The clathrin assembly protein AP180 regulates the generation of amyloid-β peptide

Fangbai Wu, Yasuji Matsuoka, Mark P. Mattson, Pamela J. Yao

Research output: Contribution to journalArticlepeer-review

Abstract

The overproduction and extracellular buildup of amyloid-β peptide (Aβ) is a critical step in the etiology of Alzheimer's disease. Recent data suggest that intracellular trafficking is of central importance in the production of Aβ. Here we use a neuronal cell line to examine two structurally similar clathrin assembly proteins, AP180 and CALM. We show that RNA interference-mediated knockdown of AP180 reduces the generation of Aβ1-40 and Aβ1-42, whereas CALM knockdown has no effect on Aβ generation. Thus AP180 is among the traffic controllers that oversee and regulate amyloid precursor protein processing pathways. Our results also suggest that AP180 and CALM, while similar in their domain structures and biochemical properties, are in fact dedicated to separate trafficking pathways in neurons.

Original languageEnglish (US)
Pages (from-to)247-250
Number of pages4
JournalBiochemical and Biophysical Research Communications
Volume385
Issue number2
DOIs
StatePublished - Jul 24 2009
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Amyloid-β peptide
  • AP180
  • APP
  • CALM
  • Clathrin assembly protein
  • Neuron

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Molecular Biology

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