The functions of the Alzheimer's -amyloid precursor protein (APP) and of its complex with the adaptor protein Fe65 are still unknown. We have demonstrated that Fe65 is also a nuclear protein and APP functions as an extranuclear anchor, thus preventing Fe65 nuclear translocation. According to this finding, it was also demonstrated that Fe65 could play a role in the regulation of transcription. In the present paper we show that the overexpression of
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