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

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

Abstract Background The expansion of 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 mech...

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Bibliographic Details
Main Authors: Pawel Sledzinski, Mateusz Nowaczyk, Marianna Iga Smielowska, Marta Olejniczak
Format: Article
Language:English
Published: BMC 2024-12-01
Series:BMC Biology
Subjects:
DNA repair
Genome editing
Short tandem repeats
TMEJ
Online Access:https://doi.org/10.1186/s12915-024-02079-6
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https://doi.org/10.1186/s12915-024-02079-6

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