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FEBS Lett. 2015 Aug 19;589(18):2394-400. doi: 10.1016/j.febslet.2015.07.017. Epub 2015 Jul 23.

Stabilization of intracellular trafficking and metabolism of amyloid β-protein precursor and Alcadein β by apolipoprotein E.

Author information

1
Laboratory of Neuroscience, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0812, Japan.
2
Laboratory of Neuroscience, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0812, Japan. Electronic address: tsuzuki@pharm.hokudai.ac.jp.

Abstract

Intracellular metabolism of amyloid β-protein precursor (APP) is important for the pathogenesis of Alzheimer's disease (AD). Alcadeins (Alcα, Alcβ, and Alcγ) are neural membrane proteins similar to APP in their localization, metabolism, and cellular function. Isoform ε4 of apolipoprotein E (ApoE) is a major risk factor for AD. We found that ApoE expression attenuated intracellular trafficking of APP and Alcβ, resulting in metabolic stabilization of both proteins. By contrast, Alcα intracellular proteolysis was facilitated by ApoE expression, which was not due to an increase in the primary cleavage of Alcα. This difference may result from binding of ApoE to membrane proteins.

KEYWORDS:

Alcadein; Alzheimer’s disease; Amyloid β-protein precursor; Apolipoprotein E

PMID:
26213366
DOI:
10.1016/j.febslet.2015.07.017
[Indexed for MEDLINE]
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