Related Experiment Video
Updated: Jun 19, 2026

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
Published on: October 17, 2015
CD74 interacts with APP and suppresses the production of Abeta
Shuji Matsuda1, Yukiko Matsuda, Luciano D'Adamio
1Albert Einstein College of Medicine, Department of Microbiology & Immunology, 1300 Morris Park Avenue, Bronx, NY 10461, USA. ldadamio@aecom.yu.edu.
Background:
Alzheimer disease (AD) is characterized by senile plaques, which are mainly composed of beta amyloid (Abeta) peptides. Abeta is cleaved off from amyloid precursor protein (APP) with consecutive proteolytic processing by beta-secretase and gamma-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 Abeta. CD74 resembles other APP interacters such as BRI2 and BRI3, since all of them reduce the level of Abeta. However, unlike BRIs, CD74 does not reduce the secretion of sAPPalpha or sAPPbeta. 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 Abeta production by interacting with and derailing normal trafficking of APP.
Related Concept Videos
Abnormal Proliferation
Inhibition of Cdk Activity
TGF - β Signaling Pathway
T Cell Activation and Clonal Selection
Naive T cells that have not yet encountered an antigen express two primary CD...
Enzyme-linked Receptors
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
