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

被引:0
作者
Jiali Li
Jianmin Chen
Christopher L Ricupero
Ronald P Hart
Melanie S Schwartz
Alexander Kusnecov
Karl Herrup
机构
[1] Nelson Biological Laboratories,Department of Cell Biology and Neuroscience
[2] Rutgers University,Department of Psychology
[3] Rutgers University,undefined
来源
Nature Medicine | 2012年 / 18卷
关键词
D O I
暂无
中图分类号
学科分类号
摘要
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.
引用
收藏
页码:783 / 790
页数:7
相关论文
共 88 条
[1]  
Barzilai A(2008)The role of the DNA damage response in neuronal development, organization and maintenance DNA Repair (Amst.) 7 1010-1027
[2]  
Biton S(1994)Clinical and genetic features of ataxia-telangiectasia Int. J. Radiat. Biol. 66 S23-S29
[3]  
Shiloh Y(1997)The genetic defect in ataxia-telangiectasia Annu. Rev. Immunol. 15 177-202
[4]  
Bundey S(1995)A single ataxia telangiectasia gene with a product similar to PI-3 kinase Science 268 1749-1753
[5]  
Lavin MF(1960)Progressive ataxia in childhood with particular reference to ataxia-telangiectasia Neurology 10 705-715
[6]  
Shiloh Y(2009)Histone deacetylases as targets for the treatment of human neurodegenerative diseases Drug News Perspect. 22 513-524
[7]  
Savitsky K(2000)Regulation of histone deacetylase 4 and 5 and transcriptional activity by 14–3-3–dependent cellular localization Proc. Natl. Acad. Sci. USA 97 7835-7840
[8]  
Sedgwick RP(2009)The many roles of histone deacetylases in development and physiology: implications for disease and therapy Nat. Rev. Genet. 10 32-42
[9]  
Boder E(2008)Class IIA HDACs in the regulation of neurodegeneration Front. Biosci. 13 1072-1082
[10]  
D'Mello SR(2008)The Rpd3/Hda1 family of lysine deacetylases: from bacteria and yeast to mice and men Nat. Rev. Mol. Cell Biol. 9 206-218