PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
3629626-3	1987	The renal toxicity of cis-DDP, indicated by increases in blood urea nitrogen (BUN), serum creatinine and urinary activity of N-acetylglucosaminidase (NAG), was significantly enhanced by a decrease in dietary selenium level.	Cisplatin	22-29	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	125-148
3629626-3	1987	The renal toxicity of cis-DDP, indicated by increases in blood urea nitrogen (BUN), serum creatinine and urinary activity of N-acetylglucosaminidase (NAG), was significantly enhanced by a decrease in dietary selenium level.	Cisplatin	22-29	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	150-153
3629626-3	1987	The renal toxicity of cis-DDP, indicated by increases in blood urea nitrogen (BUN), serum creatinine and urinary activity of N-acetylglucosaminidase (NAG), was significantly enhanced by a decrease in dietary selenium level.	Selenium	208-216	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	150-153
28664165-1	2017	Sanfilippo syndrome type B (mucopolysaccharidosis IIIB), caused by inherited deficiency of alpha-N-acetylglucosaminidase (NAGLU), required for lysosomal degradation of heparan sulfate (HS), is a pediatric neurodegenerative disorder with no approved treatment.	Heparitin Sulfate	168-183	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	91-120
33839004-1	2021	Mucopolysaccharidosis IIIB (MPS IIIB, Sanfilippo syndrome type B) is caused by a deficiency in alpha-N-acetylglucosaminidase (NAGLU) activity, which leads to the accumulation of heparan sulfate (HS).	Heparitin Sulfate	178-193	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	95-124
33839004-1	2021	Mucopolysaccharidosis IIIB (MPS IIIB, Sanfilippo syndrome type B) is caused by a deficiency in alpha-N-acetylglucosaminidase (NAGLU) activity, which leads to the accumulation of heparan sulfate (HS).	Heparitin Sulfate	178-193	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	126-131
30101150-1	2018	Sanfilippo syndrome type B (mucopolysaccharidosis type IIIB [MPS IIIB]) is a lysosomal storage disorder primarily affecting the brain that is caused by a deficiency in the enzyme alpha-N-acetylglucosaminidase (NAGLU), leading to intralysosomal accumulation of heparan sulfate.	Heparitin Sulfate	260-275	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	179-208
29186350-1	2018	Mucopolysaccharidosis IIIB is a paediatric lysosomal storage disease caused by deficiency of the enzyme alpha-N-acetylglucosaminidase (NAGLU), involved in the degradation of the glycosaminoglycan heparan sulphate.	glycosaminoglycan heparan sulphate	178-212	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	104-133
29186350-1	2018	Mucopolysaccharidosis IIIB is a paediatric lysosomal storage disease caused by deficiency of the enzyme alpha-N-acetylglucosaminidase (NAGLU), involved in the degradation of the glycosaminoglycan heparan sulphate.	glycosaminoglycan heparan sulphate	178-212	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	135-140
29186350-2	2018	Absence of NAGLU leads to accumulation of partially degraded heparan sulphate within lysosomes and the extracellular matrix, giving rise to severe CNS degeneration with progressive cognitive impairment and behavioural problems.	Heparitin Sulfate	61-77	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	11-16
29186350-11	2018	LV.NAGLU treatment led to behavioural correction, normalization of heparan sulphate and sulphation patterning, reduced inflammatory cytokine expression and correction of astrocytosis, microgliosis and lysosomal compartment size throughout the brain.	Heparitin Sulfate	67-83	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	3-8
29180785-7	2017	The deficiency of Naglu caused the accumulation of glycosaminoglycans in all studied mouse models lacking the Hsd17b1 gene.	Glycosaminoglycans	51-69	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	18-23
6832343-3	1983	Treatment with suramin resulted in marked alterations in the cell biology of the macrophage: (i) increased vacuolization and protein content, (ii) suppressed intracellular phagosome-lysosome fusion, (iii) decreased activity of the lysosomal enzymes beta-glucuronidase and N-acetyl-glucosaminidase, and (iv) enhanced exocytosis of acid phosphatase during phagocytosis.	Suramin	15-22	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	272-296
