{"created":"2024-12-12T08:08:13.819983+00:00","id":2010420,"links":{},"metadata":{"_buckets":{"deposit":"d4cbaca2-f2f3-48f9-b844-bf70fce5aa68"},"_deposit":{"created_by":7,"id":"2010420","owners":[7],"pid":{"revision_id":0,"type":"depid","value":"2010420"},"status":"published"},"_oai":{"id":"oai:tokushima-u.repo.nii.ac.jp:02010420","sets":["1713853213384:1713853296295:1716267876683:1716268551628"]},"author_link":["307","557","220"],"item_10001_alternative_title_1":{"attribute_name":"タイトル別表記","attribute_value_mlt":[{"subitem_alternative_title":"中央アミノ酸残基はプリオン蛋白質PrPCが病原性アイソフォームに変換するのに重要である","subitem_alternative_title_language":"ja"},{"subitem_alternative_title":"Central residues crucial for prion protein conversion","subitem_alternative_title_language":"en"}]},"item_10001_biblio_info_7":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2022-08-13","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"9","bibliographicPageStart":"102381","bibliographicVolumeNumber":"298","bibliographic_titles":[{"bibliographic_title":"Journal of Biological Chemistry","bibliographic_titleLang":"en"}]}]},"item_10001_description_5":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Conformational conversion of the cellular prion protein, PrPC, into the amyloidogenic isoform, PrPSc, is a key pathogenic event in prion diseases. However, the conversion mechanism remains to be elucidated. Here, we generated Tg(PrPΔ91-106)-8545/Prnp0/0 mice, which overexpress mouse PrP lacking residues 91-106. We showed that none of the mice became sick after intracerebral inoculation with RML, 22L, and FK-1 prion strains nor accumulated PrPScΔ91-106 in their brains except for a small amount of PrPScΔ91-106 detected in one 22L-inoculated mouse. However, they developed disease around 85 days after inoculation with bovine spongiform encephalopathy (BSE) prions with PrPScΔ91-106 in their brains. These results suggest that residues 91-106 are important for PrPC conversion into PrPSc in infection with RML, 22L, and FK-1 prions but not BSE prions. We then narrowed down the residues 91-106 by transducing various PrP deletional mutants into RML- and 22L-infected cells and identified that PrP mutants lacking residues 97-99 failed to convert into PrPSc in these cells. Our in vitro conversion assay also showed that RML, 22L, and FK-1 prions did not convert PrPΔ97-99 into PrPScΔ97-99, but BSE prions did. We further found that PrP mutants with proline residues at positions 97 to 99 or charged residues at positions 97 and 99 completely or almost completely lost their converting activity into PrPSc in RML- and 22L-infected cells. These results suggest that the structurally flexible and noncharged residues 97-99 could be important for PrPC conversion into PrPSc following infection with RML, 22L, and FK-1 prions but not BSE prions.","subitem_description_language":"en","subitem_description_type":"Abstract"}]},"item_10001_publisher_8":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"American Society for Biochemistry and Molecular Biology","subitem_publisher_language":"en"},{"subitem_publisher":"Elsevier","subitem_publisher_language":"en"}]},"item_10001_rights_15":{"attribute_name":"権利情報","attribute_value_mlt":[{"subitem_rights":"This is an open access article under the CCBY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).","subitem_rights_language":"en"}]},"item_10001_source_id_9":{"attribute_name":"収録物ID","attribute_value_mlt":[{"subitem_source_identifier":"00219258","subitem_source_identifier_type":"ISSN"},{"subitem_source_identifier":"AA1202441X","subitem_source_identifier_type":"NCID"}]},"item_10001_version_type_20":{"attribute_name":"出版タイプ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_be7fb7dd8ff6fe43","subitem_version_type":"NA"}]},"item_1714461018643":{"attribute_name":"報告番号","attribute_value_mlt":[{"subitem_dissertationnumber":"甲第3662号"}]},"item_1714461102074":{"attribute_name":"学位名","attribute_value_mlt":[{"subitem_degreename":"博士（医学）","subitem_degreename_language":"ja"}]},"item_1714461118377":{"attribute_name":"学位授与年月日","attribute_value_mlt":[{"subitem_dategranted":"2022-09-22"}]},"item_1714461137393":{"attribute_name":"学位授与機関","attribute_value_mlt":[{"subitem_degreegrantor":[{"subitem_degreegrantor_language":"ja","subitem_degreegrantor_name":"徳島大学"}]}]},"item_1715043197608":{"attribute_name":"アクセス権","attribute_value_mlt":[{"subitem_access_right":"open access"}]},"item_1718868208704":{"attribute_name":"備考","attribute_value_mlt":[{"subitem_textarea_language":"ja","subitem_textarea_value":"内容要旨・審査要旨・論文本文の公開\n本論文は，著者Agriani Dini Pasianaの学位論文として提出され，学位審査・授与の対象となっている。