Direct association of presenilin-1 with beta-catenin.
Families bearing mutations in the presenilin-1 (PSI) gene develop Alzheimer's disease (AD). However, the mechanism through which PS1 causes AD is unclear. The co-immunoprecipitation with PS1 in transfected COS-7 cells indicates that PSI directly interacts with endogenous beta-catenin, and the interaction requires residues 322450 of PSI and 445-676 of beta-catenin. ... Both proteins are co-localized in the endoplasmic reticulum. Over-expression of PS1 reduces the level of cytoplasmic beta-catenin, and inhibits beta-catenin-T cell factor-regulated transcription. These results indicate that PSI plays a role as inhibitor of the beta-catenin signal, which may be connected with the AD dysfunction.
Mesh Terms:
Alzheimer Disease, Animals, Binding Sites, COS Cells, Cytoplasm, Cytoskeletal Proteins, Endoplasmic Reticulum, Gene Expression, Humans, Immunosorbent Techniques, Membrane Proteins, Mutagenesis, Site-Directed, Neuroblastoma, Peptide Fragments, Presenilin-1, Signal Transduction, Structure-Activity Relationship, Trans-Activators, Transfection, Tumor Cells, Cultured, beta Catenin
Alzheimer Disease, Animals, Binding Sites, COS Cells, Cytoplasm, Cytoskeletal Proteins, Endoplasmic Reticulum, Gene Expression, Humans, Immunosorbent Techniques, Membrane Proteins, Mutagenesis, Site-Directed, Neuroblastoma, Peptide Fragments, Presenilin-1, Signal Transduction, Structure-Activity Relationship, Trans-Activators, Transfection, Tumor Cells, Cultured, beta Catenin
FEBS Lett.
Date: Aug. 14, 1998
PubMed ID: 9738936
View in: Pubmed Google Scholar
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