| ○種別 (必須): | □ | 学術論文 (審査論文)
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| ○言語 (必須): | □ | 英語
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| ○招待 (推奨): |
| ○審査 (推奨): |
| ○カテゴリ (推奨): |
| ○共著種別 (推奨): | □ | 国内共著 (徳島大学内研究者と国内(学外)研究者との共同研究 (国外研究者を含まない))
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| ○学究種別 (推奨): |
| ○組織 (推奨): |
| ○著者 (必須): | 1. | (英) Nandita Rani Das (日) (読)
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| ○学籍番号 (推奨): | □ | ****
| [ユーザ] |
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| 2. | (英) Hironori Miyata (日) (読)
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| 3. | 原 英之
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| 4. | 内山 圭司
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| [継承] |
| 5. | 千田 淳司
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| 6. | 矢野 雅司 ([徳島大学.技術支援部])
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| 7. | (英) Hitomi Watanabe (日) (読)
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| 8. | (英) Gen Kondoh (日) (読)
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| 9. | 坂口 末廣 ([徳島大学.先端酵素学研究所.基幹研究部門])
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| [継承] |
| ○題名 (必須): | □ | (英) Effects of prion protein devoid of the N-terminal residues 25-50 on prion pathogenesis in mice. (日)
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| ○要約 (任意): | □ | (英) The N-terminal polybasic region of the normal prion protein, PrP(C), which encompasses residues 23-31, is important for prion pathogenesis by affecting conversion of PrP(C) into the pathogenic isoform, PrP(Sc). We previously reported transgenic mice expressing PrP with residues 25-50 deleted in the PrP-null background, designated as Tg(PrPpreOR)/Prnp (0/0) mice. Here, we produced two new lines of Tg(PrPpreOR)/Prnp (0/0) mice, each expressing the mutant protein, PrPpreOR, 1.1 and 1.6 times more than PrP(C) in wild-type mice, and subsequently intracerebrally inoculated RML and 22L prions into them. The lower expresser showed slightly reduced susceptibility to RML prions but not to 22L prions. The higher expresser exhibited enhanced susceptibility to both prions. No prion transmission barrier was created in Tg(PrPpreOR)/Prnp (0/0) mice against full-length PrP(Sc). PrP(Sc)preOR accumulated in the brains of infected Tg(PrPpreOR)/Prnp (0/0) mice less than PrP(Sc) in control wild-type mice, although lower in RML-infected Tg(PrPpreOR)/Prnp (0/0) mice than in 22L-infected mice. Prion infectivity in infected Tg(PrPpreOR)/Prnp (0/0) mice was also lower than that in wild-type mice. These results indicate that deletion of residues 25-50 only slightly affects prion susceptibility, the conversion of PrP(C) into PrP(Sc), and prion infectivity in a strain-specific way. PrPpreOR retains residues 23-24 and lacks residues 25-31 in the polybasic region. It is thus conceivable that residues 23-24 rather than 25-31 are important for the polybasic region to support prion pathogenesis. However, other investigators have reported that residues 27-31 not 23-24 are important to support prion pathogenesis. Taken together, the polybasic region might support prion pathogenesis through multiple sites including residues 23-24 and 27-31. (日)
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| ○キーワード (推奨): | 1. | (英) Amino Acid Sequence (日) (読)
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| 2. | (英) Animals (日) (読)
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| 3. | (英) Disease Susceptibility (日) (読)
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| 4. | (英) Mice (日) (読)
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| 5. | (英) Mice, Inbred C57BL (日) (読)
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| 6. | (英) Mice, Transgenic (日) (読)
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| 7. | (英) Prion Diseases (日) (読)
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| 8. | (英) Prion Proteins (日) (読)
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| 9. | (英) Repetitive Sequences, Amino Acid (日) (読)
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| 10. | (英) Sequence Deletion (日) (読)
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| ○発行所 (推奨): |
| ○誌名 (必須): | □ | Archives of Virology (International Union of Microbiological Societies)
(pISSN: 0304-8608, eISSN: 1432-8798)
| ○ISSN (任意): | □ | 1432-8798
ISSN: 0304-8608
(pISSN: 0304-8608, eISSN: 1432-8798) Title: Archives of virologyTitle(ISO): Arch VirolSupplier: Springer Online Journal ArchivePublisher: Springer (NLM Catalog)
(Scopus)
(CrossRef)
(Scopus information is found. [need login]) | [継承] |
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| ○巻 (必須): | □ | 162
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| ○号 (必須): | □ | 7
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| ○頁 (必須): | □ | 1867 1876
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2017年 3月 2日 (平成 29年 3月 2日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1007/s00705-017-3295-3 (→Scopusで検索)
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| ○PMID (任意): | □ | 28255815 (→Scopusで検索)
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| ○CRID (任意): |
| ○Scopus (任意): | 1. | 2-s2.0-85014121673
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| ○備考 (任意): | 1. | (英) Article.ELocationID: 10.1007/s00705-017-3295-3 (日)
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| 2. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
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