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

Effective rescue of dystrophin improves cardiac function in dystrophin-deficient mice by a modified morpholino oligomer

19 Sept 2008

Abstract excerpt

Antisense oligonucleotide-mediated exon skipping is able to correct out-of-frame mutations in Duchenne muscular dystrophy and restore truncated yet functional dystrophins. However, its application is limited by low potency and inefficiency in systemic delivery, especially failure to restore dystrophin in heart. Here, we conjugate a phosphorodiamidate morpholino oligomer with a designed cell-penetrating peptide...

Read the complete abstract on PubMed

Topics

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

Share to Adipose Tissue and Metabolism
Share to Muscle Physiology and Disorders
Share to Tissue Engineering and Regenerative Medicine

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 18806224
DOI: 10.1073/pnas.0805676105

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Effective rescue of dystrophin improves cardiac function in dystrophin-deficient mice by a modified morpholino oligomerPMID 18806224Read ↗

Long-term improvement in mdx cardiomyopathy after therapy with peptide-conjugated morpholino oligomers†Semantic proximity Read ↗

Functional Rescue of Dystrophin-deficient mdx Mice by a Chimeric Peptide-PMOSemantic proximity Read ↗

Peptide-conjugate antisense based splice-correction for Duchenne muscular dystrophy and other neuromuscular diseasesSemantic proximity Read ↗

Dual Myostatin and Dystrophin Exon Skipping by Morpholino Nucleic Acid Oligomers Conjugated to a Cell-penetrating Peptide Is a Promising Therapeutic Strategy for the Treatment of Duchenne Muscular DystrophySemantic proximity Read ↗

Morpholino oligomer-mediated exon skipping averts the onset of dystrophic pathology in the mdx mouse.Semantic proximity Read ↗

Peptide conjugation of 2'-O-methyl phosphorothioate antisense oligonucleotides enhances cardiac uptake and exon skipping in mdx mice.Semantic proximity Read ↗

Heteroduplex oligonucleotide technology boosts oligonucleotide splice switching activity of morpholino oligomers in a Duchenne muscular dystrophy mouse modelSemantic proximity Read ↗

RNA Therapeutics for Duchenne Muscular Dystrophy: Exon Skipping, RNA Editing, and Translational Insights from Genome-Edited Microminipig Models.Semantic proximity Read ↗

Next steps for the optimization of exon therapy for Duchenne muscular dystrophySemantic proximity Read ↗

In-frame Dystrophin Following Exon 51-Skipping Improves Muscle Pathology and Function in the Exon 52–Deficient mdx MouseSemantic proximity Read ↗

PPMO-mediated exon skipping induces uniform sarcolemmal dystrophin rescue with dose-dependent restoration of circulating microRNA biomarkers and muscle biophysical propertiesSemantic proximity Read ↗

Systemic Delivery of Morpholinos to Skip Multiple Exons in a Dog Model of Duchenne Muscular Dystrophy.Semantic proximity Read ↗

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