Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

The Fe65s and X11s are two families of adaptor proteins that bind to the Alzheimer's disease amyloid precursor protein (APP). Although both the X11s and Fe65s bind to similar regions of APP, they have opposing effects on Abeta production and hence may represent novel therapeutic targets. However, there is no evidence that the Fe65s and X11s are present within the same cell type or cell compartment and are thus capable of competing for binding to APP. Here we show that in neurones and transfected cells, APP, Fe65 and X11beta show overlapping subcellular distributions. Furthermore, we demonstrate that Fe65 and X11beta compete for binding to APP.

More information Original publication

DOI

10.1097/00001756-200011090-00041

Type

Journal article

Publication Date

2000-11-09T00:00:00+00:00

Volume

11

Pages

3607 - 3610

Total pages

3

Keywords

Amyloid beta-Protein Precursor, Animals, Binding, Competitive, Brain, CHO Cells, Cadherins, Carrier Proteins, Cells, Cultured, Cricetinae, Gene Library, Humans, Nerve Tissue Proteins, Neurons, Nuclear Proteins, Recombinant Fusion Proteins, Recombinant Proteins, Transfection