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刘杰, Xiao-Yan Cao, Jie Liu, Zhao-Rui Lian, Marcy Clayton, Jia-Lu Hu, Ming-Hua Zhu, Dai-Ming Fan and Mark Feitelson
World J Gastroenterol 2001; 7 (4): 575-578,-0001,():
-1年11月30日
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刘杰, JONATHAN LARKIN, MARCIA M. CLAYTON, JIE LIU, AND MARK A. FEITELSON,
HEPATOLOGY Vol. 34, No.4, 2001,-0001,():
-1年11月30日
Epidemiologic observations show a higher frequency of hepatitis B virus (HBV) serologic markers in chronic alcoholics compared with the general population. This may be the result of an increased susceptibility of alcoholics to infection and/or to an ethanol-mediated stimulation of HBV gene expression and replication. To test the latter hypothesis, HBV transgenic SCID mice, which support consistent levels of virus replication, were fed with a standard Lieber-DiCarli or isocaloric diet for 5 weeks. In ethanol-fed mice, the levels of hepatitis B surface antigen (HBsAg) and viral DNA in serum increased by up to 7-fold compared with mice fed the control diet. Ethanol-treated mice also had elevated HBV-RNA levels, and increased expression of surface, core, and X antigens in the liver, especially in the pericentral regions. None of these changes were observed in transgenic mice fed isocaloric diets. Thus, chronic alcohol consumption alters the patterns of HBV gene expression and replication in the serum and liver of HBV transgenic SCID mice, and may provide a partial explanation for the increased frequency of HBV markers among alcoholics. (HEPATOLOGY 2001; 34: 792-797.)
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刘杰, N. Lale Satiroglu Tufan*, Zhaorui Llan*, MJie Liu*, Jingbo Pan*, Patrick Arbuthnot†, Michael Kew†, Marcy M Clayton*, Minghua Zhu† and Mark A Feitelson*
Neoplasia,-0001,():
-1年11月30日
Hepatitis B virus encoded X antigen (HBxAg) may contribute to the development of hepatocelIular carcin-oma (HCC) by up-or downregulating the expression of cellular genes that promote cell growth and urvival. To test this hypothesis, HBxAg-positive and-negative HepG2 cells were constructed. and the patterns of cellular gene expression compared by polymerase chain reaction select cDNA subtraction. The full-length clone of one of these upregulated genes (URG), URG4, encoded a rotein of about 104kDa. URG4 was strongly expressed jn hepatitis B-infected Iiver and in HCC cells. where it costained with HBxAg, and was weakly ex
hepatitis B virus, hepalilis Bx antigen, hepatocellular carcinoma, onccgene pathogenesin
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刘杰, ZHAORUI LIAN, JIE LIU, JINGBO PAN, N. LALE SATIROGLU TUFAN, MINGHUA ZHU, PATRICK ARBUTHNOT, MICHAEL KEW, MARCY M. CLAYTON, AND MARK A. FEITELSON,
HEPATOLOGY Vol. 34, No.1, 2001,-0001,():
-1年11月30日
Polymerase chain reaction (PCR) select complementary DNA (cDNA) subtraction of hepatitis B x antigen (HBxAg)-positive compared with -negative HepG2 cells resulted in the up-regulated expression of a cellular gene that encodes a transcript of 745 bases and a polypeptide 99 amino acids long. GenBank analysis revealed extensive homology with the amino terminal domain of cellular multidrug resistant proteins (MRP), although overexpression of this gene did not confer an MRP phenotype. In situ ybridization and immunostaining showed colocalized expression with HBxAg in the liver of hepatitis B carriers. Overexpression of this protein stimulated the growth of HepG2 cells in serum-free medium, and partially protected cells from anti-Fas-mediated killing, but did not promote growth in soft agar or tumor formation in nude mice. Introduction of the dominant negative inhibitor of nuclear factor B (I B) into HBxAgpositive HepG2 cells decreased the levels of messenger RNA (mRNA) and protein, uggesting that its up-regulation is nuclear factor B (NF-B) dependent. Hence, HBxAg activation of NF-B may result in the up-regulation of a cellular protein that promotes growth factor-ndependent survival and protects against Fas-mediated killing. This factor may contribute to the persistence of infected hepatocytes during chronic infection, which is important for the later development of epatocellular carcinoma (HCC). (HEPATOLOGY 2001; 34: 146-157.)
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【期刊论文】Activation of fibronectin gene expression by hepatitis B virus x antigen
刘杰, P. A. Norton, H. M. G. P. V. Reis, S. Prince, J. Larkin, J. Pan, J. Liu, Q. Gong, M. Zhu and M. A. Feitelson,
Journal of Viral Hepatitis, 2004, 11, 332-341,-0001,():
-1年11月30日
SUMMARY. The development of fibrosis and cirrhosis during chronic hepatitis B virus (HBV) infection correlates with the persistent expression of HBV x antigen (HBxAg), which acts in part, by stimulating selected signal transduction pathways, including nuclear factor jB (NF-jB). To identify NF-jB responsive genes that are differentially expressed in HBxAgpositive cells, HepG2 cells were stably transfected with HBxAg, and then with pZeoSV2 or pZeoSV2-IjBa. When RNAs from each culture were compared by PCR-select cDNA subtraction, fibronectin (FN) mRNA was shown to be strongly down-regulated by IjBa. Up-regulated expression of FN and co-expression between FN and HBxAg were observed in liver sections from HBV carriers that were stained for HBxAg and analysed for FN mRNA by in situ hybridization (ISH). In liver cell cultures, HBxAg increased the levels of FN mRNA and protein. This was because of the HBxAg-mediated trans-activation of the FN promoter, which was NF-jBdependent. HBxAg also antagonized the repression of the FN promoter by the tumour suppressor, p53. Hence, the FN gene may be a natural target for HBxAg trans-activation, perhaps through activation of NF-jB and inactivation of p53, thereby contributing to the accumulation of FN in the liver over the course of chronic HBV infection.
chronic HBV infection, extracellular matrix, hepatocellular carcinoma.,
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