An endosomal-lysosomal pathway for degradation of amyloid precursor protein.
We previously reported evidence for a lysosomal degradative pathway for APP and C-terminal fragments thereof, based on Western and immunocytochemical analysis of drug-treated cells. Here, we verify the existence of a lysosomal degradative pathway for APP using pulse chase immunoprecipitation analysis of drug-treated cells and fibroblasts with and without a known lysosomal hydrolase targeting defect. The results are consistent with the hypothesis that part or all of the beta-protein domain of APP is normally degraded by lysosomes. A mechanism for beta-protein deposition based on this data is hypothesized.
Cole
G M
GM
Department of Neurosciences, School of Medicine, University of California, San Diego, La Jolla 92093-0624.
Bell
L
L
Truong
Q B
QB
Saitoh
T
T
D016564:Amyloid beta-Protein Precursor / Q000378:metabolism*; D000818:Animals; D016466:CHO Cells; D006224:Cricetinae; D003720:Densitometry; D006801:Humans; D008247:Lysosomes / Q000378:metabolism*; D011233:Precipitin Tests
D016564:Amyloid beta-Protein Precursor