6832343-4	1983	Addition of suramin, in vitro, to cell lysates resulted in a reduction in the catalytic activities of acid phosphatase, beta-glucuronidase, and N-acetyl-glucosaminidase; thereby suggesting that selective interaction, in vivo, between suramin and lysosomes containing beta-glucuronidase and N-acetyl-glucosaminidase may have occurred.	Suramin	12-19	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	144-168
6832343-4	1983	Addition of suramin, in vitro, to cell lysates resulted in a reduction in the catalytic activities of acid phosphatase, beta-glucuronidase, and N-acetyl-glucosaminidase; thereby suggesting that selective interaction, in vivo, between suramin and lysosomes containing beta-glucuronidase and N-acetyl-glucosaminidase may have occurred.	Suramin	12-19	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	290-314
7157422-2	1982	Whereas others have found that nephrotoxins such as sodium salicylate and biphenyl cause increases in urinary NAG, we observed that these furans, which were shown to be nephrotoxic by histological procedures, caused significant decreases in urinary levels of the enzyme.	Sodium Salicylate	52-69	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	110-113
520650-1	1979	Cultured mouse peritoneal macrophages were shown to secrete the lysosomal enzyme N-acetyl-glucosaminidase (N-ac-Glu) in response to IgG-Sepharose and some other non-endocytosable particles without substantial release of the cytoplasmic enzyme, lactate dehydrogenase.	Sepharose	136-145	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	81-105
520650-1	1979	Cultured mouse peritoneal macrophages were shown to secrete the lysosomal enzyme N-acetyl-glucosaminidase (N-ac-Glu) in response to IgG-Sepharose and some other non-endocytosable particles without substantial release of the cytoplasmic enzyme, lactate dehydrogenase.	Sepharose	136-145	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	107-115
32111039-1	2020	Mucopolysaccharidosis IIIB (MPS IIIB) is an inherited metabolic disease due to deficiency of alpha-N-Acetylglucosaminidase (NAGLU) enzyme with subsequent storage of undegraded heparan sulfate (HS).	Heparitin Sulfate	176-191	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	124-129
32111039-1	2020	Mucopolysaccharidosis IIIB (MPS IIIB) is an inherited metabolic disease due to deficiency of alpha-N-Acetylglucosaminidase (NAGLU) enzyme with subsequent storage of undegraded heparan sulfate (HS).	Heparitin Sulfate	193-195	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	124-129
29484750-6	2018	Costunolide treatment attenuated the main components of the fibrovascular tissue, wet weight, vascularization (Hb content), macrophage recruitment (NAG activity), collagen deposition, and the levels of vascular endothelial growth factor (VEGF), interleukin (IL)-1beta, IL-6, IL-17, tumor necrosis factor (TNF)-alpha and transforming growth factor (TGF-beta).	costunolide	0-11	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	148-151
28664165-1	2017	Sanfilippo syndrome type B (mucopolysaccharidosis IIIB), caused by inherited deficiency of alpha-N-acetylglucosaminidase (NAGLU), required for lysosomal degradation of heparan sulfate (HS), is a pediatric neurodegenerative disorder with no approved treatment.	Heparitin Sulfate	185-187	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	91-120
28664165-1	2017	Sanfilippo syndrome type B (mucopolysaccharidosis IIIB), caused by inherited deficiency of alpha-N-acetylglucosaminidase (NAGLU), required for lysosomal degradation of heparan sulfate (HS), is a pediatric neurodegenerative disorder with no approved treatment.	Heparitin Sulfate	185-187	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	122-127
28664165-1	2017	Sanfilippo syndrome type B (mucopolysaccharidosis IIIB), caused by inherited deficiency of alpha-N-acetylglucosaminidase (NAGLU), required for lysosomal degradation of heparan sulfate (HS), is a pediatric neurodegenerative disorder with no approved treatment.	Heparitin Sulfate	168-183	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	122-127
20053525-5	2010	Metformin treatment attenuated the main components of the fibrovascular tissue, wet weight, vascularization (Hb content), macrophage recruitment (NAG activity), collagen deposition and the levels of transforming growth factor (TGF-beta1) intraimplant.	Metformin	0-9	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	146-149
