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Stabilization of intracellular trafficking and metabolism of amyloid β‐protein precursor and Alcadein β by apolipoprotein E
Author(s) -
Kimura Ayano,
Hata Saori,
Suzuki Toshiharu
Publication year - 2015
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2015.07.017
Subject(s) - intracellular , chemistry , intracellular transport , metabolism , amyloid (mycology) , apolipoprotein b , amyloid precursor protein , biochemistry , microbiology and biotechnology , biology , medicine , alzheimer's disease , cholesterol , disease , inorganic chemistry
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.