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. 2017 Sep 29;7:12456. doi: 10.1038/s41598-017-12334-2

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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GSK3β enhances FE65-mediated APP processing. (A) HEK293 cells were co-transfected with GAL4-APP, pFR-Luc and phRL-TK together with empty vector (EV), FE65 or FE65 + GSK3β. GSK3β potentiates the stimulatory effect of FE65 on APP-GAL4 cleavage. n = 5. *P < 0.001. Results are means ± S.D. (B) HEK293 cells were co-transfected with APP + FE65 with or without GSK3β. Levels of secreted Aβ1–40 (top graph) and 1–42 (bottom graph) were measured by corresponding Aβ ELISA kits. Overexpression of GSK3β enhances the effect of FE65 on both Aβ1–40 and 1–42 liberation. n = 5. *P < 0.001. Results are means ± S.D.