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Post-translational regulation of the β-secretase BACE1

Araki, Wataru·2016·Brain Research Bulletin
DOI 10.1016/j.brainresbull.2016.04.009
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Abstract

β-Secretase, widely known as β-site APP cleaving enzyme 1 (BACE1), is a membrane-associated protease that cleaves amyloid precursor protein (APP) to generate amyloid β-protein (Aβ). As this cleavage is a pathologically relevant event in Alzheimer's disease, BACE1 is considered a viable therapeutic target. BACE1 can be regulated at the transcriptional, post-transcriptional, translational, and post-translational levels. Elucidation of the regulatory pathways of BACE1 is critical, not only for understanding the pathological mechanisms of AD but also developing effective therapeutic strategies to inhibit activity of the protease. This mini-review focuses on the post-translational regulation of BACE1, as modulation at this level is closely associated with both physiological and pathological conditions. Current knowledge on the mechanisms underlying such BACE1 regulation and their implications for therapy are discussed.

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  • Cholesterol regulates the formation of lipid clusters and the affinity of proteins to lipid clusters, including β-secretase and γ-secretase.

    “In cellular membranes, cholesterol regulates the formation of lipid clusters (also known as lipid rafts) and the affinity of proteins to lipid clusters (7), including β-secretase and γ-secretase (8–10).”

    From Regulation of beta-amyloid production in neurons by astrocyte-derived cholesterol (2021) · cites this paper as [9]

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Authors
Araki, W.
Venue
Brain Research Bulletin
Publisher
Elsevier BV
Published
2016-09
Volume
126
Pages
170-177
ISSN
0361-9230
DOI
10.1016/j.brainresbull.2016.04.009
Cited by
26
References
17
Language
en
Licence
Funders
JSPS (22590951)

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