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

Antisense-induced exon skipping restores dystrophin expression in DMD patient derived muscle cells.

Human molecular genetics - 15 Jul 2001

van Deutekom J C, Bremmer-Bout M, Janson A A, Ginjaar I B, Baas F, den Dunnen J T, van Ommen G J

Abstract excerpt

Due to frame-shifting mutations in the DMD gene that cause dystrophin deficiency, Duchenne muscular dystrophy (DMD) patients suffer from lethal muscle degeneration. In contrast, mutations in the allelic Becker muscular dystrophy (BMD) do not disrupt the translational reading frame, resulting in a...

Read the complete abstract on PubMed

Topics

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

Share to Dystrophin
Share to Gene Deletion
Share to Microscopy, Fluorescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Muscles

Share to Muscular Dystrophy, Duchenne

Share to Oligonucleotides, Antisense

Share to Protein Biosynthesis

Source

Identifiers

PMID: 11468272
DOI: 10.1093/hmg/10.15.1547

Genes

DMD

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026. Prepared record publication-11468272-2026-09-01.1. Manifest publication-graph-cohort-2026-09-01.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Antisense-induced exon skipping restores dystrophin expression in DMD patient derived muscle cells.PMID 11468272Read ↗

Direct Reprogramming of Human DMD Fibroblasts into Myotubes for In Vitro Evaluation of Antisense-Mediated Exon Skipping and Exons 45-55 Skipping Accompanied by Rescue of Dystrophin Expression.Semantic proximity Read ↗

Therapeutic antisense-induced exon skipping in cultured muscle cells from six different DMD patients.Semantic proximity Read ↗

Biochemical characterization of patients with in-frame or out-of-frame DMD deletions pertinent to exon 44 or 45 skipping.Semantic proximity Read ↗

Antisense oligonucleotide-mediated exon skipping for Duchenne muscular dystrophy: progress and challenges.Semantic proximity Read ↗

Multiple Exon Skipping in the Duchenne Muscular Dystrophy Hot Spots: Prospects and ChallengesSemantic proximity Read ↗

Restoration of Dystrophin Protein Expression by Exon Skipping Utilizing CRISPR-Cas9 in Myoblasts Derived from DMD Patient iPS Cells.Semantic proximity Read ↗

Multiexon skipping leading to an artificial DMD protein lacking amino acids from exons 45 through 55 could rescue up to 63% of patients with Duchenne muscular dystrophy.Semantic proximity Read ↗

Molecular correction of Duchenne muscular dystrophy by splice modulation and gene editing.Semantic proximity Read ↗

Antisense-induced exon skipping and synthesis of dystrophin in the mdx mouseSemantic proximity Read ↗

Exon skipping and gene transfer restore dystrophin expression in human induced pluripotent stem cells-cardiomyocytes harboring DMD mutations.Semantic proximity Read ↗

Low-level dystrophin expression attenuating the dystrophinopathy phenotype.Semantic proximity Read ↗

Moving towards successful exon-skipping therapy for Duchenne muscular dystrophy.Semantic proximity Read ↗

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