scholarly journals Activating Transcription Factor 2 (ATF2) Down-regulates Hepatitis B Virus X Promoter Activity by the Competition for the Activating Protein 1 Binding Site and the Formation of the ATF2-Jun Heterodimer

1997 ◽  
Vol 272 (27) ◽  
pp. 16934-16939 ◽  
Author(s):  
Cheol Yong Choi ◽  
Byung Hyune Choi ◽  
Geon Tae Park ◽  
Hyune Mo Rho
Keyword(s):  
Transcription Factor ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Binding Site ◽  
Promoter Activity ◽  
B Virus ◽  
Activating Transcription Factor

Endoplasmic reticulum stress induced by hepatitis B virus X protein enhances cyclo-oxygenase 2 expression via activating transcription factor 4

2011 ◽  
Vol 435 (2) ◽  
pp. 431-439 ◽  
Author(s):  
Hyun Kook Cho ◽  
Kyu Jin Cheong ◽  
Hye Young Kim ◽  
JaeHun Cheong
Keyword(s):  
Endoplasmic Reticulum ◽  
Transcription Factor ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Critical Role ◽  
Activating Transcription Factor 4 ◽  
B Virus ◽  
Activating Transcription Factor ◽  
Transcription Factor 4 ◽  
Cox2 Expression

Chronic hepatitis B is a disease of the liver that can progress to cirrhosis and liver cancer. The HBx (hepatitis B virus X) protein of hepatitis B virus is a multifunctional regulator that induces ER (endoplasmic reticulum) stress by previously unknown mechanisms. ER stress plays a critical role in inflammatory induction and COX2 (cyclo-oxygenase 2) is an important mediator of this inflammation. In the present study, we demonstrate the molecular mechanisms of HBx on induction of ER stress and COX2 expression. In addition, HBx reduced expression of enzymes which are involved in mitochondrial β-oxidation of fatty acids and the mitochondrial inner membrane potential. The reduction in intracellular ATP levels by HBx induced the unfolded protein response and COX2 expression through the eIF2α (eukaryotic initiation factor 2α)/ATF4 (activating transcription factor 4) pathway. We confirmed that ATF4 binding to the COX2 promoter plays a critical role in HBx-mediated COX2 induction. The results of the present study suggest that HBV infection contributes to induction of hepatic inflammation through dysfunction of cellular organelles including the ER and mitochondria.

Hepatitis B virus regulation of Raf1 promoter activity through activation of transcription factor AP-2α

2012 ◽  
Vol 158 (4) ◽  
pp. 887-894 ◽  
Author(s):  
Jialin Qu ◽  
Jianbo Li ◽  
Ke Chen ◽  
Dongdong Qin ◽  
Kai Li ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Promoter Activity ◽  
Activation Of Transcription ◽  
B Virus

scholarly journals The Binding Site of Transcription Factor YY1 Is Required for Intramolecular Recombination between Terminally Repeated Sequences of Linear Replicative Hepatitis B Virus DNA

2000 ◽  
Vol 74 (20) ◽  
pp. 9471-9478 ◽  
Author(s):  
Yasuyuki Hayashi ◽  
Yoshiyuki Kitamura ◽  
Mayumi Nakanishi ◽  
Katsuro Koike
Keyword(s):  
Transcription Factor ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Binding Site ◽  
Hbv Dna ◽  
Terminal Region ◽  
Repeated Sequences ◽  
Viral Dna ◽  
B Virus ◽  
Intramolecular Recombination

