3.2.1.106	Adenocarcinoma	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1757490&form=6&db=m	Biosynthesis and transport of lysosomal alpha-glucosidase in the human colon carcinoma cell line Caco-2: secretion from the apical surface.	diagnostic usage,ongoing research,unassigned	3,4,0	
3.2.1.106	alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15659425&form=6&db=m	Clinical manifestation and natural course of late-onset Pompe's disease in 54 Dutch patients.	causal interaction,unassigned	4,0	
3.2.1.106	alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17210890&form=6&db=m	Broad spectrum of Pompe disease in patients with the same c.-32-13T->G haplotype.	causal interaction,unassigned	4,0	
3.2.1.106	alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19533645&form=6&db=m	Screening for Pompe disease using a rapid dried blood spot method: experience of a clinical diagnostic laboratory.	causal interaction,unassigned	4,0	
3.2.1.106	alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19966354&form=6&db=m	Enzyme replacement therapy for infantile Pompe disease during the critical period and identification of a novel mutation.	causal interaction,unassigned	4,0	
3.2.1.106	Anaphylaxis	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22494547&form=6&db=m	Mapping the T helper cell response to acid ?-glucosidase in Pompe mice.	therapeutic application,unassigned	1,0	
3.2.1.106	Anaphylaxis	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24897114&form=6&db=m	Immune responses and hypercoagulation in ERT for Pompe disease are mutation and rhGAA dose dependent.	causal interaction,therapeutic application,unassigned	2,2,0	
3.2.1.106	Arthritis	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32508839&form=6&db=m	Development of ImmTOR Tolerogenic Nanoparticles for the Mitigation of Anti-drug Antibodies.	ongoing research,therapeutic application,unassigned	3,1,0	
3.2.1.106	Carcinogenesis	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10734102&form=6&db=m	Allosteric activation of acid alpha-glucosidase by the human papillomavirus E7 protein.	causal interaction,ongoing research,therapeutic application,unassigned	1,4,1,0	
3.2.1.106	Carcinoma	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10734102&form=6&db=m	Allosteric activation of acid alpha-glucosidase by the human papillomavirus E7 protein.	causal interaction,ongoing research,therapeutic application,unassigned	1,4,1,0	
3.2.1.106	Carcinoma, Hepatocellular	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2434831&form=6&db=m	Differential effects of 1-deoxynojirimycin on the intracellular transport of secretory glycoproteins of human hepatoma cells in culture.	ongoing research,therapeutic application,unassigned	3,1,0	
3.2.1.106	Carcinoma, Hepatocellular	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3004419&form=6&db=m	Castanospermine inhibits glucosidase I and glycoprotein secretion in human hepatoma cells.	ongoing research,unassigned	4,0	
3.2.1.106	Carcinoma, Hepatocellular	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8054362&form=6&db=m	Effect of glycosidase inhibitors on the biosynthesis of alpha 2-plasmin inhibitor and antithrombin III in Hep G2 cells.	ongoing research,unassigned	4,0	
3.2.1.106	Cardiomegaly	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10189220&form=6&db=m	Novel mutations in African American patients with glycogen storage disease Type II. Mutations in brief no. 209. Online.	causal interaction,unassigned	4,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3288378&form=6&db=m	Km mutant of acid alpha-glucosidase in a case of cardiomyopathy without signs of skeletal muscle involvement.	causal interaction,unassigned	1,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10838256&form=6&db=m	Modulation of disease severity in mice with targeted disruption of the acid alpha-glucosidase gene.	causal interaction,unassigned	4,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11590121&form=6&db=m	Conditional tissue-specific expression of the acid alpha-glucosidase (GAA) gene in the GAA knockout mice: implications for therapy.	causal interaction,therapeutic application,unassigned	1,4,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12398843&form=6&db=m	Danon's disease (X-linked vacuolar cardiomyopathy and myopathy): a case with a novel Lamp-2 gene mutation.	unassigned	-	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12409258&form=6&db=m	Glycogen stored in skeletal but not in cardiac muscle in acid alpha-glucosidase mutant (Pompe) mice is highly resistant to transgene-encoded human enzyme.	causal interaction,unassigned	3,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14567965&form=6&db=m	Enzyme replacement therapy in the mouse model of Pompe disease.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15585405&form=6&db=m	Replacing acid alpha-glucosidase in Pompe disease: recombinant and transgenic enzymes are equipotent, but neither completely clears glycogen from type II muscle fibers.	causal interaction,ongoing research,therapeutic application,unassigned	4,2,4,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15639117&form=6&db=m	Safety and efficacy of recombinant acid alpha-glucosidase (rhGAA) in patients with classical infantile Pompe disease: results of a phase II clinical trial.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,4,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15776317&form=6&db=m	Enzyme replacement therapy in classical infantile pompe disease: results of a ten-month follow-up study.	causal interaction,unassigned	4,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16860134&form=6&db=m	Chinese hamster ovary cell-derived recombinant human acid alpha-glucosidase in infantile-onset Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	3,3,4,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16874053&form=6&db=m	Autophagy and lysosomes in Pompe disease.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17008131&form=6&db=m	Autophagy and mistargeting of therapeutic enzyme in skeletal muscle in Pompe disease.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17342521&form=6&db=m	Fractures in children with Pompe disease: a potential long-term complication.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19167256&form=6&db=m	Murine muscle cell models for Pompe disease and their use in studying therapeutic approaches.	causal interaction,diagnostic usage,ongoing research,unassigned	4,3,4,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20033064&form=6&db=m	Neonatal gene transfer using lentiviral vector for murine Pompe disease: long-term expression and glycogen reduction.	causal interaction,unassigned	4,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21637107&form=6&db=m	The impact of antibodies on clinical outcomes in diseases treated with therapeutic protein: Lessons learned from infantile Pompe disease.	causal interaction,therapeutic application,unassigned	4,3,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25763511&form=6&db=m	Postmortem Findings and Clinical Correlates in Individuals with Infantile-Onset Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Cardiomyopathies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29565424&form=6&db=m	Efficacy, safety profile, and immunogenicity of alglucosidase alfa produced at the 4,000-liter scale in US children and adolescents with Pompe disease: ADVANCE, a phase IV, open-label, prospective study.	diagnostic usage,ongoing research,therapeutic application,unassigned	2,1,4,0	
3.2.1.106	Cardiomyopathy, Hypertrophic	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16005263&form=6&db=m	Evasion of immune responses to introduced human acid alpha-glucosidase by liver-restricted expression in glycogen storage disease type II.	causal interaction,ongoing research,unassigned	4,2,0	
3.2.1.106	Cardiomyopathy, Hypertrophic	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17245350&form=6&db=m	Physiological Correction of Pompe Disease by Systemic Delivery of Adeno-associated Virus Serotype 1 Vectors.	causal interaction,unassigned	3,0	
3.2.1.106	Cardiomyopathy, Hypertrophic	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18782850&form=6&db=m	Modulation of glycogen synthesis by RNA interference: towards a new therapeutic approach for glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	Cardiomyopathy, Hypertrophic	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392195&form=6&db=m	Long-term outcome and unmet needs in infantile-onset Pompe disease.	unassigned	-	
3.2.1.106	Cleft Lip	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10377006&form=6&db=m	Increased occurrence of cleft lip in glycogen storage disease type II (GSDII): exclusion of a contiguous gene syndrome in two patients by presence of intragenic mutations including a novel nonsense mutation Gln58Stop.	causal interaction,unassigned	4,0	
3.2.1.106	Congenital Disorders of Glycosylation	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30587846&form=6&db=m	Compound heterozygous variants in MOGS inducing congenital disorders of glycosylation (CDG) IIb.	therapeutic application,unassigned	1,0	
3.2.1.106	Congenital, Hereditary, and Neonatal Diseases and Abnormalities	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12145188&form=6&db=m	Processing of N-linked carbohydrate chains in a patient with glucosidase I deficiency (CDG type IIb).	causal interaction,unassigned	4,0	
3.2.1.106	Congenital, Hereditary, and Neonatal Diseases and Abnormalities	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15383536&form=6&db=m	The Lec23 Chinese hamster ovary mutant is a sensitive host for detecting mutations in alpha-glucosidase I that give rise to congenital disorder of glycosylation IIb (CDG IIb).	unassigned	-	
3.2.1.106	Congenital, Hereditary, and Neonatal Diseases and Abnormalities	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24716661&form=6&db=m	Glycosylation, Hypogammaglobulinemia, and Resistance to Viral Infections.	causal interaction,unassigned	2,0	
3.2.1.106	Congenital, Hereditary, and Neonatal Diseases and Abnormalities	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30587846&form=6&db=m	Compound heterozygous variants in MOGS inducing congenital disorders of glycosylation (CDG) IIb.	therapeutic application,unassigned	1,0	
3.2.1.106	Congenital, Hereditary, and Neonatal Diseases and Abnormalities	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32246563&form=6&db=m	Mannosyl-oligosaccharide glucosidase - congenital disorder of glycosylation: A patient with novel variants.	causal interaction,unassigned	3,0	
3.2.1.106	Congenital, Hereditary, and Neonatal Diseases and Abnormalities	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33245474&form=6&db=m	N-Glycan Modification in Covid-19 Pathophysiology: In vitro Structural Changes with Limited Functional Effects.	unassigned	-	
3.2.1.106	Cystic Fibrosis	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3071437&form=6&db=m	Alterations in specific activity of lysosomal alpha-glucosidase in cystic fibrosis.	causal interaction,diagnostic usage,ongoing research,therapeutic application	4,3,4,4	
3.2.1.106	Cystic Fibrosis	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7030525&form=6&db=m	Activity levels and properties of acid alpha-glucosidase from liver and neutral alpha-glucosidase from sera of cystic fibrosis patients and controls.	causal interaction,diagnostic usage,ongoing research,unassigned	3,3,4,0	
3.2.1.106	Deglutition Disorders	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27344650&form=6&db=m	Swallow Prognosis and Follow-Up Protocol in Infantile Onset Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Genetic Diseases, Inborn	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22658377&form=6&db=m	Transcriptional response to GAA deficiency (Pompe disease) in infantile-onset patients.	causal interaction,unassigned	4,0	
3.2.1.106	Genetic Diseases, Inborn	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31026687&form=6&db=m	A human induced pluripotent stem cell line (TRNDi007-B) from an infantile onset Pompe patient carrying p.R854X mutation in the GAA gene.	causal interaction,unassigned	3,0	
3.2.1.106	Genetic Diseases, Inborn	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31341956&form=6&db=m	Mobility assessment using wearable technology in patients with late-onset Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Genetic Diseases, Inborn	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31867331&form=6&db=m	DeepNEU: Artificially Induced Stem Cell (aiPSC) and Differentiated Skeletal Muscle Cell (aiSkMC) Simulations of Infantile Onset POMPE Disease (IOPD) for Potential Biomarker Identification and Drug Discovery.	causal interaction,unassigned	2,0	
3.2.1.106	Genetic Diseases, Inborn	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32129012&form=6&db=m	Follow-up of late-onset Pompe disease patients with muscle magnetic resonance imaging reveals increase in fat replacement in skeletal muscles.	causal interaction,unassigned	4,0	
3.2.1.106	Glioma	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15170390&form=6&db=m	Lipoprotein receptor binding, cellular uptake, and lysosomal delivery of fusions between the receptor-associated protein (RAP) and alpha-L-iduronidase or acid alpha-glucosidase.	ongoing research,unassigned	3,0	
3.2.1.106	Glomerulonephritis, Membranous	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15466083&form=6&db=m	Nephrotic syndrome complicating alpha-glucosidase replacement therapy for Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	2,4,4,0	
3.2.1.106	glucan 1,4-alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=377133&form=6&db=m	Infantile and adult-onset acid maltase deficiency occurring in the same family.	causal interaction,unassigned	3,0	
3.2.1.106	glucan 1,4-alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1795162&form=6&db=m	Cardiomyopathy, mental retardation, and autophagic vacuolar myopathy. Abnormal MRI findings in the head.	causal interaction,unassigned	4,0	
3.2.1.106	glucan 1,4-alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2506448&form=6&db=m	Mature 98,000-dalton acid alpha-glucosidase is deficient in Japanese quails with acid maltase deficiency.	causal interaction,ongoing research,unassigned	4,4,0	
3.2.1.106	glucan 1,4-alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3090432&form=6&db=m	Developmental study of alpha-glucosidases in Japanese quails with acid maltase deficiency.	causal interaction,diagnostic usage,ongoing research,unassigned	1,3,2,0	
3.2.1.106	glucan 1,4-alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9002085&form=6&db=m	Skeletal muscle weakness and dysphagia caused by acid maltase deficiency: nutritional consequences of coincident celiac sprue.	causal interaction,unassigned	4,0	
3.2.1.106	glucan 1,4-alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9196050&form=6&db=m	Glycogen-storage disease type II (acid maltase deficiency): identification of a novel small deletion (delCC482+483) in French patients.	causal interaction,unassigned	4,0	
3.2.1.106	glucan 1,4-alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17084921&form=6&db=m	Increased aortic stiffness in glycogenosis type 2 (Pompe's disease).	causal interaction,unassigned	4,0	
3.2.1.106	glucan 1,4-alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19771425&form=6&db=m	Adult onset glycogen storage disease type II (adult onset Pompe disease): report and magnetic resonance images of two cases.	causal interaction,unassigned	4,0	
3.2.1.106	glucan 1,4-alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22676651&form=6&db=m	A cross-sectional single-centre study on Pompe disease in 42 German patients: Molecular analysis of the GAA gene, manifestation and genotype-phenotype correlations.	causal interaction,diagnostic usage,ongoing research,unassigned	4,2,4,0	
3.2.1.106	glucan 1,4-alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23305799&form=6&db=m	Detection of c. -32T>G (IVS1-13T>G) mutation of Pompe disease by real-time PCR in dried blood spot specimen.	causal interaction,unassigned	4,0	
3.2.1.106	glucan 1,4-alpha-glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24399863&form=6&db=m	Clinical features of Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4245&form=6&db=m	Physico-chemical and immunological properties of acid alpha-glucosidase from various human tissues in relation to glycogenosis type II (Pompe's disease).	ongoing research,therapeutic application,unassigned	3,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=350041&form=6&db=m	Biochemical, immunological, and cell genetic studies in glycogenosis type II.	diagnostic usage,ongoing research,unassigned	1,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=388444&form=6&db=m	Genetics of type II glycogenosis: assignment of the human gene for acid alpha-glucosidase to chromosome 17.	causal interaction,ongoing research,therapeutic application,unassigned	1,4,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=615485&form=6&db=m	Possibilities for the cytochemical diagnosis of enzymopathies.	causal interaction,therapeutic application,unassigned	1,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1418627&form=6&db=m	Recombinant human acid alpha-glucosidase generated in bacteria: antigenic, but enzymatically inactive.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1991835&form=6&db=m	Intravenous administration of phosphorylated acid alpha-glucosidase leads to uptake of enzyme in heart and skeletal muscle of mice.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2111708&form=6&db=m	Sequence of the cDNA and 5'-flanking region for human acid alpha-glucosidase, detection of an intron in the 5' untranslated leader sequence, definition of 18-bp polymorphisms, and differences with previous cDNA and amino acid sequences.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2235132&form=6&db=m	Rat heart perfusion as model system for enzyme replacement therapy in glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2256108&form=6&db=m	Leucocyte alpha-1,4- and alpha-1,6-glucosidase activities towards oligosaccharides in late onset glycogenosis type II.	diagnostic usage,ongoing research,therapeutic application,unassigned	1,1,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2403755&form=6&db=m	Adult and infantile glycogenosis type II in one family, explained by allelic diversity.	causal interaction,ongoing research,unassigned	3,3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2500669&form=6&db=m	Lysosomal glycogen storage disease without deficiency of acid alpha-glucosidase.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2506448&form=6&db=m	Mature 98,000-dalton acid alpha-glucosidase is deficient in Japanese quails with acid maltase deficiency.	causal interaction,ongoing research,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2546700&form=6&db=m	Effects of N-hydroxyethyl-1-deoxynojirimycin (BAY m 1099) on the activity of neutral- and acid alpha-glucosidases in human fibroblasts and HepG2 cells.	therapeutic application,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2662474&form=6&db=m	Partial characterization of leucocyte alpha-glucosidase in late onset glycogenosis type II.	causal interaction,diagnostic usage,ongoing research,unassigned	3,4,3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2947052&form=6&db=m	Severe course of glycogen storage disease type II (Pompe's disease) without development of cardiomegalia.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3098466&form=6&db=m	First trimester diagnosis of Pompe's disease (glycogenosis type II) with normal outcome: assay of acid alpha-glucosidase in chorionic villous biopsy using antibodies.	diagnostic usage,ongoing research,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3108320&form=6&db=m	Clinical diversity in glycogenosis type II. Biosynthesis and in situ localization of acid alpha-glucosidase in mutant fibroblasts.	causal interaction,diagnostic usage,ongoing research,unassigned	4,3,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3159730&form=6&db=m	Defects in synthesis, phosphorylation, and maturation of acid alpha-glucosidase in glycogenosis type II.	causal interaction,ongoing research,unassigned	3,3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3282727&form=6&db=m	A family with pseudodeficiency of acid alpha-glucosidase.	