Mitochondrial dysfunction in skeletal muscle of fukutin-deficient mice is resistant to exercise- and 5-aminoimidazole-4-carboxamide ribonucleotide-induced rescue.
Study shows molecular pathogenesis of muscular dystrophy-associated cardiomyopathy in mice lacking the Fktn gene. Although cardiac Fktn elimination markedly reduced alpha-dystroglycan glycosylation and dystrophin-glycoprotein complex proteins in sarcolemma at all developmental stages cardiac dysfunction was observed only in later adulthood suggesting that membrane fragility is not the sole etiology of cardiac dysfunc...
Fktn deficient mice express moderate to severe muscular dystrophy; glycosylated alpha-dystroglycan has a unique role in muscle regeneration in these mice
Mouse fukutin deletion impairs dystroglycan processing recapitulates muscular dystrophy and is relevant to modifications near the dystroglycan O-mannose sugar.
the highly hydrophobic transmembrane domain of Fukutin-1 was purified; the identity of the peptide and revealed that in hydrophobic solvents mimicking the bilayer the peptide adopts a well-structured alpha-helix as predicted from the sequence.
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