Nuclear accumulation of HDAC4 in ATM deficiency promotes neurodegeneration in ataxia telangiectasia

Ataxia-telangiectasia is a multifaceted disease that includes motor dysfunction caused by neuron death in the cerebellum. Now, Karl Herrup and colleagues report that ATM, the gene that is lost in the disease, keeps HDAC4 out of the nucleus and in the cytoplasm to maintain cerebellar neuron health. A...

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Veröffentlicht in:	Nature medicine 2012-05, Vol.18 (5), p.783-790
Hauptverfasser:	Li, Jiali, Chen, Jianmin, Ricupero, Christopher L, Hart, Ronald P, Schwartz, Melanie S, Kusnecov, Alexander, Herrup, Karl
Format:	Artikel
Sprache:	eng
Schlagworte:	692/420/2489/144 692/699/375/365 Accumulation Active Transport, Cell Nucleus Animals Ataxia telangiectasia Ataxia Telangiectasia - metabolism Ataxia Telangiectasia Mutated Proteins Biomedical and Life Sciences Biomedicine Cancer Research Cell Cycle Proteins - deficiency Cell Cycle Proteins - metabolism Cell Nucleus - metabolism Cellular biology Chromatin Cyclic AMP Response Element-Binding Protein - physiology Development and progression DNA-Binding Proteins - deficiency DNA-Binding Proteins - metabolism Female Gene expression Gene mutations Genetic aspects Genotype & phenotype Histone Deacetylases - metabolism Histones - metabolism Hydroxamic Acids - pharmacology Infectious Diseases Male MEF2 Transcription Factors Metabolic Diseases Mice Molecular Medicine Mutation Myogenic Regulatory Factors - physiology Neurodegenerative Diseases - etiology Neurological disorders Neurosciences Phosphorylation Physiological aspects Protein Phosphatase 2 - physiology Protein-Serine-Threonine Kinases - deficiency Protein-Serine-Threonine Kinases - metabolism Proteins Tumor Suppressor Proteins - deficiency Tumor Suppressor Proteins - metabolism
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