Presenilin-1 280Glu→Ala Mutation Alters C-Terminal APP Processing Yielding Longer Aβ Peptides: Implications for Alzheimer’s Disease

Molecular Medicine - United States
doi 10.2119/2007-00094.vanvickle
Full Text
Abstract

Available in full text

Date
Authors
Publisher

Springer Science and Business Media LLC

Related search

Amyloid Precursor Protein (APP) Processing and Potential Targets for Alzheimer’s Disease

Biomedical Genetics and Genomics
2019English

Involvement of WAVE Accumulation in Aβ/App Pathology-Dependent Tangle Modification in Alzheimer’s Disease

American Journal of Pathology
Forensic MedicinePathology
2009English

Modeling Alzheimer’s Disease by Induced Pluripotent Stem Cells Carrying APP D678H Mutation

Molecular Neurobiology
NeuroscienceNeurologyCellularMolecular Neuroscience
2018English

Regulation of Brain G-Protein Goby Alzheimer’s Disease Gene Presenilin-1

Journal of Biological Chemistry
BiochemistryCell BiologyMolecular Biology
1998English

APP Signaling in Alzheimer’s Disease

Aging
AgingCell Biology
2018English

Structural Investigation of the C-Terminal Catalytic Fragment of Presenilin 1

Proceedings of the National Academy of Sciences of the United States of America
Multidisciplinary
2010English

Homozygosity of the Autosomal Dominant Alzheimer Disease Presenilin 1 E280A Mutation

Neurology
Neurology
2014English

Variant Alzheimer Disease With Spastic Paraparesis: A Rare Presenilin-1 Mutation

Canadian Journal of Neurological Sciences
MedicineNeurology
2011English

Proteolytic Processing of the Alzheimer Disease-Associated Presenilin-1 Generates an in Vivo Substrate for Protein Kinase C

Proceedings of the National Academy of Sciences of the United States of America
Multidisciplinary
1997English

Amanote Research

Note-taking for researchers

Follow Amanote

© 2024 Amaplex Software S.P.R.L. All rights reserved.

Privacy PolicyRefund Policy