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 Science KeyUT 000306348900003
Related Url https://doi.org/10.1099/vir.0.040725-0 http://ousar.lib.okayama-u.ac.jp/54272
FullText URL K0005288_other.pdf
Author Sejima, Hiroe| Mori, Kyoko| Ariumi, Yasuo| Ikeda, Masanori| Kato, Nobuyuki|
Keywords HCV HCV RNA replication system Li23 cells Long-term RNA replication Upregulated host genes Downregulated host genes
Note 学位審査副論文|
Published Date 2012-07
Publication Title Virus Research
Volume volume167
Issue issue1
Publisher Elsevier Science
Start Page 74
End Page 85
ISSN 0168-1702
NCID AA10642076
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 22579597
DOI 10.1016/j.virusres.2012.04.008
Web of Science KeyUT 000305496700010
Related Url https://doi.org/10.1016/j.virusres.2012.04.008 http://ousar.lib.okayama-u.ac.jp/54271
FullText URL fulltext.pdf
Author Takahashi Nobumasa| Nojima, Ikuko| Araki, Tooru| Takasugi, Mizue| Sakane, Tomoko| Kodera, Aya| Ikeda, Masanori| Tsukahara, Hirokazu|
Keywords Norovirus false positive immunochromatography neonate rapid detection test specificity
Published Date 2015-09-03
Publication Title Journal of International Medical Research
Volume volume43
Issue issue5
Publisher Sage
Start Page 648
End Page 652
ISSN 0300-0605
NCID AA00700686
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
File Version publisher
PubMed ID 26338763
DOI 10.1177/0300060515592902
Web of Science KeyUT 000361592500006
Related Url isVersionOf https://doi.org/10.1177/0300060515592902
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 Science KeyUT 000377626300006
JaLCDOI 10.18926/AMO/54186
FullText URL 70_2_75.pdf
Author Sejima, Hiroe| Satoh, Shinya| Dansako, Hiromichi| Honda, Masao| Kaneko, Shuichi| Ikeda, Masanori| Kato, Nobuyuki|
Abstract The mechanisms of hepatitis C virus (HCV)-associated hepatocarcinogenesis and disease progression are unclear. We previously observed that the expression level of carboxypeptidase B2 (CPB2) gene was remarkably suppressed by persistent HCV RNA replication in human hepatoma cell line Li23-derived cells. The results of the present study demonstrated that the CPB2 expression in patients with chronic hepatitis C was inversely correlated with several risk factors of hepatic fibrosis or steatosis, although ectopic CPB2 expression did not suppress the expression of fibrogenic or lipogenic genes. The suppressed CPB2 expression was restored by treatment with 5-azacytidine. To clarify the mechanism underlying this phenomenon, we analyzed the CPB2 promoter, and the results revealed that (1) hepatocyte nuclear factor 1 (HNF1), especially HNF1α, was essential for the CPB2 promoter, and (2) CPB2 promoter was not methylated by persistent HCV RNA replication. The expression levels of HNF1α and HNF1β were also not changed by persistent HCV RNA replication. These results suggest the existence of 5-azacytidine-inducible or -reducible unknown factor(s) that can control the CPB2 expression. To evaluate this idea we performed a microarray analysis, and several gene candidates corresponding to the suggested factor(s) were identified.
Keywords persistent hepatitis C virus replication carboxypeptidase B2 suppression mechanism of CPB2 expression DNA methylation hepatocyte nuclear factor 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 75
End Page 88
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 27094832
Web of Science KeyUT 000377626300002
Author Kato, Nobuyuki| Sejima, Hiroe| Ueda, Youki| Mori, Kyoko| Satoh, Shinya| Dansako, Hiromichi| Ikeda, Masanori|
Published Date 2014-03-13
Publication Title PLOS ONE
Volume volume9
Issue issue3
Content Type Journal Article
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
Author Dansako, Hiromichi| Ueda, Youki| Okumura, Nobuaki| Satoh, Shinya| Sugiyama, Masaya| Mizokami, Masashi| Ikeda, Masanori| Kato, Nobuyuki|
Published Date 2015
Publication Title The FEBS journal
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 Science KeyUT 000353181700001