Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form

The mechanisms by which mutant Huntington protein Htt leads to selective neurodegeneration are not fully understood. Here, using gene editing in HD140Q knock-in mice, the authors show that exon1 Htt is a critical pathological form of the protein.

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Autores principales:	Huiming Yang, Su Yang, Liang Jing, Luoxiu Huang, Luxiao Chen, Xianxian Zhao, Weili Yang, Yongcheng Pan, Peng Yin, Zhaohui S Qin, Beisha Tang, Shihua Li, Xiao-Jiang Li
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2020
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/f7ec8fe55f5148dab5116e4f227b70c1
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spelling	oai:doaj.org-article:f7ec8fe55f5148dab5116e4f227b70c12021-12-02T15:45:30ZTruncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form10.1038/s41467-020-16318-12041-1723https://doaj.org/article/f7ec8fe55f5148dab5116e4f227b70c12020-05-01T00:00:00Zhttps://doi.org/10.1038/s41467-020-16318-1https://doaj.org/toc/2041-1723The mechanisms by which mutant Huntington protein Htt leads to selective neurodegeneration are not fully understood. Here, using gene editing in HD140Q knock-in mice, the authors show that exon1 Htt is a critical pathological form of the protein.Huiming YangSu YangLiang JingLuoxiu HuangLuxiao ChenXianxian ZhaoWeili YangYongcheng PanPeng YinZhaohui S QinBeisha TangShihua LiXiao-Jiang LiNature PortfolioarticleScienceQENNature Communications, Vol 11, Iss 1, Pp 1-15 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Huiming Yang Su Yang Liang Jing Luoxiu Huang Luxiao Chen Xianxian Zhao Weili Yang Yongcheng Pan Peng Yin Zhaohui S Qin Beisha Tang Shihua Li Xiao-Jiang Li Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form
description	The mechanisms by which mutant Huntington protein Htt leads to selective neurodegeneration are not fully understood. Here, using gene editing in HD140Q knock-in mice, the authors show that exon1 Htt is a critical pathological form of the protein.
format	article
author	Huiming Yang Su Yang Liang Jing Luoxiu Huang Luxiao Chen Xianxian Zhao Weili Yang Yongcheng Pan Peng Yin Zhaohui S Qin Beisha Tang Shihua Li Xiao-Jiang Li
author_facet	Huiming Yang Su Yang Liang Jing Luoxiu Huang Luxiao Chen Xianxian Zhao Weili Yang Yongcheng Pan Peng Yin Zhaohui S Qin Beisha Tang Shihua Li Xiao-Jiang Li
author_sort	Huiming Yang
title	Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form
title_short	Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form
title_full	Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form
title_fullStr	Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form
title_full_unstemmed	Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form
title_sort	truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form
publisher	Nature Portfolio
publishDate	2020
url	https://doaj.org/article/f7ec8fe55f5148dab5116e4f227b70c1
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Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form

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