018Article
- Inhibitory effects of resveratrol on hepatitis B virus X protein-induced hepatocellular carcinoma.Journal of veterinary science · 2017Article
- X protein variants of the autochthonous Latin American hepatitis B virus F genotype promotes human hepatocyte death by the induction of apoptosis and autophagy.Virus research · 2017Article
- Interference of Apoptosis by Hepatitis B Virus.Viruses · 2017Review
- Inhibition of apoptosis by oncogenic hepatitis B virus X protein: Implications for the treatment of hepatocellular carcinoma.World journal of hepatology · 2016Review
48 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Persistent infection with hepatitis B virus (HBV) is a leading cause of human liver disease and is strongly associated with hepatocellular carcinoma, one of the most prevalent forms of human cancer. Apoptosis (programmed cell death) is an important mediator of chronic liver disease caused by HBV infection. It is demonstrated that the HBV HBx protein acutely sensitizes cells to apoptotic killing when expressed during viral replication in cultured cells and in transfected cells independently of other HBV genes. Cells that were resistant to apoptotic killing by high doses of tumor necrosis factor alpha (TNFalpha), a cytokine associated with liver damage during HBV infection, were made sensitive to very low doses of TNFalpha by HBx. HBx induced apoptosis by prolonged stimulation of N-Myc and the stress-mediated mitogen-activated-protein kinase kinase 1 (MEKK1) pathway but not by up-regulating TNF receptors. Cell killing was blocked by inhibiting HBx stimulation of N-Myc or mitogen-activated-protein kinase kinase 1 using dominant-interfering forms or by retargeting HBx from the cytoplasm to the nucleus, which prevents HBx activation of cytoplasmic signal transduction cascades. Treatment of cells with a mitogenic growth factor produced by many virus-induced tumors impaired induction of apoptosis by HBx and TNFalpha. These results indicate that HBx might be involved in HBV pathogenesis (liver disease) during virus infection and that enhanced apoptotic killing by HBx and TNFalpha might select for neoplastic hepatocytes that survive by synthesizing mitogenic growth factors.
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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.