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Article

CRISPR deletion of the C9ORF72 promoter in ALS/FTD patient motor neurons abolishes production of dipeptide repeat proteins and rescues neurodegeneration.

Acta neuropathologica - 1 Jul 2020

Krishnan Gopinath, Zhang Yu, Gu Yuanzheng, Kankel Mark W, Gao Fen-Biao, Almeida Sandra

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Share to Amyotrophic Lateral Sclerosis
Share to C9orf72 Protein
Share to Clustered Regularly Interspaced Short Palindromic Repeats

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 32266467
DOI: 10.1007/s00401-020-02154-6
PMCID: PMC7300081

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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CRISPR deletion of the C9ORF72 promoter in ALS/FTD patient motor neurons abolishes production of dipeptide repeat proteins and rescues neurodegeneration.PMID 32266467Read ↗

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CRISPR/Cas9-mediated excision of ALS/FTD-causing hexanucleotide repeat expansion in C9ORF72 rescues major disease mechanisms in vivo and in vitroSemantic proximity Read ↗

CRISPR/Cas9-Mediated Excision of ALS/FTD-Causing Hexanucleotide Repeat Expansion in <i>C9ORF72</i> rescues major disease mechanisms <i>in vivo</i> and <i>in vitro</i>Semantic proximity Read ↗

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CRISPR-Cas9 screens in human cells and primary neurons identify modifiers of <i>C9orf72</i> dipeptide repeat protein toxicitySemantic proximity Read ↗

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CRISPR-Cas9 targeted deletion of the <i>C9orf72</i> repeat expansion mutation corrects cellular phenotypes in patient-derived iPS cellsSemantic proximity Read ↗

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