28664165-4	2017	1 day after the last dose, BMN 250 (100 mug doses) resulted in above-normal NAGLU activity levels, broad biodistribution, and uptake in all cell types, with NAGLU predominantly localized to neurons in the Naglu-/- mouse brain.	bmn	27-30	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	76-81
28664165-4	2017	1 day after the last dose, BMN 250 (100 mug doses) resulted in above-normal NAGLU activity levels, broad biodistribution, and uptake in all cell types, with NAGLU predominantly localized to neurons in the Naglu-/- mouse brain.	bmn	27-30	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	205-210
26147524-1	2015	Mucopolysaccharidosis (MPS) IIIB is a lysosomal disease due to the deficiency of the enzyme alpha-N-acetylglucosaminidase (NAGLU) required for heparan sulfate (HS) degradation.	Heparitin Sulfate	143-158	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	92-121
26147524-1	2015	Mucopolysaccharidosis (MPS) IIIB is a lysosomal disease due to the deficiency of the enzyme alpha-N-acetylglucosaminidase (NAGLU) required for heparan sulfate (HS) degradation.	Heparitin Sulfate	143-158	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	123-128
26147524-1	2015	Mucopolysaccharidosis (MPS) IIIB is a lysosomal disease due to the deficiency of the enzyme alpha-N-acetylglucosaminidase (NAGLU) required for heparan sulfate (HS) degradation.	Heparitin Sulfate	160-162	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	92-121
26147524-1	2015	Mucopolysaccharidosis (MPS) IIIB is a lysosomal disease due to the deficiency of the enzyme alpha-N-acetylglucosaminidase (NAGLU) required for heparan sulfate (HS) degradation.	Heparitin Sulfate	160-162	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	123-128
25332157-0	2015	Oxidative stress is independent of inflammation in the neurodegenerative Sanfilippo syndrome type B. Mucopolysaccharidosis (MPS) type IIIB is a genetic deficiency of alpha-N-acetylglucosaminidase, inducing accumulation of partially degraded heparan sulfate (HS) oligosaccharides in tissues.	Heparitin Sulfate	241-256	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	166-195
25332157-0	2015	Oxidative stress is independent of inflammation in the neurodegenerative Sanfilippo syndrome type B. Mucopolysaccharidosis (MPS) type IIIB is a genetic deficiency of alpha-N-acetylglucosaminidase, inducing accumulation of partially degraded heparan sulfate (HS) oligosaccharides in tissues.	Heparitin Sulfate	258-260	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	166-195
25332157-0	2015	Oxidative stress is independent of inflammation in the neurodegenerative Sanfilippo syndrome type B. Mucopolysaccharidosis (MPS) type IIIB is a genetic deficiency of alpha-N-acetylglucosaminidase, inducing accumulation of partially degraded heparan sulfate (HS) oligosaccharides in tissues.	Oligosaccharides	262-278	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	166-195
26850371-5	2016	The findings showed that subchronic TiO2 NPs exposure increased levels of urinary creatisix (Cr), N-acetyl-glucosaminidase, and vanin-1, resulted in severe renal inflammation and fibration.	titanium dioxide	36-40	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	98-122
27064211-5	2016	An immunoprecipitation method together with liquid chromatography-tandem mass spectrometry showed that alpha-N-acetylglucosaminidase (Naglu; a degradation enzyme of heparan sulfate) is one of the glycoproteins recognized by Ts4 in the epididymal spermatozoa.	Heparitin Sulfate	165-180	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	103-132
27064211-5	2016	An immunoprecipitation method together with liquid chromatography-tandem mass spectrometry showed that alpha-N-acetylglucosaminidase (Naglu; a degradation enzyme of heparan sulfate) is one of the glycoproteins recognized by Ts4 in the epididymal spermatozoa.	Heparitin Sulfate	165-180	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	134-139
27064211-10	2016	The Ts4-recognized fucosylated agalactobiantennary complex-type glycan with bisecting N-acetylglucosamine and Naglu on cauda epididymal spermatozoa may play a role in the process of fertilization.	agalactobiantennary	31-50	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	110-115
27064211-10	2016	The Ts4-recognized fucosylated agalactobiantennary complex-type glycan with bisecting N-acetylglucosamine and Naglu on cauda epididymal spermatozoa may play a role in the process of fertilization.	Polysaccharides	64-70	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	110-115
