hepatoblastoma/protease

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Protease-induced infectivity of hepatitis B virus for a human hepatoblastoma cell line.

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The human hepatoblastoma cell line HepG2 produces and secretes hepatitis B virus (HBV) after transfection of cloned HBV DNA. Intact virions do not infect these cells, although they attach to the surface of the HepG2 cell through binding sites in the pre-S1 domain. Entry of enveloped virions into the

[Prokaryotic expression, purification and activity analysis of recombinant human serine protease inhibitor Hespintor Kazal Domain].

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Hespintor is an unknown function protein that was got from hepatoblastoma cell lines HepG2 by suppression subtractive hybridization technique (SSH), sequence analysis showed that the protein is a new member of secretory type of Kazal type serine protease inhibitor (Serpin) family, and has high

Purification and identification of the Kazal domain of a novel serine protease inhibitor, Hespintor, through a bacterial (Escherichia coli) expression system.

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In this study, Hespintor, a protein with unknown function, was screened and obtained from the hepatoblastoma cell line, HepG2, using suppression subtractive hybridization (SSH). Sequence analysis demonstrated that the protein is a novel secreting member of the Kazal-type serine protease inhibitor

Niacin accelerates intracellular ApoB degradation by inhibiting triacylglycerol synthesis in human hepatoblastoma (HepG2) cells.

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The mechanism by which the potent drug niacin decreases apoB-containing atherogenic lipoproteins and prevents coronary disease is unclear. Utilizing human hepatoblastoma (HepG2) cells as an in vitro model, we have examined the effect of niacin on intracellular degradation of apoB and the regulatory

Chrysotoxene induces apoptosis of human hepatoblastoma HepG2 cells in vitro and in vivo via activation of the mitochondria-mediated apoptotic signaling pathway.

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Previous studies have indicated that chrysotoxene may be a potential drug used to treat tumors, however the effect of chrysotoxene on hepatoblastoma remains unknown. Therefore, the present study aimed to investigate the cytotoxic effect and elucidate the potential molecular mechanism of chrysotoxene

Overexpression of UHRF1 promotes silencing of tumor suppressor genes and predicts outcome in hepatoblastoma.

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Hepatoblastoma (HB) is the most common liver tumor of childhood and occurs predominantly within the first 3 years of life. In accordance to its early manifestation, HB has been described to display an extremely low mutation rate. As substitute, epigenetic modifiers seem to play an exceptional role

Inhibitory effects of the recombinant human serine protease inhibitor Hespintor on the proliferation, migration and invasion of hepatocellular carcinoma cells.

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Hespintor is a new Kazal-type serine proteinase inhibitor (Serpin) screened from the HepG2 hepatoblastoma cell line using the suppression subtractive hybridization (SSH) technique. Seprin is closely associated with the progression and remission of malignant tumors, and has certain significance in

The degradation pathway for the HBV envelope proteins involves proteolysis prior to degradation via the cytosolic proteasome.

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To study the pathway of degradation of the hepatitis B virus (HBV) middle envelope protein (M), human hepatoblastoma cells were transfected with a plasmid that specifies production of M in the absence of other viral proteins. When expressed in HepG2 cells, 90% of M protein was secreted into the

Limited proteolysis induces woodchuck hepatitis virus infectivity for human HepG2 cells.

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Previous work from our laboratory has shown that digestion of hepatitis B virus (HBV) with V8 protease rendered the virus infectious for human hepatoblastoma cell line (HepG2). It was hypothesized that the cleavage exposes a 16 amino acid region that includes a consensus 'fusion' motif necessary to

Degradation of newly synthesized apolipoprotein B-100 in a pre-Golgi compartment.

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The synthesis and secretion of apolipoprotein (apo) B-100 have been studied in a human hepatoblastoma cell line, the Hep G2 cells. Pulse-chase analysis showed that apoB-100 was not quantitatively recovered in the culture medium. To reveal the intracellular degradation of apoB-100 prior to secretion,

SV40 large T antigen directed by regulatory elements of the human alpha-1-antitrypsin gene. A transgenic mouse system that exhibits stages in liver carcinogenesis.

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SV40 large T antigen (T-ag) is a potent oncogene able to transform many cell types. The human alpha-1-antitrypsin (AAT) gene encodes the major serine protease inhibitor in plasma. The 5' flanking sequence of the AAT gene contains cis-acting elements that specify the expression of reporter genes in

Distribution of type IV collagen in pancreatic adenocarcinoma and chronic pancreatitis.

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Changes in the basement membrane are present in various neoplastic conditions such as neurofibrosarcoma, cervical carcinoma, colorectal cancers and hepatoblastoma. This study examines the expression of type IV collagen in the basement membrane, using an immunohistochemical method, in the normal

Tumor suppressor candidate TSSC5 is regulated by UbcH6 and a novel ubiquitin ligase RING105.

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The region of human chromosome 11p15.5 is linked with Beckwith-Wiedemann syndrome that is associated with susceptibility to Wilms' tumor, rhabdomyosarcoma and hepatoblastoma. TSSC5 (tumor-suppressing subchromosomal transferable fragment cDNA; also known as ORCTL2/IMPT1/BWR1A/SLC22A1L) is located in

Generation of biologically active endostatin fragments from human collagen XVIII by distinct matrix metalloproteases.

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Endostatin, a potent inhibitor of endothelial cell proliferation, migration, angiogenesis and tumor growth, is proteolytically cleaved from the C-terminal noncollagenous NC1 domain of type XVIII collagen. We investigated the endostatin formation from human collagen XVIII by several MMPs in vitro.

[Hepatic neoductules].

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Proliferation of preexisting bile ducts, ductular metaplasia of hepatocytes and proliferation and differentiation of liver stem cells are discussed in the pathogenesis of neoductular structures in the liver. Under the condition of experimental bile duct obstruction and in extrahepatic bile duct

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