NDLI: CD74 interacts with APP and suppresses the production of Aβ

Content Provider	Springer Nature : BioMed Central
Author	Matsuda, Shuji Matsuda, Yukiko D'Adamio, Luciano
Abstract	Background Alzheimer disease (AD) is characterized by senile plaques, which are mainly composed of β amyloid (Aβ) peptides. Aβ is cleaved off from amyloid precursor protein (APP) with consecutive proteolytic processing by β-secretase and γ-secretase. Results Here, we show that CD74, the invariant chain of class II major histocompatibility complex, interacts with APP and serves as a negative regulator of Aβ. CD74 resembles other APP interacters such as BRI2 and BRI3, since all of them reduce the level of Aβ. However, unlike BRIs, CD74 does not reduce the secretion of sAPPα or sAPPβ. Interestingly, in HeLa cells, over expression of CD74 steers APP, but not Notch, to large vacuoles created by CD74. Conclusion Taken together, we propose that CD74 inhibits Aβ production by interacting with and derailing normal trafficking of APP.
Related Links	https://molecularneurodegeneration.biomedcentral.com/counter/pdf/10.1186/1750-1326-4-41.pdf
Ending Page	10
Page Count	10
Starting Page	1
File Format	HTM / HTML
ISSN	17501326
DOI	10.1186/1750-1326-4-41
Journal	Molecular Neurodegeneration
Issue Number	1
Volume Number	4
Language	English
Publisher	BioMed Central
Publisher Date	2009-10-22
Access Restriction	Open
Subject Keyword	Neurosciences Neurology Molecular Medicine HeLa Cell Alzheimer Disease Amyloid Precursor Protein Cerebral Amyloid Angiopathy Alzheimer Disease Patient
Content Type	Text
Resource Type	Article
Subject	Neurology (clinical) Molecular Biology Cellular and Molecular Neuroscience
Journal Impact Factor	15.1/2023
5-Year Journal Impact Factor	16.8/2023

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