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标题: Wang-Shick Ryu 韩国延世大学——HBV相关实验室及人物介绍系列 [打印本页]

作者: marine0425030    时间: 2015-2-3 23:20
标题: Wang-Shick Ryu 韩国延世大学——HBV相关实验室及人物介绍系列

http://web.yonsei.ac.kr/virus/

Wang-Shick Ryu

Department of Biochemistry
Yonsei University
PhD: University of Wisconsin-Madison
Post-doc : Fox Chase Cancer Center

Molecular Understanding of Hepadnavirus Infection

Chronic hepatitis remains the major fatal liver diseases in many area of the globe. In particular, over 5 % of world population is chronically infected with hepatitis B virus (HBV) and these individual has a high risk of liver diseases such as hepatitis, liver cirrhosis, and liver cancer. The work in my laboratory is focused on understanding molecular aspects of hepadnaviruses infection.  We are mainly using human hepatitis B virus (HBV) as a model, a prototype of hepadnavirus family.  Although it has a DNA genome, it replicates via reverse transcription of an RNA template, pregenomic RNA (pgRNA).  In particular, we are interested in molecular aspect of viral reverse transcription.  

The major approach has been to create mutations in a cloned DNA copy of the viral genome by site-directed mutagenesis and to determine the effect of the mutations on the viral life cycle after transfer of the altered DNAs into hepatoma cells in culture.  These genetic analyses have defined the functional domains of various viral proteins and the sites of their action on viral nucleic acids.  Recently, we reported a novel strand-transfer mechanism occurring during minus-strand DNA synthesis of viral reverse transcription [(Virology 371:32-373(2008)].  In addition, we reported that HBV polymerase suppresses translation of pgRNA, implicating a regulatory role of HBV polymerase in rergulating switching from translation to genome replication [Virology 373:112-123 (2008)].  In future, we aim to define host factors that contribute to viral reverse transcription via interaction with HBV polymerase or recognition of specific sequence elements on the pgRNA.

We are also interested in defining actual role of HBx, a small viral regulatory protein in its ability in supporting the viral genome replication.  We established oncogenic potency of HBx in the context of liver cancer (Oncogene 20: 16, 2001; Hepatology 39:1683, 2004).  Establishment of a robust replicon system by using hepatoma cells in culture, that critically depends on the HBx, enables us to address how HBx stimulates the viral reverse transcription. (2008/12/24)

http://web.yonsei.ac.kr/virus/publication.htm

Lim, W.Kwon, S-H, Cho, H., Kim, S., Lee, S, Ryu, W.-S., Cho, H.  HBx targeting to mitochondria and ROS generation are necessary but insufficient for HBV-induced cyclooxygenase-2 expression. J. Mol. Med. (in press)

Kim, S., H. Wang, W.-S. Ryu. Incorporation of eukaryotic translation factor eIF4E into viral nucleocapsids via interaction with hepatitis B viral polymerase. J. Virol. (accepted)

Kim, S, J. Lee, and W.-S. Ryu. Four Conserved Cysteine Residues of the Hepatitis B Virus Polymerase are Critical for RNA Pregenome Encapsidation.  J. Virol. 83:8032-8040(2009)

Lee, J., W.-S. Ryu. Insertion or deletion mutagenesis by overlap extension PCR. In: Braman, J, ed. In Vitro
Mutagenesis Protocols. Totowa, NJ: Humana Press (In press).  

