HDAC6 rescues neurodegeneration and provides an essential link between autophagy and the UPS

A prominent feature of late-onset neurodegenerative diseases is accumulation of misfolded protein in vulnerable neurons. When levels of misfolded protein overwhelm degradative pathways, the result is cellular toxicity and neurodegeneration. Cellular mechanisms for degrading misfolded protein include...

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Veröffentlicht in:	Nature 2007-06, Vol.447 (7146), p.860-864
Hauptverfasser:	Taylor, J. Paul, Pandey, Udai Bhan, Nie, Zhiping, Batlevi, Yakup, McCray, Brett A, Ritson, Gillian P, Nedelsky, Natalia B, Schwartz, Stephanie L, DiProspero, Nicholas A, Knight, Melanie A, Schuldiner, Oren, Padmanabhan, Ranjani, Hild, Marc, Berry, Deborah L, Garza, Dan, Hubbert, Charlotte C, Yao, Tso-Pang, Baehrecke, Eric H
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Autophagy - genetics Autophagy - physiology Biological and medical sciences Cellular biology Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Degradation Disease Models, Animal Drosophila melanogaster Drosophila melanogaster - genetics Drosophila melanogaster - metabolism Drosophila Proteins - metabolism Gene expression Genetic diversity Histone Deacetylase 6 Histone Deacetylases - metabolism Humans Medical sciences Muscular Disorders, Atrophic - genetics Muscular Disorders, Atrophic - metabolism Mutation Neurodegenerative Diseases - genetics Neurodegenerative Diseases - metabolism Neurological disorders Neurology Neurons Pathology Peptides - genetics Peptides - metabolism Proteasome Endopeptidase Complex - genetics Proteasome Endopeptidase Complex - metabolism Protein folding Proteins Receptors, Androgen - genetics Receptors, Androgen - metabolism Rodents Ubiquitin - metabolism
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