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Claus J Fimmel - One of the best experts on this subject based on the ideXlab platform.
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expression of gp73 a resident golgi membrane protein in viral and nonviral liver disease
Hepatology, 2002Co-Authors: Raleigh D Kladney, Gary A Bulla, Elizabeth M Brunt, Claus J FimmelAbstract:GP73 is a novel type II Golgi membrane protein of unknown function that is expressed in the hepatocytes of patients with adult giant-Cell hepatitis (Gene 2000;249:53-65). Its expression pattern in human liver disease and the regulation of its expression in hepatocytes have not been systematically studied. The aims of the present study were to compare GP73 protein levels in viral and nonviral human liver disease and in normal livers, to identify its Cellular sources, and to study the regulation of its expression in hepatoma Cells in vitro. GP73 protein levels were quantitated in explant livers of patients with well-defined disease etiologies and compared with the levels in normal donor livers. GP73-expressing Cells were identified immunohistochemically. GP73 expression in vitro was studied by Western blotting and immunofluorescence microscopy in HepG2 and SK-Hep-1 Cells and in the HepG2-derived, hepatitis B virus (HBV)-Transfected HepG2215 and HepG2T14.1 Cell Lines. Whole organ levels of GP73 were low in normal livers. Significant increases were found in liver disease due to viral causes (HBV, HCV) or nonviral causes (alcohol-induced liver disease, autoimmune hepatitis). In normal livers, GP73 was constitutively expressed by biliary epithelial Cells but not by hepatocytes. Hepatocyte expression of GP73 was dramatically up-regulated in diseased livers, regardless of the etiology, whereas biliary epithelial Cell expression did not change appreciably. GP73 was present at high levels in HepG2215 Cells (a Cell Line that supports active HBV replication), but was absent in HepG2T14.1 Cells (an HBV-Transfected Cell Line that does not support HBV replication) and in HBV-free HepG2 Cells. In SK-Hep-1 Cells, GP73 expression was increased in response to interferon gamma (IFN-γ), and inhibited by tumor necrosis factor α (TNF-α). In conclusion, increased expression of GP73 in hepatocytes appears to be a general feature of advanced liver disease, and may be regulated via distinct pathways that involve hepatotropic viruses or cytokines. (HEPATOLOGY 2002;35:1431-1440.)
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original articlesexpression of gp73 a resident golgi membrane protein in viral and nonviral liver disease
Hepatology, 2002Co-Authors: Raleigh D Kladney, Gary A Bulla, Elizabeth M Brunt, Xiaoyen Cui, Claus J FimmelAbstract:GP73 is a novel type II Golgi membrane protein of unknown function that is expressed in the hepatocytes of patients with adult giant-Cell hepatitis (Gene 2000;249:53-65). Its expression pattern in human liver disease and the regulation of its expression in hepatocytes have not been systematically studied. The aims of the present study were to compare GP73 protein levels in viral and nonviral human liver disease and in normal livers, to identify its Cellular sources, and to study the regulation of its expression in hepatoma Cells in vitro. GP73 protein levels were quantitated in explant livers of patients with well-defined disease etiologies and compared with the levels in normal donor livers. GP73-expressing Cells were identified immunohistochemically. GP73 expression in vitro was studied by Western blotting and immunofluorescence microscopy in HepG2 and SK-Hep-1 Cells and in the HepG2-derived, hepatitis B virus (HBV)-Transfected HepG2215 and HepG2T14.1 Cell Lines. Whole organ levels of GP73 were low in normal livers. Significant increases were found in liver disease due to viral causes (HBV, HCV) or nonviral causes (alcohol-induced liver disease, autoimmune hepatitis). In normal livers, GP73 was constitutively expressed by biliary epithelial Cells but not by hepatocytes. Hepatocyte expression of GP73 was dramatically up-regulated in diseased livers, regardless of the etiology, whereas biliary epithelial Cell expression did not change appreciably. GP73 was present at high levels in HepG2215 Cells (a Cell Line that supports active HBV replication), but was absent in HepG2T14.1 Cells (an HBV-Transfected Cell Line that does not support HBV replication) and in HBV-free HepG2 Cells. In SK-Hep-1 Cells, GP73 expression was increased in response to interferon gamma (IFN-γ), and inhibited by tumor necrosis factor α (TNF-α). In conclusion, increased expression of GP73 in hepatocytes appears to be a general feature of advanced liver disease, and may be regulated via distinct pathways that involve hepatotropic viruses or cytokines. (HEPATOLOGY 2002;35:1431-1440.)
