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

Blockade of Hemichannels Normalizes the Differentiation Fate of Myoblasts and Features of Skeletal Muscles from Dysferlin-Deficient Mice

21 Aug 2020

Abstract excerpt

Dysferlinopathies are muscle dystrophies caused by mutations in the gene encoding dysferlin, a relevant protein for membrane repair and trafficking. These diseases are untreatable, possibly due to the poor knowledge of relevant molecular targets. Previously, we have shown that human myofibers from patient biopsies as well as myotubes derived from immortalized human myoblasts carrying a mutated form of dysferlin...

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 Genetic Neurodegenerative Diseases
Share to Muscle Physiology and Disorders

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 32825681
DOI: 10.3390/ijms21176025

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

Blockade of Hemichannels Normalizes the Differentiation Fate of Myoblasts and Features of Skeletal Muscles from Dysferlin-Deficient MicePMID 32825681Read ↗

Myofibers deficient in connexins 43 and 45 expression protect mice from skeletal muscle and systemic dysfunction promoted by a dysferlin mutation.Semantic proximity Read ↗

The absence of dysferlin induces the expression of functional connexin-based hemichannels in human myotubes.Semantic proximity Read ↗

Dysferlin and Animal Models for DysferlinopathySemantic proximity Read ↗

Disruption of muscle membrane and phenotype divergence in two novel mouse models of dysferlin deficiency.Semantic proximity Read ↗

Portrait of Dysferlinopathy: Diagnosis and Development of TherapySemantic proximity Read ↗

Dysferlin-deficient immortalized human myoblasts and myotubes as a useful tool to study dysferlinopathySemantic proximity Read ↗

Dysferlin function in skeletal muscle: Possible pathological mechanisms and therapeutical targets in dysferlinopathies.Semantic proximity Read ↗

The Dysferlinopathies Conundrum: Clinical Spectra, Disease Mechanism and Genetic Approaches for Treatments.Semantic proximity Read ↗

Myogenesis in dysferlin-deficient myoblasts is inhibited by an intrinsic inflammatory response.Semantic proximity Read ↗

Early pathological signs in young <i> dysf <sup>−/−</sup> </i> mice are improved by halofuginoneSemantic proximity Read ↗

Translational research and therapeutic perspectives in dysferlinopathies.Semantic proximity Read ↗

The Dysferlinopathies Conundrum: Clinical Spectra, Disease Mechanism and Genetic Approaches for TreatmentsSemantic proximity Read ↗

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