causal interaction,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3302116&form=6&db=m	Breakdown of lysosomal glycogen in cultured fibroblasts from glycogenosis type II patients after uptake of acid alpha-glucosidase.	diagnostic usage,ongoing research,unassigned	3,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3304722&form=6&db=m	A simple differential immunoprecipitation assay of urinary acid and neutral alpha-glucosidases for glycogenosis II.	diagnostic usage,therapeutic application,unassigned	4,2,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3519597&form=6&db=m	Isolation and characterization of three alpha-glucosidases from the Japanese quail.	ongoing research,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3899727&form=6&db=m	Bovine generalised glycogenosis type II. Uptake of lysosomal alpha-glucosidase by cultured skeletal muscle and reversal of glycogen accumulation.	ongoing research,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3935646&form=6&db=m	Neutral oligosaccharides in the urine of a patient with glycogen storage disease type II.	unassigned	-	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6237928&form=6&db=m	Uptake and stability of human and bovine acid alpha-glucosidase in cultured fibroblasts and skeletal muscle cells from glycogenosis type II patients.	diagnostic usage,ongoing research,unassigned	3,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6304667&form=6&db=m	Glycogen storage disease. Studies related to the mechanism of glycogenosome formation.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6391168&form=6&db=m	Biochemical genetics of the Lapland dog model of glycogen storage disease type II (acid alpha-glucosidase deficiency).	causal interaction,diagnostic usage,ongoing research,therapeutic application	3,3,4,2	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6754447&form=6&db=m	Adult forms of glycogenosis type II. A defect in an early stage of acid alpha-glucosidase realization.	causal interaction,diagnostic usage,ongoing research,unassigned	4,3,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6761145&form=6&db=m	Biosynthesis of acid alpha-glucosidase in late-onset forms of glycogenosis type II (Pompe's disease).	causal interaction,diagnostic usage,ongoing research,unassigned	1,3,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7603531&form=6&db=m	Genetic defects in patients with glycogenosis type II (acid maltase deficiency).	causal interaction,diagnostic usage,unassigned	3,3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7717400&form=6&db=m	Leaky splicing mutation in the acid maltase gene is associated with delayed onset of glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8173350&form=6&db=m	Bovine glycogenosis type II: the molecular defect in Shorthorn cattle.	unassigned	-	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8411709&form=6&db=m	[Pompe's disease--acid alpha-glucosidase deficiency--a review]	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8439343&form=6&db=m	Biochemical genetics of glycogenosis type II in Brahman cattle.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8575451&form=6&db=m	Isolation and characterisation of a recombinant, precursor form of lysosomal acid alpha-glucosidase.	causal interaction,ongoing research,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8577039&form=6&db=m	[Glycogenosis type II; acid alpha-glucosidase deficiency]	unassigned	-	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8843344&form=6&db=m	Expression of catalytically active human multifunctional glycogen-debranching enzyme and lysosomal acid alpha-glucosidase in insect cells.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8884087&form=6&db=m	Homozygous deletion of exon 18 leads to degradation of the lysosomal alpha-glucosidase precursor and to the infantile form of glycogen storage disease type II.	ongoing research,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9259196&form=6&db=m	Glycogenosis type II: a juvenile-specific mutation with an unusual splicing pattern and a shared mutation in African Americans.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9266392&form=6&db=m	A novel acid alpha-glucosidase mutation identified in a Pakistani family with glycogen storage disease type II.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9322088&form=6&db=m	Retroviral transfer of acid alpha-glucosidase cDNA to enzyme-deficient myoblasts results in phenotypic spread of the genotypic correction by both secretion and fusion.	causal interaction,therapeutic application,unassigned	3,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9384603&form=6&db=m	Generalized glycogen storage and cardiomegaly in a knockout mouse model of Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	4,1,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9505277&form=6&db=m	Recombinant human acid alpha-glucosidase corrects acid alpha-glucosidase-deficient human fibroblasts, quail fibroblasts, and quail myoblasts.	causal interaction,therapeutic application,unassigned	3,3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9535769&form=6&db=m	Glycogen storage disease type II: identification of four novel missense mutations (D645N, G648S, R672W, R672Q) and two insertions/deletions in the acid alpha-glucosidase locus of patients of differing phenotype.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9668092&form=6&db=m	Targeted disruption of the acid alpha-glucosidase gene in mice causes an illness with critical features of both infantile and adult human glycogen storage disease type II.	causal interaction,ongoing research,unassigned	1,3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9736771&form=6&db=m	Adenovirus-mediated transfer of the acid alpha-glucosidase gene into fibroblasts, myoblasts and myotubes from patients with glycogen storage disease type II leads to high level expression of enzyme and corrects glycogen accumulation.	causal interaction,ongoing research,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9736785&form=6&db=m	Recombinant human acid alpha-glucosidase: high level production in mouse milk, biochemical characteristics, correction of enzyme deficiency in GSDII KO mice.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10071199&form=6&db=m	A large Alu-mediated deletion, identified by PCR, as the molecular basis for glycogen storage disease type II (GSDII).	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10377006&form=6&db=m	Increased occurrence of cleft lip in glycogen storage disease type II (GSDII): exclusion of a contiguous gene syndrome in two patients by presence of intragenic mutations including a novel nonsense mutation Gln58Stop.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10545593&form=6&db=m	Human acid alpha-glucosidase from rabbit milk has therapeutic effect in mice with glycogen storage disease type II.	diagnostic usage,ongoing research,therapeutic application,unassigned	3,4,3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10838256&form=6&db=m	Modulation of disease severity in mice with targeted disruption of the acid alpha-glucosidase gene.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10840383&form=6&db=m	Towards a molecular therapy for glycogen storage disease type II (Pompe disease).	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10899751&form=6&db=m	Evidence for a founder effect in Sicilian patients with glycogen storage disease type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11286229&form=6&db=m	Recombinant human acid alpha-glucosidase enzyme therapy for infantile glycogen storage disease type II: results of a phase I/II clinical trial.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11343339&form=6&db=m	Aberrant splicing at catalytic site as cause of infantile onset glycogen storage disease type II (GSDII): molecular identification of a novel IVS9 (+2GT-->GC) in combination with rare IVS10 (+1GT-->CT).	unassigned	-	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11552029&form=6&db=m	Intractable fever and cortical neuronal glycogen storage in glycogenosis type 2.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11738358&form=6&db=m	Identification of six novel mutations in the acid alpha-glucosidase gene in three Spanish patients with infantile onset glycogen storage disease type II (Pompe disease).	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11949932&form=6&db=m	Acid alpha-glucosidase deficiency (glycogenosis type II, Pompe disease).	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12075008&form=6&db=m	Muscle as a putative producer of acid alpha-glucosidase for glycogenosis type II gene therapy.	therapeutic application,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12115977&form=6&db=m	Impaired performance of skeletal muscle in alpha-glucosidase knockout mice.	unassigned	-	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12601120&form=6&db=m	Juvenile-onset glycogen storage disease type II with novel mutations in acid alpha-glucosidase gene.	unassigned	-	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12727109&form=6&db=m	Packaging of an AAV vector encoding human acid alpha-glucosidase for gene therapy in glycogen storage disease type II with a modified hybrid adenovirus-AAV vector.	ongoing research,therapeutic application,unassigned	2,2,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14643388&form=6&db=m	New GAA mutations in Japanese patients with GSDII (Pompe disease).	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14695532&form=6&db=m	Twenty-two novel mutations in the lysosomal alpha-glucosidase gene (GAA) underscore the genotype-phenotype correlation in glycogen storage disease type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14707516&form=6&db=m	Efficacy of multidisciplinary approach in the treatment of two cases of nonclassical infantile glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14972326&form=6&db=m	Glycogenosis type II: identification and expression of three novel mutations in the acid alpha-glucosidase gene causing the infantile form of the disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15031984&form=6&db=m	[Therapy for myopathies: from management to genetic treatment: introductory remarks]	ongoing research,therapeutic application,unassigned	1,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15057961&form=6&db=m	Detection of a homozygous D645E mutation of the acid alpha-glucosidase gene and glycogen deposition in tissues in a second-trimester fetus with infantile glycogen storage disease type II.	unassigned	-	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15169761&form=6&db=m	Rescue of enzyme deficiency in embryonic diaphragm in a mouse model of metabolic myopathy: Pompe disease.	causal interaction,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15366815&form=6&db=m	Infantile-onset glycogen storage disease type II (Pompe disease): report of a case with genetic diagnosis and pathological findings.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15659425&form=6&db=m	Clinical manifestation and natural course of late-onset Pompe's disease in 54 Dutch patients.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15668445&form=6&db=m	Mutations in the acid alpha-glucosidase gene (M. Pompe) in a patient with an unusual phenotype.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15703490&form=6&db=m	Impact of humoral immune response on distribution and efficacy of recombinant adeno-associated virus-derived acid alpha-glucosidase in a model of glycogen storage disease type II.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15920463&form=6&db=m	Sustained correction of glycogen storage disease type II using adeno-associated virus serotype 1 vectors.	unassigned	-	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15922959&form=6&db=m	Correction of glycogen storage disease type II by an adeno-associated virus vector containing a muscle-specific promoter.	causal interaction,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16005263&form=6&db=m	Evasion of immune responses to introduced human acid alpha-glucosidase by liver-restricted expression in glycogen storage disease type II.	causal interaction,ongoing research,unassigned	4,2,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16372321&form=6&db=m	Age-related morphological changes in skeletal muscle cells of acid alpha-glucosidase knockout mice.	unassigned	-	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16702879&form=6&db=m	Electrocardiographic response to enzyme replacement therapy for Pompe disease.	causal interaction,diagnostic usage,ongoing research,therapeutic application	4,2,4,2	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16917947&form=6&db=m	Mutation profile of the GAA gene in 40 Italian patients with late onset glycogen storage disease type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16987711&form=6&db=m	Enhanced efficacy of an AAV vector encoding chimeric, highly secreted acid alpha-glucosidase in glycogen storage disease type II.	causal interaction,therapeutic application,unassigned	3,2,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17084921&form=6&db=m	Increased aortic stiffness in glycogenosis type 2 (Pompe's disease).	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17092519&form=6&db=m	Two new missense mutations of GAA in late onset glycogen storage disease type II.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17095274&form=6&db=m	Chemical chaperones improve transport and enhance stability of mutant alpha-glucosidases in glycogen storage disease type II.	causal interaction,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17210890&form=6&db=m	Broad spectrum of Pompe disease in patients with the same c.-32-13T->G haplotype.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17616415&form=6&db=m	Glycogen storage disease type II in Spanish patients: high frequency of c.1076-1G>C mutation.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17723315&form=6&db=m	Development of a clinical assay for detection of GAA mutations and characterization of the GAA mutation spectrum in a Canadian cohort of individuals with glycogen storage disease, type II.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17915575&form=6&db=m	Molecular genetics of late onset glycogen storage disease II in Italy.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18176891&form=6&db=m	Adult glycogenosis type II (Pompe's disease): morphological abnormalities in muscle and skin biopsies compared with acid alpha-glucosidase activity.	ongoing research,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18425781&form=6&db=m	Update of the Pompe disease mutation database with 107 sequence variants and a format for severity rating.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18458862&form=6&db=m	Identification of eight novel mutations of the acid alpha-glucosidase gene causing the infantile or juvenile form of glycogen storage disease type II.	unassigned	-	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18505932&form=6&db=m	Hematopoietic contribution to skeletal muscle regeneration in acid alpha-glucosidase knockout mice.	ongoing research,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18508267&form=6&db=m	Eight years experience with enzyme replacement therapy in two children and one adult with Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18535739&form=6&db=m	Report of the first Brazilian infantile Pompe disease patient to be treated with recombinant human acid alpha-glucosidase.	ongoing research,therapeutic application,unassigned	3,2,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18560415&form=6&db=m	Correction of multiple striated muscles in murine Pompe disease through adeno-associated virus-mediated gene therapy.	causal interaction,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18704279&form=6&db=m	Enzyme replacement therapy in severe adult-onset glycogen storage disease type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18782850&form=6&db=m	Modulation of glycogen synthesis by RNA interference: towards a new therapeutic approach for glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18810562&form=6&db=m	Correction of glycogenosis type 2 by muscle-specific lentiviral vector.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19019308&form=6&db=m	Therapeutic approaches in glycogen storage disease type II/Pompe Disease.	causal interaction,therapeutic application,unassigned	4,3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19263466&form=6&db=m	Partial phenotypic correction and immune tolerance induction to enzyme replacement therapy after hematopoietic stem cell gene transfer of alpha-glucosidase in Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	3,2,2,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19362502&form=6&db=m	High frequency of acid alpha-glucosidase pseudodeficiency complicates newborn screening for glycogen storage disease type II in the Japanese population.	causal interaction,diagnostic usage,ongoing research,therapeutic application	2,3,3,1	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19533645&form=6&db=m	Screening for Pompe disease using a rapid dried blood spot method: experience of a clinical diagnostic laboratory.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19649685&form=6&db=m	Enzyme replacement therapy with alglucosidase alfa in 44 patients with late-onset glycogen storage disease type 2: 12-month results of an observational clinical trial.	causal interaction,ongoing research,therapeutic application,unassigned	4,2,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19665008&form=6&db=m	Immortalization of murine muscle cells from lysosomal alpha-glucosidase deficient mice: a new tool to study pathophysiology and assess therapeutic strategies for Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	3,4,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19707330&form=6&db=m	A review of treatment of Pompe disease in infants.	causal interaction,ongoing research,therapeutic application,unassigned	4,1,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19771425&form=6&db=m	Adult onset glycogen storage disease type II (adult onset Pompe disease): report and magnetic resonance images of two cases.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19959526&form=6&db=m	Restoration of muscle functionality by genetic suppression of glycogen synthesis in a murine model of Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19966354&form=6&db=m	Enzyme replacement therapy for infantile Pompe disease during the critical period and identification of a novel mutation.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20441705&form=6&db=m	[Establishment and clinical application of dried blood spots and mixed leukocytes for determination of acid alpha-glucosidase activity.]	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20554235&form=6&db=m	Inhibition of glycogen biosynthesis via mTORC1 suppression as an adjunct therapy for Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20838899&form=6&db=m	Long-term observational, non-randomized study of enzyme replacement therapy in late-onset glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22253254&form=6&db=m	Autophagy and mitochondria in Pompe disease: nothing is so new as what has long been forgotten.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22572506&form=6&db=m	Two cases of Pompe's disease: case report and review of literature.	causal interaction,diagnostic usage,therapeutic application,unassigned	4,3,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22926164&form=6&db=m	Enzyme replacement therapy in late-onset Pompe disease: a systematic literature review.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23606558&form=6&db=m	Transcription factor EB (TFEB) is a new therapeutic target for Pompe disease.	causal interaction,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23839583&form=6&db=m	Enzyme Replacement Therapy Improves Respiratory Outcomes in Patients with Late-Onset Type II Glycogenosis and High Ventilator Dependency.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24169249&form=6&db=m	[Clinical features and acid alpha-glucosidase gene mutation in 7 Chinese patients with glycogen storage disease type II].	