| Literature DB >> 15629783 |
Takayuki Murata1, Takayuki Ohshima, Masashi Yamaji, Masahiro Hosaka, Yusuke Miyanari, Makoto Hijikata, Kunitada Shimotohno.
Abstract
Hepatitis C virus (HCV) is one of the major causative agents of liver diseases, such as liver inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma. Using an efficient HCV subgenomic replicon system, we demonstrate that transforming growth factor-beta (TGF-beta) suppresses viral RNA replication and protein expression from the HCV replicon. We further show that the anti-viral effect of this cytokine is associated with cellular growth arrest in a manner dependent on Smad signaling, not mitogen-activated protein kinase (MAPK) signaling. These results suggest a novel insight into the mechanisms of liver diseases caused by HCV.Entities:
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Year: 2005 PMID： 15629783 DOI： 10.1016/j.virol.2004.10.036
Source DB: PubMed Journal: Virology ISSN： 0042-6822 Impact factor: 3.616