scholarly journals Accurately mapping the location of the binding site for the interaction between hepatitis B virus X protein and cytochrome c oxidase III

2014 ◽  
Vol 35 (2) ◽  
pp. 319-324 ◽  
Author(s):  
DAN LI ◽  
JIAN DING ◽  
ZHIXIN CHEN ◽  
YUN CHEN ◽  
NA LIN ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Cytochrome C ◽  
Hepatitis B ◽  
Binding Site ◽  
Cytochrome C Oxidase ◽  
X Protein ◽  
B Virus

scholarly journals Regulation of Hepatitis B Virus Core Promoter by Transcription Factors HNF1 and HNF4 and the Viral X Protein

2004 ◽  
Vol 78 (13) ◽  
pp. 6908-6914 ◽  
Author(s):  
Yanyan Zheng ◽  
Jie Li ◽  
Jing-hsiung Ou
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Binding Site ◽  
Nuclear Receptors ◽  
Double Mutant ◽  
Core Promoter ◽  
X Protein ◽  
Double Mutation ◽  
The Core ◽  
B Virus

ABSTRACT Hepatitis B virus (HBV) core promoter contains a binding site for nuclear receptors. A natural double mutation in this binding site, which changes nucleotide (nt) 1765 from A to T and nt 1767 from G to A, selectively abolishes the binding of several nuclear receptors without affecting that of HNF4. This double mutation also creates a binding site for the transcription factor HNF1 and changes two amino acids in the overlapping X protein sequence. In this study, we have examined the roles of HNF1, HNF4, and the X protein in the regulation of the core promoter activities in Huh7 hepatoma cells. Our results indicate that HNF4 could stimulate the expression of the precore RNA and the core RNA from the core promoter of both the wild-type (WT) HBV and the double mutant, although its effect on the former was more prominent. In contrast, HNF1, which did not affect the WT core promoter, suppressed the precore RNA expression of the double mutant. Further analysis using HBV genomic constructs, with and without the ability to express the X protein, indicates that the X protein did not affect the HNF4 activity on the core promoter and affected the HNF1 activity on the core promoter of only the double mutant. Thus, our results indicate that the phenotypic differences of HBV WT and double-mutant core promoters are at least partially due to the differential activities of HNF1, HNF4, and the X protein on these two promoters.

Mo1527 Defects of Cytochrome C Oxidase in Hepatitis B Virus Related Liver Cirrhosis

2012 ◽  
Vol 142 (5) ◽  
pp. S-987-S-988
Author(s):  
Wey-Ran Lin ◽  
Chau-Ting Yeh ◽  
Cheng-Tang Chiu
Keyword(s):  
Liver Cirrhosis ◽  
Hepatitis B Virus ◽  
Cytochrome C ◽  
Hepatitis B ◽  
Cytochrome C Oxidase ◽  
B Virus

A novel hepatitis B virus X-interactive protein: Cytochrome C oxidase III

2006 ◽  
Vol 21 (4) ◽  
pp. 711-715 ◽  
Author(s):  
Xiao Zhong Wang ◽  
Dan Li ◽  
Qi Min Tao ◽  
Na Lin ◽  
Zhi Xin Chen
Keyword(s):  
Hepatitis B Virus ◽  
Cytochrome C ◽  
Hepatitis B ◽  
Cytochrome C Oxidase ◽  
B Virus

scholarly journals Altered Binding Site Selection of p53 Transcription Cassettes by Hepatitis B Virus X Protein

2012 ◽  
Vol 33 (3) ◽  
pp. 485-497 ◽  
Author(s):  
Cheryl Chan ◽  
Yu Wang ◽  
Pierce K. H. Chow ◽  
Alexander Y. F. Chung ◽  
London L. P. J. Ooi ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Binding Site ◽  
Transcription Regulation ◽  
Site Selection ◽  
Regulatory Region ◽  
X Protein ◽  
Aberrant Expression ◽  
B Virus ◽  
Selection Of

ABSTRACTThe key cellular regulator p53 is a common target of viral oncoproteins. However, the mechanism by which p53 transcription regulation is modulated by hepatitis B virus X protein (HBx), a transcription cofactor implicated in hepatitis B virus-associated hepatocellular carcinoma (HCC), is poorly understood. By integrating p53 chromatin immunoprecipitation (ChIP)-on-chip and expression profiling of an HBx-expressing cell culture system, we report that HBx alters p53 binding site selectivity in the regulatory regions of genes, and this is associated with their aberrant expression. Using an HBx-deregulated gene,p53AIP1, as a model, we show that HBx aberrantly increasesp53AIP1expression by conferring p53 selectivity for a more conserved binding site in its regulatory region. We further demonstrate that HBx-deregulated increasedp53AIP1expression is relevant in HCC livers and define a functional role forp53AIP1in mediating HBx-induced apoptosisin vitro. Significantly, we provide evidence that specific p53-associated transcription cofactors and coregulators are differentially recruited in the presence of HBx, effecting a PCAF-mediated “p53 Lys320 acetylation switch” that results in altered binding site selection of distinct p53 transcription cassettes. The findings here clarify the role of HBx in modulating p53 transcription regulation and provide a novel mechanistic insight into this deregulation.

scholarly journals Hepatitis B virus X protein regulates the mEZH2 promoter via the E2F1-binding site in AML12 cells

2011 ◽  
Vol 30 (4) ◽  
pp. 273-279 ◽  
Author(s):  
Xiao-Yan Shi ◽  
Ying-Ying Zhang ◽  
Xiao-Wei Zhou ◽  
Jian-Sheng Lu ◽  
Ze-Kun Guo ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Binding Site ◽  
X Protein ◽  
B Virus
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