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J. Biol. Chem., Vol. 277, Issue 42, 39634-39641, October 18, 2002
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From the The core protein of hepatitis C virus (HCV) is a
major component of the viral nucleocapsid. The HCV core protein
includes nuclear localization signal-like sequences and has various
effects on cellular metabolism, playing roles, for example, in the
regulation of transcription, apoptosis, and transformation. To examine
the possibility of an effect of the core protein on nucleocytoplasmic transport, we used the yeast Saccharomyces cerevisiae as a
model system. The core protein (p23) is processed to p21 and is
localized in both the cytoplasm and nucleus in yeast cells, similar to
that observed in mammalian cells in several cases. The nuclear import of the core protein requires the activity of small GTPase Ran/Gsp1p and
is mediated by Kap123p in yeast cells. When the core protein was
expressed in yeast cells, the import of the yeast AP1-like transcription factor Yap1p into the nucleus was inhibited. Experiments in vitro involving Kap121p, also known as Pse1p, a receptor
for the nuclear import of Yap1p, indicated that the amount of Yap1p bound to Kap121p was reduced in the presence of core protein. These results suggest that the HCV core protein affects cellular metabolism by disturbing transport of proteins to the nucleus.
The Core Protein of Hepatitis C Virus Is Imported into the
Nucleus by Transport Receptor Kap123p but Inhibits
Kap121p-dependent Nuclear Import of Yeast AP1-like
Transcription Factor in Yeast Cells*
§,¶
, and
Department of Microbiology, Graduate School
of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo
113-0033 and the ¶ Laboratory of Molecular and Biochemical
Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku
University, Aza-Aoba, Aoba-ku, Sendai, Miyagi 980-8578, Japan
*
This work was supported in part by a grant-in-aid from the
Ministry of Education, Science, Sports, and Culture of Japan.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Laboratory of
Molecular and Biochemical Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University, Aza-Aoba, Aoba-ku, Sendai, Miyagi 980-8578, Japan. Tel.: 81-22-217-6872; Fax: 81-22-217-6872;
E-mail: skuge@mail.pharm.tohoku.ac.jp.
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