Oxidative stress promotes JNK-dependent amyloidogenic processing of normally expressed human APP by differential modification of α-, β- and γ-secretase expression
Authors:
- Ricardo Quiroz-BaezRicardo Quiroz-Baez
- Emilio RojasEmilio Rojas
- Clorinda AriasCAClorinda Arias
- 1 December 2009
- journal article
- research article
- Published by Elsevier in Neurochemistry International
- Vol. 55 (7) , 662-670
Abstract
No abstract availableKeywords
This publication has 59 references indexed in Scilit:
- Regulation of Amyloid β-Protein Precursor by Phosphorylation and Protein InteractionsJournal of Biological Chemistry, 2008
- Sequential expression of cell‐cycle regulators and Alzheimer's disease–related proteins in entorhinal cortex after hippocampal excitotoxic damageJournal of Neuroscience Research, 2007
- Physiological Mouse Brain Aβ Levels Are Not Related to the Phosphorylation State of Threonine-668 of Alzheimer's APPPLOS ONE, 2006
- Energy Inhibition Elevates β-Secretase Levels and Activity and Is Potentially Amyloidogenic in APP Transgenic Mice: Possible Early Events in Alzheimer's Disease PathogenesisThe Journal of Neuroscience, 2005
- Pin1 promotes production of Alzheimer’s amyloid β from β-cleaved amyloid precursor proteinBiochemical and Biophysical Research Communications, 2005
- Amyloid‐β in Alzheimer's disease: the horse or the cart? Pathogenic or protective?International Journal of Experimental Pathology, 2005
- APH1, PEN2, and Nicastrin increase Aβ levels and γ-secretase activityBiochemical and Biophysical Research Communications, 2003
- NADPH Oxidase Activity in Preeclampsia With Immortalized Lymphoblasts Used as ModelsHypertension, 2003
- Putative function of ADAM9, ADAM10, and ADAM17 as APP -secretaseBiochemical and Biophysical Research Communications, 2003
- Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's diseaseNature, 1991