TY - JOUR
T1 - Suppression of hepatitis C virus replicon by TGF-β
AU - Murata, Takayuki
AU - Ohshima, Takayuki
AU - Yamaji, Masashi
AU - Hosaka, Masahiro
AU - Miyanari, Yusuke
AU - Hijikata, Makoto
AU - Shimotohno, Kunitada
N1 - Funding Information:
We would like to thank Dr. K. Miyazono for the FLAG-tagged human Smad2, Smad4, TβR-I(T/D) expression plasmids and p3TP-Luc. pCALNL5/pBR and I377/NS3- 3′ sequence were kindly provided by Dr. M. Kohara and Dr. R. Bartenschlager, respectively. This work was supported by grants-in-aid for cancer research and by the second-term comprehensive 10-year strategy for cancer control, and by the Ministry of Health, Labor, and Welfare, as well as grants-in-aid for scientific research from the Ministry of Education, Culture, Sports, Science, and Technology, grants-in-aid by the Japanese Society for the Promotion of Science (JSPS), and by the Program for Promotion of Fundamental Studies in Health Science of the Organization for Pharmaceutical Safety and Research (OPSR) of Japan. T. M. is a recipient of a JSPS Postdoctoral Fellowship.
PY - 2005/1/20
Y1 - 2005/1/20
N2 - 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-β) 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.
AB - 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-β) 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.
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U2 - 10.1016/j.virol.2004.10.036
DO - 10.1016/j.virol.2004.10.036
M3 - Article
C2 - 15629783
AN - SCOPUS:11344275986
SN - 0042-6822
VL - 331
SP - 407
EP - 417
JO - Virology
JF - Virology
IS - 2
ER -
