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- Material Type
- 文書・図像類
- Author/Editor
- 武田, 泰生
- Author Heading
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- Alternative Title
- Analysis for molecular mechanism of contactin associated protein on intractable epilepsy
- Text Language Code
- jpn
- Subject Heading
- Target Audience
- 一般
- Note (General)
- 2008-2010年度科学研究費補助金(基盤研究(C))研究成果報告書 課題番号：20590149 研究代表者：武田泰生 (鹿児島大学医学部・歯学部附属病院准教授)跳躍伝導のKチャネルの局在に関与するCaspr2の細胞内部分と直接結合する分子として小胞体への蛋白質パッケージングに関わるcarboxypeptidase E(CPE)を同定した。これら両者間の相互作用を検討した結果、Caspr2とCPEはともにラット大脳皮質2, 3層のapical dendritesに共存し、細胞内のゴルジ/小胞体に共局在しており、Caspr2の膜輸送はCPEを介したtrans-Golgi networkによることを明らかにした。To investigate the molecular mechanism for trafficking of Contactin-associated protein (Caspr) 2 to the cem membrane, we identified carboxypeptidase E (CPE) as a binding partner of Caspr2. Both Caspr2- and CPE-like immunoreactivities (IR) were found to co-localize in the apical dendrites and cell bodies of rat cortical neurons. In subcellular localization analysis, Caspr2- and CPE-like IRs were comigrated in the fractions of Golgi/ER. When Caspr2 cDNA was transfected into COS-7 cells with or without CPE cDNA, Caspr2 localized only in Golgi/ER without CPE, but localized in both Golgi/ER and plasma membrane with CPE. Our data suggest that CPE may be a key molecule to regulate Caspr2 trafficking to the cell membrane.