PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
6240800-11	1984	Although the patient was not examined enzymatically, the structure of urinary GAG suggested a defect of alpha-N-acetylglucosaminidase in the patient.	Glycosaminoglycans	78-81	N-acetyl-alpha-glucosaminidase	Homo sapiens	104-133	
6402508-7	1983	When lysosomes deficient in the enzyme alpha-N-acetylglucosaminidase were incubated at 37 degrees C with [3H]acetyl-CoA, tritium was incorporated primarily into glycosaminoglycans.	Glycosaminoglycans	161-179	N-acetyl-alpha-glucosaminidase	Homo sapiens	39-68	
29881562-1	2018	Homozygous or compound heterozygous mutation in the gene encoding N-alpha-acetylglucosaminidase (NAGLU) on chromosome 17q21 results in Sanfilippo B, resulting in excess accumulation of intralysosomal glycosaminoglycans (mucopolysaccharides) in various tissues.	Glycosaminoglycans	220-239	N-acetyl-alpha-glucosaminidase	Homo sapiens	66-95	
29881562-1	2018	Homozygous or compound heterozygous mutation in the gene encoding N-alpha-acetylglucosaminidase (NAGLU) on chromosome 17q21 results in Sanfilippo B, resulting in excess accumulation of intralysosomal glycosaminoglycans (mucopolysaccharides) in various tissues.	Glycosaminoglycans	220-239	N-acetyl-alpha-glucosaminidase	Homo sapiens	97-102	
19399896-1	2009	Sanfilippo syndrome type B (MPS III B) is caused by a deficiency of alpha-N-acetylglucosaminidase enzyme (Naglu), leading to accumulation of heparan sulfate (HS), a glycosaminoglycan (GAG), within lysosomes and to eventual progressive cerebral and systemic multiple organ abnormalities.	Glycosaminoglycans	165-182	N-acetyl-alpha-glucosaminidase	Homo sapiens	28-37	
24266751-6	2014	Glycosaminoglycan storage was reduced by 60% (P<0.001) to near background levels in MPS IIIB cells after treatment with rhNAGLU-IGF-II, with half-maximal correction at concentrations of 3-12 pM.	Glycosaminoglycans	0-17	N-acetyl-alpha-glucosaminidase	Homo sapiens	87-95	
19399896-1	2009	Sanfilippo syndrome type B (MPS III B) is caused by a deficiency of alpha-N-acetylglucosaminidase enzyme (Naglu), leading to accumulation of heparan sulfate (HS), a glycosaminoglycan (GAG), within lysosomes and to eventual progressive cerebral and systemic multiple organ abnormalities.	Glycosaminoglycans	184-187	N-acetyl-alpha-glucosaminidase	Homo sapiens	28-37	
24692796-12	2008	Urinary GAG concentration decreased significantly in all 5 patients with MPS IIIA and in 2 patients with MPS IIIB (P = 0.028).	Glycosaminoglycans	8-11	N-acetyl-alpha-glucosaminidase	Homo sapiens	105-113	
10649686-0	1998	The effect of N-acetylglucosamine as a substrate for in vitro synthesis of glycosaminoglycans by human peritoneal mesothelial cells and fibroblasts.	Glycosaminoglycans	75-93	N-acetyl-alpha-glucosaminidase	Homo sapiens	14-33	
16137227-0	2005	Transplantation of human umbilical cord blood cells benefits an animal model of Sanfilippo syndrome type B. Sanfilippo syndrome type B is caused by alpha-N-acetylglucosaminidase (Naglu) enzyme deficiency leading to an accumulation of undegraded heparan sulfate, a glycosaminoglycan (GAG).	Glycosaminoglycans	283-286	N-acetyl-alpha-glucosaminidase	Homo sapiens	179-184	
10649686-5	1998	Our results demonstrate that NAG is an effective stimulator of the in vitro glycosaminoglycans synthesis by human peritoneal mesothelial cells and fibroblasts.	Glycosaminoglycans	76-94	N-acetyl-alpha-glucosaminidase	Homo sapiens	29-32	
34411609-2	2021	Deficiency in NAGLU results in lysosomal accumulation of glycosaminoglycans (GAGs) and neurological symptoms.	Glycosaminoglycans	57-75	N-acetyl-alpha-glucosaminidase	Homo sapiens	14-19	
34411609-5	2021	MPS IIIB neural stem cells exhibited NAGLU deficiency accompanied with GAG accumulation, as well as lysosomal enlargement and secondary lipid accumulation.	Glycosaminoglycans	71-74	N-acetyl-alpha-glucosaminidase	Homo sapiens	0-8	
2556907-5	1989	In the patients with MPS IIA and MPS IIIB, the white matter did not show the proper signal intensity, which suggested that myelination was insufficient and that infiltration or deposition of glycosaminoglycan had occurred; this was consistent with the association of these two types with mental retardation.	Glycosaminoglycans	191-208	N-acetyl-alpha-glucosaminidase	Homo sapiens	33-41