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

U7 snRNAs induce correction of mutated dystrophin pre-mRNA by exon skipping.

Cellular and molecular life sciences : CMLS - 1 Mar 2003

Brun C, Suter D, Pauli C, Dunant P, Lochmüller H, Burgunder J M, Schümperli D, Weis J

Abstract excerpt

Most cases of Duchenne muscular dystrophy are caused by dystrophin gene mutations that disrupt the mRNA reading frame. Artificial exclusion (skipping) of a single exon would often restore the reading frame, giving rise to a shorter, but still functional dystrophin protein. Here, we analyzed the ability of antisense U7 small nuclear (sn)RNA derivatives to alter dystrophin pre-mRNA splicing. As a proof of...

Read the complete abstract on PubMed

Topics

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

Share to Dystrophin
Share to Genetic Therapy
Share to Mice, Inbred mdx

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Muscular Dystrophy, Duchenne

Share to RNA, Antisense

Share to RNA Precursors

Share to RNA, Small Nuclear

Share to RNA Splicing

Source

Open in PubMed Open full text

Identifiers

PMID: 12737315
DOI: 10.1007/s000180300047
PMCID: PMC11138867

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

U7 snRNAs induce correction of mutated dystrophin pre-mRNA by exon skipping.PMID 12737315Read ↗

Rescue of dystrophic muscle through U7 snRNA-mediated exon skipping.Semantic proximity Read ↗

Genetic therapies for RNA mis-splicing diseases.Semantic proximity Read ↗

Spinal Muscular Atrophy: SMN2 Pre-mRNA Splicing Corrected by a U7 snRNA Derivative Carrying a Splicing Enhancer SequenceSemantic proximity Read ↗

Improvement of SMN2 Pre-mRNA Processing Mediated by Exon-Specific U1 Small Nuclear RNASemantic proximity Read ↗

Rescue of severely affected dystrophin/utrophin-deficient mice through scAAV-U7snRNA-mediated exon skipping.Semantic proximity Read ↗

The Cellular Processing Capacity Limits the Amounts of Chimeric U7 snRNA Available for Antisense DeliverySemantic proximity Read ↗

U7 snRNA: A tool for gene therapySemantic proximity Read ↗

Efficient Modulation of Exon Skipping via Antisense Circular RNAsSemantic proximity Read ↗

Specific removal of the nonsense mutation from the mdx dystrophin mRNA using antisense oligonucleotides.Semantic proximity Read ↗

Exon Skipping Through Chimeric Antisense U1 snRNAs to Correct Retinitis Pigmentosa GTPase-Regulator (RPGR) Splice Defect.Semantic proximity Read ↗

Exon skipping via chimeric antisense U1 snRNAs to correct Retinitis Pigmentosa GTPase-Regulator (RPGR) splice defectSemantic proximity Read ↗

Towards a therapeutic inhibition of dystrophin exon 23 splicing in mdx mouse muscle induced by antisense oligoribonucleotides (splicomers): target sequence optimisation using oligonucleotide arrays.Semantic proximity Read ↗

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