diagnostic usage,ongoing research,unassigned	2,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24399863&form=6&db=m	Clinical features of Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24399865&form=6&db=m	Non-muscle involvement in late-onset glycogenosis II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24495340&form=6&db=m	Glycogenosome accumulation in the arrector pili muscle in Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25323875&form=6&db=m	Late-onset Glycogen Storage Disease type 2.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25336838&form=6&db=m	A complex craniovertebral junction malformation in a patient with late onset glycogenosis 2.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26353478&form=6&db=m	Use of Polylactide-Co-Glycolide-Nanoparticles for Lysosomal Delivery of a Therapeutic Enzyme in Glycogenosis Type II Fibroblasts.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28629821&form=6&db=m	Glycogen Reduction in Myotubes of Late-Onset Pompe Disease Patients Using Antisense Technology.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28694071&form=6&db=m	First clinical and genetic description of a family diagnosed with late-onset Pompe disease from Costa Rica.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29435968&form=6&db=m	[A new phenotype of infantile-onset Pompe disease].	unassigned	-	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30770309&form=6&db=m	Reevaluating the pathogenicity of the mutation c.1194 +5 G>A in GAA gene by functional analysis of RNA in a 61-year-old woman diagnosed with Pompe disease by muscle biopsy.	causal interaction,diagnostic usage,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31439017&form=6&db=m	Comprehensive approach to weaning in difficult-to-wean infantile and juvenile-onset glycogen-storage disease type II patients: a case series.	unassigned	-	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31713816&form=6&db=m	Molecular Approaches for the Treatment of Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32962155&form=6&db=m	Pompe Disease: New Developments in an Old Lysosomal Storage Disorder.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34220802&form=6&db=m	Immune Tolerance-Adjusted Personalized Immunogenicity Prediction for Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4245&form=6&db=m	Physico-chemical and immunological properties of acid alpha-glucosidase from various human tissues in relation to glycogenosis type II (Pompe's disease).	ongoing research,therapeutic application,unassigned	3,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34626&form=6&db=m	Characterization of the molecular defect in infantile and adult acid alpha-glucosidase deficiency fibroblasts.	causal interaction,diagnostic usage,ongoing research,therapeutic application	3,4,4,2	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=36157&form=6&db=m	Use of immobilized antibodies in investigating acid alpha-glucosidase in urine in relation to Pompe's disease.	diagnostic usage,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=60470&form=6&db=m	Acid maltase deficiency in non-identical adult twins. A morphological and biochemical study.	ongoing research,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=350041&form=6&db=m	Biochemical, immunological, and cell genetic studies in glycogenosis type II.	diagnostic usage,ongoing research,unassigned	1,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=352582&form=6&db=m	Pompe's disease: diagnosis in kidney and leucocytes using 4-methylumbelliferyl-alpha-D-glucopyranoside.	diagnostic usage,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=377133&form=6&db=m	Infantile and adult-onset acid maltase deficiency occurring in the same family.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=788807&form=6&db=m	Glycogen storage diseases.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1418627&form=6&db=m	Recombinant human acid alpha-glucosidase generated in bacteria: antigenic, but enzymatically inactive.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1795162&form=6&db=m	Cardiomyopathy, mental retardation, and autophagic vacuolar myopathy. Abnormal MRI findings in the head.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1822357&form=6&db=m	Natural bone marrow transplantation in cattle with Pompe's disease.	therapeutic application,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1991835&form=6&db=m	Intravenous administration of phosphorylated acid alpha-glucosidase leads to uptake of enzyme in heart and skeletal muscle of mice.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2111708&form=6&db=m	Sequence of the cDNA and 5'-flanking region for human acid alpha-glucosidase, detection of an intron in the 5' untranslated leader sequence, definition of 18-bp polymorphisms, and differences with previous cDNA and amino acid sequences.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2235132&form=6&db=m	Rat heart perfusion as model system for enzyme replacement therapy in glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2256108&form=6&db=m	Leucocyte alpha-1,4- and alpha-1,6-glucosidase activities towards oligosaccharides in late onset glycogenosis type II.	diagnostic usage,ongoing research,therapeutic application,unassigned	1,1,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2403755&form=6&db=m	Adult and infantile glycogenosis type II in one family, explained by allelic diversity.	causal interaction,ongoing research,unassigned	3,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2506448&form=6&db=m	Mature 98,000-dalton acid alpha-glucosidase is deficient in Japanese quails with acid maltase deficiency.	causal interaction,ongoing research,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2546700&form=6&db=m	Effects of N-hydroxyethyl-1-deoxynojirimycin (BAY m 1099) on the activity of neutral- and acid alpha-glucosidases in human fibroblasts and HepG2 cells.	therapeutic application,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2662474&form=6&db=m	Partial characterization of leucocyte alpha-glucosidase in late onset glycogenosis type II.	causal interaction,diagnostic usage,ongoing research,unassigned	3,4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2947052&form=6&db=m	Severe course of glycogen storage disease type II (Pompe's disease) without development of cardiomegalia.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3063423&form=6&db=m	[Adult Pompe disease with normal acid alpha-glucosidase activity in leukocytes]	causal interaction,diagnostic usage,ongoing research,unassigned	4,1,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3090432&form=6&db=m	Developmental study of alpha-glucosidases in Japanese quails with acid maltase deficiency.	causal interaction,diagnostic usage,ongoing research,unassigned	1,3,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3093639&form=6&db=m	Acid maltase deficiency: a case study and review of the pathophysiological changes and proposed therapeutic measures.	causal interaction,therapeutic application,unassigned	2,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3098466&form=6&db=m	First trimester diagnosis of Pompe's disease (glycogenosis type II) with normal outcome: assay of acid alpha-glucosidase in chorionic villous biopsy using antibodies.	diagnostic usage,ongoing research,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3108320&form=6&db=m	Clinical diversity in glycogenosis type II. Biosynthesis and in situ localization of acid alpha-glucosidase in mutant fibroblasts.	causal interaction,diagnostic usage,ongoing research,unassigned	4,3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3152090&form=6&db=m	[Acid alpha-glucosidase deficiency: Pompe's disease]	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3159730&form=6&db=m	Defects in synthesis, phosphorylation, and maturation of acid alpha-glucosidase in glycogenosis type II.	causal interaction,ongoing research,unassigned	3,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3282727&form=6&db=m	A family with pseudodeficiency of acid alpha-glucosidase.	causal interaction,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3302116&form=6&db=m	Breakdown of lysosomal glycogen in cultured fibroblasts from glycogenosis type II patients after uptake of acid alpha-glucosidase.	diagnostic usage,ongoing research,unassigned	3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3519597&form=6&db=m	Isolation and characterization of three alpha-glucosidases from the Japanese quail.	ongoing research,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3549635&form=6&db=m	Subcellular distribution of acid alpha-glucosidase in fibroblasts and of antigenically cross-reactive material in Pompe's disease fibroblasts.	causal interaction,diagnostic usage,ongoing research,unassigned	1,3,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3899727&form=6&db=m	Bovine generalised glycogenosis type II. Uptake of lysosomal alpha-glucosidase by cultured skeletal muscle and reversal of glycogen accumulation.	ongoing research,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3935646&form=6&db=m	Neutral oligosaccharides in the urine of a patient with glycogen storage disease type II.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4611528&form=6&db=m	Enzyme replacement in Pompe disease: an attempt with purified human acid alpha-glucosidase.	ongoing research,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6237928&form=6&db=m	Uptake and stability of human and bovine acid alpha-glucosidase in cultured fibroblasts and skeletal muscle cells from glycogenosis type II patients.	diagnostic usage,ongoing research,unassigned	3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6347982&form=6&db=m	Immunohistochemical demonstration of acid alpha-glucosidase in muscle in Pompe's disease.	ongoing research,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6391168&form=6&db=m	Biochemical genetics of the Lapland dog model of glycogen storage disease type II (acid alpha-glucosidase deficiency).	causal interaction,diagnostic usage,ongoing research,therapeutic application	3,3,4,2	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6401921&form=6&db=m	Genetic heterogeneity in acid alpha-glucosidase deficiency.	causal interaction,diagnostic usage,ongoing research,therapeutic application	2,3,2,1	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6418414&form=6&db=m	Acid alpha-glucosidase deficiency in cultured fibroblasts with phenotype 2 of acid alpha-glucosidase.	causal interaction,diagnostic usage,ongoing research,unassigned	4,3,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6435005&form=6&db=m	The effect of age on biochemical and morphological changes in the semitendinosus muscle of cattle with generalized glycogenosis type II.	diagnostic usage,ongoing research,unassigned	4,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6442343&form=6&db=m	Demonstration of acid alpha-glucosidase in different types of Pompe disease by use of an immunochemical method.	ongoing research,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6754447&form=6&db=m	Adult forms of glycogenosis type II. A defect in an early stage of acid alpha-glucosidase realization.	causal interaction,diagnostic usage,ongoing research,unassigned	4,3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6761145&form=6&db=m	Biosynthesis of acid alpha-glucosidase in late-onset forms of glycogenosis type II (Pompe's disease).	causal interaction,diagnostic usage,ongoing research,unassigned	1,3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7037230&form=6&db=m	Human amniotic fluid alpha-glucosidase.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7603531&form=6&db=m	Genetic defects in patients with glycogenosis type II (acid maltase deficiency).	causal interaction,diagnostic usage,unassigned	3,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8173350&form=6&db=m	Bovine glycogenosis type II: the molecular defect in Shorthorn cattle.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8214335&form=6&db=m	Computed tomography and magnetic resonance imaging of affected muscle in childhood acid alpha-glucosidase deficiency: a case report.	causal interaction,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8411709&form=6&db=m	[Pompe's disease--acid alpha-glucosidase deficiency--a review]	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8439343&form=6&db=m	Biochemical genetics of glycogenosis type II in Brahman cattle.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8552676&form=6&db=m	High-level production of recombinant human lysosomal acid alpha-glucosidase in Chinese hamster ovary cells which targets to heart muscle and corrects glycogen accumulation in fibroblasts from patients with Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8575451&form=6&db=m	Isolation and characterisation of a recombinant, precursor form of lysosomal acid alpha-glucosidase.	causal interaction,ongoing research,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8577039&form=6&db=m	[Glycogenosis type II; acid alpha-glucosidase deficiency]	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8834250&form=6&db=m	Acid alpha-glucosidase deficiency: identification and expression of a missense mutation (S529V) in a Japanese adult phenotype.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8870826&form=6&db=m	Pathological study of Japanese quail embryo with acid alpha-glucosidase deficiency during early development.	ongoing research,therapeutic application,unassigned	2,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8884087&form=6&db=m	Homozygous deletion of exon 18 leads to degradation of the lysosomal alpha-glucosidase precursor and to the infantile form of glycogen storage disease type II.	ongoing research,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8986097&form=6&db=m	[Chronic respiratory failure in a case with juvenile-onset acid alpha-glucosidase deficiency; successful therapy with nasal intermittent positive pressure ventilation (NIPPV)]	causal interaction,therapeutic application,unassigned	4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9002085&form=6&db=m	Skeletal muscle weakness and dysphagia caused by acid maltase deficiency: nutritional consequences of coincident celiac sprue.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9196050&form=6&db=m	Glycogen-storage disease type II (acid maltase deficiency): identification of a novel small deletion (delCC482+483) in French patients.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9259196&form=6&db=m	Glycogenosis type II: a juvenile-specific mutation with an unusual splicing pattern and a shared mutation in African Americans.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9266392&form=6&db=m	A novel acid alpha-glucosidase mutation identified in a Pakistani family with glycogen storage disease type II.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9352080&form=6&db=m	Purification of recombinant human precursor acid alpha-glucosidase.	ongoing research,therapeutic application,unassigned	2,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9382133&form=6&db=m	Nosology of lysosomal glycogen storage diseases without in vitro acid maltase deficiency. Delineation of a neonatal form.	causal interaction,diagnostic usage,therapeutic application,unassigned	4,3,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9384603&form=6&db=m	Generalized glycogen storage and cardiomegaly in a knockout mouse model of Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	4,1,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9466978&form=6&db=m	Clinical and metabolic correction of pompe disease by enzyme therapy in acid maltase-deficient quail.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9505277&form=6&db=m	Recombinant human acid alpha-glucosidase corrects acid alpha-glucosidase-deficient human fibroblasts, quail fibroblasts, and quail myoblasts.	causal interaction,therapeutic application,unassigned	3,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9535769&form=6&db=m	Glycogen storage disease type II: identification of four novel missense mutations (D645N, G648S, R672W, R672Q) and two insertions/deletions in the acid alpha-glucosidase locus of patients of differing phenotype.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9614571&form=6&db=m	Complete correction of acid alpha-glucosidase deficiency in Pompe disease fibroblasts in vitro, and lysosomally targeted expression in neonatal rat cardiac and skeletal muscle.	causal interaction,ongoing research,therapeutic application,unassigned	3,2,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9668092&form=6&db=m	Targeted disruption of the acid alpha-glucosidase gene in mice causes an illness with critical features of both infantile and adult human glycogen storage disease type II.	causal interaction,ongoing research,unassigned	1,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9736771&form=6&db=m	Adenovirus-mediated transfer of the acid alpha-glucosidase gene into fibroblasts, myoblasts and myotubes from patients with glycogen storage disease type II leads to high level expression of enzyme and corrects glycogen accumulation.	causal interaction,ongoing research,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9736785&form=6&db=m	Recombinant human acid alpha-glucosidase: high level production in mouse milk, biochemical characteristics, correction of enzyme deficiency in GSDII KO mice.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9883081&form=6&db=m	[Treatment of Pompe's disease with recombinant enzymes]	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10071199&form=6&db=m	A large Alu-mediated deletion, identified by PCR, as the molecular basis for glycogen storage disease type II (GSDII).	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10189220&form=6&db=m	Novel mutations in African American patients with glycogen storage disease Type II. Mutations in brief no. 209. Online.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10338092&form=6&db=m	Molecular genetic study of Pompe disease in Chinese patients in Taiwan.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10377006&form=6&db=m	Increased occurrence of cleft lip in glycogen storage disease type II (GSDII): exclusion of a contiguous gene syndrome in two patients by presence of intragenic mutations including a novel nonsense mutation Gln58Stop.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10545593&form=6&db=m	Human acid alpha-glucosidase from rabbit milk has therapeutic effect in mice with glycogen storage disease type II.	diagnostic usage,ongoing research,therapeutic application,unassigned	3,4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10838256&form=6&db=m	Modulation of disease severity in mice with targeted disruption of the acid alpha-glucosidase gene.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10840383&form=6&db=m	Towards a molecular therapy for glycogen storage disease type II (Pompe disease).	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10899751&form=6&db=m	Evidence for a founder effect in Sicilian patients with glycogen storage disease type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10973860&form=6&db=m	Determination of acid alpha-glucosidase protein: evaluation as a screening marker for Pompe disease and other lysosomal storage disorders.	diagnostic usage,ongoing research,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11027569&form=6&db=m	Correction of glycogen storage disease type II by enzyme replacement with a recombinant human acid maltase produced by over-expression in a CHO-DHFR(neg) cell line.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11078593&form=6&db=m	Liquid chromatographic assay for a glucose tetrasaccharide, a putative biomarker for the diagnosis of Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11268285&form=6&db=m	Intercellular transfer of the virally derived precursor form of acid alpha-glucosidase corrects the enzyme deficiency in inherited cardioskeletal myopathy Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11286229&form=6&db=m	Recombinant human acid alpha-glucosidase enzyme therapy for infantile glycogen storage disease type II: results of a phase I/II clinical trial.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11328962&form=6&db=m	Cardiac remodeling and contractile function in acid alpha-glucosidase knockout mice.