25267636-2	2014	The cause is mutation in the gene encoding alpha-N-acetylglucosaminidase (NAGLU), deficiency of NAGLU, and accumulation of heparan sulfate.	Heparitin Sulfate	123-138	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	43-72
25267636-4	2014	To overcome the first impediment, a fusion protein of recombinant NAGLU and a fragment of insulin-like growth factor II (IGFII) was prepared for endocytosis by the mannose 6-phosphate/IGFII receptor.	mannose-6-phosphate	164-183	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	66-71
24419745-5	2014	Xanthones significantly ameliorated the severity of AA indicated by the physical parameters changes, and reverted the abnormal changes of MDA, GSH, NAG and SA in liver.	Xanthones	0-9	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	148-151
23395890-6	2013	Strychnine treatment attenuated the main components of the fibrovascular tissue, wet weight, vascularization (Hb content), macrophage recruitment (NAG activity), collagen deposition and the levels of vascular endothelial growth factor (VEGF), tumour necrosis factor (TNF)-alpha and transforming growth factor (TGF-beta).	Strychnine	0-10	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	147-150
22867887-1	2012	Mucopolysaccharidosis type IIIB (MPS IIIB) is a neuropathic lysosomal storage disorder (LSD) resulting from an inherited deficiency of N-acetyl-alpha-D-glucosaminidase (Naglu) activity, an enzyme required to degrade the glycosaminoglycan heparan sulfate (HS).	Glycosaminoglycans	220-237	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	135-167
22867887-1	2012	Mucopolysaccharidosis type IIIB (MPS IIIB) is a neuropathic lysosomal storage disorder (LSD) resulting from an inherited deficiency of N-acetyl-alpha-D-glucosaminidase (Naglu) activity, an enzyme required to degrade the glycosaminoglycan heparan sulfate (HS).	Glycosaminoglycans	220-237	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	169-174
22867887-1	2012	Mucopolysaccharidosis type IIIB (MPS IIIB) is a neuropathic lysosomal storage disorder (LSD) resulting from an inherited deficiency of N-acetyl-alpha-D-glucosaminidase (Naglu) activity, an enzyme required to degrade the glycosaminoglycan heparan sulfate (HS).	Heparitin Sulfate	238-253	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	135-167
22867887-1	2012	Mucopolysaccharidosis type IIIB (MPS IIIB) is a neuropathic lysosomal storage disorder (LSD) resulting from an inherited deficiency of N-acetyl-alpha-D-glucosaminidase (Naglu) activity, an enzyme required to degrade the glycosaminoglycan heparan sulfate (HS).	Heparitin Sulfate	238-253	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	169-174
22867887-1	2012	Mucopolysaccharidosis type IIIB (MPS IIIB) is a neuropathic lysosomal storage disorder (LSD) resulting from an inherited deficiency of N-acetyl-alpha-D-glucosaminidase (Naglu) activity, an enzyme required to degrade the glycosaminoglycan heparan sulfate (HS).	Heparitin Sulfate	255-257	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	135-167
22867887-1	2012	Mucopolysaccharidosis type IIIB (MPS IIIB) is a neuropathic lysosomal storage disorder (LSD) resulting from an inherited deficiency of N-acetyl-alpha-D-glucosaminidase (Naglu) activity, an enzyme required to degrade the glycosaminoglycan heparan sulfate (HS).	Heparitin Sulfate	255-257	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	169-174
22867887-2	2012	A deficiency in Naglu activity leads to lysosomal accumulation of HS as a primary storage substrate, and the gangliosides GM2 and GM3 as secondary accumulation products.	Gangliosides	109-121	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	16-21
22536363-4	2012	O-GlcNAcylation is dynamically regulated by O-GlcNAc transferase, the enzyme catalyzing the transfer of GlcNAc to proteins, and N-acetylglucosaminidase (OGA), the enzyme catalyzing the removal of GlcNAc from proteins.	2-acetamido-2-deoxy-4-O-(beta-2-acetamid-2-deoxyglucopyranosyl)glucopyranose	2-8	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	128-151
21618584-1	2011	The accumulation of heparan sulfate (HS) in lysosomes is the primary consequence of the enzyme defect (alpha-N-acetylglucosaminidase) in mucopolysaccharidosis type IIIB.	Heparitin Sulfate	20-35	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	103-132
