Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic f...
Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form
About this item
Full title
Author / Creator
Publisher
London: Nature Publishing Group UK
Journal title
Language
English
Formats
Publication information
Publisher
London: Nature Publishing Group UK
Subjects
More information
Scope and Contents
Contents
Polyglutamine expansion in proteins can cause selective neurodegeneration, although the mechanisms are not fully understood. In Huntington’s disease (HD), proteolytic processing generates toxic N-terminal huntingtin (HTT) fragments that preferentially kill striatal neurons. Here, using CRISPR/Cas9 to truncate full-length mutant HTT in HD140Q knock-...
Alternative Titles
Full title
Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form
Authors, Artists and Contributors
Identifiers
Primary Identifiers
Record Identifier
TN_cdi_doaj_primary_oai_doaj_org_article_f7ec8fe55f5148dab5116e4f227b70c1
Permalink
https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_f7ec8fe55f5148dab5116e4f227b70c1
Other Identifiers
ISSN
2041-1723
E-ISSN
2041-1723
DOI
10.1038/s41467-020-16318-1
