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ID 48557
JaLCDOI
フルテキストURL
著者
Tanabe, Kenji Department of Neuroscience, Okayama University Graduate School of Medicine
Takei, Kohji Department of Neuroscience, Okayama University Graduate School of Medicine
抄録
Charcot-Marie-Tooth disease (CMT) is an inherited neuronal disorder, and is induced by mutations of various genes associated with intracellular membrane traffic and cytoskeleton. A large GTPase, dynamin, which is known as a fission protein for endocytic vesicles, was identified as a gene responsible for dominant-intermediate CMT type 2B (DI-CMT2B). Of these mutants, the PH domain, which is required for interaction with phosphoinositides, was mutated in several families. Interestingly, the expression of a deletion mutant, 551Δ3, did not impair endocytosis, but induced abnormal accumulation of microtubules. Recent evidence has shown that dynamin 2 regulates the dynamic instability of microtubules, and 551Δ3 lacks this function. We propose a model for the regulation of the dynamic instability of microtubules by dynamin 2 and discuss the relationship between dynamin 2 and CMT.
キーワード
neuropathy
Charcot-Marie-Tooth disease
membrane traffic
dynamin
microtubules
Amo Type
Review
発行日
2012-06
出版物タイトル
Acta Medica Okayama
66巻
3号
出版者
Okayama University Medical School
開始ページ
183
終了ページ
190
ISSN
0386-300X
NCID
AA00508441
資料タイプ
学術雑誌論文
言語
English
著作権者
CopyrightⒸ 2012 by Okayama University Medical School
論文のバージョン
publisher
査読
有り
PubMed ID
Web of Sience KeyUT