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11343339&form=6&db=m	Aberrant splicing at catalytic site as cause of infantile onset glycogen storage disease type II (GSDII): molecular identification of a novel IVS9 (+2GT-->GC) in combination with rare IVS10 (+1GT-->CT).	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11405345&form=6&db=m	Enzyme therapy for pompe disease with recombinant human alpha-glucosidase from rabbit milk.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11425943&form=6&db=m	Surprises of genetic engineering: a possible model of polyglucosan body disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11468225&form=6&db=m	Determination of acid alpha-glucosidase activity in blood spots as a diagnostic test for Pompe disease.	causal interaction,diagnostic usage,therapeutic application,unassigned	4,4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11590121&form=6&db=m	Conditional tissue-specific expression of the acid alpha-glucosidase (GAA) gene in the GAA knockout mice: implications for therapy.	causal interaction,therapeutic application,unassigned	1,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11738358&form=6&db=m	Identification of six novel mutations in the acid alpha-glucosidase gene in three Spanish patients with infantile onset glycogen storage disease type II (Pompe disease).	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11949932&form=6&db=m	Acid alpha-glucosidase deficiency (glycogenosis type II, Pompe disease).	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12075008&form=6&db=m	Muscle as a putative producer of acid alpha-glucosidase for glycogenosis type II gene therapy.	therapeutic application,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12115977&form=6&db=m	Impaired performance of skeletal muscle in alpha-glucosidase knockout mice.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12188423&form=6&db=m	Clinical, pathological, and electron microscopic findings in two Thai children with Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12398843&form=6&db=m	Danon's disease (X-linked vacuolar cardiomyopathy and myopathy): a case with a novel Lamp-2 gene mutation.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12409258&form=6&db=m	Glycogen stored in skeletal but not in cardiac muscle in acid alpha-glucosidase mutant (Pompe) mice is highly resistant to transgene-encoded human enzyme.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12601120&form=6&db=m	Juvenile-onset glycogen storage disease type II with novel mutations in acid alpha-glucosidase gene.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12727109&form=6&db=m	Packaging of an AAV vector encoding human acid alpha-glucosidase for gene therapy in glycogen storage disease type II with a modified hybrid adenovirus-AAV vector.	ongoing research,therapeutic application,unassigned	2,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14643388&form=6&db=m	New GAA mutations in Japanese patients with GSDII (Pompe disease).	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14695532&form=6&db=m	Twenty-two novel mutations in the lysosomal alpha-glucosidase gene (GAA) underscore the genotype-phenotype correlation in glycogen storage disease type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14707516&form=6&db=m	Efficacy of multidisciplinary approach in the treatment of two cases of nonclassical infantile glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14972326&form=6&db=m	Glycogenosis type II: identification and expression of three novel mutations in the acid alpha-glucosidase gene causing the infantile form of the disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15031984&form=6&db=m	[Therapy for myopathies: from management to genetic treatment: introductory remarks]	ongoing research,therapeutic application,unassigned	1,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15048888&form=6&db=m	Enzyme replacement therapy in late-onset Pompe's disease: a three-year follow-up.	causal interaction,ongoing research,therapeutic application,unassigned	3,1,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15057961&form=6&db=m	Detection of a homozygous D645E mutation of the acid alpha-glucosidase gene and glycogen deposition in tissues in a second-trimester fetus with infantile glycogen storage disease type II.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15145338&form=6&db=m	A case of childhood Pompe disease demonstrating phenotypic variability of p.Asp645Asn.	diagnostic usage,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15169761&form=6&db=m	Rescue of enzyme deficiency in embryonic diaphragm in a mouse model of metabolic myopathy: Pompe disease.	causal interaction,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15292070&form=6&db=m	Direct multiplex assay of lysosomal enzymes in dried blood spots for newborn screening.	causal interaction,therapeutic application,unassigned	1,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15313146&form=6&db=m	Glycogen storage disease type II: enzymatic screening in dried blood spots on filter paper.	causal interaction,ongoing research,unassigned	4,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15366815&form=6&db=m	Infantile-onset glycogen storage disease type II (Pompe disease): report of a case with genetic diagnosis and pathological findings.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15383547&form=6&db=m	Conjugation of mannose 6-phosphate-containing oligosaccharides to acid alpha-glucosidase improves the clearance of glycogen in pompe mice.	causal interaction,diagnostic usage,therapeutic application,unassigned	4,2,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15466083&form=6&db=m	Nephrotic syndrome complicating alpha-glucosidase replacement therapy for Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	2,4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15520017&form=6&db=m	Lysosomal acid alpha-glucosidase consists of four different peptides processed from a single chain precursor.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15585405&form=6&db=m	Replacing acid alpha-glucosidase in Pompe disease: recombinant and transgenic enzymes are equipotent, but neither completely clears glycogen from type II muscle fibers.	causal interaction,ongoing research,therapeutic application,unassigned	4,2,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15637339&form=6&db=m	High-resolution light microscopy (HRLM) and digital analysis of Pompe disease pathology.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15639117&form=6&db=m	Safety and efficacy of recombinant acid alpha-glucosidase (rhGAA) in patients with classical infantile Pompe disease: results of a phase II clinical trial.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15659425&form=6&db=m	Clinical manifestation and natural course of late-onset Pompe's disease in 54 Dutch patients.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15668445&form=6&db=m	Mutations in the acid alpha-glucosidase gene (M. Pompe) in a patient with an unusual phenotype.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15703490&form=6&db=m	Impact of humoral immune response on distribution and efficacy of recombinant adeno-associated virus-derived acid alpha-glucosidase in a model of glycogen storage disease type II.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15839836&form=6&db=m	Carbohydrate-remodelled acid alpha-glucosidase with higher affinity for the cation-independent mannose 6-phosphate receptor demonstrates improved delivery to muscles of Pompe mice.	causal interaction,diagnostic usage,therapeutic application,unassigned	1,1,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15886040&form=6&db=m	Glucose tetrasaccharide as a biomarker for monitoring the therapeutic response to enzyme replacement therapy for Pompe disease.	causal interaction,diagnostic usage,ongoing research,therapeutic application	1,3,4,4	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15920463&form=6&db=m	Sustained correction of glycogen storage disease type II using adeno-associated virus serotype 1 vectors.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15922959&form=6&db=m	Correction of glycogen storage disease type II by an adeno-associated virus vector containing a muscle-specific promoter.	causal interaction,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15993875&form=6&db=m	Correlation of acid alpha-glucosidase and glycogen content in skin fibroblasts with age of onset in Pompe disease.	causal interaction,ongoing research,unassigned	4,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16005263&form=6&db=m	Evasion of immune responses to introduced human acid alpha-glucosidase by liver-restricted expression in glycogen storage disease type II.	causal interaction,ongoing research,unassigned	4,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16133732&form=6&db=m	The natural course of non-classic Pompe's disease; a review of 225 published cases.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16372321&form=6&db=m	Age-related morphological changes in skeletal muscle cells of acid alpha-glucosidase knockout mice.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16531044&form=6&db=m	Juvenile onset acid maltase deficiency presenting as a rigid spine syndrome.	causal interaction,diagnostic usage,therapeutic application,unassigned	3,3,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16532490&form=6&db=m	Dysfunction of endocytic and autophagic pathways in a lysosomal storage disease.	causal interaction,diagnostic usage,therapeutic application,unassigned	4,3,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16702879&form=6&db=m	Electrocardiographic response to enzyme replacement therapy for Pompe disease.	causal interaction,diagnostic usage,ongoing research,therapeutic application	4,2,4,2	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16702880&form=6&db=m	Comparison of maltose and acarbose as inhibitors of maltase-glucoamylase activity in assaying acid alpha-glucosidase activity in dried blood spots for the diagnosis of infantile Pompe disease.	causal interaction,diagnostic usage,therapeutic application,unassigned	1,2,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16702881&form=6&db=m	The use of acarbose inhibition in the measurement of acid alpha-glucosidase activity in blood lymphocytes for the diagnosis of Pompe disease.	diagnostic usage,ongoing research,therapeutic application,unassigned	3,3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16702882&form=6&db=m	Ambulatory electrocardiogram analysis in infants treated with recombinant human acid alpha-glucosidase enzyme replacement therapy for Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	4,3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16702883&form=6&db=m	Physical therapy management of Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16737883&form=6&db=m	A retrospective, multinational, multicenter study on the natural history of infantile-onset Pompe disease.	diagnostic usage,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16763908&form=6&db=m	Direct multiplex assay of enzymes in dried blood spots by tandem mass spectrometry for the newborn screening of lysosomal storage disorders.	diagnostic usage,therapeutic application,unassigned	3,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16782080&form=6&db=m	A novel missense mutation in the acid alpha-glucosidase gene causing the classic infantile form of Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16860134&form=6&db=m	Chinese hamster ovary cell-derived recombinant human acid alpha-glucosidase in infantile-onset Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	3,3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16874053&form=6&db=m	Autophagy and lysosomes in Pompe disease.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16898258&form=6&db=m	Pompe disease (glycogen storage disease type II): clinical features and enzyme replacement therapy.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16917947&form=6&db=m	Mutation profile of the GAA gene in 40 Italian patients with late onset glycogen storage disease type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16987711&form=6&db=m	Enhanced efficacy of an AAV vector encoding chimeric, highly secreted acid alpha-glucosidase in glycogen storage disease type II.	causal interaction,therapeutic application,unassigned	3,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17008131&form=6&db=m	Autophagy and mistargeting of therapeutic enzyme in skeletal muscle in Pompe disease.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17075580&form=6&db=m	Characterization of pre- and post-treatment pathology after enzyme replacement therapy for Pompe disease.	causal interaction,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17084921&form=6&db=m	Increased aortic stiffness in glycogenosis type 2 (Pompe's disease).	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17092519&form=6&db=m	Two new missense mutations of GAA in late onset glycogen storage disease type II.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17095274&form=6&db=m	Chemical chaperones improve transport and enhance stability of mutant alpha-glucosidases in glycogen storage disease type II.	causal interaction,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17151339&form=6&db=m	Recombinant human acid [alpha]-glucosidase: major clinical benefits in infantile-onset Pompe disease.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17175893&form=6&db=m	Monitoring cardiac function by B-type natriuretic peptide (BNP) in patients with infantile Pompe's disease treated with recombinant alpha-glucosidase.	ongoing research,therapeutic application,unassigned	1,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17210890&form=6&db=m	Broad spectrum of Pompe disease in patients with the same c.-32-13T->G haplotype.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17217857&form=6&db=m	Acid alpha-glucosidase deficiency (Pompe disease).	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17245350&form=6&db=m	Physiological Correction of Pompe Disease by Systemic Delivery of Adeno-associated Virus Serotype 1 Vectors.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17270480&form=6&db=m	Rapid diagnosis of late-onset Pompe disease by fluorometric assay of alpha-glucosidase activities in dried blood spots.	diagnostic usage,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17293352&form=6&db=m	N-glycans of recombinant human acid alpha-glucosidase expressed in the milk of transgenic rabbits.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17342521&form=6&db=m	Fractures in children with Pompe disease: a potential long-term complication.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17510371&form=6&db=m	Optimized preservation of CNS morphology for the identification of glycogen in the Pompe mouse model.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17546777&form=6&db=m	[Clinical development of acid alpha-glucosidase for the treatment of Pompe disease]	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17592248&form=6&db=m	Deconstructing pompe disease by analyzing single muscle fibers: to see a world in a grain of sand...''.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17596219&form=6&db=m	Cardiac arrhythmias following anesthesia induction in infantile-onset Pompe disease: a case series.	ongoing research,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17616415&form=6&db=m	Glycogen storage disease type II in Spanish patients: high frequency of c.1076-1G>C mutation.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17690063&form=6&db=m	Long-term enzyme replacement therapy for pompe disease with recombinant human alpha-glucosidase derived from chinese hamster ovary cells.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17723315&form=6&db=m	Development of a clinical assay for detection of GAA mutations and characterization of the GAA mutation spectrum in a Canadian cohort of individuals with glycogen storage disease, type II.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17805474&form=6&db=m	Structural and biochemical studies on Pompe disease and a "pseudodeficiency of acid alpha-glucosidase".	causal interaction,diagnostic usage,therapeutic application,unassigned	1,3,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17879614&form=6&db=m	[Enzyme replacement therapy in a patient with Pompe disease]	causal interaction,ongoing research,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17915569&form=6&db=m	Role of autophagy in the pathogenesis of Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17915575&form=6&db=m	Molecular genetics of late onset glycogen storage disease II in Italy.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18033029&form=6&db=m	[New approaches for the treatment of metabolic myopathies]	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18078773&form=6&db=m	Methods for a prompt and reliable laboratory diagnosis of Pompe disease: report from an international consensus meeting.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18176891&form=6&db=m	Adult glycogenosis type II (Pompe's disease): morphological abnormalities in muscle and skin biopsies compared with acid alpha-glucosidase activity.	ongoing research,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18285536&form=6&db=m	Molecular pathology and enzyme processing in various phenotypes of acid maltase deficiency.	diagnostic usage,ongoing research,therapeutic application,unassigned	3,2,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18301443&form=6&db=m	p.[G576S; E689K]: pathogenic combination or polymorphism in Pompe disease?	causal interaction,ongoing research,therapeutic application,unassigned	3,1,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18307520&form=6&db=m	Immune tolerance induction to enzyme-replacement therapy by co-administration of short-term, low-dose methotrexate in a murine Pompe disease model.	ongoing research,therapeutic application,unassigned	1,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18425781&form=6&db=m	Update of the Pompe disease mutation database with 107 sequence variants and a format for severity rating.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18458862&form=6&db=m	Identification of eight novel mutations of the acid alpha-glucosidase gene causing the infantile or juvenile form of glycogen storage disease type II.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18505932&form=6&db=m	Hematopoietic contribution to skeletal muscle regeneration in acid alpha-glucosidase knockout mice.	ongoing research,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18508267&form=6&db=m	Eight years experience with enzyme replacement therapy in two children and one adult with Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18519449&form=6&db=m	Early detection of Pompe disease by newborn screening is feasible: results from the Taiwan screening program.	causal interaction,diagnostic usage,ongoing research,unassigned	4,4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18535739&form=6&db=m	Report of the first Brazilian infantile Pompe disease patient to be treated with recombinant human acid alpha-glucosidase.	ongoing research,therapeutic application,unassigned	3,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18538603&form=6&db=m	Biochemical and pharmacological characterization of different recombinant acid alpha-glucosidase preparations evaluated for the treatment of Pompe disease.	causal interaction,diagnostic usage,ongoing research,therapeutic application	4,2,2,4	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18560415&form=6&db=m	Correction of multiple striated muscles in murine Pompe disease through adeno-associated virus-mediated gene therapy.	causal interaction,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18648322&form=6&db=m	Temporal neuropathologic and behavioral phenotype of 6neo/6neo Pompe disease mice.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18661169&form=6&db=m	Cardiac remodeling after enzyme replacement therapy with acid alpha-glucosidase for infants with Pompe disease.	causal interaction,diagnostic usage,ongoing research,therapeutic application	4,1,1,4	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18703766&form=6&db=m	Newborn screening for Pompe disease by measuring acid alpha-glucosidase activity using tandem mass spectrometry.	