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

ABSTRACT: 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 hemaggl

SUBMITTER: Oba M 

PROVIDER: S-EPMC8220321 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature