%0 PDF %T BACE1 elevation engendered by GGA3 deletion increases β-amyloid pathology in association with APP elevation and decreased CHL1 processing in 5XFAD mice. %A Kim, WonHee.; Ma, Liang.; Lomoio, Selene.; Willen, Rachel.; Lombardo, Sylvia.; Dong, Jinghui.; Haydon, Philip G.; Tesco, Giuseppina. %D 2018-02-05T09:54:27.796-05:00 %8 2018-02-05 %R http://localhost/files/1257b4783 %X Background: β-site amyloid precursor protein cleaving enzyme 1 (BACE1) is the rate-limiting enzyme in the production of amyloid beta (Aβ), the toxic peptide that accumulates in the brains of Alzheimer's disease (AD) patients. Our previous studies have shown that the clathrin adaptor Golgi-localized γ-ear-containing ARF binding protein 3 (GGA3) plays a key role in the trafficking of BACE1 to lysosomes, where it is normally degraded. GGA3 depletion results in BACE1 stabilization both in vitro and in vivo. Moreover, levels of GGA3 are reduced and inversely related to BACE1 levels in post-mortem brains of AD patients.; Keywords: Alzheimer disease, Amyloid-beta (Aβ), Beta-secretase 1 (BACE1), Golgi-localized γ-ear-containing ARF binding protein 3 (GGA3), Amyloid precursor protein (APP), Cell adhesion molecule L1 like protein (CHL1), Down syndrome.; Springer Open. %[ 2018-10-10 %9 Text %~ Tufts Digital Library %W Institution