causal interaction,diagnostic usage,unassigned	4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18704279&form=6&db=m	Enzyme replacement therapy in severe adult-onset glycogen storage disease type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18757064&form=6&db=m	Cardiac evaluation in children and adults with Pompe disease sharing the common c.-32-13T>G genotype rarely reveals abnormalities.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18782850&form=6&db=m	Modulation of glycogen synthesis by RNA interference: towards a new therapeutic approach for glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18810562&form=6&db=m	Correction of glycogenosis type 2 by muscle-specific lentiviral vector.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18929906&form=6&db=m	Pompe's disease.	causal interaction,ongoing research,therapeutic application,unassigned	2,3,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18975241&form=6&db=m	[A case of Pompe disease treated with acid alpha-glucosidase]	causal interaction,therapeutic application,unassigned	4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19003770&form=6&db=m	[Adult form of Pompe disease]	causal interaction,diagnostic usage,ongoing research,therapeutic application	4,4,3,1	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19019308&form=6&db=m	Therapeutic approaches in glycogen storage disease type II/Pompe Disease.	causal interaction,therapeutic application,unassigned	4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19047572&form=6&db=m	Diagnosis of glycogenosis type II.	causal interaction,diagnostic usage,unassigned	3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19131232&form=6&db=m	Pompe disease: a neuromuscular disease with respiratory muscle involvement.	causal interaction,ongoing research,therapeutic application,unassigned	4,1,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19167256&form=6&db=m	Murine muscle cell models for Pompe disease and their use in studying therapeutic approaches.	causal interaction,diagnostic usage,ongoing research,unassigned	4,3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19263466&form=6&db=m	Partial phenotypic correction and immune tolerance induction to enzyme replacement therapy after hematopoietic stem cell gene transfer of alpha-glucosidase in Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	3,2,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19277015&form=6&db=m	Glycoengineered Acid alpha-Glucosidase With Improved Efficacy at Correcting the Metabolic Aberrations and Motor Function Deficits in a Mouse Model of Pompe Disease.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19293774&form=6&db=m	The Pharmacological Chaperone N-butyldeoxynojirimycin Enhances Enzyme Replacement Therapy in Pompe Disease Fibroblasts.	causal interaction,ongoing research,therapeutic application,unassigned	3,4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19343043&form=6&db=m	Structural modeling of mutant alpha-glucosidases resulting in a processing/transport defect in Pompe disease.	causal interaction,therapeutic application,unassigned	1,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19362502&form=6&db=m	High frequency of acid alpha-glucosidase pseudodeficiency complicates newborn screening for glycogen storage disease type II in the Japanese population.	causal interaction,diagnostic usage,ongoing research,therapeutic application	2,3,3,1	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19472353&form=6&db=m	A novel mutation of the GAA gene in a Finnish late-onset Pompe disease patient: clinical phenotype and follow-up with enzyme replacement therapy.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19533645&form=6&db=m	Screening for Pompe disease using a rapid dried blood spot method: experience of a clinical diagnostic laboratory.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19588081&form=6&db=m	Pompe disease in a Brazilian series: clinical and molecular analyses with identification of nine new mutations.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19649685&form=6&db=m	Enzyme replacement therapy with alglucosidase alfa in 44 patients with late-onset glycogen storage disease type 2: 12-month results of an observational clinical trial.	causal interaction,ongoing research,therapeutic application,unassigned	4,2,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19665008&form=6&db=m	Immortalization of murine muscle cells from lysosomal alpha-glucosidase deficient mice: a new tool to study pathophysiology and assess therapeutic strategies for Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	3,4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19690517&form=6&db=m	Immunomodulatory Gene Therapy Prevents Antibody Formation and Lethal Hypersensitivity Reactions in Murine Pompe Disease.	causal interaction,therapeutic application,unassigned	2,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19707330&form=6&db=m	A review of treatment of Pompe disease in infants.	causal interaction,ongoing research,therapeutic application,unassigned	4,1,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19771425&form=6&db=m	Adult onset glycogen storage disease type II (adult onset Pompe disease): report and magnetic resonance images of two cases.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19775921&form=6&db=m	Cross-reactive immunologic material status affects treatment outcomes in Pompe disease infants.	causal interaction,diagnostic usage,unassigned	4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19862843&form=6&db=m	The pharmacological chaperone 1-deoxynojirimycin increases the activity and lysosomal trafficking of multiple mutant forms of acid alpha-glucosidase.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19959526&form=6&db=m	Restoration of muscle functionality by genetic suppression of glycogen synthesis in a murine model of Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19966354&form=6&db=m	Enzyme replacement therapy for infantile Pompe disease during the critical period and identification of a novel mutation.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20033064&form=6&db=m	Neonatal gene transfer using lentiviral vector for murine Pompe disease: long-term expression and glycogen reduction.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20033296&form=6&db=m	Diagnostic efficacy of the fluorometric determination of enzyme activity for Pompe disease from dried blood specimens compared with lymphocytes-possibility for newborn screening.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20080426&form=6&db=m	Genetic heterozygosity and pseudodeficiency in the Pompe disease newborn screening pilot program.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20206419&form=6&db=m	Evaluation of 2-thioxo-2,3,5,6,7,8-hexahydropyrimido[4,5-d]pyrimidin-4(1H)-one analogues as GAA activators.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20223998&form=6&db=m	Impaired organization and function of myofilaments in single muscle fibers from a mouse model of Pompe disease.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20350966&form=6&db=m	Screening of Late-Onset Pompe Disease in a Sample of Mexican Patients With Myopathies of Unknown Etiology: Identification of a Novel Mutation in the Acid {alpha}-glucosidase Gene.	causal interaction,diagnostic usage,unassigned	4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20441705&form=6&db=m	[Establishment and clinical application of dried blood spots and mixed leukocytes for determination of acid alpha-glucosidase activity.]	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20464284&form=6&db=m	Homozygotic intronic GAA mutation in three siblings with late-onset Pompe's disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20554235&form=6&db=m	Inhibition of glycogen biosynthesis via mTORC1 suppression as an adjunct therapy for Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20601298&form=6&db=m	Low bone mass in Pompe disease: muscular strength as a predictor of bone mineral density.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20801068&form=6&db=m	Differences in the predominance of lysosomal and autophagic pathologies between infants and adults with Pompe disease: implications for therapy.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20817528&form=6&db=m	Effect of enzyme therapy in juvenile patients with Pompe disease: A three-year open-label study.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20861693&form=6&db=m	Suppression of autophagy permits successful enzyme replacement therapy in a lysosomal storage disorder-murine Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20882352&form=6&db=m	CRIM-negative infantile Pompe disease: 42-month treatment outcome.	causal interaction,therapeutic application,unassigned	1,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21179212&form=6&db=m	Fiber type conversion by PGC-1? activates lysosomal and autophagosomal biogenesis in both unaffected and Pompe skeletal muscle.	causal interaction,therapeutic application,unassigned	3,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21477922&form=6&db=m	24-Months results in two adults with Pompe disease on enzyme replacement therapy.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21518733&form=6&db=m	Pompe disease gene therapy.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21550241&form=6&db=m	Recombinant human acid alpha-glucosidase (rhGAA) in adult patients with severe respiratory failure due to Pompe disease.	causal interaction,ongoing research,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21763167&form=6&db=m	Rate of progression and predictive factors for pulmonary outcome in children and adults with Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21926084&form=6&db=m	Human Pompe disease-induced pluripotent stem cells for pathogenesis modeling, drug testing and disease marker identification.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21963784&form=6&db=m	Newborn screening for Pompe disease in Japan.	causal interaction,diagnostic usage,ongoing research,therapeutic application	4,2,2,1	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22154081&form=6&db=m	?2 Agonists enhance the efficacy of simultaneous enzyme replacement therapy in murine Pompe disease.	ongoing research,therapeutic application,unassigned	1,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22173792&form=6&db=m	Consensus treatment recommendations for late-onset Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22252923&form=6&db=m	Predicting cross-reactive immunological material (CRIM) status in Pompe disease using GAA mutations: lessons learned from 10 years of clinical laboratory testing experience.	causal interaction,therapeutic application,unassigned	2,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22252961&form=6&db=m	Assessing disease severity in Pompe disease: the roles of a urinary glucose tetrasaccharide biomarker and imaging techniques.	causal interaction,diagnostic usage,therapeutic application,unassigned	4,4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22253254&form=6&db=m	Autophagy and mitochondria in Pompe disease: nothing is so new as what has long been forgotten.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22365055&form=6&db=m	Persistence of high sustained antibodies to enzyme replacement therapy despite extensive immunomodulatory therapy in an infant with Pompe disease: Need for agents to target antibody-secreting plasma cells.	causal interaction,therapeutic application,unassigned	3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22521436&form=6&db=m	Quantitative computed tomography for enzyme replacement therapy in Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22572506&form=6&db=m	Two cases of Pompe's disease: case report and review of literature.	causal interaction,diagnostic usage,therapeutic application,unassigned	4,3,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22616199&form=6&db=m	Genetic counseling in Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22658377&form=6&db=m	Transcriptional response to GAA deficiency (Pompe disease) in infantile-onset patients.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22676651&form=6&db=m	A cross-sectional single-centre study on Pompe disease in 42 German patients: Molecular analysis of the GAA gene, manifestation and genotype-phenotype correlations.	causal interaction,diagnostic usage,ongoing research,unassigned	4,2,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22981821&form=6&db=m	Fat and carbohydrate metabolism during exercise in late-onset Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23305799&form=6&db=m	Detection of c. -32T>G (IVS1-13T>G) mutation of Pompe disease by real-time PCR in dried blood spot specimen.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23430500&form=6&db=m	In vivo bone architecture in pompe disease using high-resolution peripheral computed tomography.	therapeutic application,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23430847&form=6&db=m	Immune Modulation Therapy in a CRIM-Positive and IgG Antibody-Positive Infant with Pompe Disease Treated with Alglucosidase Alfa: A Case Report.	causal interaction,diagnostic usage,therapeutic application,unassigned	4,3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23570273&form=6&db=m	Phase I/II trial of adeno-associated virus-mediated alpha-glucosidase gene therapy to the diaphragm for chronic respiratory failure in Pompe disease: initial safety and ventilatory outcomes.	causal interaction,therapeutic application,unassigned	3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23601496&form=6&db=m	B-Cell Depletion and Immunomodulation before Initiation of Enzyme Replacement Therapy Blocks the Immune Response to Acid Alpha-Glucosidase in Infantile-Onset Pompe Disease.	causal interaction,therapeutic application,unassigned	2,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23606558&form=6&db=m	Transcription factor EB (TFEB) is a new therapeutic target for Pompe disease.	causal interaction,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23749294&form=6&db=m	Swiss national guideline for reimbursement of enzyme replacement therapy in late-onset Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23787031&form=6&db=m	Skeletal muscle pathology of infantile Pompe disease during long-term enzyme replacement therapy.	causal interaction,ongoing research,unassigned	4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23839583&form=6&db=m	Enzyme Replacement Therapy Improves Respiratory Outcomes in Patients with Late-Onset Type II Glycogenosis and High Ventilator Dependency.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24008051&form=6&db=m	The French Pompe registry. Baseline characteristics of a cohort of 126 patients with adult Pompe disease.	diagnostic usage,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24008937&form=6&db=m	[Two new mutations in the gene that codes for acid alpha-glucosidase in an adolescent with late-onset Pompe disease].	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24021025&form=6&db=m	Preclinical Toxicology and Biodistribution Studies of Recombinant Adeno-Associated Virus 1 Human Acid ?-Glucosidase.	diagnostic usage,ongoing research,therapeutic application,unassigned	3,3,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24269976&form=6&db=m	Clinical and molecular genetic study of infantile-onset Pompe disease in Chinese patients: identification of 6 novel mutations.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24273659&form=6&db=m	The Identification of Pompe Disease Mutations in Archival Tissues and Development of a Rapid Molecular-based Test.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24337590&form=6&db=m	Effects of immune modulation therapy in the first Croatian infant diagnosed with Pompe disease: a 3-year follow-up study.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24383498&form=6&db=m	The value of muscle biopsies in Pompe disease: identifying lipofuscin inclusions in juvenile- and adult-onset patients.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24399863&form=6&db=m	Clinical features of Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24399865&form=6&db=m	Non-muscle involvement in late-onset glycogenosis II.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24399866&form=6&db=m	A novel homozygous mutation at the GAA gene in Mexicans with early-onset Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24495340&form=6&db=m	Glycogenosome accumulation in the arrector pili muscle in Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24897114&form=6&db=m	Immune responses and hypercoagulation in ERT for Pompe disease are mutation and rhGAA dose dependent.	causal interaction,therapeutic application,unassigned	2,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24923245&form=6&db=m	Cessation and resuming of alglucosidase alfa in Pompe disease: a retrospective analysis.	causal interaction,ongoing research,therapeutic application,unassigned	3,1,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25036864&form=6&db=m	The pharmacological chaperone AT2220 increases the specific activity and lysosomal delivery of mutant acid alpha-glucosidase, and promotes glycogen reduction in a transgenic mouse model of Pompe disease.	ongoing research,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25085280&form=6&db=m	Methods of diagnosis of patients with Pompe disease: Data from the Pompe Registry.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25183957&form=6&db=m	Pompe disease: from pathophysiology to therapy and back again.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25238277&form=6&db=m	Phase I/II trial of diaphragm delivery of recombinant adeno-associated virus acid alpha-glucosidase (rAAaV1-CMV-GAA) gene vector in patients with Pompe disease.	ongoing research,therapeutic application,unassigned	4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25345093&form=6&db=m	New therapeutic approaches for Pompe disease: enzyme replacement therapy and beyond.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25569118&form=6&db=m	Ampakines Stimulate Respiratory Motor Output and Ventilation in a Murine Model of Pompe Disease.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25673129&form=6&db=m	Clinical and molecular aspects of 30 patients with late-onset Pompe disease (LOPD): unusual features and response to treatment.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25681082&form=6&db=m	Baseline Urinary Glucose Tetrasaccharide Concentrations in Patients with Infantile- and Late-Onset Pompe Disease Identified by Newborn Screening.	causal interaction,diagnostic usage,therapeutic application,unassigned	1,1,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25763511&form=6&db=m	Postmortem Findings and Clinical Correlates in Individuals with Infantile-Onset Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26031770&form=6&db=m	Successful combined liver/kidney transplantation from a donor with Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26053072&form=6&db=m	Oral delivery of Acid Alpha Glucosidase epitopes expressed in plant chloroplasts suppresses antibody formation in treatment of Pompe mice.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26353478&form=6&db=m	Use of Polylactide-Co-Glycolide-Nanoparticles for Lysosomal Delivery of a Therapeutic Enzyme in Glycogenosis Type II Fibroblasts.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26390092&form=6&db=m	Evaluation of Readministration of a Recombinant Adeno-Associated Virus Vector Expressing Acid Alpha-Glucosidase in Pompe Disease: Preclinical to Clinical Planning.	causal interaction,ongoing research,therapeutic application,unassigned	3,2,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26502468&form=6&db=m	[Thymic neuroendocrine carcinoma with Pompe's disease of the adult].	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26503317&form=6&db=m	[Variability in the clinical presentation of Pompe disease: development following enzyme replacement therapy].	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26510925&form=6&db=m	Lack of robust satellite cell activation and muscle regeneration during the progression of Pompe disease.	