scholarly journals Development of PCR-ELISA for the detection of hepatitis B virus x gene expression and clinical application

2005 ◽  
Vol 19 (4) ◽  
pp. 139-145 ◽  
Author(s):  
Jong-Wan Kim ◽  
Jung-Hyun Shim ◽  
Joo-Won Park ◽  
Won-Cheol Jang ◽  
H.K. Chang ◽  
...  
1999 ◽  
Vol 257 (3) ◽  
pp. 759-765 ◽  
Author(s):  
Young Kyeung Kim ◽  
Ensung Junn ◽  
Inwon Park ◽  
Younghoon Lee ◽  
Changwon Kang ◽  
...  

2001 ◽  
Vol 353 (3) ◽  
pp. 701 ◽  
Author(s):  
Ritu GOILA ◽  
Akhil C. BANERJEA

1999 ◽  
Vol 73 (12) ◽  
pp. 10399-10405 ◽  
Author(s):  
Kurt Reifenberg ◽  
Heike Wilts ◽  
Jürgen Löhler ◽  
Petra Nusser ◽  
Ralph Hanano ◽  
...  

ABSTRACT The function of the X protein in the life cycle of mammalian hepadnaviruses is unclear. Based on tissue culture experiments it has been suggested that this protein represents a transcriptional transactivator which might be essential for the expression of the viral core gene. Here we have examined whether the activity of the human hepatitis B virus (HBV) core gene in vivo depends on X coexpression. To this end we compared core gene expression between four lineages of transgenic mice carrying the HBV core gene in cisarrangement with the X gene (cex lineage) and six lineages containing a modified construct in which the start codon of the X gene had been deleted (ce lineage). Whereas all cex lineages consistently exhibited a high-level hepatic core gene expression, the liver-specific core gene expression pattern of the ce lineages was heterogenous with four lineages virtually not expressing the core gene. This defect was due to a strongly reduced transcription since no core mRNA could be detected by Northern blotting. To test whether core gene expression could be restored by providing an intact X gene in trans, we crossbred mice of two lines which expressed no core mRNA or core protein with transgenic mice expressing the X-gene product under the transcriptional regulation of the liver-specific major-urinary-protein promoter/enhancer (MUP-X mice). The introduction of the MUP-X transgene induced core mRNA expression and core protein biosynthesis in the livers of the double-transgenic mice. This demonstrates that the X-gene product has the capacity to transactivate HBV core gene expression in vivo.


Virology ◽  
1990 ◽  
Vol 174 (1) ◽  
pp. 299-304 ◽  
Author(s):  
Massimo Levrero ◽  
O. Jean-Jean ◽  
C. Balsano ◽  
H. Will ◽  
M. Perricaudet

1999 ◽  
Vol 259 (1) ◽  
pp. 231
Author(s):  
Young Kyeung Kim ◽  
Ensung Junn ◽  
Inwon Park ◽  
Younghoon Lee ◽  
Changwon Kang ◽  
...  

2000 ◽  
Vol 33 (1) ◽  
pp. 142-151 ◽  
Author(s):  
Marc Weinberg ◽  
Marc Passman ◽  
Michael Kew ◽  
Patrick Arbuthnot

2006 ◽  
Vol 72 (3) ◽  
pp. 190-196 ◽  
Author(s):  
Wei Hou ◽  
Qin Ni ◽  
Jianer Wo ◽  
Minwei Li ◽  
Kezhou Liu ◽  
...  

2001 ◽  
Vol 75 (18) ◽  
pp. 8400-8406 ◽  
Author(s):  
Jie Li ◽  
Jing-hsiung Ou

ABSTRACT The expression of hepatitis B virus (HBV) genes is regulated by a number of transcription factors. One such factor, Sp1, has two binding sites in the core promoter and one in its upstream regulatory element, which is also known as the ENII enhancer. In this study, we have analyzed the effects of these three Sp1 binding sites on the expression of HBV genes. Our results indicate that both Sp1 binding sites in the core promoter are important for the transcription of the core RNA and the precore RNA. Moreover, while the downstream Sp1 site (the Sp1-1 site) in the core promoter did not affect the transcription of the S gene and the X gene, the upstream Sp1 site (the Sp1-2 site) in the core promoter was found to negatively regulate the transcription of the S gene and the X gene, as removal of the latter led to enhancement of transcription of these two genes. The Sp1 binding site in the ENII enhancer (the Sp1-3 site) positively regulates the expression of all of the HBV genes, as its removal by mutation suppressed the expression of all of the HBV genes. However, the suppressive effect of the Sp1-3 site mutation on the expression of the S gene and the X gene was abolished if the two Sp1 sites in the core promoter were also mutated. These results indicate that Sp1 can serve both as a positive regulator and as a negative regulator for the expression of HBV genes. This dual activity may be important for the differential regulation of HBV gene expression.


2001 ◽  
Vol 353 (3) ◽  
pp. 701-708 ◽  
Author(s):  
Ritu GOILA ◽  
Akhil C. BANERJEA

Two mono- and a di-RNA-cleaving DNA enzymes with the 10–23 catalytic motif were synthesized that were targeted to cleave at the conserved site/sites of the X gene of the hepatitis B virus. In each case, protein-independent but Mg2+-dependent cleavage of in vitro-synthesized full-length X RNA was obtained. Specific cleavage products were obtained with two different mono- and a di-DNA enzyme, with the latter giving rise to multiple RNA fragments that retained the cleavage specificity of the mono-DNA enzymes. A relatively less efficient cleavage was also obtained under simulated physiological conditions by the two mono-DNA enzymes but the efficiency of the di-DNA enzyme was significantly reduced. A single nucleotide change (G to C) in the 10–23 catalytic motif of the DNA enzyme 307 abolished its ability to cleave target RNA completely. Both, mono- and di-DNA enzymes, when introduced into a mammalian cell, showed specific inhibition of X-gene-mediated transactivation of reporter-gene expression. This decrease was due to the ability of these DNA enzymes to cleave X RNA intracellularly, which was also reflected by significant reduction in the levels of X protein in a liver-specific cell line, HepG2. Ribonuclease protection assay confirmed the specific reduction of X RNA in DNA-enzyme-treated cells. Potential in vivo applications of mono- and di-DNA enzymes in interfering specifically with the X-gene-mediated pathology are discussed.


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