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37 results on '"Zhou, Tianlun"'

4. HBsAg mRNA degradation induced by a dihydroquinolizinone compound depends on the HBV posttranscriptional regulatory element

Author

Zhou, Tianlun, Block, Timothy, Liu, Fei, Kondratowicz, Andrew S., Sun, Liren, Rawat, Siddhartha, Branson, Jeffrey, Guo, Fang, Steuer, Holly Micolochick, Liang, Hongyan, Bailey, Lauren, Moore, Chris, Wang, Xiaohe, Cuconatti, Andy, Gao, Min, Lee, Amy C.H., Harasym, Troy, Chiu, Tim, Gotchev, Dimitar, Dorsey, Bruce, Rijnbrand, Rene, and Sofia, Michael J.

Published
2018
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13. The Dihydroquinolizinone Compound RG7834 Inhibits the Polyadenylase Function of PAPD5 and PAPD7 and Accelerates the Degradation of Matured Hepatitis B Virus Surface Protein mRNA

Author

Sun, Liren, primary, Zhang, Fang, additional, Guo, Fang, additional, Liu, Fei, additional, Kulsuptrakul, Jessie, additional, Puschnik, Andreas, additional, Gao, Min, additional, Rijnbrand, Rene, additional, Sofia, Michael, additional, Block, Timothy, additional, and Zhou, Tianlun, additional

Published
2020
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14. Scalable Synthesis, In Vitro cccDNA Reduction, and In Vivo Antihepatitis B Virus Activity of a Phosphonomethoxydeoxythreosyl Adenine Prodrug

Author

Luo, Min, primary, Wu, Shuo, additional, Kalkeri, Raj, additional, Ptak, Roger G., additional, Zhou, Tianlun, additional, Van Mellaert, Lieve, additional, Wang, Chuanmin, additional, Dumbre, Shrinivas G., additional, Block, Timothy, additional, Groaz, Elisabetta, additional, De Jonghe, Steven, additional, Li, Yuhuan, additional, and Herdewijn, Piet, additional

Published
2020
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17. Proteomic analysis of primary duck hepatocytes infected with duck hepatitis B virus

Author

Zhou Tianlun, Ye Rong, Lou Qiang, Zhou Shuangcheng, Xu Bin, Yan Liang, Zhou Xinwen, Qu Su, Ben Haijing, Zhao Yanfeng, Yang Pengyuan, and Qu Di

Subjects
Cytology, QH573-671
Abstract

Abstract Background Hepatitis B virus (HBV) is a major cause of liver infection in human. Because of the lack of an appropriate cell culture system for supporting HBV infection efficiently, the cellular and molecular mechanisms of hepadnavirus infection remain incompletely understood. Duck heptatitis B virus (DHBV) can naturally infect primary duck hepatocytes (PDHs) that provide valuable model systems for studying hepadnavirus infection in vitro. In this report, we explored global changes in cellular protein expression in DHBV infected PDHs by two-dimension gel electrophoresis (2-DE) combined with MALDI-TOF/TOF tandem mass spectrometry (MS/MS). Results The effects of hepadnavirus infection on hepatocytes were investigated in DHBV infected PDHs by the 2-DE analysis. Proteomic profile of PDHs infected with DHBV were analyzed at 24, 72 and 120 h post-infection by comparing with uninfected PDHs, and 75 differentially expressed protein spots were revealed by 2-DE analysis. Among the selected protein spots, 51 spots were identified corresponding to 42 proteins by MS/MS analysis; most of them were matched to orthologous proteins of Gallus gallus, Anas platyrhynchos or other avian species, including alpha-enolase, lamin A, aconitase 2, cofilin-2 and annexin A2, etc. The down-regulated expression of beta-actin and annexin A2 was confirmed by Western blot analysis, and potential roles of some differentially expressed proteins in the virus-infected cells have been discussed. Conclusions Differentially expressed proteins of DHBV infected PDHs revealed by 2-DE, are involved in carbohydrate metabolism, amino acid metabolism, stress responses and cytoskeleton processes etc, providing the insight to understanding of interactions between hepadnavirus and hepatocytes and molecular mechanisms of hepadnavirus pathogenesis.

