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- W2322035504 abstract "The processing of amyloid precursor protein (APP) into β-amyloid peptide (Aβ) is a key step in the pathogenesis of Alzheimer’s disease (AD), and trafficking dysregulations of APP and its secretases contribute significantly to altered APP processing. Here we show that the cell polarity protein Par3 plays an important role in APP processing and trafficking. We found that the expression of full length Par3 is significantly decreased in AD patients. Overexpression of Par3 promotes non-amyloidogenic APP processing, while depletion of Par3 induces intracellular accumulation of Aβ. We further show that Par3 functions by regulating APP trafficking. Loss of Par3 decreases surface expression of APP by targeting APP to the late endosome/lysosome pathway. Finally, we show that the effects of Par3 are mediated through the endocytic adaptor protein Numb, and Par3 functions by interfering with the interaction between Numb and APP. Together, our studies show a novel role for Par3 in regulating APP processing and trafficking." @default.
- W2322035504 created "2016-06-24" @default.
- W2322035504 creator A5008475267 @default.
- W2322035504 creator A5036259640 @default.
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- W2322035504 date "2016-09-01" @default.
- W2322035504 modified "2023-10-15" @default.
- W2322035504 title "The polarity protein Par3 regulates APP trafficking and processing through the endocytic adaptor protein Numb" @default.
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- W2322035504 doi "https://doi.org/10.1016/j.nbd.2016.03.022" @default.
- W2322035504 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4930744" @default.
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