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Clinical features of Pompe disease.

Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology (2014-01-09)
Fiore Manganelli, Lucia Ruggiero
ABSTRACT

Glycogen storage disease type II - also called Pompe disease or acid maltase deficiency - is an autosomal recessive metabolic disorder, caused by an accumulation of glycogen in the lysosome due to deficiency of the lysosomal acid alpha-glucosidase enzyme. Pompe disease is transmitted as an autosomal recessive trait and is caused by mutations in the gene encoding the acid α-glucosidase (GAA), located on chromosome 17q25.2-q25.3. The different disease phenotypes are related to the levels of residual GAA activity in muscles. The clinical spectrum ranging from the classical form with early onset and severe phenotype to not-classical form with later onset and milder phenotype is described.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
α-Glucosidase from Saccharomyces cerevisiae, recombinant, expressed in proprietary host, lyophilized powder, ≥100 units/mg protein
Sigma-Aldrich
α-Glucosidase from Saccharomyces cerevisiae, Type I, lyophilized powder, ≥10 units/mg protein (using p-nitrophenyl α-D-glucoside as substrate.)
Sigma-Aldrich
α-Glucosidase from rice, Type V, ammonium sulfate suspension, 40-80 units/mg protein
Sigma-Aldrich
Glycogen from mussel, Mytilus genus, ≥85% anhydrous basis (enzymatic)
Sigma-Aldrich
Glycogen from rabbit liver, ≥85% dry basis (enzymatic)
Sigma-Aldrich
Glycogen from oyster, ≥75% dry basis
Sigma-Aldrich
Glycogen from bovine liver, ≥85% dry basis (enzymatic)
Sigma-Aldrich
α-Glucosidase from Bacillus stearothermophilus, lyophilized powder, ≥50 units/mg protein