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Bibliographic Record
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- Material Type
- 文書・図像類
- Author/Editor
- 佐野, 輝
- Author Heading
- Publication, Distribution, etc.
- Alternative Title
- Autophagic neurodegeneration inn molecular pathogenesis of chores-accanthocytosis
- Text Language Code
- jpn
- Target Audience
- 一般
- Note (General)
- 2011-2013年度科学研究費助成事業（基盤研究（B））研究成果報告書 課題番号：23390291 研究代表者：佐野輝（鹿児島大学・医歯（薬）学総合研究科・教授）有棘赤血球舞踏病の責任タンパク質であるコレインを強制発現させた培養細胞を用いた研究の結果、コレインはα-チューブリン、ヒストン脱アセチル化酵素6（HDAC6）と相互作用し、α-チューブリンの脱アセチル化を促進する可能性が示された。また、コレインは飢餓誘発性細胞死に対し抑制的に働くが、HDAC6阻害剤を培養液に添加するとこの作用が弱まる。HDAC6は、飢餓誘発性オートファジーとも関わることが報告されている。飢餓誘発性オートファジーに関わる細胞死抑制機構の破綻が有棘赤血球舞踏病の分子病態の一つである可能性が示唆された。Co-immunopreticipation assay using extracts from chorein-overexpressing cells showed that chorein, the protein responsible for chorea-acanthocytosis (ChAc), co-precipitated with alpha-tubulin and HDAC6, probably leading to facilitation of alpha-tubulin deacetylation. Cell viability assay revealed that cells stably expressing chorein, significantly preserved cell viability during nutrient deprivation. These results suggest that chorein interacts with the cytoskeletal proteins and may play an important role in autophagic process, including in the protection against starvation-induced cell damages. Disruption of this cell protection mechanism may involved in molecular pathogenesis of ChAc.