glycogen storage disease type ii/arginina

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Nutrition and exercise in Pompe disease.

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The current standard of care for Pompe disease (PD) is the administration of enzyme replacement therapy (ERT). Exercise and nutrition are often considered as complementary strategies rather than "treatments" per se. Nutritional assessment is important in patients with locomotor

Mutations in GAA Gene in Tunisian Families with Infantile Onset Pompe Disease: Novel Mutation and Structural Modeling Investigations.

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Pompe disease, a rare, autosomal, recessive, inherited, lysosomal storage disorder, is caused by mutations in the acid α-glucosidase (GAA) gene leading to a deficiency of the lysosomal GAA enzyme. Some GAA mutations eliminate all enzymatic activities, causing severe infantile Pompe disease; others

Modulation of mTOR signaling as a strategy for the treatment of Pompe disease.

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Mechanistic target of rapamycin (mTOR) coordinates biosynthetic and catabolic processes in response to multiple extracellular and intracellular signals including growth factors and nutrients. This serine/threonine kinase has long been known as a critical regulator of muscle mass. The recent finding

Expression and routeing of human lysosomal alpha-glucosidase in transiently transfected mammalian cells.

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Previously isolated lysosomal alpha-glucosidase cDNA clones were ligated to full-length constructs for expression in vitro and in mammalian cells. One of these constructs (pSHAG1) did not code for functional enzyme, due to an arginine residue instead of a tryptophan residue at amino acid position

CARM1/PRMT4 is necessary for the glycogen gene expression programme in skeletal muscle cells.

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CARM1 (co-activator-associated arginine methyltransferase 1)/PRMT4 (protein arginine methyltransferase 4), functions as a co-activator for transcription factors that are regulators of muscle fibre type and oxidative metabolism, including PGC (peroxisome-proliferator-activated receptor γ

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