Kim, Jin-SookBareiss, SonjaKim, Kyung KeunTatum, RodneyHan, Jeong-RanJin, Yun HyeKim, HangunLu, QunKim, Kwonseop2011-04-152011-05-172011-04-152011-05-172006-12-29Biochemical and Biophysical Research Communications; 351:4 p. 903-908http://hdl.handle.net/10342/3325Although delta-catenin/neural plakophilin-related armadillo protein (NPRAP) was reported to interact with presenilin-1 (PS-1), the effects of PS-1 on delta-catenin have not been established. In this study, we report that overexpression of PS-1 inhibits the delta-catenin-induced dendrite-like morphological changes in NIH 3T3 cells and promotes delta-catenin processing and turnover. The effects of PS-1 on endogenous delta-catenin processing were confirmed in hippocampal neurons overexpressing PS-1, as well as in the transgenic mice expressing the disease-causing mutant PS-1 (M146V). In addition, disease-causing mutant PS-1 (M146V and L286V) enhanced delta-catenin processing, whereas PS-1/gamma-secretase inhibitors could block the formation of processed forms of delta-catenin. Together, our findings suggest that PS-1 can affect delta-catenin-induced morphogenesis possibly through the regulation of its processing and stability. Originally published Biochem Biophys Res Commun, Vol. 351, No. 4, Dec 2006en-USAuthor notified of opt-out rights by Cammie Jennings prior to upload of this article.Alzheimer's disease[Delta]-catenin/NPRAPPresenilin/gamma-secretaseδ-catenin/NPRAPPresenilin-1 inhibits delta-catenin-induced cellular branching and promotes delta-catenin processing and turnoverArticlePMC1800877