Back to search

Article

CRISPR/Cas9-induced double-strand breaks in huntingtin locus lead to CAG repeat contraction through the extensive DNA end resection and homology-mediated repair

2023-11-24

Abstract excerpt

<h4>ABSTRACT</h4> Expansion of the CAG/CTG repeats in functionally unrelated genes is a causative factor in many inherited neurodegenerative disorders, including Huntington’s disease (HD), spinocerebellar ataxias (SCAs) and myotonic dystrophy type 1 (DM1). Despite many years of research, the mechanism responsible for repeat instability is unknown, and recent findings indicate the key role of DNA repair in this pr...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work
b32bd00b-5152-5727-953b-0ce9f3771b13
DOI
10.1101/2023.11.24.568568
Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest
Interactive article relationship graphSelect a related publication card to move it into the centre and load its closest explainable connections. Solid lines are source-backed structured connections. Dashed lines are semantic discovery signals and are not scientific evidence.
CRISPR/Cas9-induced double-strand breaks in huntingtin locus lead to CAG repeat contraction through the extensive DNA end resection and homology-mediated repairDOI 10.1101/2023.11.24.568568
Select a neighboring publication to make it the new centre.