ongoing research,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26603344&form=6&db=m	Copackaged AAV9 Vectors Promote Simultaneous Immune Tolerance and Phenotypic Correction of Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26873529&form=6&db=m	Observational clinical study of 22 adult-onset Pompe disease patients undergoing enzyme replacement therapy over 5years.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26894045&form=6&db=m	The infantile-onset form of Pompe disease: an autopsy diagnosis.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27017193&form=6&db=m	Salmeterol enhances the cardiac response to gene therapy in Pompe disease.	therapeutic application,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27055517&form=6&db=m	Pompe Disease: Diagnosis and Management. Evidence-Based Guidelines from a Canadian Expert Panel.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27142047&form=6&db=m	Severe Cardiomyopathy as the Isolated Presenting Feature in an Adult with Late-Onset Pompe Disease: A Case Report.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27344650&form=6&db=m	Swallow Prognosis and Follow-Up Protocol in Infantile Onset Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27362911&form=6&db=m	Pompe disease in adulthood: effects of antibody formation on enzyme replacement therapy.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27488899&form=6&db=m	Phosphatidylserine Converts Immunogenic Recombinant Human Acid Alpha-Glucosidase to a Tolerogenic Form in a Mouse Model of Pompe Disease.	ongoing research,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27614205&form=6&db=m	Transcriptome assessment of the Pompe (Gaa-/-) mouse spinal cord indicates widespread neuropathology.	causal interaction,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27629975&form=6&db=m	A Senile Case of Late-onset Pompe's Disease.	causal interaction,diagnostic usage,unassigned	1,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27637292&form=6&db=m	SWORD: A simplified desensitization protocol for enzyme replacement therapy in adult Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27692944&form=6&db=m	Alglucosidase alfa enzyme replacement therapy as a therapeutic approach for a patient presenting with a PRKAG2 mutation.	diagnostic usage,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27858617&form=6&db=m	Long-Term Interruption of Enzyme Replacement Therapy with rhGAA in Pompe Disease Leads to Irreversible Clinical Decline.	causal interaction,ongoing research,therapeutic application,unassigned	1,2,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28045567&form=6&db=m	Disruption of the gaa Gene in Zebrafish Fails to Generate the Phenotype of Classical Pompe Disease.	diagnostic usage,ongoing research,unassigned	3,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28077463&form=6&db=m	Novel method for detection of glycogen in cells.	ongoing research,therapeutic application,unassigned	3,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28154884&form=6&db=m	Antibody-mediated enzyme replacement therapy targeting both lysosomal and cytoplasmic glycogen in Pompe disease.	causal interaction,therapeutic application,unassigned	3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28265479&form=6&db=m	Clinical Analysis of Algerian Patients with Pompe Disease.	causal interaction,therapeutic application,unassigned	3,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28336814&form=6&db=m	Airway smooth muscle dysfunction in Pompe (Gaa-/-) mice.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28480166&form=6&db=m	Albuterol as an adjunctive treatment to enzyme replacement therapy in infantile-onset Pompe disease.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28629821&form=6&db=m	Glycogen Reduction in Myotubes of Late-Onset Pompe Disease Patients Using Antisense Technology.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28648664&form=6&db=m	High dose IVIG successfully reduces high rhGAA IgG antibody titers in a CRIM-negative infantile Pompe disease patient.	ongoing research,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28694071&form=6&db=m	First clinical and genetic description of a family diagnosed with late-onset Pompe disease from Costa Rica.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28761815&form=6&db=m	A pilot study on using rapamycin-carrying synthetic vaccine particles (SVP) in conjunction with enzyme replacement therapy to induce immune tolerance in Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28838325&form=6&db=m	A study on the safety and efficacy of reveglucosidase alfa in patients with late-onset Pompe disease.	causal interaction,diagnostic usage,ongoing research,therapeutic application	4,1,2,2	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28856460&form=6&db=m	Late-onset Pompe disease: a genetic-radiological correlation on cerebral vascular anomalies.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29051784&form=6&db=m	Delivery and postpartum management of a patient with Pompe disease: Case report and review of the literature.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29102549&form=6&db=m	Lipidic Nanoparticles Comprising Phosphatidylinositol Mitigate Immunogenicity and Improve Efficacy of Recombinant Human Acid Alpha-Glucosidase in a Murine Model of Pompe Disease.	causal interaction,ongoing research,therapeutic application,unassigned	1,4,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29118420&form=6&db=m	AAV-mediated transcription factor EB (TFEB) gene delivery ameliorates muscle pathology and function in the murine model of Pompe Disease.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29155436&form=6&db=m	Enzyme replacement therapy for infantile-onset Pompe disease.	causal interaction,therapeutic application,unassigned	4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29274340&form=6&db=m	Four unreported types of glycans containing mannose-6-phosphate are heterogeneously attached at three sites (including newly found Asn 233) to recombinant human acid alpha-glucosidase that is the only approved treatment for Pompe disease.	causal interaction,therapeutic application,unassigned	3,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29295737&form=6&db=m	Immunomodulatory, liver depot gene therapy for Pompe disease.	causal interaction,ongoing research,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29428273&form=6&db=m	High Sustained Antibody Titers in Patients with Classic Infantile Pompe Disease Following Immunomodulation at Start of Enzyme Replacement Therapy.	diagnostic usage,ongoing research,therapeutic application,unassigned	1,4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29435968&form=6&db=m	[A new phenotype of infantile-onset Pompe disease].	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29451150&form=6&db=m	Identification of Seven Novel Mutations in the Acid Alpha-glucosidase Gene in Five Chinese Patients with Late-onset Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29565424&form=6&db=m	Efficacy, safety profile, and immunogenicity of alglucosidase alfa produced at the 4,000-liter scale in US children and adolescents with Pompe disease: ADVANCE, a phase IV, open-label, prospective study.	diagnostic usage,ongoing research,therapeutic application,unassigned	2,1,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29649469&form=6&db=m	Phosphatidylserine Is Not Just a Cleanup Crew but Also a Well-Meaning Teacher.	causal interaction,ongoing research,therapeutic application,unassigned	1,1,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29742245&form=6&db=m	Late-onset Pompe disease: what is the prevalence of limb-girdle muscular weakness presentation?	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29755837&form=6&db=m	Chagasic cardiomyopathy and Pompe disease: case report.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29901418&form=6&db=m	Systemic Delivery of AAVB1-GAA Clears Glycogen and Prolongs Survival in a Mouse Model of Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30049495&form=6&db=m	Cardiac outcome in classic infantile Pompe disease after 13?years of treatment with recombinant human acid alpha-glucosidase.	therapeutic application,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30179846&form=6&db=m	[Argentine consensus on late-onset Pompe's disease].	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30232608&form=6&db=m	36-Months follow-up assessment after cessation and resuming of enzyme replacement therapy in late onset Pompe disease: data from the Swiss Pompe Registry.	causal interaction,therapeutic application,unassigned	2,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30360039&form=6&db=m	Clinical and molecular characterization of Korean children with infantile and late-onset Pompe disease: 10 years of experience with enzyme replacement therapy at a single center.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30382921&form=6&db=m	Satellite cells fail to contribute to muscle repair but are functional in Pompe disease (glycogenosis type II).	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30711607&form=6&db=m	HLA- and genotype-based risk assessment model to identify infantile onset pompe disease patients at high-risk of developing significant anti-drug antibodies (ADA).	causal interaction,therapeutic application,unassigned	3,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30770309&form=6&db=m	Reevaluating the pathogenicity of the mutation c.1194 +5 G>A in GAA gene by functional analysis of RNA in a 61-year-old woman diagnosed with Pompe disease by muscle biopsy.	causal interaction,diagnostic usage,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30809555&form=6&db=m	Intravenous Injection of an AAV-PHP.B Vector Encoding Human Acid ?-Glucosidase Rescues Both Muscle and CNS Defects in Murine Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31026687&form=6&db=m	A human induced pluripotent stem cell line (TRNDi007-B) from an infantile onset Pompe patient carrying p.R854X mutation in the GAA gene.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31193175&form=6&db=m	Characterization of immune response in Cross-Reactive Immunological Material (CRIM)-positive infantile Pompe disease patients treated with enzyme replacement therapy.	causal interaction,therapeutic application,unassigned	2,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31254424&form=6&db=m	Extension of the Pompe mutation database by linking disease-associated variants to clinical severity.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31281600&form=6&db=m	Rehabilitation management of Pompe disease, from childhood trough adulthood: A systematic review of the literature.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31301153&form=6&db=m	Assessment of the functional impact on the pre-mRNA splicing process of 28 nucleotide variants associated with Pompe disease in GAA exon 2 and their recovery using antisense technology.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31341956&form=6&db=m	Mobility assessment using wearable technology in patients with late-onset Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392188&form=6&db=m	Variable clinical features and genotype-phenotype correlations in 18 patients with late-onset Pompe disease.	causal interaction,diagnostic usage,ongoing research,therapeutic application	4,3,1,3	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392189&form=6&db=m	Assessing metabolic profiles in human myoblasts from patients with late-onset Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	3,4,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392190&form=6&db=m	Molecular genetics of Pompe disease: a comprehensive overview.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392193&form=6&db=m	Newborn screening: Taiwanese experience.	causal interaction,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392195&form=6&db=m	Long-term outcome and unmet needs in infantile-onset Pompe disease.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392197&form=6&db=m	Immunological challenges and approaches to immunomodulation in Pompe disease: a literature review.	causal interaction,diagnostic usage,therapeutic application,unassigned	4,3,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392198&form=6&db=m	Diagnostic tools in late onset Pompe disease (LOPD).	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392199&form=6&db=m	Progress and challenges of gene therapy for Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392202&form=6&db=m	Pompe disease gene therapy: neural manifestations require consideration of CNS directed therapy.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392203&form=6&db=m	Challenges in treating Pompe disease: an industry perspective.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392204&form=6&db=m	Pompe disease: what are we missing?	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31439017&form=6&db=m	Comprehensive approach to weaning in difficult-to-wean infantile and juvenile-onset glycogen-storage disease type II patients: a case series.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31510962&form=6&db=m	Clinical course, mutations and its functional characteristics of infantile-onset Pompe disease in Thailand.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31713816&form=6&db=m	Molecular Approaches for the Treatment of Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31867331&form=6&db=m	DeepNEU: Artificially Induced Stem Cell (aiPSC) and Differentiated Skeletal Muscle Cell (aiSkMC) Simulations of Infantile Onset POMPE Disease (IOPD) for Potential Biomarker Identification and Drug Discovery.	causal interaction,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31904026&form=6&db=m	Higher dosing of alglucosidase alfa improves outcomes in children with Pompe disease: a clinical study and review of the literature.	causal interaction,diagnostic usage,ongoing research,therapeutic application	4,2,2,4	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32044029&form=6&db=m	Profiles of plant core-fucosylated N-glycans of acid alpha-glucosidases produced in transgenic rice cell suspension cultures treated with eight different conditions.	ongoing research,therapeutic application,unassigned	2,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32065100&form=6&db=m	Feasibility Study for Bedside Production of Recombinant Human Acid ?-Glucosidase: Technical and Financial Considerations.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32129012&form=6&db=m	Follow-up of late-onset Pompe disease patients with muscle magnetic resonance imaging reveals increase in fat replacement in skeletal muscles.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32290314&form=6&db=m	Moss-Derived Human Recombinant GAA Provides an Optimized Enzyme Uptake in Differentiated Human Muscle Cells of Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32504392&form=6&db=m	GAA gene mutation detection following clinical evaluation and enzyme activity analysis in Azeri Turkish patients with Pompe disease.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32508839&form=6&db=m	Development of ImmTOR Tolerogenic Nanoparticles for the Mitigation of Anti-drug Antibodies.	ongoing research,therapeutic application,unassigned	3,1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32579304&form=6&db=m	[The long-term follow-up of enzyme replacement treatment in late onset Pompe disease].	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32587263&form=6&db=m	CRISPR-Cas9 generated Pompe knock-in murine model exhibits early-onset hypertrophic cardiomyopathy and skeletal muscle weakness.	causal interaction,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32671132&form=6&db=m	Enzyme Replacement Therapy Can Reverse Pathogenic Cascade in Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32775491&form=6&db=m	Lentiviral Hematopoietic Stem Cell Gene Therapy Rescues Clinical Phenotypes in a Murine Model of Pompe Disease.	causal interaction,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32932790&form=6&db=m	Pregnancy Outcomes in Late Onset Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32962155&form=6&db=m	Pompe Disease: New Developments in an Old Lysosomal Storage Disorder.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33039711&form=6&db=m	Gene therapy with secreted acid alpha-glucosidase rescues Pompe disease in a novel mouse model with early-onset spinal cord and respiratory defects.	therapeutic application,unassigned	3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33073007&form=6&db=m	The First Year Experience of Newborn Screening for Pompe Disease in California.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33073019&form=6&db=m	A Newborn Screening, Presymptomatically Identified Infant With Late-Onset Pompe Disease: Case Report, Parental Experience, and Recommendations.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33155691&form=6&db=m	Skeletal muscle magnetic resonance imaging in Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33162552&form=6&db=m	Enzymatic diagnosis of Pompe disease: lessons from 28 years of experience.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33205401&form=6&db=m	Expansion of immature, nucleated red blood cells by transient low-dose methotrexate immune tolerance induction in mice.	causal interaction,unassigned	2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33375166&form=6&db=m	Modeling CNS Involvement in Pompe Disease Using Neural Stem Cells Generated from Patient-Derived Induced Pluripotent Stem Cells.	causal interaction,ongoing research,unassigned	4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33554498&form=6&db=m	Advances in diagnosis and management of Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33561046&form=6&db=m	The First Year Experience of Newborn Screening for Pompe Disease in California.	unassigned	-	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33762497&form=6&db=m	[Selenoprotein-related myopathy in a patient with old-age-onset type 2 respiratory failure: a case report].	diagnostic usage,unassigned	1,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33807278&form=6&db=m	Rare Variants in Autophagy and Non-Autophagy Genes in Late-Onset Pompe Disease: Suggestions of Their Disease-Modifying Role in Two Italian Families.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33953320&form=6&db=m	Three-dimensional tissue-engineered human skeletal muscle model of Pompe disease.	causal interaction,therapeutic application,unassigned	4,3,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33971197&form=6&db=m	Endolysosomal N-glycan processing is critical to attain the most active form of the enzyme acid alpha-glucosidase.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33977033&form=6&db=m	Uptake of moss-derived human recombinant GAA in Gaa -/- mice.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34191636&form=6&db=m	Case Studies in Neuroscience: Neuropathology and diaphragm dysfunction in ventilatory failure from late-onset Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34220802&form=6&db=m	Immune Tolerance-Adjusted Personalized Immunogenicity Prediction for Pompe Disease.	causal interaction,unassigned	4,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34357340&form=6&db=m	Experience with the Urinary Tetrasaccharide Metabolite for Pompe Disease in the Diagnostic Laboratory.	causal interaction,diagnostic usage,unassigned	2,2,0	
3.2.1.106	Glycogen Storage Disease Type II	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34501319&form=6&db=m	Molecular Diagnosis of Pompe Disease in the Genomic Era: Correlation with Acid Alpha-Glucosidase Activity in Dried Blood Spots.	diagnostic usage,therapeutic application,unassigned	3,1,0	
3.2.1.106	Glycogen Storage Disease Type III	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8843344&form=6&db=m	Expression of catalytically active human multifunctional glycogen-debranching enzyme and lysosomal acid alpha-glucosidase in insect cells.	causal interaction,unassigned	3,0	
3.2.1.106	Heart Failure	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2235132&form=6&db=m	Rat heart perfusion as model system for enzyme replacement therapy in glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	Hemophilia A	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32508839&form=6&db=m	Development of ImmTOR Tolerogenic Nanoparticles for the Mitigation of Anti-drug Antibodies.	ongoing research,therapeutic application,unassigned	3,1,0	
