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COPS5 protein overexpression increases amyloid plaque burden, decreases spinophilin-immunoreactive puncta, and exacerbates learning and memory deficits in the mouse brain.

J. Biol. Chem.. 2015-04; 
WangRuizhi,WangHongjie,CarreraIvan,XuShaohua,LakshmanaMadepal
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Monoclonal Antibody Services … The polyclonal antibody 1704, recognizing the cytoplasmic domain of human LRP, has been described previously Mouse monoclonal antibody against β-actin (catalog no A00702) was purchased from Genscript USA Inc (Piscataway, NJ) Anti-spinophilin (catalog no … Get A Quote

摘要

Brain accumulation of neurotoxic amyloid β (Aβ) peptide because of increased processing of amyloid precursor protein (APP), resulting in loss of synapses and neurodegeneration, is central to the pathogenesis of Alzheimer disease (AD). Therefore, the identification of molecules that regulate Aβ generation and those that cause synaptic damage is crucial for future therapeutic approaches for AD. We demonstrated previously that COPS5 regulates Aβ generation in neuronal cell lines in a RanBP9-dependent manner. Consistent with the data from cell lines, even by 6 months, COPS5 overexpression in APΔE9 mice (APΔE9/COPS5-Tg) significantly increased Aβ40 levels by 32% (p < 0.01) in the cortex and by 28% (... More

关键词

Alzheimer Disease,Amyloid Plaque Burden,Amyloid Precursor Protein (APP),COPS5,Jab1,Learning and Memory,Protein Processing,Spinophilin,Synaptic Plasticity,amyloid β