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Activity-dependent cleavage of dyskinesia-related proline-rich transmembrane protein 2 (PRRT2) by calpain in mouse primary cortical neurons
http://hdl.handle.net/10069/39661
http://hdl.handle.net/10069/3966182b70a0c-5320-4658-b055-8b19d3fee851
名前 / ファイル | ライセンス | アクション |
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FASEB34_180.pdf (3.2 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2020-11-20 | |||||
タイトル | ||||||
タイトル | Activity-dependent cleavage of dyskinesia-related proline-rich transmembrane protein 2 (PRRT2) by calpain in mouse primary cortical neurons | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | proteolysis | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | NMDA receptor | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | glutamate | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | calcium signaling | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | neuronal excitation | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Hatta, Daisuke
× Hatta, Daisuke× Shirotani, Keiro× Hori, Yuma× Kurotaki, Naohiro× Iwata, Nobuhisa |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Mutations of PRRT2 (proline-rich transmembrane protein 2) cause several neurological disorders, represented by paroxysmal kinesigenic dyskinesia (PKD), which is characterized by attacks of involuntary movements triggered by sudden voluntary movements. PRRT2 is reported to suppress neuronal excitation, but it is unclear how the function of PRRT2 is modulated during neuronal excitation. We found that PRRT2 is processed to a 12 kDa carboxy-terminal fragment (12K-CTF) by calpain, a calcium-activated cysteine protease, in a neuronal activity-dependent manner, predominantly via NMDA receptors or voltage-gated calcium channels. Furthermore, we clarified that 12K-CTF is generated by sequential cleavages at Q220 and S244. The amino-terminal fragment (NTF) of PRRT2, which corresponds to PKD-related truncated mutants, is not detected, probably due to rapid cleavage at multiple positions. Given that 12K-CTF lacks most of the proline-rich domain, this cleavage might be involved in the activity-dependent enhancement of neuronal excitation perhaps through transient retraction of PRRT2's function. Therefore, PRRT2 might serve as a buffer for neuronal excitation, and lack of this function in PKD patients might cause neuronal hyperexcitability in their motor circuits. | |||||
書誌情報 |
The FASEB Journal 巻 34, 号 1, p. 180-191, 発行日 2019-11-20 |
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出版者 | ||||||
出版者 | Wiley | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 08926638 | |||||
EISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 15306860 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1096/fj.201902148R | |||||
権利 | ||||||
権利情報 | c 2019 Federation of American Societies for Experimental Biology. This is the peer reviewed version of the following article: FASEB journal: official publication of the Federation of American Societies for Experimental Biology, 34(1), pp.180-191; 2020, which has been published in final form at 10.1096/fj.201902148R. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | FASEB journal, 34(1), pp.180-191; 2020 |