3.2.1.106	Hepatitis B	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15664065&form=6&db=m	Assays for glucosidase inhibitors with potential antiviral activities: secreted alkaline phosphatase as a surrogate marker.	causal interaction,therapeutic application,unassigned	2,4,0	
3.2.1.106	Hepatitis B	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20618459&form=6&db=m	Hepatitis B virus surface antigen interacts with acid alpha-glucosidase and alters glycogen metabolism.	diagnostic usage,ongoing research,therapeutic application,unassigned	1,1,1,0	
3.2.1.106	Hepatomegaly	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10189220&form=6&db=m	Novel mutations in African American patients with glycogen storage disease Type II. Mutations in brief no. 209. Online.	causal interaction,unassigned	4,0	
3.2.1.106	Hypersensitivity	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20882352&form=6&db=m	CRIM-negative infantile Pompe disease: 42-month treatment outcome.	causal interaction,therapeutic application,unassigned	1,2,0	
3.2.1.106	Infections	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2472115&form=6&db=m	Antibody-independent, complement-mediated enhancement of HIV-1 infection by mannosidase I and II inhibitors.	causal interaction,therapeutic application,unassigned	1,4,0	
3.2.1.106	Infections	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19649930&form=6&db=m	Celgosivir, an alpha-glucosidase I inhibitor for the potential treatment of HCV infection.	causal interaction,therapeutic application,unassigned	3,4,0	
3.2.1.106	Influenza, Human	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6232135&form=6&db=m	Inhibition of N-linked oligosaccharide trimming does not interfere with surface expression of certain integral membrane proteins.	ongoing research,therapeutic application,unassigned	2,1,0	
3.2.1.106	Influenza, Human	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6538079&form=6&db=m	Inhibition of processing of plant N-linked oligosaccharides by castanospermine.	causal interaction,unassigned	1,0	
3.2.1.106	Influenza, Human	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9023540&form=6&db=m	Inhibition of glycoprotein processing by L-fructose and L-xylulose.	causal interaction,ongoing research,unassigned	2,1,0	
3.2.1.106	Intellectual Disability	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12398843&form=6&db=m	Danon's disease (X-linked vacuolar cardiomyopathy and myopathy): a case with a novel Lamp-2 gene mutation.	unassigned	-	
3.2.1.106	Leukemia	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2078038&form=6&db=m	Inhibition of glycoprotein processing and HIV replication by castanospermine analogues.	diagnostic usage,ongoing research,therapeutic application,unassigned	1,3,2,0	
3.2.1.106	Leukemia	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2957325&form=6&db=m	Effect of glycoprotein-processing inhibitors on the mouse IgE binding capacity of rat basophilic leukemia cells.	ongoing research,unassigned	4,0	
3.2.1.106	Lymphoma	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3924028&form=6&db=m	The effect of castanospermine on the oligosaccharide structures of glycoproteins from lymphoma cell lines.	ongoing research,unassigned	4,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2947052&form=6&db=m	Severe course of glycogen storage disease type II (Pompe's disease) without development of cardiomegalia.	causal interaction,unassigned	4,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3159730&form=6&db=m	Defects in synthesis, phosphorylation, and maturation of acid alpha-glucosidase in glycogenosis type II.	causal interaction,ongoing research,unassigned	3,3,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6754447&form=6&db=m	Adult forms of glycogenosis type II. A defect in an early stage of acid alpha-glucosidase realization.	causal interaction,diagnostic usage,ongoing research,unassigned	4,3,4,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8575451&form=6&db=m	Isolation and characterisation of a recombinant, precursor form of lysosomal acid alpha-glucosidase.	causal interaction,ongoing research,unassigned	4,4,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11949932&form=6&db=m	Acid alpha-glucosidase deficiency (glycogenosis type II, Pompe disease).	causal interaction,unassigned	4,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15668445&form=6&db=m	Mutations in the acid alpha-glucosidase gene (M. Pompe) in a patient with an unusual phenotype.	causal interaction,unassigned	4,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15703490&form=6&db=m	Impact of humoral immune response on distribution and efficacy of recombinant adeno-associated virus-derived acid alpha-glucosidase in a model of glycogen storage disease type II.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,3,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20206419&form=6&db=m	Evaluation of 2-thioxo-2,3,5,6,7,8-hexahydropyrimido[4,5-d]pyrimidin-4(1H)-one analogues as GAA activators.	causal interaction,unassigned	4,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24273659&form=6&db=m	The Identification of Pompe Disease Mutations in Archival Tissues and Development of a Rapid Molecular-based Test.	causal interaction,unassigned	4,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24495340&form=6&db=m	Glycogenosome accumulation in the arrector pili muscle in Pompe disease.	causal interaction,unassigned	3,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26353478&form=6&db=m	Use of Polylactide-Co-Glycolide-Nanoparticles for Lysosomal Delivery of a Therapeutic Enzyme in Glycogenosis Type II Fibroblasts.	causal interaction,unassigned	4,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26502468&form=6&db=m	[Thymic neuroendocrine carcinoma with Pompe's disease of the adult].	causal interaction,unassigned	4,0	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29755837&form=6&db=m	Chagasic cardiomyopathy and Pompe disease: case report.	unassigned	-	
3.2.1.106	Lysosomal Storage Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32962155&form=6&db=m	Pompe Disease: New Developments in an Old Lysosomal Storage Disorder.	causal interaction,unassigned	4,0	
3.2.1.106	Mania	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28457156&form=6&db=m	Robert Lowell, Setting the River on Fire: A Study of Genius, Mania, and Characterby Kay Redfield Jamison, Ph.D. New York, Alfred A Knopf, 2017, 544 pp., $29.95 (hardcover).	unassigned	-	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34626&form=6&db=m	Characterization of the molecular defect in infantile and adult acid alpha-glucosidase deficiency fibroblasts.	causal interaction,diagnostic usage,ongoing research,therapeutic application	3,4,4,2	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=60470&form=6&db=m	Acid maltase deficiency in non-identical adult twins. A morphological and biochemical study.	ongoing research,unassigned	2,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1991835&form=6&db=m	Intravenous administration of phosphorylated acid alpha-glucosidase leads to uptake of enzyme in heart and skeletal muscle of mice.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2235132&form=6&db=m	Rat heart perfusion as model system for enzyme replacement therapy in glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2403755&form=6&db=m	Adult and infantile glycogenosis type II in one family, explained by allelic diversity.	causal interaction,ongoing research,unassigned	3,3,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3093639&form=6&db=m	Acid maltase deficiency: a case study and review of the pathophysiological changes and proposed therapeutic measures.	causal interaction,therapeutic application,unassigned	2,1,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3108320&form=6&db=m	Clinical diversity in glycogenosis type II. Biosynthesis and in situ localization of acid alpha-glucosidase in mutant fibroblasts.	causal interaction,diagnostic usage,ongoing research,unassigned	4,3,4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3152090&form=6&db=m	[Acid alpha-glucosidase deficiency: Pompe's disease]	unassigned	-	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3159730&form=6&db=m	Defects in synthesis, phosphorylation, and maturation of acid alpha-glucosidase in glycogenosis type II.	causal interaction,ongoing research,unassigned	3,3,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3935646&form=6&db=m	Neutral oligosaccharides in the urine of a patient with glycogen storage disease type II.	unassigned	-	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6391168&form=6&db=m	Biochemical genetics of the Lapland dog model of glycogen storage disease type II (acid alpha-glucosidase deficiency).	causal interaction,diagnostic usage,ongoing research,therapeutic application	3,3,4,2	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6401921&form=6&db=m	Genetic heterogeneity in acid alpha-glucosidase deficiency.	causal interaction,diagnostic usage,ongoing research,therapeutic application	2,3,2,1	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6418414&form=6&db=m	Acid alpha-glucosidase deficiency in cultured fibroblasts with phenotype 2 of acid alpha-glucosidase.	causal interaction,diagnostic usage,ongoing research,unassigned	4,3,1,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7037230&form=6&db=m	Human amniotic fluid alpha-glucosidase.	causal interaction,unassigned	3,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8214335&form=6&db=m	Computed tomography and magnetic resonance imaging of affected muscle in childhood acid alpha-glucosidase deficiency: a case report.	causal interaction,unassigned	1,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8439343&form=6&db=m	Biochemical genetics of glycogenosis type II in Brahman cattle.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8577039&form=6&db=m	[Glycogenosis type II; acid alpha-glucosidase deficiency]	unassigned	-	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8834250&form=6&db=m	Acid alpha-glucosidase deficiency: identification and expression of a missense mutation (S529V) in a Japanese adult phenotype.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8870826&form=6&db=m	Pathological study of Japanese quail embryo with acid alpha-glucosidase deficiency during early development.	ongoing research,therapeutic application,unassigned	2,1,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8986097&form=6&db=m	[Chronic respiratory failure in a case with juvenile-onset acid alpha-glucosidase deficiency; successful therapy with nasal intermittent positive pressure ventilation (NIPPV)]	causal interaction,therapeutic application,unassigned	4,3,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9143306&form=6&db=m	Recombinant HIV envelope expressed in an alpha-glucosidase I-deficient CHO cell line and its parental cell line in the presence of 1-deoxynojirimycin is functional.	ongoing research,therapeutic application,unassigned	4,3,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9384603&form=6&db=m	Generalized glycogen storage and cardiomegaly in a knockout mouse model of Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	4,1,1,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9614571&form=6&db=m	Complete correction of acid alpha-glucosidase deficiency in Pompe disease fibroblasts in vitro, and lysosomally targeted expression in neonatal rat cardiac and skeletal muscle.	causal interaction,ongoing research,therapeutic application,unassigned	3,2,3,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9736785&form=6&db=m	Recombinant human acid alpha-glucosidase: high level production in mouse milk, biochemical characteristics, correction of enzyme deficiency in GSDII KO mice.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,1,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10377006&form=6&db=m	Increased occurrence of cleft lip in glycogen storage disease type II (GSDII): exclusion of a contiguous gene syndrome in two patients by presence of intragenic mutations including a novel nonsense mutation Gln58Stop.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10545593&form=6&db=m	Human acid alpha-glucosidase from rabbit milk has therapeutic effect in mice with glycogen storage disease type II.	diagnostic usage,ongoing research,therapeutic application,unassigned	3,4,3,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10788335&form=6&db=m	A novel disorder caused by defective biosynthesis of N-linked oligosaccharides due to glucosidase I deficiency.	causal interaction,ongoing research,unassigned	3,4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10838256&form=6&db=m	Modulation of disease severity in mice with targeted disruption of the acid alpha-glucosidase gene.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11949932&form=6&db=m	Acid alpha-glucosidase deficiency (glycogenosis type II, Pompe disease).	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12145188&form=6&db=m	Processing of N-linked carbohydrate chains in a patient with glucosidase I deficiency (CDG type IIb).	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12398843&form=6&db=m	Danon's disease (X-linked vacuolar cardiomyopathy and myopathy): a case with a novel Lamp-2 gene mutation.	unassigned	-	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14695532&form=6&db=m	Twenty-two novel mutations in the lysosomal alpha-glucosidase gene (GAA) underscore the genotype-phenotype correlation in glycogen storage disease type II.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14707516&form=6&db=m	Efficacy of multidisciplinary approach in the treatment of two cases of nonclassical infantile glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15048888&form=6&db=m	Enzyme replacement therapy in late-onset Pompe's disease: a three-year follow-up.	causal interaction,ongoing research,therapeutic application,unassigned	3,1,3,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16702880&form=6&db=m	Comparison of maltose and acarbose as inhibitors of maltase-glucoamylase activity in assaying acid alpha-glucosidase activity in dried blood spots for the diagnosis of infantile Pompe disease.	causal interaction,diagnostic usage,therapeutic application,unassigned	1,2,2,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16737883&form=6&db=m	A retrospective, multinational, multicenter study on the natural history of infantile-onset Pompe disease.	diagnostic usage,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17210890&form=6&db=m	Broad spectrum of Pompe disease in patients with the same c.-32-13T->G haplotype.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17217857&form=6&db=m	Acid alpha-glucosidase deficiency (Pompe disease).	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18285536&form=6&db=m	Molecular pathology and enzyme processing in various phenotypes of acid maltase deficiency.	diagnostic usage,ongoing research,therapeutic application,unassigned	3,2,1,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18301443&form=6&db=m	p.[G576S; E689K]: pathogenic combination or polymorphism in Pompe disease?	causal interaction,ongoing research,therapeutic application,unassigned	3,1,1,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18425781&form=6&db=m	Update of the Pompe disease mutation database with 107 sequence variants and a format for severity rating.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18929906&form=6&db=m	Pompe's disease.	causal interaction,ongoing research,therapeutic application,unassigned	2,3,1,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21763167&form=6&db=m	Rate of progression and predictive factors for pulmonary outcome in children and adults with Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22676651&form=6&db=m	A cross-sectional single-centre study on Pompe disease in 42 German patients: Molecular analysis of the GAA gene, manifestation and genotype-phenotype correlations.	causal interaction,diagnostic usage,ongoing research,unassigned	4,2,4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23839583&form=6&db=m	Enzyme Replacement Therapy Improves Respiratory Outcomes in Patients with Late-Onset Type II Glycogenosis and High Ventilator Dependency.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24273659&form=6&db=m	The Identification of Pompe Disease Mutations in Archival Tissues and Development of a Rapid Molecular-based Test.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24399865&form=6&db=m	Non-muscle involvement in late-onset glycogenosis II.	causal interaction,unassigned	4,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26510925&form=6&db=m	Lack of robust satellite cell activation and muscle regeneration during the progression of Pompe disease.	ongoing research,unassigned	3,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29051784&form=6&db=m	Delivery and postpartum management of a patient with Pompe disease: Case report and review of the literature.	causal interaction,unassigned	3,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29118420&form=6&db=m	AAV-mediated transcription factor EB (TFEB) gene delivery ameliorates muscle pathology and function in the murine model of Pompe Disease.	unassigned	-	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30382921&form=6&db=m	Satellite cells fail to contribute to muscle repair but are functional in Pompe disease (glycogenosis type II).	causal interaction,unassigned	3,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392193&form=6&db=m	Newborn screening: Taiwanese experience.	causal interaction,unassigned	2,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32504392&form=6&db=m	GAA gene mutation detection following clinical evaluation and enzyme activity analysis in Azeri Turkish patients with Pompe disease.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	mannosyl-oligosaccharide glucosidase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33375166&form=6&db=m	Modeling CNS Involvement in Pompe Disease Using Neural Stem Cells Generated from Patient-Derived Induced Pluripotent Stem Cells.	causal interaction,ongoing research,unassigned	4,3,0	
3.2.1.106	Melanoma	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3093061&form=6&db=m	Inhibition of experimental metastasis by castanospermine in mice: blockage of two distinct stages of tumor colonization by oligosaccharide processing inhibitors.	ongoing research,therapeutic application,unassigned	1,4,0	
3.2.1.106	Mesothelioma	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32508839&form=6&db=m	Development of ImmTOR Tolerogenic Nanoparticles for the Mitigation of Anti-drug Antibodies.	ongoing research,therapeutic application,unassigned	3,1,0	
3.2.1.106	Mucolipidoses	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2846524&form=6&db=m	Intracellular transport of acid alpha-glucosidase in human fibroblasts: evidence for involvement of phosphomannosyl receptor-independent system.	diagnostic usage,unassigned	3,0	
3.2.1.106	Mucolipidoses	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2935398&form=6&db=m	The subcellular localization of soluble and membrane-bound lysosomal enzymes in I-cell fibroblasts: a comparative immunocytochemical study.	diagnostic usage,ongoing research,unassigned	1,4,0	
3.2.1.106	Muscle Hypotonia	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10189220&form=6&db=m	Novel mutations in African American patients with glycogen storage disease Type II. Mutations in brief no. 209. Online.	causal interaction,unassigned	4,0	