ABSTRACT In the replication cycle of hepadnavirus DNA, the double-stranded linear form of viral DNA is generated as a minor replicative intermediate, which is efficiently converted to covalently closed circular DNA (cccDNA) by intramolecular recombination (W. Yang and J. Summers, J. Virol. 69:4029–4036, 1995). We previously found a binding site of transcription factor Yin and Yang 1 (YY1) in one terminal region of the double-stranded linear replicative hepatitis B virus (HBV) DNA (M. Nakanishi-Matsui, Y. Hayashi, Y. Kitamura, and K. Koike, J. Virol. 74:5562–5568, 2000). However, it is not known whether the YY1-binding site is required for the intramolecular recombination of HBV DNA. In this study, we established an HBV-producing system in which the cccDNA appeared to be generated from the transfected linear DNA or the linear replicative DNA by nonhomologous end joining (NHEJ) or by both NHEJ and homologous recombination between terminally repeated sequences, respectively. When the YY1-binding site in the terminal region of transfected linear viral DNA was mutated, the cccDNA was generated merely by NHEJ. Results suggest that the YY1-binding site in the terminal region of linear replicative HBV DNA is required for intramolecular recombination between terminally repeated sequences.

scholarly journals Hepatitis B virus X protein impedes the DNA repair via its association with transcription factor, TFIIH

2011 ◽  
Vol 11 (1) ◽  
pp. 48 ◽  
Author(s):  
Ishtiaq Qadri ◽  
Kaneez Fatima ◽  
Hany AbdeL-Hafiz
Keyword(s):  
Dna Repair ◽  
Transcription Factor ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
X Protein ◽  
B Virus

scholarly journals Hepatitis B virus X protein promotes human hepatoma cell growth via upregulation of transcription factor AP2α and sphingosine kinase 1

2015 ◽  
Vol 36 (10) ◽  
pp. 1228-1236 ◽  
Author(s):  
Zhan-ping Lu ◽  
Ze-lin Xiao ◽  
Zhe Yang ◽  
Jiong Li ◽  
Guo-xing Feng ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Hepatitis B Virus ◽  
Cell Growth ◽  
Hepatitis B ◽  
Hepatoma Cell ◽  
Sphingosine Kinase ◽  
Human Hepatoma ◽  
Sphingosine Kinase 1 ◽  
Human Hepatoma Cell ◽  
B Virus

scholarly journals Creation of a Six-fingered Artificial Transcription Factor That Represses the Hepatitis B Virus HBx Gene Integrated into a Human Hepatocellular Carcinoma Cell Line

2012 ◽  
Vol 18 (4) ◽  
pp. 378-387 ◽  
Author(s):  
Xinghui Zhao ◽  
Zhanzhong Zhao ◽  
Junwei Guo ◽  
Peitang Huang ◽  
Xudong Zhu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Transcription Factor ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Cell Line ◽  
Hbv Infection ◽  
Luciferase Reporter ◽  
Artificial Transcription Factor ◽  
Chronic Hepatitis B Virus ◽  
B Virus

Chronic hepatitis B virus (HBV) infection is an independent risk factor for the development of hepatocellular carcinoma (HCC). The HBV HBx gene is frequently identified as an integrant in the chromosomal DNA of patients with HCC. HBx encodes the X protein (HBx), a putative viral oncoprotein that affects transcriptional regulation of several cellular genes. Therefore, HBx may be an ideal target to impede the progression of HBV infection–related HCC. In this study, integrated HBx was transcriptionally downregulated using an artificial transcription factor (ATF). Two three-fingered Cys2-His2 zinc finger (ZF) motifs that specifically recognized two 9-bp DNA sequences regulating HBx expression were identified from a phage-display library. The ZF domains were linked into a six-fingered protein that specified an 18-bp DNA target in the Enhancer I region upstream of HBx. This DNA-binding domain was fused with a Krüppel-associated box (KRAB) transcriptional repression domain to produce an ATF designed to downregulate HBx integrated into the Hep3B HCC cell line. The ATF significantly repressed HBx in a luciferase reporter assay. Stably expressing the ATF in Hep3B cells resulted in significant growth arrest, whereas stably expressing the ATF in an HCC cell line lacking integrated HBx (HepG2) had virtually no effect. The targeted downregulation of integrated HBx is a promising novel approach to inhibiting the progression of HBV infection–related HCC.

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