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Loss of CDC50A function drives Aβ/p3 production via increased β/α-secretase processing of APP

Tambini, M. D.; D'Adamio, L.

2020-11-12 molecular biology
10.1101/2020.11.12.379636 bioRxiv
Show abstract

The Amyloid Precursor Protein (APP) undergoes extensive proteolytic processing to produce several biologically active metabolites which affect Alzheimers disease (AD) pathogenesis. Sequential cleavage of APP by {beta}- and {gamma}-secretases results in A{beta}, while cleavage by - and {gamma}-secretases produces the smaller p3 peptide. Here we report that in cells in which the P4-ATPase flippase subunit CDC50A has been knocked out, large increases in the products of {beta}- and -secretase cleavage of APP (sAPP{beta}/{beta}CTF and sAPP/CTF, respectively) and the downstream metabolites A{beta} and p3 are seen. These data indicate that APP cleavage by {beta}/-secretase are increased and suggest that phospholipid asymmetry plays an important role in APP metabolism and A{beta} production.

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