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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.


Journal article



Publication Date





3607 - 3610


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