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

Inhibition of nonsense-mediated mRNA decay may improve stop codon read-through therapy for Duchenne muscular dystrophy.

Human molecular genetics - 20 Jul 2023

Amar-Schwartz Adi, Cohen Yuval, Elhaj Antony, Ben-Hur Vered, Siegfried Zahava, Karni Rotem, Dor Talya

Abstract excerpt

Duchene muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are genetic neuromuscular disorders that affect skeletal and cardiac muscle resulting from mutations in the dystrophin gene (DMD), coding for dystrophin protein. Read-through therapies hold great promise for the treatment of genetic diseases harboring nonsense mutations, such as DMD/BMD, as they enable a complete translation of the affected...

Read the complete abstract on PubMed

Topics

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

Share to Codon, Terminator
Share to Dystrophin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Muscle Physiology and Disorders

Share to Muscular Dystrophy, Duchenne

Share to Mutation

Share to Nonsense Mediated mRNA Decay

Share to RNA Research and Splicing

Share to Viral Infections and Immunology Research

Source

Identifiers

PMID: 37145099
DOI: 10.1093/hmg/ddad072

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

Inhibition of nonsense-mediated mRNA decay may improve stop codon read-through therapy for Duchenne muscular dystrophy.PMID 37145099Read ↗

Read-through strategies for suppression of nonsense mutations in Duchenne/ Becker muscular dystrophy: aminoglycosides and ataluren (PTC124).Semantic proximity Read ↗

Readthrough Activators and Nonsense-Mediated mRNA Decay Inhibitor Molecules: Real Potential in Many Genetic Diseases Harboring Premature Termination CodonsSemantic proximity Read ↗

Nonsense Suppression as an Approach to Treat Lysosomal Storage DiseasesSemantic proximity Read ↗

Emerging genetic therapies to treat Duchenne muscular dystrophy.Semantic proximity Read ↗

Therapeutic approaches for Duchenne muscular dystrophy.Semantic proximity Read ↗

Inhibition of nonsense-mediated mRNA decay rescues the phenotype in Ullrich's disease.Semantic proximity Read ↗

Introducing sense into nonsense in treatments of human genetic diseases.Semantic proximity Read ↗

Targeting Nonsense Mutations in Diseases with Translational Read-Through-Inducing Drugs (TRIDs).Semantic proximity Read ↗

Attenuation of Nonsense-Mediated mRNA Decay Enhances In Vivo Nonsense SuppressionSemantic proximity Read ↗

Combining Translation Readthrough Inducing Drugs and Nonsense Mediated Decay Pathway Inhibition to Rescue of CFTRW1282X in Cystic Fibrosis Cell Model SystemSemantic proximity Read ↗

Readthrough approach by NV translational readthrough inducing drugs (TRIDs): a study of the possible off-target effects on natural termination codons (NTCs) on TP53 and housekeeping genes expression.Semantic proximity Read ↗

Effect of Readthrough Treatment in Fibroblasts of Patients Affected by Lysosomal Diseases Caused by Premature Termination Codons.Semantic proximity Read ↗

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