PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
7896015-2	1995	AGU patients are deficient in glycosylasparaginase (GA), which results in accumulation of aspartylglucosamine in body fluids and tissues.	N-acetylglucosaminylasparagine	90-109	aspartylglucosaminidase	Homo sapiens	30-50	
7896015-2	1995	AGU patients are deficient in glycosylasparaginase (GA), which results in accumulation of aspartylglucosamine in body fluids and tissues.	N-acetylglucosaminylasparagine	90-109	aspartylglucosaminidase	Homo sapiens	52-54	
7896015-6	1995	Supplementation of culture medium with either isoform cleared AGU lymphoblasts of stored aspartylglucosamine when glycosylasparaginase activity in the cells reached 3-4% of that in normal lymphoblasts.	N-acetylglucosaminylasparagine	89-108	aspartylglucosaminidase	Homo sapiens	114-134	
1138532-2	1975	Aspartylglycosaminuria (AGU) is a hereditary metabolic disorder characterized by slowly progressive mental deterioration from infancy, urinary excretion of large amounts of aspartylglycosamine, and decreased activity of the lysosomal enzyme aspartylglcosamine amido hydrolase in various body tissues and fluids.	N-acetylglucosaminylasparagine	173-192	aspartylglucosaminidase	Homo sapiens	24-27	
27906067-4	2016	Progressive intellectual and physical disability is the main symptom leading to death usually before the age of 50 years.The disease is caused by the deficient activity of the lysosomal enzyme glycosylasparaginase (aspartylglucosaminidase, AGA), which leads to a disorder in the degradation of glycoasparagines - aspartylglucosamine or other glycoconjugates with an aspartylglucosamine moiety at their reducing end - and accumulation of these undegraded glycoasparagines in tissues and body fluids.	N-acetylglucosaminylasparagine	313-332	aspartylglucosaminidase	Homo sapiens	240-243