our data support the concept that expanded ATXN2 undergoes progressive insolubility and affects PABPC1 by a toxic gain-of-function mechanism with tissue-specific effects which may be partially alleviated by the induction of FBXW8.
Depletion of FBXW8 caused a significant accumulation of cyclin D1 as well as sequestration of CDK1 in the cytoplasm. This resulted in a severe reduction of cell proliferation.
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