Raleigh D Kladney - One of the best experts on this subject based on the ideXlab platform.
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expression of gp73 a resident golgi membrane protein in viral and nonviral liver disease
Hepatology, 2002Co-Authors: Raleigh D Kladney, Gary A Bulla, Elizabeth M Brunt, Claus J FimmelAbstract:GP73 is a novel type II Golgi membrane protein of unknown function that is expressed in the hepatocytes of patients with adult giant-Cell hepatitis (Gene 2000;249:53-65). Its expression pattern in human liver disease and the regulation of its expression in hepatocytes have not been systematically studied. The aims of the present study were to compare GP73 protein levels in viral and nonviral human liver disease and in normal livers, to identify its Cellular sources, and to study the regulation of its expression in hepatoma Cells in vitro. GP73 protein levels were quantitated in explant livers of patients with well-defined disease etiologies and compared with the levels in normal donor livers. GP73-expressing Cells were identified immunohistochemically. GP73 expression in vitro was studied by Western blotting and immunofluorescence microscopy in HepG2 and SK-Hep-1 Cells and in the HepG2-derived, hepatitis B virus (HBV)-Transfected HepG2215 and HepG2T14.1 Cell Lines. Whole organ levels of GP73 were low in normal livers. Significant increases were found in liver disease due to viral causes (HBV, HCV) or nonviral causes (alcohol-induced liver disease, autoimmune hepatitis). In normal livers, GP73 was constitutively expressed by biliary epithelial Cells but not by hepatocytes. Hepatocyte expression of GP73 was dramatically up-regulated in diseased livers, regardless of the etiology, whereas biliary epithelial Cell expression did not change appreciably. GP73 was present at high levels in HepG2215 Cells (a Cell Line that supports active HBV replication), but was absent in HepG2T14.1 Cells (an HBV-Transfected Cell Line that does not support HBV replication) and in HBV-free HepG2 Cells. In SK-Hep-1 Cells, GP73 expression was increased in response to interferon gamma (IFN-γ), and inhibited by tumor necrosis factor α (TNF-α). In conclusion, increased expression of GP73 in hepatocytes appears to be a general feature of advanced liver disease, and may be regulated via distinct pathways that involve hepatotropic viruses or cytokines. (HEPATOLOGY 2002;35:1431-1440.)
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original articlesexpression of gp73 a resident golgi membrane protein in viral and nonviral liver disease
Hepatology, 2002Co-Authors: Raleigh D Kladney, Gary A Bulla, Elizabeth M Brunt, Xiaoyen Cui, Claus J FimmelAbstract:GP73 is a novel type II Golgi membrane protein of unknown function that is expressed in the hepatocytes of patients with adult giant-Cell hepatitis (Gene 2000;249:53-65). Its expression pattern in human liver disease and the regulation of its expression in hepatocytes have not been systematically studied. The aims of the present study were to compare GP73 protein levels in viral and nonviral human liver disease and in normal livers, to identify its Cellular sources, and to study the regulation of its expression in hepatoma Cells in vitro. GP73 protein levels were quantitated in explant livers of patients with well-defined disease etiologies and compared with the levels in normal donor livers. GP73-expressing Cells were identified immunohistochemically. GP73 expression in vitro was studied by Western blotting and immunofluorescence microscopy in HepG2 and SK-Hep-1 Cells and in the HepG2-derived, hepatitis B virus (HBV)-Transfected HepG2215 and HepG2T14.1 Cell Lines. Whole organ levels of GP73 were low in normal livers. Significant increases were found in liver disease due to viral causes (HBV, HCV) or nonviral causes (alcohol-induced liver disease, autoimmune hepatitis). In normal livers, GP73 was constitutively expressed by biliary epithelial Cells but not by hepatocytes. Hepatocyte expression of GP73 was dramatically up-regulated in diseased livers, regardless of the etiology, whereas biliary epithelial Cell expression did not change appreciably. GP73 was present at high levels in HepG2215 Cells (a Cell Line that supports active HBV replication), but was absent in HepG2T14.1 Cells (an HBV-Transfected Cell Line that does not support HBV replication) and in HBV-free HepG2 Cells. In SK-Hep-1 Cells, GP73 expression was increased in response to interferon gamma (IFN-γ), and inhibited by tumor necrosis factor α (TNF-α). In conclusion, increased expression of GP73 in hepatocytes appears to be a general feature of advanced liver disease, and may be regulated via distinct pathways that involve hepatotropic viruses or cytokines. (HEPATOLOGY 2002;35:1431-1440.)
