ArticleVirus genes2003
A carboxy-terminal region of the hepatitis B virus X protein promotes DNA interaction of CREB and mimics the native protein for transactivation function.
Article in Virus genes, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- The Intrinsically Disordered Region of HBx and Virus-Host Interactions: Uncovering New Therapeutic Approaches for HBV and Cancer.International journal of molecular sciences · 2025Review
- Pre- and Post-Transcriptional Control of HBV Gene Expression: The Road Traveled towards the New Paradigm of HBx, Its Isoforms, and Their Diverse Functions.Biomedicines · 2023Review
- Pathogenicity and virulence of Hepatitis B virus.Virulence · 2022Review
- Canonical and Divergent N-Terminal HBx Isoform Proteins Unveiled: Characteristics and Roles during HBV Replication.Biomedicines · 2021Article
- Antibody-dependent enhancement infection facilitates dengue virus-regulated signaling of IL-10 production in monocytes.PLoS neglected tropical diseases · 2014Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Earlier we had shown that the conserved region E (residues 120-140) of HBV X protein (HBx) is crucial for transactivation. To investigate this region further, its oligomerisation was considered necessary to augment intracellular biochemical stability. Two to ten unit long tandem repeats of the E region (X16-n) were generated and their expression vectors constructed. Transient transfection of the E expression vectors along with different CAT constructs showed increase in the reporter activity. Interestingly a direct correlation was observed between the number of E repeat units in an expression vector and the level of transactivation. The transactivation levels with decameric X16 on different reporter constructs were comparable to those of the wild type HBx. Co-expression of X16 in a stable CHO-K1 cell line expressing the native HBx, showed co-operativity for transactivation. Further, X16 facilitated the binding of cAMP response element binding protein (CREB) to its responsive element just like the native HBx. The present study suggests that the C-terminal 'E' region of HBx represents its transactivation domain that acts by promoting the interaction of transcription factors to their cognate response elements.
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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.