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

Increased Apoptosis of Myoblasts in Drosophila Model for the Walker-Warburg Syndrome

13 Jul 2010

Abstract excerpt

Walker-Warburg syndrome, a progressive muscular dystrophy, is a severe disease with various kinds of symptoms such as muscle weakness and occasional seizures. The genes of protein O-mannosyltransferases 1 and 2 (POMT1 and POMT2), fukutin, and fukutin-related protein are responsible for this syndrome. In our previous study, we cloned Drosophila orthologs of human POMT1 and POMT2 and identified their activity....

Read the complete abstract on PubMed

Topics

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

Share to Cardiomyopathy and Myosin Studies
Share to Muscle Physiology and Disorders
Share to RNA Research and Splicing

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 20644630
DOI: 10.1371/journal.pone.0011557

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Increased Apoptosis of Myoblasts in Drosophila Model for the Walker-Warburg SyndromePMID 20644630Read ↗

The twisted abdomen phenotype of Drosophila POMT1 and POMT2 mutants coincides with their heterophilic protein O-mannosyltransferase activity.Semantic proximity Read ↗

Protein O-Mannosyltransferases Affect Sensory Axon Wiring and Dynamic Chirality of Body Posture in the Drosophila Embryo.Semantic proximity Read ↗

The twisted gene encodes Drosophila protein O-mannosyltransferase 2 and genetically interacts with the rotated abdomen gene encoding Drosophila protein O-mannosyltransferase 1.Semantic proximity Read ↗

Extracellular matrix and nuclear abnormalities in skeletal muscle of a patient with Walker–Warburg syndrome caused by POMT1 mutationSemantic proximity Read ↗

Generation of induced pluripotent stem (iPS) cells derived from a murine model of Pompe disease and differentiation of Pompe-iPS cells into skeletal muscle cells.Semantic proximity Read ↗

Characterization of novel dystonia musculorum mutant mice: Implications for central nervous system abnormality.Semantic proximity Read ↗

Identification of a Human Homolog of the Drosophila rotated abdomen Gene (POMT1) Encoding a Putative Protein O-Mannosyl-Transferase, and Assignment to Human Chromosome 9q34.1Semantic proximity Read ↗

Fukutin mutations in non-Japanese patients with congenital muscular dystrophy: less severe mutations predominate in patients with a non-Walker-Warburg phenotype.Semantic proximity Read ↗

A novel missense mutation in POMT1 modulates the severe congenital muscular dystrophy phenotype associated with POMT1 nonsense mutations.Semantic proximity Read ↗

Loss of p21-activated kinase Mbt/PAK4 causes Parkinson-like phenotypes in Drosophila.Semantic proximity Read ↗

Increased autophagy and apoptosis contribute to muscle atrophy in a myotonic dystrophy type 1 <i>Drosophila</i> modelSemantic proximity Read ↗

The expanding phenotype of POMT1 mutations: from Walker-Warburg syndrome to congenital muscular dystrophy, microcephaly, and mental retardation.Semantic proximity Read ↗

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