\n学位授与者所属 : 徳島大学大学院医学研究科（医学専攻）"}]},"item_1718868303842":{"attribute_name":"学位記番号","attribute_value_mlt":[{"subitem_text_language":"ja","subitem_text_value":"甲医第1544号"}]},"item_1722929371688":{"attribute_name":"出版社版DOI","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_language":"ja","subitem_relation_name_text":"10.1016/j.jbc.2022.102381"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://doi.org/10.1016/j.jbc.2022.102381","subitem_relation_type_select":"DOI"}}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"パシアナ, アグリアニ ディニ","creatorNameLang":"ja"},{"creatorName":"パシアナ, アグリアニ ディニ","creatorNameLang":"ja-Kana"},{"creatorName":"Pasiana, Agriani Dini","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"ミヤタ, ヒロノリ","creatorNameLang":"ja"},{"creatorName":"ミヤタ, ヒロノリ","creatorNameLang":"ja-Kana"},{"creatorName":"Miyata, Hironori","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"千田, 淳司","creatorNameLang":"ja"}],"nameIdentifiers":[{"nameIdentifier":"307","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"原, 英之","creatorNameLang":"ja"}],"nameIdentifiers":[{"nameIdentifier":"557","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"イマムラ, モリカズ","creatorNameLang":"ja"},{"creatorName":"イマムラ, モリカズ","creatorNameLang":"ja-Kana"},{"creatorName":"Imamura, Morikazu","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"アタラシ, リュウイチロウ","creatorNameLang":"ja"},{"creatorName":"アタラシ, リュウイチロウ","creatorNameLang":"ja-Kana"},{"creatorName":"Atarashi, Ryuichiro","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"坂口, 末廣","creatorNameLang":"ja"}],"nameIdentifiers":[{"nameIdentifier":"220","nameIdentifierScheme":"WEKO"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_access","date":[{"dateType":"Available","dateValue":"2022-10-31"}],"displaytype":"detail","filename":"k3662_abstract.pdf","filesize":[{"value":"128 KB"}],"format":"application/pdf","mimetype":"application/pdf","url":{"objectType":"abstract","url":"https://tokushima-u.repo.nii.ac.jp/record/2010420/files/k3662_abstract.pdf"},"version_id":"a9bf818f-00ab-43f1-882f-a662ffc1f549"},{"accessrole":"open_access","date":[{"dateType":"Available","dateValue":"2022-10-31"}],"displaytype":"detail","filename":"k3662_review.pdf","filesize":[{"value":"117 KB"}],"format":"application/pdf","mimetype":"application/pdf","url":{"objectType":"other","url":"https://tokushima-u.repo.nii.ac.jp/record/2010420/files/k3662_review.pdf"},"version_id":"64c8dbde-bfec-4edf-82c7-1b4a0d9a10a8"},{"accessrole":"open_access","date":[{"dateType":"Available","dateValue":"2022-10-31"}],"displaytype":"detail","filename":"k3662_fulltext.pdf","filesize":[{"value":"1.29 MB"}],"format":"application/pdf","mimetype":"application/pdf","url":{"objectType":"fulltext","url":"https://tokushima-u.repo.nii.ac.jp/record/2010420/files/k3662_fulltext.pdf"},"version_id":"d7df2257-7868-4e67-aa92-c7b7d89c4daf"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"prion","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"prion disease","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"protein misfolding","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"structure-function","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"transgenic mice","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"neurodegenerative disease","subitem_subject_language":"en","subitem_subject_scheme":"Other"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"eng"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"doctoral thesis","resourceuri":"http://purl.org/coar/resource_type/c_db06"}]},"item_title":"Central Residues in Prion Protein PrPC Are Crucial for Its Conversion into the Pathogenic Isoform","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Central Residues in Prion Protein PrPC Are Crucial for Its Conversion into the Pathogenic Isoform","subitem_title_language":"en"}]},"item_type_id":"40001","owner":"7","path":["1716268551628"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2022-10-31"},"publish_date":"2022-10-31","publish_status":"0","recid":"2010420","relation_version_is_last":true,"title":["Central Residues in Prion Protein PrPC Are Crucial for Its Conversion into the Pathogenic Isoform"],"weko_creator_id":"7","weko_shared_id":-1},"updated":"2024-12-12T08:08:25.341078+00:00"}