Generation and Characterization of Knock-in Mouse Models Expressing Versions of Huntingtin with Either an N17 or a Combined PolyQ and Proline-Rich Region Deletion-Reference-Cited by-同舟云学术

Generation and Characterization of Knock-in Mouse Models Expressing Versions of Huntingtin with Either an N17 or a Combined PolyQ and Proline-Rich Region Deletion

Published:2017-03-28 Issue:1 Volume:6 Page:47-62
ISSN:1879-6397
Container-title:Journal of Huntington's Disease
language:
Short-container-title:JHD

Author:

André Emily A.,Braatz Elise M.,Liu Jeh-Ping,Zeitlin Scott O.

Publisher

IOS Press

Subject

Cellular and Molecular Neuroscience,Neurology (clinical)

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1. Huntingtin exon 1 deletion does not alter the subcellular distribution of huntingtin and gene transcription in mice;Frontiers in Cellular Neuroscience;2022-11-10

2. Temporal Phenotypic Changes in Huntington’s Disease Models for Preclinical Studies;Journal of Huntington's Disease;2022-03-01

3. Huntingtin structure is orchestrated by HAP40 and shows a polyglutamine expansion-specific interaction with exon 1;Communications Biology;2021-12

4. Characterization of a Knock-In Mouse Model with a Huntingtin Exon 1 Deletion;Journal of Huntington's Disease;2021-11-09

5. Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form;Nature Communications;2020-05-22