. Up-regulation of inhibitors of protein phosphatase-2A in Alzheimer's disease. Am J Pathol. 2005 Jun;166(6):1761-71. PubMed.


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  1. The observation of the relocalization of I2PPA2/SET/TAF-1 from the nucleus to the cytoplasm in AD neurons is of particular interest because of the possible role of this phosphatase inhibitor in the hyperphosphorylation of tau. Furthermore, we have recently demonstrated (Telese et al., 2005) that SET is responsible for the activation of transcription under the control of AICD/Fe65. Thus, it can be speculated that the relocation of SET in AD could affect the transcription of the genes dependent on the APP cleavage. Could this phenomenon contribute to the AD phenotype? Is it an attempt to counteract the increased production of AICD?


    . Transcription regulation by the adaptor protein Fe65 and the nucleosome assembly factor SET. EMBO Rep. 2005 Jan;6(1):77-82. PubMed.

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  1. San Francisco: Making Tau Toxic—Post-translational Changes Galore