PS1 activates PI3K thus inhibiting GSK-3 activity and tau overphosphorylation: effects of FAD mutations-Reference-Cited by-同舟云学术

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PS1 activates PI3K thus inhibiting GSK-3 activity and tau overphosphorylation: effects of FAD mutations

Published:2004-06-10 Issue:13 Volume:23 Page:2586-2596
ISSN:0261-4189
Container-title:The EMBO Journal
language:
Short-container-title:EMBO J

Author:

Baki Lia,Shioi Junichi,Wen Paul,Shao Zhiping,Schwarzman Alexander,Gama-Sosa Miguel,Neve Rachael,Robakis Nikolaos K

Publisher

Wiley

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,Molecular Biology,General Neuroscience

Reference43 articles.

1. Presenilin-1 binds cytoplasmic epithelial cadherin, inhibits cadherin/p120 association, and regulates stability and function of the cadherin/catenin adhesion complex

2. Transcription-dependent and -independent control of neuronal survival by the PI3K–Akt signaling pathway

3. Overexpression in Neurons of Human Presenilin-1 or a Presenilin-1 Familial Alzheimer Disease Mutant Does Not Enhance Apoptosis

4. AKT/PKB and Other D3 Phosphoinositide-Regulated Kinases: Kinase Activation by Phosphoinositide-Dependent Phosphorylation

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