Published
2010
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21. Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53

Author

Fei, Qi, primary, Shang, Ke, additional, Zhang, Jianhua, additional, Chuai, Shannon, additional, Kong, Desheng, additional, Zhou, Tianlun, additional, Fu, Shijun, additional, Liang, Ying, additional, Li, Chong, additional, Chen, Zhi, additional, Zhao, Yuan, additional, Yu, Zhengtian, additional, Huang, Zheng, additional, Hu, Min, additional, Ying, Haiyan, additional, Chen, Zhui, additional, Zhang, Yun, additional, Xing, Feng, additional, Zhu, Jidong, additional, Xu, Haiyan, additional, Zhao, Kehao, additional, Lu, Chris, additional, Atadja, Peter, additional, Xiao, Zhi-Xiong, additional, Li, En, additional, and Shou, Jianyong, additional

Published
2015
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22. Novel Woodchuck Hepatitis Virus (WHV) Transgene Mouse Models Show Sex-Dependent WHV Replicative Activity and Development of Spontaneous Immune Responses to WHV Proteins

Author

Meng, Zhongji, primary, Ma, Zhiyong, additional, Zhang, Ejuan, additional, Kosinska, Anna D., additional, Liu, Jia, additional, Zhang, Xiaoyong, additional, Zhou, Tianlun, additional, Wu, Jun, additional, Dahmen, Uta, additional, Dirsch, Olaf, additional, Yang, Dongliang, additional, Roggendorf, Michael, additional, and Lu, Mengji, additional

Published
2014
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32. Combination Therapy with Lamivudine and Adenovirus Causes Transient Suppression of Chronic Woodchuck Hepatitis Virus Infections

Author

Zhou, Tianlun, primary, Guo, Juo-Tao, additional, Nunes, Frederick A., additional, Molnar-Kimber, Katherine L., additional, Wilson, James M., additional, Aldrich, Carol E., additional, Saputelli, Jeffry, additional, Litwin, Sam, additional, Condreay, Lynn D., additional, Seeger, Christoph, additional, and Mason, William S., additional

Published
2000
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34. Mutations of the Woodchuck Hepatitis Virus Polymerase Gene That Confer Resistance to Lamivudine and 2'-Fluoro-5-Methyl-ß-l-Arabinofuranosyluracil

Author

Yamamoto, Toshiki, Litwin, Samuel, Zhou, Tianlun, Zhu, Yuao, Condreay, Lynn, Furman, Phillip, and Mason, William S.

Abstract

ABSTRACTAdministration of either lamivudine (2'-deoxy-3'-thiacytidine) or l-FMAU (2'-fluoro-5-methyl-ß-l-arabinofuranosyluracil) to woodchucks chronically infected with woodchuck hepatitis virus (WHV) induces a transient decline in virus titers. However, within 6 to 12 months, virus titers begin to increase towards pretreatment levels. This is associated with the emergence of virus strains with mutations of the B and C regions of the viral DNA polymerase (T. Zhou et al., Antimicrob. Agents Chemother. 43:1947–1954, 1999; Y. Zhu et al., J. Virol. 75:311–322, 2001). The present study was carried out to determine which of the mutants that we have identified conferred resistance to lamivudine and/or to l-FMAU. When inserted into a laboratory strain of WHV, each of the mutations, or combinations of mutations, of regions B and C produced a DNA replication-competent virus and typically conferred resistance to both nucleoside analogs in cell culture. Sequencing of the polymerase active site also occasionally revealed other mutations, but these did not appear to contribute to drug resistance. Moreover, in transfected cells, most of the mutants synthesized viral DNA nearly as efficiently as wild-type WHV. Computational models suggested that persistence of several of the WHV mutants as prevalent species in the serum and, by inference, liver for up to 6 months following drug withdrawal required a replication efficiency of at least 10 to 30% of that of the wild type. However, their delayed emergence during therapy suggested replication efficiency in the presence of the drug that was still well below that of wild-type WHV in the absence of the drug.

Published
2002
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35. Histone methyltransferase SETDB1 regulates liver cancer cell growth through methylation of p53.

