Expression of AHI1 Rescues Amyloidogenic Pathology in Alzheimer’s Disease Model Cells

A hallmark of Alzheimer’s disease (AD) pathogenesis is the accumulation of extracellular plaques mainly composed of amyloid-β (Aβ) derived from amyloid precursor protein (APP) cleavage. Recent reports suggest that transport of APP in vesicles with huntingtin-associated protein-1 (HAP1) negatively re...

Ausführliche Beschreibung

Gespeichert in:

Bibliographische Detailangaben
Veröffentlicht in:	Molecular neurobiology 2019-11, Vol.56 (11), p.7572-7582
Hauptverfasser:	Ting, Lai-Lei, Lu, Hsien-Tsung, Yen, Shu-Fen, Ngo, Thi Huong, Tu, Fang-Yu, Tsai, I-Shih, Tsai, Yi-Hua, Chang, Fu-Yen, Li, Xiao-Jiang, Li, Shihua, Lee, Ching-Kuo, Kao, Shu-Huei, Kuo, Yu-Min, Lin, Yung-Feng
Format:	Artikel
Sprache:	eng
Schlagworte:	Adaptor Proteins, Vesicular Transport - metabolism Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid - metabolism Amyloid beta-Protein Precursor - metabolism Amyloid precursor protein Amyloidogenesis Animals Axonogenesis Biomedical and Life Sciences Biomedicine Brain Cell Biology Cell culture Cell Differentiation Cell Line Cell Survival Culture media Extracellular signal-regulated kinase Genotypes Hap1 protein Humans Huntingtin Lysates Mental disorders Mice, Inbred C57BL Models, Biological Nerve Growth Factors - metabolism Neurobiology Neuroblastoma Neurodevelopmental disorders Neurology Neuroprotection Neurosciences Pathology Plaques Protein Binding Translocation Tropomyosin
Online-Zugang:	Volltext
Tags:	Tag hinzufügen Keine Tags, Fügen Sie den ersten Tag hinzu!

Schreiben Sie den ersten Kommentar!