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作 者:Xiaodan Zhang Xue Wen Ismael Al-Ramahi Juan Botas Boxun Lu Yuhua Fu
机构地区:[1]School of Life Sciences,Fudan University,Shanghai,200438,China [2]Department of Molecular and Human Genetics,Baylor College of Medicine,Houston,77030,USA [3]Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital,Houston,77030,USA
出 处:《Neuroscience Bulletin》2022年第1期99-103,共5页神经科学通报(英文版)
基 金:This work was supported by the National Natural Science Foundation of China(31970748,92049301,and 81870990)and the Research Start-up Fund of Fudan University,China.
摘 要:Dear Editor,Accumulation of misfolded and aggregation-prone proteins is the common hallmark of many neurodegenerative disorders,and lowering the levels of these proteins may provide promising strategies for the potential treatment of some of these diseases[1,2].Among them,Huntington’s disease(HD)is a monogenic disease caused by mutation of the HTT(huntingtin)gene[3],which encodes the mutant HTT protein(mHTT)with an expanded polyglutamine tract(polyQ).
关 键 词:HUNTINGTON APOPTOSIS diseases
分 类 号:R741[医药卫生—神经病学与精神病学]
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