Dataset on the effect of Rubicon overexpression on polyglutamine-induced locomotor dysfunction in Drosophila

Masaki Oba, Koji Fukui, Kazunori Sango, Mari Suzuki

研究成果査読

抄録

The accumulation of pathogenic misfolded proteins is believed to be a common mechanism of generation of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and polyglutamine (polyQ) diseases. The autophagy–lysosome degradation system has been considered as a potential therapeutic target against these disorders, as it is able to degrade large protein aggregates. Previously, we focused on Rubicon, a negative regulator of autophagy, and demonstrated that knockdown of the Drosophila homolog of Rubicon (dRubicon) suppressed locomotor dysfunction in a fly model of polyQ disease. This suppression was associated with increased autophagic activity and a marked reduction in the number of polyQ inclusion bodies [1]. We generated transgenic fly lines expressing hemagglutinin-tagged dRubicon wild-type (WT) or dRubicon in which the RUN [after RPIP8 (RaP2 interacting protein 8), UNC-14 and NESCA (new molecule containing SH3 at the carboxyl-terminus)] domain was deleted (ΔRUN). We provide data regarding the effect of WT and ΔRUN dRubicon co-expression on polyQ-induced locomotor dysfunction in Drosophila.

本文言語English
論文番号107222
ジャーナルData in Brief
37
DOI
出版ステータスPublished - 2021 8

ASJC Scopus subject areas

  • 一般

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