Mechanistic study of neurite outgrowth stimulated by the amyloid precursor protein interactor FE65
Refereed conference paper presented and published in conference proceedings


Alzheimer’s disease is a devastating neurodegenerative disorder that affecting millions of people worldwide. Severe neurite degeneration is observed in Alzheimer’s disease which is suggested to be associated with cognitive decline in the disease. FE65 is a brain enriched multi-domain adaptor protein which is shown to interact with the Alzheimer’s disease amyloid precursor protein (APP) and to alter APP metabolism. Moreover, recent evidence reveals that FE65 is also involved in other neurophysiological processes including neurite development. However, the mechanism(s) by which FE65 stimulates neurite outgrowth is still largely unknown. As an adaptor protein, FE65 functions in recruiting various interactors to form biological complexes. Hence, identification of the full complement of FE65 interacting proteins is an important step for improving our understanding of FE65 in various processes including neurite development. In this project, we have identified several small GTPases interact with FE65 including ARF6 and Rac1 and their corresponding regulators. ARF6-Rac1 signaling has been implicated in neurite outgrowth via regulation of cytoskeleton remodeling. In fact, FE65 stimulates neurite outgrowth in primary neurons via activation of ARF6 and its downstream GTPase Rac1. Additionally, we also found that the regulators of ARF6 and Rac1 are required for FE65-mediated neurite extension. Our work suggests that FE65 functions as an adaptor to recruit

著者W Li, H Cheung, KF Lau
會議名稱Neuroscience 2016
會議地點San Diego

上次更新時間 2018-21-01 於 21:38