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

Four-week rapamycin treatment improves muscular dystrophy in a fukutin-deficient mouse model of dystroglycanopathy.

Skeletal muscle - 1 Jan 2016

Foltz Steven J, Luan Junna, Call Jarrod A, Patel Ankit, Peissig Kristen B, Fortunato Marisa J, Beedle Aaron M

Abstract excerpt

BACKGROUND: Secondary dystroglycanopathies are a subset of muscular dystrophy caused by abnormal glycosylation of α-dystroglycan (αDG). Loss of αDG functional glycosylation prevents it from binding to laminin and other extracellular matrix receptors, causing muscular dystrophy. Mutations in a number of genes, including FKTN (fukutin), disrupt αDG glycosylation. METHODS: We analyzed conditional Fktn knockout (Fktn...

Read the complete abstract on PubMed

Topics

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

Share to Biomechanical Phenomena
Share to Dystroglycans

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Electric Stimulation

Share to Muscle Strength

Share to Muscular Dystrophy, Animal

Share to Myogenic Regulatory Factor 5

Share to Sirolimus

Share to Transferases

Source

Open in PubMed Open full text

Identifiers

PMID: 27257474
DOI: 10.1186/s13395-016-0091-9
PMCID: PMC4890530

Genes

FKTN

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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

Four-week rapamycin treatment improves muscular dystrophy in a fukutin-deficient mouse model of dystroglycanopathy.PMID 27257474Read ↗

Mitochondrial dysfunction in skeletal muscle of fukutin deficient mice is resistant to exercise- and AICAR-induced rescueSemantic proximity Read ↗

Mouse fukutin deletion impairs dystroglycan processing and recapitulates muscular dystrophy.Semantic proximity Read ↗

A New Mouse Model of Limb-Girdle Muscular Dystrophy Type 2I Homozygous for the Common L276I Mutation Mimicking the Mild Phenotype in Humans.Semantic proximity Read ↗

mTORC1 Promotes Denervation-Induced Muscle Atrophy Through a Mechanism Involving the Activation of FoxO and E3 Ubiquitin LigasesSemantic proximity Read ↗

Abnormal Skeletal Muscle Regeneration plus Mild Alterations in Mature Fiber Type Specification in Fktn-Deficient Dystroglycanopathy Muscular Dystrophy Mice.Semantic proximity Read ↗

Defective autophagy and increased apoptosis contribute toward the pathogenesis of FKRP-associated muscular dystrophies.Semantic proximity Read ↗

Progressive Dystrophic Pathology in Diaphragm and Impairment of Cardiac Function in FKRP P448L Mutant Mice.Semantic proximity Read ↗

Elimination of fukutin reveals cellular and molecular pathomechanisms in muscular dystrophy-associated heart failureSemantic proximity Read ↗

Muscle and Heart Function Restoration in a Limb Girdle Muscular Dystrophy 2I (LGMD2I) Mouse Model by Systemic FKRP Gene DeliverySemantic proximity Read ↗

Rapamycin-induced autophagy aggravates pathology and weakness in a mouse model of VCP-associated myopathySemantic proximity Read ↗

FKRP-dependent glycosylation of fibronectin regulates muscle pathology in muscular dystrophy.Semantic proximity Read ↗

Break Down of the Complexity and Inconsistency Between Levels of Matriglycan and Disease Phenotype in FKRP-Related Dystroglycanopathies: A Review and Model of Interpretation.Semantic proximity Read ↗

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