Kinesin light chain 1 suppression impairs human embryonic stem cell neural differentiation and amyloid precursor protein metabolism

The etiology of sporadic Alzheimer disease (AD) is largely unknown, although evidence implicates the pathological hallmark molecules amyloid beta (Aβ) and phosphorylated Tau. Work in animal models suggests that altered axonal transport caused by Kinesin-1 dysfunction perturbs levels of both Aβ and p...

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Veröffentlicht in:	PloS one 2012-01, Vol.7 (1), p.e29755-e29755
Hauptverfasser:	Killian, Rhiannon L, Flippin, Jessica D, Herrera, Cheryl M, Almenar-Queralt, Angels, Goldstein, Lawrence S B
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer's disease Amyloid beta-protein Amyloid beta-Protein Precursor - metabolism Amyloid precursor protein Animal models Antigens, Surface - metabolism Axonal transport Biology Biosynthesis Blotting, Western Cell culture Cell Differentiation Cell growth Cell Line Cell Proliferation Cell surface Chains Differentiation (biology) Drosophila Embryo cells Embryonic stem cells Embryonic Stem Cells - cytology Embryonic Stem Cells - metabolism Etiology Flow Cytometry Humans Insects Karyotyping Kinases Kinesin Light Light levels Localization Medicine Metabolism Microtubule-Associated Proteins - genetics Microtubule-Associated Proteins - metabolism Nerve tissue proteins Nervous system Nervous system diseases Neural stem cells Neural Stem Cells - cytology Neural Stem Cells - metabolism Neurites - metabolism Neurodegenerative diseases Neurodevelopmental disorders Neurological diseases Neuronal-glial interactions Neurons Neurons - cytology Neurons - metabolism Octamer Transcription Factor-3 - metabolism Penicillin Physiological aspects Pluripotency Pluripotent Stem Cells - cytology Pluripotent Stem Cells - metabolism Precursors Progeny Protein metabolism Protein turnover Proteins RNA Interference Rodents Stem cell transplantation Stem cells Surface markers Tau protein tau Proteins - metabolism Tissues Transgenic animals Transport
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