Presenilin-1 inhibits delta-catenin-induced cellular branching and promotes delta-catenin processing and turnover

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)

Sonja Bareiss (Creator)

Jeong-Ran Han (Creator)

Yun Hye Jin (Creator)

Hangun Kim (Creator)

Jin-Sook Kim (Creator)

Kwonseop Kim (Creator)

Kyung Keun Kim (Creator)

Qun Lu (Creator)

Rodney Tatum (Creator)

Institution

East Carolina University (ECU )

Web Site: http://www.ecu.edu/lib/

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

Additional Information

Publication

Other

Biochemical and Biophysical Research Communications. 351:4(December 2006) p. 903-908.

Language: English

Date: 2011

Keywords

Alzheimer's disease, delta-catenin/NPRAP, presenilin/gamma-secretase

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