21618584-1	2011	The accumulation of heparan sulfate (HS) in lysosomes is the primary consequence of the enzyme defect (alpha-N-acetylglucosaminidase) in mucopolysaccharidosis type IIIB.	Heparitin Sulfate	37-39	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	103-132
21408219-1	2011	BACKGROUND: Sanfilippo syndrome type B (MPS III B) is caused by a deficiency of alpha-N-acetylglucosaminidase enzyme, leading to accumulation of heparan sulfate within lysosomes and eventual progressive cerebral and systemic multiple organ abnormalities.	Heparitin Sulfate	145-160	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	80-109
2165995-2	1990	The administration of CDDP alone at doses of 50 mumols/kg caused the increase of blood urea nitrogen (BUN) and urinary N-acetylglucosaminidase (NAG) and the degeneration of proximal tubule cells pathologically.	Cisplatin	22-26	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	119-142
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.	Heparitin Sulfate	141-156	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	68-104
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.	Heparitin Sulfate	141-156	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	106-111
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.	Heparitin Sulfate	158-160	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	68-104
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.	Heparitin Sulfate	158-160	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	106-111
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	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	68-104
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	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	106-111
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	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	68-104
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	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	106-111
17185018-1	2007	The neurodegenerative disease MPS III B (Sanfilippo syndrome type B) is caused by mutations in the gene encoding the lysosomal enzyme alpha-N-acetylglucosaminidase, with a resulting block in heparan sulfate degradation.	Heparitin Sulfate	191-206	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	134-163
15581054-2	2004	Using an in vivo tumor model, we report that thalidomide (100 mg kg(-1)day(-1)) or clotrimazole (120 mg kg(-1) day(-1)), inhibit blood vessel formation (determined by hemoglobin content), leukocyte recruitment [myeloperoxidase (MPO) activity; N-acetylglucosa-minidase (NAG) activity], and vascular endothelial growth factor production.	Thalidomide	45-56	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	243-267
15581054-2	2004	Using an in vivo tumor model, we report that thalidomide (100 mg kg(-1)day(-1)) or clotrimazole (120 mg kg(-1) day(-1)), inhibit blood vessel formation (determined by hemoglobin content), leukocyte recruitment [myeloperoxidase (MPO) activity; N-acetylglucosa-minidase (NAG) activity], and vascular endothelial growth factor production.	Thalidomide	45-56	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	269-272
15581054-2	2004	Using an in vivo tumor model, we report that thalidomide (100 mg kg(-1)day(-1)) or clotrimazole (120 mg kg(-1) day(-1)), inhibit blood vessel formation (determined by hemoglobin content), leukocyte recruitment [myeloperoxidase (MPO) activity; N-acetylglucosa-minidase (NAG) activity], and vascular endothelial growth factor production.	Clotrimazole	83-95	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	243-267
15581054-2	2004	Using an in vivo tumor model, we report that thalidomide (100 mg kg(-1)day(-1)) or clotrimazole (120 mg kg(-1) day(-1)), inhibit blood vessel formation (determined by hemoglobin content), leukocyte recruitment [myeloperoxidase (MPO) activity; N-acetylglucosa-minidase (NAG) activity], and vascular endothelial growth factor production.	Clotrimazole	83-95	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	269-272
15581054-5	2004	Thalidomide was able to reduce the inflammatory reaction (MPO and NAG activities) by 50% to 70%, but was unable to delay tumor development.	Thalidomide	0-11	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	66-69
10814850-4	2000	Nodularin induces the activity of beta-D-glucuronidase, alpha-glucosidase, lysosomal esterase and N-acetyl-glucosaminidase and influenced on the labilization of endoplasmatic reticulum membranes.	nodularin	0-9	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	98-122
