CELLULAR, MOLECULAR AND DEVELOPMENTAL NEUROSCIENCEAn X11α/FSBP complex represses transcription of the GSK3β gene promoterLau, Kwok-Faia; Perkinton, Michael S.b; Rodriguez, Liliab; McLoughlin, Declan M.c; Miller, Christopher C.J.bAuthor Information aDepartment of Biochemistry (Science), The Chinese University of Hong Kong, Shatin NT, Hong Kong SAR bMRC Centre for Neurodegeneration Research, King's College London, Institute of Psychiatry, London, UK cDepartment of Psychiatry and Trinity College Institute of Neuroscience, Trinity College Dublin, St Patrick's Hospital, Dublin, Ireland Correspondence to Dr Kwok-Fai Lau, The Chinese University of Hong Kong, Rm 291, Science Centre, Shatin, NT, Hong Kong Tel: +852 26921106; fax: +852 26037732; e-mail: [email protected] Received 13 April 2010 accepted 11 May 2010 NeuroReport: August 4, 2010 - Volume 21 - Issue 11 - p 761-766 doi: 10.1097/WNR.0b013e32833bfca0 Buy Metrics Abstract X11α is a neuronal adaptor protein that interacts with the amyloid precursor protein (APP) through a centrally located phosphotyrosine binding domain to inhibit the production of Aβ peptide that is deposited in Alzheimer's disease brains. X11α also contains two C-terminal postsynaptic density-95, large discs, zona occludens 1 (PDZ) domains, and we show here that through its PDZ domains, X11α interacts with a novel transcription factor, fibrinogen silencer binding protein. Moreover, we show that an X11α/fibrinogen silencer binding protein complex signals to the nucleus to repress glycogen synthase kinase-3β promoter activity. Glycogen synthase kinase-3β is a favoured candidate kinase for phosphorylating tau in Alzheimer's disease. Our findings show a new function for X11α that may impact on Alzheimer's disease pathogenesis. © 2010 Lippincott Williams & Wilkins, Inc.