3.2.1.106	Muscle Hypotonia	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10788335&form=6&db=m	A novel disorder caused by defective biosynthesis of N-linked oligosaccharides due to glucosidase I deficiency.	causal interaction,ongoing research,unassigned	3,4,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2235132&form=6&db=m	Rat heart perfusion as model system for enzyme replacement therapy in glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14695532&form=6&db=m	Twenty-two novel mutations in the lysosomal alpha-glucosidase gene (GAA) underscore the genotype-phenotype correlation in glycogen storage disease type II.	causal interaction,unassigned	4,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15639117&form=6&db=m	Safety and efficacy of recombinant acid alpha-glucosidase (rhGAA) in patients with classical infantile Pompe disease: results of a phase II clinical trial.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,4,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16005263&form=6&db=m	Evasion of immune responses to introduced human acid alpha-glucosidase by liver-restricted expression in glycogen storage disease type II.	causal interaction,ongoing research,unassigned	4,2,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17075580&form=6&db=m	Characterization of pre- and post-treatment pathology after enzyme replacement therapy for Pompe disease.	causal interaction,unassigned	1,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17095274&form=6&db=m	Chemical chaperones improve transport and enhance stability of mutant alpha-glucosidases in glycogen storage disease type II.	causal interaction,unassigned	2,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19472353&form=6&db=m	A novel mutation of the GAA gene in a Finnish late-onset Pompe disease patient: clinical phenotype and follow-up with enzyme replacement therapy.	causal interaction,unassigned	4,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19588081&form=6&db=m	Pompe disease in a Brazilian series: clinical and molecular analyses with identification of nine new mutations.	causal interaction,unassigned	4,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20033064&form=6&db=m	Neonatal gene transfer using lentiviral vector for murine Pompe disease: long-term expression and glycogen reduction.	causal interaction,unassigned	4,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23430500&form=6&db=m	In vivo bone architecture in pompe disease using high-resolution peripheral computed tomography.	therapeutic application,unassigned	1,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26454691&form=6&db=m	A beta-blocker, propranolol, decreases the efficacy from enzyme replacement therapy in Pompe disease.	ongoing research,therapeutic application,unassigned	3,1,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27692944&form=6&db=m	Alglucosidase alfa enzyme replacement therapy as a therapeutic approach for a patient presenting with a PRKAG2 mutation.	diagnostic usage,unassigned	4,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29326002&form=6&db=m	Prevalence of adult Pompe disease in patients with proximal myopathic syndrome and undiagnosed muscle biopsy.	diagnostic usage,ongoing research,therapeutic application,unassigned	4,1,1,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392195&form=6&db=m	Long-term outcome and unmet needs in infantile-onset Pompe disease.	unassigned	-	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33155691&form=6&db=m	Skeletal muscle magnetic resonance imaging in Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Muscle Weakness	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33953320&form=6&db=m	Three-dimensional tissue-engineered human skeletal muscle model of Pompe disease.	causal interaction,therapeutic application,unassigned	4,3,0	
3.2.1.106	Muscular Atrophy	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33762497&form=6&db=m	[Selenoprotein-related myopathy in a patient with old-age-onset type 2 respiratory failure: a case report].	diagnostic usage,unassigned	1,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8552676&form=6&db=m	High-level production of recombinant human lysosomal acid alpha-glucosidase in Chinese hamster ovary cells which targets to heart muscle and corrects glycogen accumulation in fibroblasts from patients with Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,1,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9466978&form=6&db=m	Clinical and metabolic correction of pompe disease by enzyme therapy in acid maltase-deficient quail.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10840383&form=6&db=m	Towards a molecular therapy for glycogen storage disease type II (Pompe disease).	causal interaction,unassigned	4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11268285&form=6&db=m	Intercellular transfer of the virally derived precursor form of acid alpha-glucosidase corrects the enzyme deficiency in inherited cardioskeletal myopathy Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11286229&form=6&db=m	Recombinant human acid alpha-glucosidase enzyme therapy for infantile glycogen storage disease type II: results of a phase I/II clinical trial.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11405345&form=6&db=m	Enzyme therapy for pompe disease with recombinant human alpha-glucosidase from rabbit milk.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,3,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11590121&form=6&db=m	Conditional tissue-specific expression of the acid alpha-glucosidase (GAA) gene in the GAA knockout mice: implications for therapy.	causal interaction,therapeutic application,unassigned	1,4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11738358&form=6&db=m	Identification of six novel mutations in the acid alpha-glucosidase gene in three Spanish patients with infantile onset glycogen storage disease type II (Pompe disease).	causal interaction,unassigned	4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12398843&form=6&db=m	Danon's disease (X-linked vacuolar cardiomyopathy and myopathy): a case with a novel Lamp-2 gene mutation.	unassigned	-	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12409258&form=6&db=m	Glycogen stored in skeletal but not in cardiac muscle in acid alpha-glucosidase mutant (Pompe) mice is highly resistant to transgene-encoded human enzyme.	causal interaction,unassigned	3,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14567965&form=6&db=m	Enzyme replacement therapy in the mouse model of Pompe disease.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15585405&form=6&db=m	Replacing acid alpha-glucosidase in Pompe disease: recombinant and transgenic enzymes are equipotent, but neither completely clears glycogen from type II muscle fibers.	causal interaction,ongoing research,therapeutic application,unassigned	4,2,4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15659425&form=6&db=m	Clinical manifestation and natural course of late-onset Pompe's disease in 54 Dutch patients.	causal interaction,unassigned	4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15776317&form=6&db=m	Enzyme replacement therapy in classical infantile pompe disease: results of a ten-month follow-up study.	causal interaction,unassigned	4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16702879&form=6&db=m	Electrocardiographic response to enzyme replacement therapy for Pompe disease.	causal interaction,diagnostic usage,ongoing research,therapeutic application	4,2,4,2	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16874053&form=6&db=m	Autophagy and lysosomes in Pompe disease.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16898258&form=6&db=m	Pompe disease (glycogen storage disease type II): clinical features and enzyme replacement therapy.	causal interaction,unassigned	4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17008131&form=6&db=m	Autophagy and mistargeting of therapeutic enzyme in skeletal muscle in Pompe disease.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17592248&form=6&db=m	Deconstructing pompe disease by analyzing single muscle fibers: to see a world in a grain of sand...''.	causal interaction,unassigned	3,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17690063&form=6&db=m	Long-term enzyme replacement therapy for pompe disease with recombinant human alpha-glucosidase derived from chinese hamster ovary cells.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,2,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18704279&form=6&db=m	Enzyme replacement therapy in severe adult-onset glycogen storage disease type II.	causal interaction,unassigned	4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18975241&form=6&db=m	[A case of Pompe disease treated with acid alpha-glucosidase]	causal interaction,therapeutic application,unassigned	4,3,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19167256&form=6&db=m	Murine muscle cell models for Pompe disease and their use in studying therapeutic approaches.	causal interaction,diagnostic usage,ongoing research,unassigned	4,3,4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19293774&form=6&db=m	The Pharmacological Chaperone N-butyldeoxynojirimycin Enhances Enzyme Replacement Therapy in Pompe Disease Fibroblasts.	causal interaction,ongoing research,therapeutic application,unassigned	3,4,1,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20350966&form=6&db=m	Screening of Late-Onset Pompe Disease in a Sample of Mexican Patients With Myopathies of Unknown Etiology: Identification of a Novel Mutation in the Acid {alpha}-glucosidase Gene.	causal interaction,diagnostic usage,unassigned	4,3,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20464284&form=6&db=m	Homozygotic intronic GAA mutation in three siblings with late-onset Pompe's disease.	causal interaction,unassigned	3,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20601298&form=6&db=m	Low bone mass in Pompe disease: muscular strength as a predictor of bone mineral density.	causal interaction,unassigned	4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21179212&form=6&db=m	Fiber type conversion by PGC-1? activates lysosomal and autophagosomal biogenesis in both unaffected and Pompe skeletal muscle.	causal interaction,therapeutic application,unassigned	3,1,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21518733&form=6&db=m	Pompe disease gene therapy.	causal interaction,unassigned	4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22926164&form=6&db=m	Enzyme replacement therapy in late-onset Pompe disease: a systematic literature review.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23305799&form=6&db=m	Detection of c. -32T>G (IVS1-13T>G) mutation of Pompe disease by real-time PCR in dried blood spot specimen.	causal interaction,unassigned	4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23606558&form=6&db=m	Transcription factor EB (TFEB) is a new therapeutic target for Pompe disease.	causal interaction,unassigned	1,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24008937&form=6&db=m	[Two new mutations in the gene that codes for acid alpha-glucosidase in an adolescent with late-onset Pompe disease].	causal interaction,unassigned	3,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24383498&form=6&db=m	The value of muscle biopsies in Pompe disease: identifying lipofuscin inclusions in juvenile- and adult-onset patients.	causal interaction,unassigned	3,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24991319&form=6&db=m	Recent developments, utilization, and spending trends for pompe disease therapies.	causal interaction,unassigned	3,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26510925&form=6&db=m	Lack of robust satellite cell activation and muscle regeneration during the progression of Pompe disease.	ongoing research,unassigned	3,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28265479&form=6&db=m	Clinical Analysis of Algerian Patients with Pompe Disease.	causal interaction,therapeutic application,unassigned	3,1,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28480166&form=6&db=m	Albuterol as an adjunctive treatment to enzyme replacement therapy in infantile-onset Pompe disease.	causal interaction,therapeutic application,unassigned	4,4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29118420&form=6&db=m	AAV-mediated transcription factor EB (TFEB) gene delivery ameliorates muscle pathology and function in the murine model of Pompe Disease.	unassigned	-	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32587263&form=6&db=m	CRISPR-Cas9 generated Pompe knock-in murine model exhibits early-onset hypertrophic cardiomyopathy and skeletal muscle weakness.	causal interaction,unassigned	1,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32962155&form=6&db=m	Pompe Disease: New Developments in an Old Lysosomal Storage Disorder.	causal interaction,unassigned	4,0	
3.2.1.106	Muscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34357340&form=6&db=m	Experience with the Urinary Tetrasaccharide Metabolite for Pompe Disease in the Diagnostic Laboratory.	causal interaction,diagnostic usage,unassigned	2,2,0	
3.2.1.106	Muscular Dystrophies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3282727&form=6&db=m	A family with pseudodeficiency of acid alpha-glucosidase.	causal interaction,unassigned	1,0	
3.2.1.106	Muscular Dystrophies	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16987711&form=6&db=m	Enhanced efficacy of an AAV vector encoding chimeric, highly secreted acid alpha-glucosidase in glycogen storage disease type II.	causal interaction,therapeutic application,unassigned	3,2,0	
3.2.1.106	Neoplasm Metastasis	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3093061&form=6&db=m	Inhibition of experimental metastasis by castanospermine in mice: blockage of two distinct stages of tumor colonization by oligosaccharide processing inhibitors.	ongoing research,therapeutic application,unassigned	1,4,0	
3.2.1.106	Neoplasms	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7540952&form=6&db=m	The alpha-glucosidase I inhibitor castanospermine alters endothelial cell glycosylation, prevents angiogenesis, and inhibits tumor growth.	causal interaction,ongoing research,therapeutic application,unassigned	3,3,3,0	
3.2.1.106	Neoplasms	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10734102&form=6&db=m	Allosteric activation of acid alpha-glucosidase by the human papillomavirus E7 protein.	causal interaction,ongoing research,therapeutic application,unassigned	1,4,1,0	
3.2.1.106	Nephrotic Syndrome	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15466083&form=6&db=m	Nephrotic syndrome complicating alpha-glucosidase replacement therapy for Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	2,4,4,0	
3.2.1.106	Neuromuscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23570273&form=6&db=m	Phase I/II trial of adeno-associated virus-mediated alpha-glucosidase gene therapy to the diaphragm for chronic respiratory failure in Pompe disease: initial safety and ventilatory outcomes.	causal interaction,therapeutic application,unassigned	3,4,0	
3.2.1.106	Neuromuscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392189&form=6&db=m	Assessing metabolic profiles in human myoblasts from patients with late-onset Pompe disease.	causal interaction,ongoing research,therapeutic application,unassigned	3,4,2,0	
3.2.1.106	Neuromuscular Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31392202&form=6&db=m	Pompe disease gene therapy: neural manifestations require consideration of CNS directed therapy.	causal interaction,unassigned	3,0	
3.2.1.106	Niemann-Pick Diseases	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29369793&form=6&db=m	Alpha galactosidase A activity in Parkinson's disease.	causal interaction,diagnostic usage,ongoing research,unassigned	4,3,1,0	
3.2.1.106	Pancreatic Neoplasms	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33931930&form=6&db=m	Suppression of lysosomal acid alpha-glucosidase impacts the modulation of transcription factor EB translocation in pancreatic cancer.	causal interaction,unassigned	1,0	
3.2.1.106	pullulanase deficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3161667&form=6&db=m	Debranching enzyme in fibroblasts, amniotic fluid cells and chorionic villi: pre- and postnatal diagnosis of glycogenosis type III.	causal interaction,diagnostic usage,unassigned	4,1,0	
3.2.1.106	Respiratory Insufficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8986097&form=6&db=m	[Chronic respiratory failure in a case with juvenile-onset acid alpha-glucosidase deficiency; successful therapy with nasal intermittent positive pressure ventilation (NIPPV)]	causal interaction,therapeutic application,unassigned	4,3,0	
3.2.1.106	Respiratory Insufficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15639117&form=6&db=m	Safety and efficacy of recombinant acid alpha-glucosidase (rhGAA) in patients with classical infantile Pompe disease: results of a phase II clinical trial.	causal interaction,ongoing research,therapeutic application,unassigned	4,4,4,0	
3.2.1.106	Respiratory Insufficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16005263&form=6&db=m	Evasion of immune responses to introduced human acid alpha-glucosidase by liver-restricted expression in glycogen storage disease type II.	causal interaction,ongoing research,unassigned	4,2,0	
3.2.1.106	Respiratory Insufficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17245350&form=6&db=m	Physiological Correction of Pompe Disease by Systemic Delivery of Adeno-associated Virus Serotype 1 Vectors.	causal interaction,unassigned	3,0	
3.2.1.106	Respiratory Insufficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18782850&form=6&db=m	Modulation of glycogen synthesis by RNA interference: towards a new therapeutic approach for glycogenosis type II.	causal interaction,unassigned	4,0	
3.2.1.106	Respiratory Insufficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21550241&form=6&db=m	Recombinant human acid alpha-glucosidase (rhGAA) in adult patients with severe respiratory failure due to Pompe disease.	causal interaction,ongoing research,unassigned	4,4,0	
3.2.1.106	Respiratory Insufficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21763167&form=6&db=m	Rate of progression and predictive factors for pulmonary outcome in children and adults with Pompe disease.	causal interaction,unassigned	4,0	
3.2.1.106	Respiratory Insufficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24399865&form=6&db=m	Non-muscle involvement in late-onset glycogenosis II.	causal interaction,unassigned	4,0	
3.2.1.106	Respiratory Insufficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25323875&form=6&db=m	Late-onset Glycogen Storage Disease type 2.	causal interaction,therapeutic application,unassigned	4,1,0	
3.2.1.106	Respiratory Insufficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28838325&form=6&db=m	A study on the safety and efficacy of reveglucosidase alfa in patients with late-onset Pompe disease.	causal interaction,diagnostic usage,ongoing research,therapeutic application	4,1,2,2	
3.2.1.106	Respiratory Insufficiency	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33953320&form=6&db=m	Three-dimensional tissue-engineered human skeletal muscle model of Pompe disease.	causal interaction,therapeutic application,unassigned	4,3,0	
3.2.1.106	Sarcoma	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2539799&form=6&db=m	Inhibition of glycosylation processing alters the growth parameters of cells transformed by the oncogene of simian sarcoma virus.	ongoing research,therapeutic application,unassigned	3,1,0	
3.2.1.106	Speech Disorders	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28039015&form=6&db=m	Longitudinal follow-up to evaluate speech disorders in early-treated patients with infantile-onset Pompe disease.	causal interaction,therapeutic application,unassigned	2,4,0	
3.2.1.106	Spinocerebellar Ataxias	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22992774&form=6&db=m	Pentanucleotide repeat-primed PCR for genetic diagnosis of spinocerebellar ataxia type 31.	unassigned	-	
3.2.1.106	Spinocerebellar Ataxias	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26663503&form=6&db=m	Voiding Dysfunction in Spinocerebellar Ataxia Type 31.	diagnostic usage,unassigned	3,0	
3.2.1.106	Starvation	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1582534&form=6&db=m	Heterogeneity of glycogen synthesis upon refeeding following starvation.	unassigned	-	
3.2.1.106	Starvation	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8330029&form=6&db=m	Processing and secretion of lysosomal acid alpha-glucosidase in Tetrahymena wild type and secretion-deficient mutant cells.	ongoing research,unassigned	4,0	
3.2.1.106	Vesicular Stomatitis	http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6232135&form=6&db=m	Inhibition of N-linked oligosaccharide trimming does not interfere with surface expression of certain integral membrane proteins.	ongoing research,therapeutic application,unassigned	2,1,0