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COPS5 (Jab1) increases β-site processing of amyloid precursor protein and Aβ generation by stabilizing RanBP9 protein levels.

J Biol Chem.. 2013-8; 
Hongjie Wang, Debleena Dey, Ivan Carrera, Dmitriy Minond, Elisabetta Bianchi, Shaohua Xu, Madepalli K. Lakshmana. Torrey Pines Institute for Molecular Studies, United States.
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摘要

Increased processing of amyloid precursor protein (APP) and accumulation of neurotoxic amyloid β-peptide (Aβ) in the brain is central to the pathogenesis of Alzheimers disease (AD). Therefore identification of molecules that regulate Aβ generation is crucial for future therapeutic approaches for AD. We previously demonstrated that RanBP9 regulates Aβ generation in a number of cell lines and primary neuronal cultures, by forming tripartite protein complexes with APP, LRP and BACE1, consequently leading to increased amyloid plaque burden in the brain. RanBP9 is a scaffold protein that exists and functions in multiprotein complexes. In order to identify other proteins that may bind RanBP9 and r... More

关键词

Alzheimers disease; Amyloid; Amyloid precursor protein; Protein complexes; Protein degradation; Protein stability.