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Induction of Proliferation-Related Signals by Hepatitis C Virus,tion on hepatocytes, the effects of HCV proteins on intracellular signal transduction pathways were investigated. The effects of seven HCV proteins (core, nonstructural [NS]2, NS3, NS4A, NS4B, NS5A, and NS5B) on cyclic AMP response element (CRE)-, serum response element (SRE)-, nuclear factor (NF)-κ
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https://doi.org/10.1007/978-3-322-80348-1LH factor, .uman homologue of .aid (HHM), from a human fetal liver cDNA library. HHM is composed of 360 amino acids (aa). The HHM has an HLH region (150–184 aa) with a leucine zipper motif (240–260 aa) lacking the basic region. The homology of the HLH region for HHM shared 82% identity with that for
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https://doi.org/10.1007/978-3-663-08085-5binds to its respective receptor, it initiates parallel cascades leading to either apoptosis or the induction of antiapoptotic proteins. The transcription factor NF-κB is a critical mediator of antiapoptosis in the liver in vivo and in cultured hepatocytes. The mechanisms by which NF-κB blocks the a
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,Zusammenfassung und Schlußfolgerungen,induced and modulated by signal transduction governing cell growth and differentiation. We found that when normal rat hepatocyte growth was induced by hepatocyte growth factor (HGF), HGF receptor (MET) was activated, with association of MET with growth factor receptor-bound protein (GRB)-2, which is
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