論文

査読有り
2011年3月

Interaction of ataxin-3 with huntingtin-associated protein 1 through Josephin domain

NEUROREPORT
  • Yukio Takeshita
  • ,
  • Ryutaro Fujinaga
  • ,
  • Keiji Kokubu
  • ,
  • Md. Nabiul Islam
  • ,
  • Mir Rubayet Jahan
  • ,
  • Akie Yanai
  • ,
  • Akira Kakizuka
  • ,
  • Koh Shinoda

22
5
開始ページ
232
終了ページ
238
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1097/WNR.0b013e32834505f4
出版者・発行元
LIPPINCOTT WILLIAMS & WILKINS

Huntingtin-associated protein 1 (HAP1) is an essential component of the stigmoid body (STB) and known as a possible neuroprotective interactor with causative proteins for Huntington's disease, spinal and bulbar muscular atrophy, spinocerebellar ataxia type 17 (SCA17), and Joubert syndrome. To clarify what other causative molecules HAP1/STB could interact with, we cloned normal causative genes for several neural disorders from human brain RNA library and evaluated their subcellular interaction with HAP1/STB by immunocytochemistry and immunoprecipitation after cotransfection into Neuro2a cells. The results clearly showed that HAP1/STB interacts with the normal ataxin-3 through Josephin domain and polyglutamine-expanded mutants derived from SCA3 as well. The findings suggest that HAP1/STB could modify the physiological function of normal ataxin-3 and pathogenesis of SCA3 attributable to the mutant ataxin-3. NeuroReport 22:232-238 (C) 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.

Web of Science ® 被引用回数 : 11

リンク情報
DOI
https://doi.org/10.1097/WNR.0b013e32834505f4
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/21386698
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000288155900008&DestApp=WOS_CPL

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