{"created":"2023-05-15T09:59:01.349705+00:00","id":3099,"links":{},"metadata":{"_buckets":{"deposit":"498c3799-fb1c-4b54-9c04-1a0d6059a7ef"},"_deposit":{"created_by":5,"id":"3099","owner":"5","owners":[5],"pid":{"revision_id":0,"type":"depid","value":"3099"},"status":"published"},"_oai":{"id":"oai:miyazaki-u.repo.nii.ac.jp:00003099","sets":["72","72:40"]},"author_link":["8738"],"item_10007_description_13":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"アルツハイマー病、パーキンソン病などの神経変性疾患の治療法開発を目標に、脳神経細胞で起こる小胞体ストレス応答の全貌解明を目指している。本年度得られた成果は以下のとおりである。 1、新規小胞体ストレスセンサーの同定と機能解析;小胞体ストレスセンサーATF6やOASISに構造的に類似するBBF2H7を同定した。BBF2H7は転写因子として機能し、分子シャペロンBiPの発現を促進する可能性を見出した。さらにこの分子はストレス時に翻訳レベルで誘導され、小胞体ストレス誘導性細胞死から救済する機能をもつことがわかった。 2、小胞体ストレス誘導性オートファジーの分子機構;小胞体ストレス時に二重膜でつつまれたオートファゴゾームが多数出現すること、このオートファゴゾーム形成にはIRE1-TRAF-JNKパスウェーが必須であること、さらには活性化したオートファジーは異常タンパク質の排除に働く可能性を見出した。 3、小胞体分子シャペロンBiP誘導剤の作用機序解明と薬効評価;低分子化合物BIXは小胞体ストレスを誘発することなくBiPのみを特異的に転写・翻訳させることが分かった。また、in vitroおよびin vivoにおいて小胞体ストレス誘導性の細胞死を抑制することも明らかにした。 4、神経細胞の樹状突起における小胞体ストレス:樹状突起に局在する小胞体におけるストレス応答について検討した。その結果、樹状突起内で小胞体ストレスセンサーIRE1, PERKおよびATF6がストレス依存的に活性化し下流シグナルもそれに応答することが明らかになった。","subitem_description_language":"ja","subitem_description_type":"Abstract"}]},"item_10007_description_14":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"平成17年度～平成19年度科学研究費補助金\n(基盤研究(A)) 研究成果報告書","subitem_description_language":"ja","subitem_description_type":"Other"}]},"item_10007_relation_17":{"attribute_name":"関連サイト","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"http://dx.doi.org/10.1038/sj.cdd.4402276"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://dx.doi.org/10.1038/sj.cdd.4402276","subitem_relation_type_select":"DOI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"http://dx.doi.org/10.1128/MCB.01552-06"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://dx.doi.org/10.1128/MCB.01552-06","subitem_relation_type_select":"DOI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"http://dx.doi.org/10.1093/hmg/ddm239"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://dx.doi.org/10.1093/hmg/ddm239","subitem_relation_type_select":"DOI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"http://dx.doi.org/10.1016/j.neuroscience.2007.01.069"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://dx.doi.org/10.1016/j.neuroscience.2007.01.069","subitem_relation_type_select":"DOI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"http://dx.doi.org/10.1128/MCB.01453-06"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://dx.doi.org/10.1128/MCB.01453-06","subitem_relation_type_select":"DOI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"http://dx.doi.org/10.1016/j.bbrc.2006.03.173"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://dx.doi.org/10.1016/j.bbrc.2006.03.173","subitem_relation_type_select":"DOI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"http://dx.doi.org/10.1111/j.1471-4159.2005.03596.x"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://dx.doi.org/10.1111/j.1471-4159.2005.03596.x","subitem_relation_type_select":"DOI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"http://dx.doi.org/10.1038/ncb1213"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://dx.doi.org/10.1038/ncb1213","subitem_relation_type_select":"DOI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"http://dx.doi.org/10.1016/j.bbrc.2005.04.039"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://dx.doi.org/10.1016/j.bbrc.2005.04.039","subitem_relation_type_select":"DOI"}}]},"item_10007_textarea_26":{"attribute_name":"目次情報","attribute_value_mlt":[{"subitem_textarea_language":"ja","subitem_textarea_value":"○ はしがき\n○ 研究組織\n○ 交付決定額(配分額)\n1. 研究の背景および目的\n2. 研究内容\n3. 研究成果、考察、展望\n4. 研究発表\n    1)論文\n    2)学会発表\n    3)研究成果による産業財産権の出願・取得状況\n \n 主要論文\n○ Kudo, T., Kanemoto, S., Hara, H., Morimoto, N., Morihara, T., Kimura, R., et al. (2008). A molecular chaperone inducer protects neurons from ER stress. Cell Death and Differentiation, 15(2),364-375\n http://dx.doi.org/10.1038/sj.cdd.4402276\n○ Kondo, S., Saito, A., Hino, S. -., Murakami, T., Ogata, M., Kanemoto, S., et al. (2007). BBF2H7, a novel transmembrane bZIP transcription factor, is a new type of endoplasmic reticulum stress transducer. Molecular and Cellular Biology, 27(5),1716-1729\n http://dx.doi.org/10.1128/MCB.01552-06\n○ Hino, S. -., Kondo, S., Sekiya, H., Saito, A., Kanemoto, S., Murakami, T., et al. (2007). Molecular mechanisms responsible for aberrant splicing of SERCA1 in myotonic dystrophy type 1. Human Molecular Genetics, 16(23),2834-2843\n http://dx.doi.org/10.1093/hmg/ddm239\n○ Murakami, T., Hino, S. -., Saito, A., & Imaizumi, K. (2007). Endoplasmic reticulum stress response in dendrites of cultured primary neurons. Neuroscience, 146(1),1-8\n http://dx.doi.org/10.1016/j.neuroscience.2007.01.069\n○ Ogata, M., Hino, S. -., Saito, A., Morikawa, K., Kondo, S., Kanemoto, S., et al. (2006). Autophagy is activated for cell survival after endoplasmic reticulum stress. Molecular and Cellular Biology, 26(24),9220-9231\n http://dx.doi.org/10.1128/MCB.01453-06\n○ Kudo, T., Okumura, M., Imaizumi, K., Araki, W., Morihara, T., Tanimukai, H., et al. (2006). Altered localization of amyloid precursor protein under endoplasmic reticulum stress. Biochemical and Biophysical Research Communications, 344(2),525-530\n http://dx.doi.org/10.1016/j.bbrc.2006.03.173\n○ Murakami, T., Kondo, S., Ogata, M., Kanemoto, S., Saito, A., Wanaka, A., et al. (2006). Cleavage of the membrane-bound transcription factor OASIS in response to endoplasmic reticulum stress. Journal of Neurochemistry, 96(4),1090-1100\n http://dx.doi.org/10.1111/j.1471-4159.2005.03596.x\n○ Kondo, S., Murakami, T., Tatsumi, K., Ogata, M., Kanemoto, S., Otori, K., et al. (2005). OASIS, a CREB/ATF-family member, modulates UPR signalling in astrocytes. Nature Cell Biology, 7(2),186-194\n http://dx.doi.org/10.1038/ncb1213\n○ Kanemoto, S., Kondo, S., Ogata, M., Murakami, T., Urano, F., & Imaizumi, K. (2005). XBP1 activates the transcription of its target genes via an ACGT core sequence under ER stress. Biochemical and Biophysical Research Communications, 331(4),1146-1153\n http://dx.doi.org/10.1016/j.bbrc.2005.04.039"}]},"item_10007_version_type_20":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2020-06-21"}],"displaytype":"detail","filename":"H-24_imaizumi-kaken-17200026.pdf","filesize":[{"value":"693.3 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"H-24_imaizumi-kaken-17200026.pdf","url":"https://miyazaki-u.repo.nii.ac.jp/record/3099/files/H-24_imaizumi-kaken-17200026.pdf"},"version_id":"d679b038-e353-4dad-aa60-ec9add055e5e"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"神経変性疾患, 小胞体ストレス, 神経細胞死, 転写因子, OASIS, オートファジー, 化合物, 分子シャペロン","subitem_subject_language":"ja","subitem_subject_scheme":"Other"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_researcher":{"attribute_name":"研究代表者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"今泉, 和則","creatorNameLang":"ja"},{"creatorName":"イマイズミ, カズノリ","creatorNameLang":"ja-Kana"}],"nameIdentifiers":[{"nameIdentifier":"8738","nameIdentifierScheme":"WEKO"}]}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"research report","resourceuri":"http://purl.org/coar/resource_type/c_18ws"}]},"item_title":"小胞体ストレス応答機構の制御による神経細胞死防御法の開発","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"小胞体ストレス応答機構の制御による神経細胞死防御法の開発","subitem_title_language":"ja"}]},"item_type_id":"10007","owner":"5","path":["72","40"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2009-10-15"},"publish_date":"2009-10-15","publish_status":"0","recid":"3099","relation_version_is_last":true,"title":["小胞体ストレス応答機構の制御による神経細胞死防御法の開発"],"weko_creator_id":"5","weko_shared_id":-1},"updated":"2024-01-30T04:25:12.020636+00:00"}