Kenneth O Lloyd - One of the best experts on this subject based on the ideXlab platform.
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analysis of melanoma Cells stably Transfected with β1 4galnac transferase gm2 gd2synthase cdna relative glycosyltransferase levels play a dominant role in determining ganglioside expression
Archives of Biochemistry and Biophysics, 1995Co-Authors: Shutian Ruan, Mohan Raj, Koichi Furukawa, Kenneth O LloydAbstract:Previous studies (Y. Nagata, S. Yamashiro, J. Yodoi, K. O. Lloyd, H. Shiku, and K. Furukawa (1992) J. Biol. Chem. 267, 12082-12089) had isolated a putative cDNA coding for beta 1,4 N-acetylgalactosaminyltransferase (GM2/GD2 synthase) and demonstrated the presence of GM2 and/or GD2 gangliosides in melanoma Cell Lines stably Transfected with this gene. We have now measured the levels of glycosyltransferase activities and mRNA levels in five Transfected Cell Lines in comparison with their parent Cell Lines (mouse melanoma B16 and human melanoma MeWo). Membrane preparations from the Transfected Cell Lines demonstrated de novo synthesis of GM2 or GD2 in in vitro assays using GM3 or GD3, respectively, as ganglioside acceptors. The enzyme levels, however, varied considerably among the different transfectants, as did the mRNA levels for the beta 1,4 Gal-NAc-transferase. The effect of the Transfected gene on levels of preexisting glycosyltransferases involved in ganglioside biosynthesis was also measured and the ganglioside composition of the Cell Lines was determined. The level of beta 1,4 GalNAc-transferase expressed in the different Cell Lines was found to dramatically influence the overall ganglioside composition of the Cell. In the Transfected Cell Line with the highest levels of the transferase, for example, biosynthesis was almost completely redirected away from the b pathway to the a pathway with the resulting expression of only GM2. These data from this family of related Cell Lines clearly demonstrate the primary roles that relative glycosyltransferase levels play in determining the ganglioside composition of Cells.
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analysis of melanoma Cells stably Transfected with beta 1 4galnac transferase gm2 gd2 synthase cdna relative glycosyltransferase levels play a dominant role in determining ganglioside expression
Archives of Biochemistry and Biophysics, 1995Co-Authors: Shutian Ruan, Koichi Furukawa, Mohan B K Raj, Kenneth O LloydAbstract:Previous studies (Y. Nagata, S. Yamashiro, J. Yodoi, K. O. Lloyd, H. Shiku, and K. Furukawa (1992) J. Biol. Chem. 267, 12082-12089) had isolated a putative cDNA coding for beta 1,4 N-acetylgalactosaminyltransferase (GM2/GD2 synthase) and demonstrated the presence of GM2 and/or GD2 gangliosides in melanoma Cell Lines stably Transfected with this gene. We have now measured the levels of glycosyltransferase activities and mRNA levels in five Transfected Cell Lines in comparison with their parent Cell Lines (mouse melanoma B16 and human melanoma MeWo). Membrane preparations from the Transfected Cell Lines demonstrated de novo synthesis of GM2 or GD2 in in vitro assays using GM3 or GD3, respectively, as ganglioside acceptors. The enzyme levels, however, varied considerably among the different transfectants, as did the mRNA levels for the beta 1,4 Gal-NAc-transferase. The effect of the Transfected gene on levels of preexisting glycosyltransferases involved in ganglioside biosynthesis was also measured and the ganglioside composition of the Cell Lines was determined. The level of beta 1,4 GalNAc-transferase expressed in the different Cell Lines was found to dramatically influence the overall ganglioside composition of the Cell. In the Transfected Cell Line with the highest levels of the transferase, for example, biosynthesis was almost completely redirected away from the b pathway to the a pathway with the resulting expression of only GM2. These data from this family of related Cell Lines clearly demonstrate the primary roles that relative glycosyltransferase levels play in determining the ganglioside composition of Cells.
Elizabeth M Brunt - One of the best experts on this subject based on the ideXlab platform.