Wang, H.F., S. Kim, W.-S. Ryu.  DDX3 DEAD-box RNA helicase inhibits hepatitis B viral reverse transcription by incorporation into nucleocapsids. J. Virol. 83:5815-5824(2009)

Hussain, Z. H.-S. Jung, D.-K., Ryu, and W.-S. Ryu. Genetic dissection of naturally occurring basal core promoter mutations of hepatitis B virus reveals the silent phenotype in the overlapping X gene. J. Gen. Virol. 90:2272-2281(2009)

Cha, M.-Y, D.-K. Ryu, H.-S. Jung, H.-E, Chang, W.-S. Ryu.  Stimulation of Hepatitis B Virus Genome Replication by HBx is Linked to Both Nuclear and Cytoplasmic HBx Expression. J. Gen. Virol. 90:978-986(2009)

Lee, H.-J. J. Lee , M. K. Shin and W.-S. Ryu.  Polyadenylation is dispensable for hepadnaviral reverse transcription. Mol. Cells. 25: 545-552 (2008)

Ryu, D.-K., S. Kim, and W.-S. Ryu. Hepatitis B virus polymerase suppresses translation of pregenomic RNA via a mechanism involving its interaction with 5' stem-loop structure. Virology 373:112-123 (2008)

Shin, M.-K., J.-H. Kim, D.-K. Ryu, and W.-S. Ryu. Circularization of an RNA template via long-range base pairing is critical for hepadnaviral reverse transcription. Virology 371:362-373 (2008)

Sohn, S.-Y., J.-H. Kim, K.-W. Baek, W.-S. Ryu, and B.-Y. Ahn. Turnover of hepatitis B virus X protein is facilitated by Hdji, a human Hsp40/DnaJ protein. BBRC 347: 764-768 (2006)

Cha, M.-Y., C.-M. kim, Y.-M. Park, and W.-S. Ryu. Hepatitis B virus X protein is essential for the activation of Wnt/β-catenin signaling in hepatoma cell. Hepatology 39:1683-1693 (2004)            

Shin, M.-K. J. Lee, and W.-S. Ryu. A Novel cis-acting Element Facilitates Minus-Strand DNA Synthesis During Reverse Transcription of the Hepatitis B Viruses Genome. J. Virol. 78:6252-6262 (2004)   

Lee, J., M.-K Shin, H.-J. Lee, and W.-S. Ryu. Identification of three novel cis-acting elements required for efficient plus-strand DNA synthesis of hepatitis B virus genome. J. Virol. 78:7455-7464 (2004)  

Lee, J., H.-J. Lee, M.-K Shin. and W.-S. Ryu. Versatile PCR-mediated insertion or deletion mutagenesis. BioTechniques 36:398-400 (2004)


