Mol. Cells 2019; 42(): 1081
Effects of δ-Catenin on APP by Its Interaction with Presenilin-1
Weiye Dai1,3, Taeyong Ryu1,3, Hangun Kim2, Yun Hye Jin1, Young-Chang Cho1, and Kwonseop Kim1,*
1College of Pharmacy and Research Institute for Drug Development, Chonnam National University, Gwangju 61186, Korea, 2College of Pharmacy and Research Institute of Life and Pharmaceutical Sciences, Sunchon National University, Sunchon 57922, Korea, 3These authors contributed equally to this work.
Received June 25, 2018; Revised October 16, 2018; Accepted October 18, 2018.; Published online January 2, 2019.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit (
Alzheimer’s disease (AD) is the most frequent age-related human neurological disorder. The characteristics of AD include
senile plaques, neurofibrillary tangles, and loss of synapses and neurons in the brain. β-Amyloid (Aβ) peptide is the
predominant proteinaceous component of senile plaques. The “amyloid hypothesis” states that Aβ initiates the cascade
of events that result in AD. Amyloid precursor protein (APP) processing plays an important role in Aβ production, which
initiates synaptic and neuronal damage. δ-Catenin is known to be bound to presenilin-1 (PS-1), which is the main component of the γ-secretase complex that regulates APP cleavage. Because PS-1 interacts with both APP and δ-catenin, it is worth studying their interactive mechanism and/or effects on each other. Our immunoprecipitation data showed that there was no physical association between δ-catenin and APP. However, we observed that δ-catenin could reduce the binding between PS-1 and APP, thus decreasing the PS-1 mediated APP processing activity. Furthermore, δ-catenin reduced PS-1-mediated stabilization of APP. The results suggest that δ-catenin can influence the APP processing and its level by interacting with PS-1, which may eventually play a protective role in the degeneration of an Alzheimer’s disease patient. 
Keywords: Alzheimer’s disease, APP, δ-catenin, presenilin

Current Issue

31 December 2018 Volume 41,
Number 12, pp. 993~1081

This Article

Cited By Articles
  • CrossRef (0)

Social Network Service

Indexed in

  • Science Central
  • CrossMark