Aβ induces cell death by direct interaction with its cognate extracellular domain on APP (APP 597–624)
Open Access
- 24 April 2006
- journal article
- fj express-summary
- Published by Wiley in The FASEB Journal
- Vol. 20 (8) , 1254-1256
- https://doi.org/10.1096/fj.05-5032fje
Abstract
Click on the article title to read more.Keywords
Funding Information
- National Institutes of Health (AG05131)
- Alzheimer's Association
This publication has 45 references indexed in Scilit:
- Deposition of amyloid fibrils promotes cell-surface accumulation of amyloid β precursor proteinNeurobiology of Disease, 2004
- The Proteolytic Processing of the Amyloid Precursor Protein Gene Family Members APLP-1 and APLP-2 Involves α-, β-, γ-, and ϵ-Like CleavagesJournal of Biological Chemistry, 2004
- C‐terminal fragments of amyloid precursor protein exert neurotoxicity by inducing glycogen synthase kinase‐3β expressionThe FASEB Journal, 2003
- Processing of β-Amyloid Precursor-like Protein-1 and -2 by γ-Secretase Regulates TranscriptionJournal of Biological Chemistry, 2002
- Alzheimer's Disease Is a Synaptic FailureScience, 2002
- Localization of a Fibrillar Amyloid β-Protein Binding Domain on Its PrecursorJournal of Biological Chemistry, 2002
- The caspase‐derived C‐terminal fragment of βAPP induces caspase‐independent toxicity and triggers selective increase of Aβ42 in mammalian cellsJournal of Neurochemistry, 2001
- Retention of the Alzheimer's Amyloid Precursor Fragment C99 in the Endoplasmic Reticulum Prevents Formation of Amyloid β-PeptideJournal of Biological Chemistry, 2001
- The cell biology of β-amyloid precursor protein and presenilin in Alzheimer's diseaseTrends in Cell Biology, 1998
- Isolation and characterization of APLP2 encoding a homologue of the Alzheimer's associated amyloid β protein precursorNature Genetics, 1993