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. 1998 Nov;21(5):1213-21.
doi: 10.1016/s0896-6273(00)80637-6.

Effects of PS1 deficiency on membrane protein trafficking in neurons

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Free article

Effects of PS1 deficiency on membrane protein trafficking in neurons

S Naruse et al. Neuron. 1998 Nov.
Free article

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.

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