FullText URL K0005289_other1.pdf
Author Takeda, Midori| Ikeda, Masanori| Ariumi, Yasuo| Wakita, Takaji| Kato, Nobuyuki|
Note 学位審査副論文
Published Date 2012-07
Publication Title Journal of General Virology
Volume volume93
Issue issue7
Publisher Cambridge Univ. Press for the Society for General Microbiology
Start Page 1422
End Page 1431
ISSN 0022-1317
NCID AA00698722
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
File Version author
PubMed ID 22456614
DOI 10.1099/vir.0.040725-0
Web of Sience KeyUT 000306348900003
Related Url https://doi.org/10.1099/vir.0.040725-0 http://ousar.lib.okayama-u.ac.jp/54272
JaLCDOI 10.18926/AMO/54190
FullText URL 70_2_111.pdf
Author Takeda, Midori| Ikeda, Masanori| Satoh, Shinya| Dansako, Hiromichi| Wakita, Takaji| Kato, Nobuyuki|
Abstract Membrane transport probably participates in the lifecycle of hepatitis C virus (HCV). Rab proteins are essential host factors for HCV RNA replication, but these proteins’ roles in other steps of the HCV lifecycle are not clear. The tight junction (TJ) plays a key role in HCV infection. Rab13 regulates the endocytic recycling of the TJ-associated proteins. Here we investigated whether Rab13 is involved in the HCV entry step. We used HuH-7-derived RSc cells and Li23-derived D7 cells. To evaluate the effect of Rab13 in HCV infection, we transfected the cells with siRNA targeting Rab13 before HCV infection. The down-regulation of Rab13 inhibited HCV infection. The D7 cells had showed a greater inhibitory effect against HCV infection compared to that in the RSc cells by Rab13 knockdown. Next, to evaluate the effect of Rab13 after infection, we inoculated the cells with HCV before transfection of the siRNA. The down-regulation of Rab13 did not show any effects after HCV infection. We further examined whether Rab13 would influence HCV RNA replication by using HCV replicon-harboring cells. The results revealed that Rab13 did not affect the step of HCV RNA replication. These results suggest that Rab13 plays an important role in the step of HCV entry.
Keywords hepatitis C virus Rab13 occludin claudin 1
Amo Type Original Article
Published Date 2016-04
Publication Title Acta Medica Okayama
Volume volume70
Issue issue2
Publisher Okayama University Medical School
Start Page 111
End Page 118
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2016 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 27094836
Web of Sience KeyUT 000377626300006
Author Ueda, Youki| Takeda, Midori| Mori, Kyoko| Dansako, Hiromichi| Wakita, Takaji| Kim, Hye-Sook| Sato, Akira| Wataya, Yusuke| Ikeda, Masanori| Kato, Nobuyuki|
Published Date 2013-08-30
Publication Title PLOS ONE
Volume volume8
Issue issue8
Content Type Journal Article
JaLCDOI 10.18926/AMO/53335
FullText URL 69_2_71.pdf
Author Hiramoto, Hiroki| Dansako, Hiromichi| Takeda, Midori| Satoh, Shinya| Wakita, Takaji| Ikeda, Masanori| Kato, Nobuyuki|
Abstract Persistent infection with hepatitis C virus (HCV) often causes chronic hepatitis, and then shows a high rate of progression to liver cirrhosis and hepatocellular carcinoma. To clarify the mechanism of the persistent HCV infection is considered to be important for the discovery of new target(s) for the development of anti-HCV strategies. In the present study, we found that the expression level of annexin A1 (ANXA1) in human hepatoma cell line Li23-derived D7 cells was remarkably lower than that in parental Li23 cells, whereas the susceptibility of D7 cells to HCV infection was much higher than that of Li23 cells. Therefore, we hypothesized that ANXA1 negatively regulates persistent HCV infection through the inhibition of viral RNA replication. The results revealed that HCV production was significantly inhibited without a concomitant reduction in the amount of lipid droplets in the D7 cells stably expressing exogenous ANXA1. Further, we demonstrated that ANXA1 negatively regulated the step of viral RNA replication rather than that of viral entry in human hepatocytes. These results suggest that ANXA1 would be a novel target for the development of anti-HCV strategies.
Keywords HCV annexin A1 Li23 cell line Li23-derived D7 cells HCV-JFH-1
Amo Type Original Article
Published Date 2015-04
Publication Title Acta Medica Okayama
Volume volume69
Issue issue2
Publisher Okayama University Medical School
Start Page 71
End Page 78
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2015 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 25899628
Web of Sience KeyUT 000353181700001
Author Kuroki, Misao| Ariumi, Yasuo| Hijikata, Makoto| Ikeda, Masanori| Dansako, Hiromichi| Wakita, Takaji| Shimotohno, Kunitada| Kato, Nobuyuki|
Published Date 2013-01-11
Publication Title Biochemical and Biophysical Research Communications
Volume volume430
Issue issue2
Content Type Journal Article