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Article

Allele-selective inhibition of mutant huntingtin expression with antisense oligonucleotides targeting the expanded CAG repeat.

Biochemistry - 30 Nov 2010

Gagnon Keith T, Pendergraff Hannah M, Deleavey Glen F, Swayze Eric E, Potier Pierre, Randolph John, Roesch Eric B, Chattopadhyaya Jyoti, Damha Masad J, Bennett C Frank, Montaillier Christophe, Lemaitre Marc, Corey David R

Abstract excerpt

Huntington's disease (HD) is a currently incurable neurodegenerative disease caused by the expansion of a CAG trinucleotide repeat within the huntingtin (HTT) gene. Therapeutic approaches include selectively inhibiting the expression of the mutated HTT allele while conserving function of the normal allele. We have evaluated a series of antisense oligonucleotides (ASOs) targeted to the expanded CAG repeat within...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 21028906
DOI: 10.1021/bi101208k
PMCID: PMC2991413

Genes

HTT

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

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Allele-selective inhibition of mutant huntingtin expression with antisense oligonucleotides targeting the expanded CAG repeat.PMID 21028906Read ↗

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Personalized gene silencing therapeutics for Huntington disease.Semantic proximity Read ↗

Allele-specific suppression of mutant huntingtin using antisense oligonucleotides: providing a therapeutic option for all Huntington disease patients.Semantic proximity Read ↗

Allele-selective inhibition of huntingtin expression by switching to an miRNA-like RNAi mechanism.Semantic proximity Read ↗

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