IndraLab

Statements


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"Downregulation of ATXN3 enhanced AKT inhibitors (perifosine or MK-2206) induced cell death by BIM, but decreased the cell death induced by chemotherapeutic drugs (etoposide or cisplatin) via Bcl-xl."

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"These results are in complete agreement with previous reports showing that both depletion of ATXN3 and overexpression of pathogenic polyQ ATXN3 alleles caused disorganization of cytoskeleton and increased cell death in cultured cells (Neves-Carvalho et al., 2015; Rodrigues et al., 2010)."

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"In our cellular model, full-length expanded ataxin-3 that leads to neurodegenerative disorders significantly impaired the expression of Bcl-2 protein, which may be, at least in part, responsible for the weak tolerance to polyglutamine toxicity at the early stage of disease and ultimately resulted in an increase of stress induced cell death upon apoptotic stress."

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"Overexpression of ATXN3 in polyQ neurodegeneration models in Drosophila suppresses toxicity and cell death, implying that ATXN3 is a neuroprotective protein; its neuroprotective action, moreover, depends both on its DUB activity and proper functioning of the proteasome."