Presenilin, Notch, and the genesis and treatment of Alzheimer's disease
Author:
Publisher
Proceedings of the National Academy of Sciences
Subject
Multidisciplinary
Reference37 articles.
1. Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice
2. Transition-state analogue inhibitors of γ-secretase bind directly to presenilin-1
3. The Transmembrane Aspartates in Presenilin 1 and 2 Are Obligatory for γ-Secretase Activity and Amyloid β-Protein Generation
4. Two transmembrane aspartates in presenilin-1 required for presenilin endoproteolysis and γ-secretase activity
5. Peptidomimetic Probes and Molecular Modeling Suggest That Alzheimer's γ-Secretase Is an Intramembrane-Cleaving Aspartyl Protease
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