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J. Biol. Chem., Vol. 281, Issue 34, 24521-24530, August 25, 2006

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FE65 Interaction with the ApoE Receptor ApoEr2^*

Hyang-Sook Hoe¹, Laura Ann Magill¹, Suzanne Guenette, Zhanyan Fu^¶, Stefano Vicini^¶, and G. William Rebeck²

From the Department of Neuroscience and the ^¶Department of Physiology and Biophysics, Georgetown University Medical Center, Washington, D. C. 20057-1464 and Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Charlestown, Massachusetts 02129

The adaptor protein FE65 interacts with the -amyloid precursor protein (APP) via its C-terminal phosphotyrosine binding (PTB) domain and affects APP processing and A production. Our previous data demonstrate that the apoE receptor ApoEr2 co-precipitated with APP and suggest that there are extracellular and intracellular interactions between these two transmembrane proteins. We hypothesized that FE65 acts as an intracellular link between ApoEr2 and APP. Co-immunoprecipitation experiments in COS7 cells demonstrated an interaction between ApoEr2 and FE65 that depended on the N-terminal PTB domain of FE65. Full-length FE65 increased co-immunoprecipitation of ApoEr2 and APP. Full-length FE65 also increased surface expression of ApoEr2, as determined by surface protein biotinylation and live cell surface staining. Constructs containing both the C- and N-terminal PTB domains of FE65 increased secreted APP, secreted ApoEr2, APP C-terminal fragment, and ApoEr2 C-terminal fragment, but constructs containing only single PTB domains did not affect APP or ApoEr2 processing. In addition, full-length FE65 decreased A to a significantly greater extent than individual FE65 domains. These data suggest that FE65 can bind APP and ApoEr2 at the same time and affect the processing of each.

Received for publication, January 24, 2006 , and in revised form, March 30, 2006.

^* This work was supported by National Institutes of Health Grant AG14473. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Both authors contributed equally to this article.

² To whom correspondence should be addressed: Dept. of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Rd. NW, Washington, D. C. 20057-14. Tel.: 202-687-1534; Fax: 202-687-0617; E-mail: gwr2{at}georgetown.edu.

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