Author

Fei, Qi, Shang, Ke, Zhang, Jianhua, Chuai, Shannon, Kong, Desheng, Zhou, Tianlun, Fu, Shijun, Liang, Ying, Li, Chong, Chen, Zhi, Zhao, Yuan, Yu, Zhengtian, Huang, Zheng, Hu, Min, Ying, Haiyan, Chen, Zhui, Zhang, Yun, Xing, Feng, Zhu, Jidong, and Xu, Haiyan

Subjects
HISTONE methyltransferases, LIVER cancer, P53 antioncogene, GENES, METHYLATION, MELANOMA
Abstract

SETDB1 is a histone H3K9 methyltransferase that has a critical role in early development. It is located within a melanoma susceptibility locus and facilitates melanoma formation. However, the mechanism by which SETDB1 regulates tumorigenesis remains unknown. Here we report the molecular interplay between SETDB1 and the well-known hotspot gain-of-function (GOF) TP53 R249S mutation. We show that in hepatocellular carcinoma (HCC) SETDB1 is overexpressed with moderate copy number gain, and GOF TP53 mutations including R249S associate with this overexpression. Inactivation of SETDB1 in HCC cell lines bearing the R249S mutation suppresses cell growth. The TP53 mutation status renders cancer cells dependent on SETDB1. Moreover, SETDB1 forms a complex with p53 and catalyses p53K370 di-methylation. SETDB1 attenuation reduces the p53K370me2 level, which subsequently leads to increased recognition and degradation of p53 by MDM2. Together, we provide both genetic and biochemical evidence for a mechanism by which SETDB1 regulates cancer cell growth via methylation of p53. [ABSTRACT FROM AUTHOR]

Published
2015
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36. Evolving New Strategies for the Medical Management of Chronic Hepatitis B Virus Infection.

Author

Block TM, Zhou T, Anbarasan N, and Gish R

Abstract

Is a cure for chronic hepatitis B virus (HBV) infection possible? Hepatitis C virus infection is now routinely cured medically. There is a growing expectation that new drugs for the management of chronic HBV infection should provide substantial benefit over and above that of current chronic HBV medications, if not be curative. Although the definition of medically induced cure for chronic HBV infection varies, most include sustained off-drug absence of viremia and negativity for other virologic markers. There are currently more than 29 drugs in the pipeline being tested for the management of chronic HBV infection. This article discusses the potential drugs with respect to their possible contributions to achieving medically induced cure.

Published
2016

37. Mutations of the woodchuck hepatitis virus polymerase gene that confer resistance to lamivudine and 2'-fluoro-5-methyl-beta-L-arabinofuranosyluracil.

Author

Yamamoto T, Litwin S, Zhou T, Zhu Y, Condreay L, Furman P, and Mason WS

Subjects
Amino Acid Sequence, Animals, Arabinofuranosyluracil analogs & derivatives, Binding Sites, DNA-Directed DNA Polymerase genetics, Genes, Viral physiology, Hepatitis B Virus, Woodchuck drug effects, Hepatitis B Virus, Woodchuck genetics, Hepatitis B Virus, Woodchuck physiology, Humans, Marmota, Molecular Sequence Data, Mutagenesis, Mutagenesis, Insertional, Sequence Homology, Amino Acid, Time Factors, Tumor Cells, Cultured, Virus Replication, Antiviral Agents pharmacology, Arabinofuranosyluracil pharmacology, DNA-Directed DNA Polymerase physiology, Drug Resistance, Multiple, Viral, Drug Resistance, Viral, Hepatitis B Virus, Woodchuck enzymology, Lamivudine pharmacology
Abstract

Administration of either lamivudine (2'-deoxy-3'-thiacytidine) or L-FMAU (2'-fluoro-5-methyl-beta-L-arabinofuranosyluracil) to woodchucks chronically infected with woodchuck hepatitis virus (WHV) induces a transient decline in virus titers. However, within 6 to 12 months, virus titers begin to increase towards pretreatment levels. This is associated with the emergence of virus strains with mutations of the B and C regions of the viral DNA polymerase (T. Zhou et al., Antimicrob. Agents Chemother. 43:1947-1954, 1999; Y. Zhu et al., J. Virol. 75:311-322, 2001). The present study was carried out to determine which of the mutants that we have identified conferred resistance to lamivudine and/or to L-FMAU. When inserted into a laboratory strain of WHV, each of the mutations, or combinations of mutations, of regions B and C produced a DNA replication-competent virus and typically conferred resistance to both nucleoside analogs in cell culture. Sequencing of the polymerase active site also occasionally revealed other mutations, but these did not appear to contribute to drug resistance. Moreover, in transfected cells, most of the mutants synthesized viral DNA nearly as efficiently as wild-type WHV. Computational models suggested that persistence of several of the WHV mutants as prevalent species in the serum and, by inference, liver for up to 6 months following drug withdrawal required a replication efficiency of at least 10 to 30% of that of the wild type. However, their delayed emergence during therapy suggested replication efficiency in the presence of the drug that was still well below that of wild-type WHV in the absence of the drug.

Published
2002
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