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PMID:17097608

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Citation

Kim, JS, Bareiss, S, Kim, KK, Tatum, R, Han, JR, Jin, YH, Kim, H, Lu, Q and Kim, K (2006) Presenilin-1 inhibits delta-catenin-induced cellular branching and promotes delta-catenin processing and turnover. Biochem. Biophys. Res. Commun. 351:903-8

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.

Links

PubMed PMC1800877 Online version:10.1016/j.bbrc.2006.10.135

Keywords

Alzheimer Disease/enzymology; Alzheimer Disease/genetics; Amyloid Precursor Protein Secretases/antagonists & inhibitors; Animals; Catenins; Cell Adhesion Molecules/genetics; Cell Adhesion Molecules/metabolism; Dendrites/enzymology; Dendrites/ultrastructure; Enzyme Inhibitors/pharmacology; Fibroblasts/enzymology; Hippocampus/cytology; Hippocampus/enzymology; Mice; Mice, Transgenic; NIH 3T3 Cells; Neurons/metabolism; Phosphoproteins/genetics; Phosphoproteins/metabolism; Presenilin-1/antagonists & inhibitors; Presenilin-1/genetics; Presenilin-1/metabolism; Transcriptional Activation

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


See also

References

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