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Publication : Effects of PS1 deficiency on membrane protein trafficking in neurons.

First Author  Naruse S Year  1998
Journal  Neuron Volume  21
Issue  5 Pages  1213-21
PubMed ID  9856475 Mgi Jnum  J:111807
Mgi Id  MGI:3654873 Doi  10.1016/s0896-6273(00)80637-6
Citation  Naruse S, et al. (1998) Effects of PS1 deficiency on membrane protein trafficking in neurons. Neuron 21(5):1213-21
abstractText  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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