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expression of gp73 a resident golgi membrane protein in viral and nonviral liver disease
Hepatology, 2002Co-Authors: Raleigh D Kladney, Gary A Bulla, Elizabeth M Brunt, Claus J FimmelAbstract:GP73 is a novel type II Golgi membrane protein of unknown function that is expressed in the hepatocytes of patients with adult giant-Cell hepatitis (Gene 2000;249:53-65). Its expression pattern in human liver disease and the regulation of its expression in hepatocytes have not been systematically studied. The aims of the present study were to compare GP73 protein levels in viral and nonviral human liver disease and in normal livers, to identify its Cellular sources, and to study the regulation of its expression in hepatoma Cells in vitro. GP73 protein levels were quantitated in explant livers of patients with well-defined disease etiologies and compared with the levels in normal donor livers. GP73-expressing Cells were identified immunohistochemically. GP73 expression in vitro was studied by Western blotting and immunofluorescence microscopy in HepG2 and SK-Hep-1 Cells and in the HepG2-derived, hepatitis B virus (HBV)-Transfected HepG2215 and HepG2T14.1 Cell Lines. Whole organ levels of GP73 were low in normal livers. Significant increases were found in liver disease due to viral causes (HBV, HCV) or nonviral causes (alcohol-induced liver disease, autoimmune hepatitis). In normal livers, GP73 was constitutively expressed by biliary epithelial Cells but not by hepatocytes. Hepatocyte expression of GP73 was dramatically up-regulated in diseased livers, regardless of the etiology, whereas biliary epithelial Cell expression did not change appreciably. GP73 was present at high levels in HepG2215 Cells (a Cell Line that supports active HBV replication), but was absent in HepG2T14.1 Cells (an HBV-Transfected Cell Line that does not support HBV replication) and in HBV-free HepG2 Cells. In SK-Hep-1 Cells, GP73 expression was increased in response to interferon gamma (IFN-γ), and inhibited by tumor necrosis factor α (TNF-α). In conclusion, increased expression of GP73 in hepatocytes appears to be a general feature of advanced liver disease, and may be regulated via distinct pathways that involve hepatotropic viruses or cytokines. (HEPATOLOGY 2002;35:1431-1440.)
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original articlesexpression of gp73 a resident golgi membrane protein in viral and nonviral liver disease
Hepatology, 2002Co-Authors: Raleigh D Kladney, Gary A Bulla, Elizabeth M Brunt, Xiaoyen Cui, Claus J FimmelAbstract:GP73 is a novel type II Golgi membrane protein of unknown function that is expressed in the hepatocytes of patients with adult giant-Cell hepatitis (Gene 2000;249:53-65). Its expression pattern in human liver disease and the regulation of its expression in hepatocytes have not been systematically studied. The aims of the present study were to compare GP73 protein levels in viral and nonviral human liver disease and in normal livers, to identify its Cellular sources, and to study the regulation of its expression in hepatoma Cells in vitro. GP73 protein levels were quantitated in explant livers of patients with well-defined disease etiologies and compared with the levels in normal donor livers. GP73-expressing Cells were identified immunohistochemically. GP73 expression in vitro was studied by Western blotting and immunofluorescence microscopy in HepG2 and SK-Hep-1 Cells and in the HepG2-derived, hepatitis B virus (HBV)-Transfected HepG2215 and HepG2T14.1 Cell Lines. Whole organ levels of GP73 were low in normal livers. Significant increases were found in liver disease due to viral causes (HBV, HCV) or nonviral causes (alcohol-induced liver disease, autoimmune hepatitis). In normal livers, GP73 was constitutively expressed by biliary epithelial Cells but not by hepatocytes. Hepatocyte expression of GP73 was dramatically up-regulated in diseased livers, regardless of the etiology, whereas biliary epithelial Cell expression did not change appreciably. GP73 was present at high levels in HepG2215 Cells (a Cell Line that supports active HBV replication), but was absent in HepG2T14.1 Cells (an HBV-Transfected Cell Line that does not support HBV replication) and in HBV-free HepG2 Cells. In SK-Hep-1 Cells, GP73 expression was increased in response to interferon gamma (IFN-γ), and inhibited by tumor necrosis factor α (TNF-α). In conclusion, increased expression of GP73 in hepatocytes appears to be a general feature of advanced liver disease, and may be regulated via distinct pathways that involve hepatotropic viruses or cytokines. (HEPATOLOGY 2002;35:1431-1440.)
Gary A Bulla - One of the best experts on this subject based on the ideXlab platform.
