Reference - Detail
| RRC ID | 73819 |
|---|---|
| Author | Oba M, Fukui K, Sango K, Suzuki M. |
| Title | Dataset on the effect of Rubicon overexpression on polyglutamine-induced locomotor dysfunction in Drosophila. |
| Journal | Data Brief |
| 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 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. |
| Volume | 37 |
| Pages | 107222 |
| Published | 2021-8-1 |
| DOI | 10.1016/j.dib.2021.107222 |
| PII | S2352-3409(21)00506-0 |
| PMID | 34189208 |
| PMC | PMC8220321 |
| Altmetric score |
オルトメトリクス指標項目
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| The most frequently cited source | News |
| Total number of mentions | 2 |
| Altmetric score changes over past 6months | 0.0 |
| Resource | |
| Drosophila | DGRC#118835 DGRC#118836 DGRC#118837 DGRC#118838 |