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KAKEN_15K09323seika.pdf
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Download
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:192.9 KB
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| Last updated |
:Nov 12, 2018 |
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Total downloads since Nov 12, 2018 : 230
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| Title |
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ALS/FTLDの治療ターゲット同定を目指した分子病態の解明
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ALS/FTLD ノ チリョウ ターゲット ドウテイ オ メザシタ ブンシ ビョウタイ ノ カイメイ
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ALS/FTLD no chiryō tāgetto dōtei o mezashita bunshi byōtai no kaimei
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Establishment of treatment target for ALS/FTLD
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伊東, 大介
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イトウ, ダイスケ
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Ito, Daisuke
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| Affiliation |
慶應義塾大学・医学部(信濃町)・講師
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Research team head
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科研費研究者番号 : 80286450
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2018
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科学研究費補助金研究成果報告書
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2017
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1)家族性ALSに関与する2つの異なる分子UBQLN2, OPTNが共に蛋白分解に関わるendosomal vesicleに関与しており, endosomeとautopahgyをつなぐ機能を持ち, late-endosomeとは独立したendosomeの新規の蛋白品質管理機構を形成していることを確認した。2)GGGGCC異常伸長反復配列からのnon ATG翻訳によるDRP(dipeptidere peat protein)の中で塩基性の強いpoly-PRをHela細胞に導入するとgemini of coiled bodyが有意に減少させ, ALSの病態を反映しているものと考えられた。
1) Two different molecules involved in familial ALS, UBQLN 2 and OPTN are both involved in endosomal vesicles involved in proteolysis, have the function of connecting enodosome and autopahgy, and formed a novel protein quality control mechanism in endosome. 2) In DRP (dipeptidere peat protein) by non-AUG (RAN) translation from abnormal elongation GGGGCC repetitive sequence, expression of poly-PR, which is strongly basic, significantly reduces gemini of coiled bodies and Cajal bodies into Hela cells and suggested that it reflects the pathology of ALS.
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研究種目 : 基盤研究(C)(一般)
研究期間 : 2015～2017
課題番号 : 15K09323
研究分野 : 神経内科
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