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

Our study provides new insights into the complex mechanisms of CRISPR/Cas9-induced shortening of CAG repeats in human cells.

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Publication Details

Journal
BMC Biology
Published
2024-12-03
DOI
https://doi.org/10.1186/s12915-024-02079-6
Citations
4
Primary Topic
Genetic Neurodegenerative Diseases
Type
article
Field-Weighted Citation Impact
1.07

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article

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

Paweł Śledziński, Marta Olejniczak, Mateusz Nowaczyk, Marianna Iga Smielowska
4 citations
BMC Biology
Genetic Neurodegenerative Diseases
1.07
article

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

Paweł Śledziński, Marta Olejniczak, Mateusz Nowaczyk, Marianna Iga Smielowska
article en
4 citations

Abstract

Our study provides new insights into the complex mechanisms of CRISPR/Cas9-induced shortening of CAG repeats in human cells.

BMC BiologyVol. 22(1)
Institute of Bioorganic Chemistry, Polish Academy of Sciences (PL)
European Regional Development Fund
Good health and well-being
Openalex Percentile: Top 23%
Genetic Neurodegenerative Diseases
1.07
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