An X11alpha/FSBP complex represses transcription of the GSK3beta gene promoter.
Authors
Lau, Kwok-FaiPerkinton, Michael S
Rodriguez, Lilia
McLoughlin, Declan M
Miller, Christopher C J
Affiliation
Department of Biochemistry Science, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR. kflau@cuhk.edu.hkIssue Date
2010-08-04MeSH
Adaptor Proteins, Signal TransducingAlzheimer Disease
Animals
Blotting, Northern
Brain
CHO Cells
Cricetinae
Cricetulus
Gene Expression Regulation
Glycogen Synthase Kinase 3
Humans
Multiprotein Complexes
Nerve Tissue Proteins
Promoter Regions, Genetic
Rats
Transcription Factors
Transcription, Genetic
Transfection
Two-Hybrid System Techniques
Metadata
Show full item recordCitation
An X11alpha/FSBP complex represses transcription of the GSK3beta gene promoter. 2010, 21 (11):761-6 NeuroreportJournal
NeuroreportDOI
10.1097/WNR.0b013e32833bfca0PubMed ID
20531236Additional Links
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896363/?tool=pubmedAbstract
X11alpha 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 Abeta peptide that is deposited in Alzheimer's disease brains. X11alpha also contains two C-terminal postsynaptic density-95, large discs, zona occludens 1 (PDZ) domains, and we show here that through its PDZ domains, X11alpha interacts with a novel transcription factor, fibrinogen silencer binding protein. Moreover, we show that an X11alpha/fibrinogen silencer binding protein complex signals to the nucleus to repress glycogen synthase kinase-3beta promoter activity. Glycogen synthase kinase-3beta is a favoured candidate kinase for phosphorylating tau in Alzheimer's disease. Our findings show a new function for X11alpha that may impact on Alzheimer's disease pathogenesis.Item Type
ArticleLanguage
enISSN
1473-558Xae974a485f413a2113503eed53cd6c53
10.1097/WNR.0b013e32833bfca0
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