ArticleOncogene2000
UVDDB p127-binding modulates activities and intracellular distribution of hepatitis B virus X protein.
Article in Oncogene, 2000. 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
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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
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Conserved Yet Divergent Smc5/6 Complex Degradation by Mammalian Hepatitis B Virus X Proteins.International journal of molecular sciences · 2025Article
- JunB-HBZ nuclear translocation by TGF-β is a key driver in HTLV-1-mediated leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Antagonism of BST2/Tetherin, a new restriction factor of respiratory syncytial virus, requires the viral NS1 protein.PLoS pathogens · 2024Article
- Novel Approaches to Inhibition of HBsAg Expression from cccDNA and Chromosomal Integrants: A Review.Journal of clinical and translational hepatology · 2023Review
- Tampering of Viruses and Bacteria with Host DNA Repair: Implications for Cellular Transformation.Cancers · 2021Review
- Spatiotemporal Analysis of Hepatitis B Virus X Protein in Primary Human Hepatocytes.Journal of virology · 2019Article
- Post-translational Modification Control of HBV Biological Processes.Frontiers in microbiology · 2018Review
- A Mass Spectrometry-Based Profiling of Interactomes of Viral DDB1- and Cullin Ubiquitin Ligase-Binding Proteins Reveals NF-κB Inhibitory Activity of the HIV-2-Encoded Vpx.Frontiers in immunology · 2018Article
- Identifying and Characterizing Interplay between Hepatitis B Virus X Protein and Smc5/6.Viruses · 2017Review
- Hepatitis B virus X protein identifies the Smc5/6 complex as a host restriction factor.Nature · 2016Article
- Cullin E3 ligases and their rewiring by viral factors.Biomolecules · 2014Review
- Methyltransferase PRMT1 is a binding partner of HBx and a negative regulator of hepatitis B virus transcription.Journal of virology · 2013Article
- The viral transactivator HBx protein exhibits a high potential for regulation via phosphorylation through an evolutionarily conserved mechanism.Infectious agents and cancer · 2012Article
- Hepatitis B virus X gene and hepatocarcinogenesis.Journal of gastroenterology · 2011Review
- Molecular insight into how HIV-1 Vpr protein impairs cell growth through two genetically distinct pathways.The Journal of biological chemistry · 2011Article
- The human immunodeficiency virus type 2 Vpx protein usurps the CUL4A-DDB1 DCAF1 ubiquitin ligase to overcome a postentry block in macrophage infection.Journal of virology · 2009Article
- HIV-1 Vpr: mechanisms of G2 arrest and apoptosis.Experimental and molecular pathology · 2008Review
- Hepatitis B virus-cell interactions and pathogenesis.Journal of cellular physiology · 2008Review
- Human immunodeficiency virus type 1 Vpr links proteasomal degradation and checkpoint activation.Journal of virology · 2008Review
- HIV-1 Vpr function is mediated by interaction with the damage-specific DNA-binding protein DDB1.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
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
Mammalian hepatitis B viruses encode a unique regulatory protein termed X, which is essential for infection and likely plays a role in the carcinogenic process associated with hepadnaviral infection. Among the numerous properties ascribed to X protein, two have been widely documented: promiscuous transcriptional transactivation and proapoptosis. However, full understanding of the mechanisms underlying these activities requires the identification of the genuine X partners among the multiple X-binding host proteins. Here we show that (i) mutations in X protein, which markedly alter affinity for the host protein UVDDBp127, inactivate both transactivation and proapoptosis; (ii) ectopic fusion of a functional UVDDB-binding domain to a deficient binding X mutant restored its activity; (iii) in contrast to the loss-of-binding mutants, a mutant with a strong gain-of-binding exerted trans-dominant negative effects on wt X activity and localized in the nucleus and (iv) increase in intracellular UVDDB concentration enhanced both wt X-mediated transactivation and apoptosis. Taken together, our data provide strong evidence for a common upstream step in X mode of action, consisting of its productive interaction with UVDDB, via a structurally and functionally autonomous module. In addition, they underscore a nuclear location step of the viral protein that depends on its ability to bind UVDDB.
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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.