Presenilin-1 inhibits delta-catenin-induced cellular branching and promotes delta-catenin processing and turnover
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Date
2006-12-29
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Authors
Kim, Jin-Sook
Bareiss, Sonja
Kim, Kyung Keun
Tatum, Rodney
Han, Jeong-Ran
Jin, Yun Hye
Kim, Hangun
Lu, Qun
Kim, Kwonseop
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Publisher
East Carolina University
Abstract
Although 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 2006
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Citation
Biochemical and Biophysical Research Communications; 351:4 p. 903-908