Direct association of presenilin-1 with β-catenin

Miyuki Murayama, Shoji Tanaka, James Palacino, Ohoshi Murayama, Toshiyuki Honda, Xiaoyan Sun, Kaori Yasutake, Naomi Nihonmatsu, Benjamin Wolozin, Akihiko Takashima

Research output: Contribution to journalArticlepeer-review

145 Scopus citations


Families bearing mutations in the presenilin-1 (PS1) 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 PS1 directly interacts with endogenous β-catenin, and the interaction requires residues 322-450 of PS1 and 445-676 of β-catenin. Both proteins are co-localized in the endoplasmic reticulum. Over-expression of PS1 reduces the level of cytoplasmic β-catenin, and inhibits β-catenin-T cell factor-regulated transcription. These results indicate that PS1 plays a role as inhibitor of the β-catenin signal, which may be connected with the AD dysfunction. Copyright (C) 1998 Federation of European Biochemical Societies.

Original languageEnglish (US)
Pages (from-to)73-77
Number of pages5
JournalFEBS letters
Issue number1-2
StatePublished - Aug 14 1998
Externally publishedYes


  • Alzheimer's disease
  • Glycogen synthase kinase 3β
  • Presenilin-1
  • β-Catenin

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology


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