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expression of gp73 a resident golgi membrane protein in viral and nonviral liver disease
Hepatology, 2002Co-Authors: Raleigh D Kladney, Gary A Bulla, Elizabeth M Brunt, Claus J FimmelAbstract:GP73 is a novel type II Golgi membrane protein of unknown function that is expressed in the hepatocytes of patients with adult giant-Cell hepatitis (Gene 2000;249:53-65). Its expression pattern in human liver disease and the regulation of its expression in hepatocytes have not been systematically studied. The aims of the present study were to compare GP73 protein levels in viral and nonviral human liver disease and in normal livers, to identify its Cellular sources, and to study the regulation of its expression in hepatoma Cells in vitro. GP73 protein levels were quantitated in explant livers of patients with well-defined disease etiologies and compared with the levels in normal donor livers. GP73-expressing Cells were identified immunohistochemically. GP73 expression in vitro was studied by Western blotting and immunofluorescence microscopy in HepG2 and SK-Hep-1 Cells and in the HepG2-derived, hepatitis B virus (HBV)-Transfected HepG2215 and HepG2T14.1 Cell Lines. Whole organ levels of GP73 were low in normal livers. Significant increases were found in liver disease due to viral causes (HBV, HCV) or nonviral causes (alcohol-induced liver disease, autoimmune hepatitis). In normal livers, GP73 was constitutively expressed by biliary epithelial Cells but not by hepatocytes. Hepatocyte expression of GP73 was dramatically up-regulated in diseased livers, regardless of the etiology, whereas biliary epithelial Cell expression did not change appreciably. GP73 was present at high levels in HepG2215 Cells (a Cell Line that supports active HBV replication), but was absent in HepG2T14.1 Cells (an HBV-Transfected Cell Line that does not support HBV replication) and in HBV-free HepG2 Cells. In SK-Hep-1 Cells, GP73 expression was increased in response to interferon gamma (IFN-γ), and inhibited by tumor necrosis factor α (TNF-α). In conclusion, increased expression of GP73 in hepatocytes appears to be a general feature of advanced liver disease, and may be regulated via distinct pathways that involve hepatotropic viruses or cytokines. (HEPATOLOGY 2002;35:1431-1440.)
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original articlesexpression of gp73 a resident golgi membrane protein in viral and nonviral liver disease
Hepatology, 2002Co-Authors: Raleigh D Kladney, Gary A Bulla, Elizabeth M Brunt, Xiaoyen Cui, Claus J FimmelAbstract:GP73 is a novel type II Golgi membrane protein of unknown function that is expressed in the hepatocytes of patients with adult giant-Cell hepatitis (Gene 2000;249:53-65). Its expression pattern in human liver disease and the regulation of its expression in hepatocytes have not been systematically studied. The aims of the present study were to compare GP73 protein levels in viral and nonviral human liver disease and in normal livers, to identify its Cellular sources, and to study the regulation of its expression in hepatoma Cells in vitro. GP73 protein levels were quantitated in explant livers of patients with well-defined disease etiologies and compared with the levels in normal donor livers. GP73-expressing Cells were identified immunohistochemically. GP73 expression in vitro was studied by Western blotting and immunofluorescence microscopy in HepG2 and SK-Hep-1 Cells and in the HepG2-derived, hepatitis B virus (HBV)-Transfected HepG2215 and HepG2T14.1 Cell Lines. Whole organ levels of GP73 were low in normal livers. Significant increases were found in liver disease due to viral causes (HBV, HCV) or nonviral causes (alcohol-induced liver disease, autoimmune hepatitis). In normal livers, GP73 was constitutively expressed by biliary epithelial Cells but not by hepatocytes. Hepatocyte expression of GP73 was dramatically up-regulated in diseased livers, regardless of the etiology, whereas biliary epithelial Cell expression did not change appreciably. GP73 was present at high levels in HepG2215 Cells (a Cell Line that supports active HBV replication), but was absent in HepG2T14.1 Cells (an HBV-Transfected Cell Line that does not support HBV replication) and in HBV-free HepG2 Cells. In SK-Hep-1 Cells, GP73 expression was increased in response to interferon gamma (IFN-γ), and inhibited by tumor necrosis factor α (TNF-α). In conclusion, increased expression of GP73 in hepatocytes appears to be a general feature of advanced liver disease, and may be regulated via distinct pathways that involve hepatotropic viruses or cytokines. (HEPATOLOGY 2002;35:1431-1440.)
