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• W2958303039 abstract "Fused in sarcoma (FUS) is a DNA/RNA-binding protein associated with amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration. The exact molecular mechanisms by which FUS results in neurotoxicity have not yet been fully elucidated. Here, we found that parkin is a genetic suppressor of defective phenotypes induced by exogenous human wild type FUS in Drosophila. Although parkin overexpression did not modulate the FUS protein expression level, the locomotive defects in FUS-expressing larvae and adult flies were rescued by parkin expression. We found that FUS expression in muscle tissues resulted in a reduction of the levels and assembly of mitochondrial complex I and III subunits, as well as decreased ATP. Remarkably, expression of parkin suppressed these mitochondrial dysfunctions. Our results indicate parkin as a neuroprotective regulator of FUS-induced proteinopathy by recovering the protein levels of mitochondrial complexes I and III. Our findings on parkin-mediated neuroprotection may expand our understanding of FUS-induced ALS pathogenesis." @default.
• W2958303039 created "2019-07-23" @default.
• W2958303039 creator A5001302287 @default.
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• W2958303039 date "2019-07-12" @default.
• W2958303039 modified "2023-10-14" @default.
• W2958303039 title "Parkin expression reverses mitochondrial dysfunction in fused in sarcoma‐induced amyotrophic lateral sclerosis" @default.
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• W2958303039 doi "https://doi.org/10.1111/imb.12608" @default.
• W2958303039 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31290213" @default.
• W2958303039 hasPublicationYear "2019" @default.
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