作者: bigben446    时间: 2016-5-10 21:11
Lee, S. and W. Kim, et al. (2016). "Hepatitis B virus X protein enhances Myc stability by inhibiting SCF(Skp2) ubiquitin E3 ligase-mediated Myc ubiquitination and contributes to oncogenesis." Oncogene 35(14): 1857-67.
Ryu, D. K. and Y. Ahn, et al. (2015). "Development of a novel hepatitis B virus encapsidation detection assay by viral nucleocapsid-captured quantitative RT-PCR." Biotechniques 59(5): 287-93.
Ko, C. and Y. C. Shin, et al. (2014). "Residues Arg703, Asp777, and Arg781 of the RNase H domain of hepatitis B virus polymerase are critical for viral DNA synthesis." J Virol 88(1): 154-63.
Ko, C. and S. Lee, et al. (2014). "DDX3 DEAD-box RNA helicase is a host factor that restricts hepatitis B virus replication at the transcriptional level." J Virol 88(23): 13689-98.
Park, I. H. and Y. C. Kwon, et al. (2014). "Inhibition of hepatitis B virus replication by ligand-mediated activation of RNase L." Antiviral Res 104: 118-27.
Shin, Y. C. and C. Ko, et al. (2011). "Hydrophobic residues of terminal protein domain of hepatitis B virus polymerase contribute to distinct steps in viral genome replication." FEBS Lett 585(24): 3964-8.
Shin, Y. C. and S. Park, et al. (2011). "A conserved arginine residue in the terminal protein domain of hepatitis B virus  polymerase is critical for RNA pre-genome encapsidation." J Gen Virol 92(Pt 8): 1809-16.
Ryu, D. K. and B. Y. Ahn, et al. (2010). "Proximity between the cap and 5' epsilon stem-loop structure is critical for the  suppression of pgRNA translation by the hepatitis B viral polymerase." Virology 406(1): 56-64.
Wang, H. and W. S. Ryu (2010). "Hepatitis B virus polymerase blocks pattern recognition receptor signaling via interaction with DDX3: implications for immune evasion." PLoS Pathog 6(7): e1000986.
Kim, S. and H. Wang, et al. (2010). "Incorporation of eukaryotic translation initiation factor eIF4E into viral nucleocapsids via interaction with hepatitis B virus polymerase." J Virol 84(1): 52-8.
Kim, S. and J. Lee, et al. (2009). "Four conserved cysteine residues of the hepatitis B virus polymerase are critical for RNA pregenome encapsidation." J Virol 83(16): 8032-40.
Hussain, Z. and H. S. Jung, et al. (2009). "Genetic dissection of naturally occurring basal core promoter mutations of hepatitis B virus reveals a silent phenotype in the overlapping X gene." J Gen Virol 90(Pt 9): 2272-81.
Cha, M. Y. and D. K. Ryu, et al. (2009). "Stimulation of hepatitis B virus genome replication by HBx is linked to both nuclear and cytoplasmic HBx expression." J Gen Virol 90(Pt 4): 978-86.
Wang, H. and S. Kim, et al. (2009). "DDX3 DEAD-Box RNA helicase inhibits hepatitis B virus reverse transcription by incorporation into nucleocapsids." J Virol 83(11): 5815-24.
Lee, H. J. and J. Lee, et al. (2008). "Polyadenylation is dispensable for encapsidation and reverse transcription of hepatitis B viral pregenomic RNA." Mol Cells 25(4): 545-52.
Ryu, D. K. and S. Kim, et al. (2008). "Hepatitis B virus polymerase suppresses translation of pregenomic RNA via a mechanism involving its interaction with 5' stem-loop structure." Virology 373(1): 112-23.
Sohn, S. Y. and J. H. Kim, et al. (2006). "Turnover of hepatitis B virus X protein is facilitated by Hdj1, a human Hsp40/DnaJ protein." Biochem Biophys Res Commun 347(3): 764-8.
Lee, J. and M. K. Shin, et al. (2004). "Three novel cis-acting elements required for efficient plus-strand DNA synthesis  of the hepatitis B virus genome." J Virol 78(14): 7455-64.
Cha, M. Y. and C. M. Kim, et al. (2004). "Hepatitis B virus X protein is essential for the activation of Wnt/beta-catenin signaling in hepatoma cells." Hepatology 39(6): 1683-93.
Shin, M. K. and J. Lee, et al. (2004). "A novel cis-acting element facilitates minus-strand DNA synthesis during reverse  transcription of the hepatitis B virus genome." J Virol 78(12): 6252-62.
Ryu, W. S. (2003). "Molecular aspects of hepatitis B viral infection and the viral carcinogenesis." J Biochem Mol Biol 36(1): 138-43.
Joo, H. Y. and K. H. Han, et al. (2002). "[Gene expression profile in response to hepatitis B virus X gene by using an adenoviral vector]." Taehan Kan Hakhoe Chi 8(4): 371-80.
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Paik, Y. H. and H. Y. Chung, et al. (2001). "Emergence of YMDD motif mutant of hepatitis B virus during short-term lamivudine  therapy in South Korea." J Hepatol 35(1): 92-8.
Kim, Y. C. and K. S. Song, et al. (2001). "Activated ras oncogene collaborates with HBx gene of hepatitis B virus to transform cells by suppressing HBx-mediated apoptosis." Oncogene 20(1): 16-23.
Jeong, J. K. and G. S. Yoon, et al. (2000). "Evidence that the 5'-end cap structure is essential for encapsidation of hepatitis B virus pregenomic RNA." J Virol 74(12): 5502-8.
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