Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Allele-selective inhibition of trinucleotide repeat genes.

Drug discovery today - 1 May 2012

Matsui Masayuki, Corey David R

Abstract excerpt

Expanded trinucleotide repeats cause Huntington's disease (HD) and many other neurodegenerative disorders. There are no cures for these devastating illnesses and treatments are urgently needed. Each trinucleotide repeat disorder is the result of the mutation of just one gene, and agents that block expression of the mutant gene offer a promising option for treatment. Therapies that block expression of both mutant...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alleles
Share to Gene Silencing
Share to Neurodegenerative Diseases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Nucleic Acids

Share to Polymorphism, Genetic

Share to Trinucleotide Repeat Expansion

Source

Open in PubMed Open full text

Identifiers

PMID: 22285529
DOI: 10.1016/j.drudis.2012.01.006
PMCID: PMC3468950

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Allele-selective inhibition of trinucleotide repeat genes.PMID 22285529Read ↗

Limits of using oligonucleotides for allele-selective inhibition at trinucleotide repeat sequences - targeting the CAG repeat within ataxin-1.Semantic proximity Read ↗

Allele-selective inhibition of mutant atrophin-1 expression by duplex and single-stranded RNAs.Semantic proximity Read ↗

Rational design of antisense oligonucleotides targeting single nucleotide polymorphisms for potent and allele selective suppression of mutant Huntingtin in the CNS.Semantic proximity Read ↗

Possibilities and limitations of antisense oligonucleotide therapies for the treatment of monogenic disordersSemantic proximity Read ↗

Gene targeting techniques for Huntington's disease.Semantic proximity Read ↗

Towards Personalized Allele-Specific Antisense Oligonucleotide Therapies for Toxic Gain-of-Function Neurodegenerative DiseasesSemantic proximity Read ↗

Antisense oligonucleotides and their applications in rare neurological diseasesSemantic proximity Read ↗

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

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

Allele-selective inhibition of mutant huntingtin by peptide nucleic acid-peptide conjugates, locked nucleic acid, and small interfering RNA.Semantic proximity Read ↗

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

Repeat expansion diseases: when a good RNA turns bad.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.