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1 used by a deficiency of the lysosomal enzyme acid alpha-glucosidase.
2 imum at pH 4.3, classifying the enzyme as an acid alpha-glucosidase.
3 y of the glycogen-degrading lysosomal enzyme acid-alpha glucosidase.
4 ic muscle disorder caused by a deficiency of acid alpha-glucosidase, a glycogen-degrading lysosomal e
5 The physiological relevance of acid maltase (acid alpha-glucosidase, an enzyme that degrades lysosoma
7 ed by the deficiency of the lysosomal enzyme acid alpha-glucosidase and results in cellular lysosomal
8 ed a plasmid containing a 5'-shortened human acid alpha-glucosidase cDNA driven by the cytomegaloviru
9 disease (PD) is a metabolic myopathy due to acid alpha-glucosidase deficiency and characterized by e
10 CI-MPR-mediated uptake of recombinant human acid-alpha-glucosidase during ERT in mice with Pompe dis
11 isingly, we also found that, unlike mammals, acid alpha-glucosidase from zebrafish and medaka does no
12 ding the glycogen-degrading lysosomal enzyme acid alpha -glucosidase (GAA) (also called "acid maltase
13 oss of lysosomal glycogen-hydrolyzing enzyme acid alpha-glucosidase (GAA) activity, which results in
16 transported to and degraded in lysosomes by acid alpha-glucosidase (GAA) in mammals, but it is uncle
19 ation of a modified Ad vector encoding human acid alpha-glucosidase (GAA) resulted in efficient hepat
20 e generated by treating the lysosomal enzyme acid alpha-glucosidase (GAA) with recombinant GlcNAc-pho
21 e type II (GSDII), caused by a deficiency in acid alpha-glucosidase (GAA), leads to lysosomal accumul
22 y and cardiomyopathy caused by deficiency of acid alpha-glucosidase (GAA), skeletal muscle seems an o
23 ting system to improve lysosomal delivery of acid alpha-glucosidase (GAA), the enzyme deficient in pa
24 ity is directly related to the deficiency of acid alpha-glucosidase (GAA), which degrades glycogen in
25 has resisted enzyme replacement therapy with acid alpha-glucosidase (GAA), which has been attributed
28 metabolic disorder characterized by lack of acid-alpha glucosidase (GAA) resulting in ubiquitous lys
29 rome), mice homozygous for disruption of the acid alpha-glucosidase gene (6(neo)/6(neo)) lack enzyme
30 g the expression and regulation of the human acid alpha-glucosidase gene as well as other lysosomal e
31 have previously demonstrated that the human acid alpha-glucosidase gene expression is regulated by a
34 (Delta6/Delta6), like the recently published acid alpha-glucosidase knockout with disruption of exon
35 t relatively high doses of recombinant human acid alpha-glucosidase (rhGAA) may be required to reduce
36 tion system now exists for recombinant human acid alpha-glucosidase targeted to heart and capable of
38 ed these residues were not acquired on human acid alpha-glucosidase when expressed in zebrafish embry
39 man lysosomal enzymes alpha-l-iduronidase or acid alpha-glucosidase with the receptor-associated prot
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