Effects of PS1 Deficiency on Membrane Protein Trafficking in Neurons
NeuronPublished 1 November 1998Open access
Satoshi Naruse, Gopal Thinakaran, Jin Jun Luo, John W. Kusiak, Taisuke Tomita, Takeshi Iwatsubo
Citations358
SJR quartileQ1
SJR score6.75
SNIP2.95
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TL;DR
It is concluded that PS1 plays an essential role in modulating trafficking and metabolism of a selected set of membrane and secretory proteins in neurons.
Abstract
We have examined the trafficking and metabolism of the beta-amyloid precursor protein (APP), an APP homolog (APLP1), and TrkB in neurons that lack PS1. We report that PS1-deficient neurons fail to secrete Abeta, and that the rate of appearance of soluble APP derivatives in the conditioned medium is increased. Remarkably, carboxyl-terminal fragments (CTFs) derived from APP and APLP1 accumulate in PS1-deficient neurons. Hence, PS1 plays a role in promoting intramembrane cleavage and/or degradation of membrane-bound CTFs. Moreover, the maturation of TrkB and BDNF-inducible TrkB autophosphorylation is severely compromised in neurons lacking PS1. We conclude that PS1 plays an essential role in modulating trafficking and metabolism of a selected set of membrane and secretory proteins in neurons.
Keywords
MedicineBiochemistry, Genetics and Molecular Biology
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