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Biochemistry, Biophysics, and Structural Biology Commons

Open Access. Powered by Scholars. Published by Universities.®

Physiology

2011

Series

Amyloid beta-Protein Precursor; Animals; Animals, Newborn; Apoptosis; Cells, Cultured; Enzyme Activation; Humans; JNK Mitogen-Activated Protein Kinases; Mice; Mice, Transgenic; Neurons; Plaque, Amyloid

Articles 1 - 1 of 1

Full-Text Articles in Biochemistry, Biophysics, and Structural Biology

The Loss Of C-Jun N-Terminal Protein Kinase Activity Prevents The Amyloidogenic Cleavage Of Amyloid Precursor Protein And The Formation Of Amyloid Plaques In Vivo, Sonia Mazzitelli, Ping Xu, Isidre Ferrer, Roger J. Davis, Cathy Tournier Nov 2011

The Loss Of C-Jun N-Terminal Protein Kinase Activity Prevents The Amyloidogenic Cleavage Of Amyloid Precursor Protein And The Formation Of Amyloid Plaques In Vivo, Sonia Mazzitelli, Ping Xu, Isidre Ferrer, Roger J. Davis, Cathy Tournier

Davis Lab Publications

Phosphorylation plays a central role in the dynamic regulation of the processing of the amyloid precursor protein (APP) and the production of amyloid-beta (Abeta), one of the clinically most important factors that determine the onset of Alzheimer's disease (AD). This has led to the hypothesis that aberrant Abeta production associated with AD results from regulatory defects in signal transduction. However, conflicting findings have raised a debate over the identity of the signaling pathway that controls APP metabolism. Here, we demonstrate that activation of the c-Jun N-terminal protein kinase (JNK) is essential for mediating the apoptotic response of neurons to ...