8933637-11	1996	In male and female mice of the 20% erythritol group, the creatinine-normalized urinary excretion of protein, K-glutamyltransferase (GGT), and electrolytes (Na+, K+, Ca2+, Pi, citrate) was significantly increased while urinary N-acetylglucosaminidase (NAG) remained unchanged.	Erythritol	35-45	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	226-249
8933637-11	1996	In male and female mice of the 20% erythritol group, the creatinine-normalized urinary excretion of protein, K-glutamyltransferase (GGT), and electrolytes (Na+, K+, Ca2+, Pi, citrate) was significantly increased while urinary N-acetylglucosaminidase (NAG) remained unchanged.	Erythritol	35-45	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	251-254
8933637-11	1996	In male and female mice of the 20% erythritol group, the creatinine-normalized urinary excretion of protein, K-glutamyltransferase (GGT), and electrolytes (Na+, K+, Ca2+, Pi, citrate) was significantly increased while urinary N-acetylglucosaminidase (NAG) remained unchanged.	Creatinine	57-67	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	226-249
8933637-11	1996	In male and female mice of the 20% erythritol group, the creatinine-normalized urinary excretion of protein, K-glutamyltransferase (GGT), and electrolytes (Na+, K+, Ca2+, Pi, citrate) was significantly increased while urinary N-acetylglucosaminidase (NAG) remained unchanged.	Creatinine	57-67	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	251-254
8933637-13	1996	In rats, the creatinine-normalized urinary excretion of GGT, NAG, and some electrolytes (Na+, K+, and Ca2+) was increased in some erythritol groups but a clear dose-response relationship was evident only for calcium.	Creatinine	13-23	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	61-64
8933637-13	1996	In rats, the creatinine-normalized urinary excretion of GGT, NAG, and some electrolytes (Na+, K+, and Ca2+) was increased in some erythritol groups but a clear dose-response relationship was evident only for calcium.	Erythritol	130-140	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	61-64
20017592-7	2010	O(3) exposure enhanced the Ova-induced increase in inflammatory cell infiltration and N-acetylglucosaminidase (NAG) in the lung, but had no effect on R(L) or E(L).	Ozone	0-4	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	86-109
19524658-9	2009	Intraplantar injection of costunolide also reduced the paw oedema, myeloperoxidase and N-acetyl-glucosaminidase activity induced by Cg in mice.	costunolide	26-37	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	87-111
19524658-9	2009	Intraplantar injection of costunolide also reduced the paw oedema, myeloperoxidase and N-acetyl-glucosaminidase activity induced by Cg in mice.	Carrageenan	132-134	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	87-111
19416848-8	2009	P-tau was found in MEC of Naglu(-/-) mice, in the same neurons as lysozyme.	p-tau	0-5	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	26-31
19232362-11	2009	However, NAG activity was reduced by pentoxifylline, but not by cilostazol.	Pentoxifylline	37-51	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	9-12
15649123-1	2005	The Sanfilippo syndrome type B (mucopolysaccharidosis IIIB) is an autosomal recessive disorder due to mutations in the gene encoding NAGLU (alpha-N-acetylglucosaminidase), one of the enzymes required for the degradation of the GAG (glycosaminoglycan) heparan sulphate.	gag (glycosaminoglycan) heparan sulphate	227-267	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	133-138
15649123-1	2005	The Sanfilippo syndrome type B (mucopolysaccharidosis IIIB) is an autosomal recessive disorder due to mutations in the gene encoding NAGLU (alpha-N-acetylglucosaminidase), one of the enzymes required for the degradation of the GAG (glycosaminoglycan) heparan sulphate.	gag (glycosaminoglycan) heparan sulphate	227-267	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	140-169
15649123-7	2005	Expression of 1% normal NAGLU activity in liver resulted in a 77% decrease in the GAG content; more remarkably, an expression of 0.16% normal activity in lung was capable of decreasing the GAG level by 29%.	Glycosaminoglycans	82-85	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	24-29
15649123-7	2005	Expression of 1% normal NAGLU activity in liver resulted in a 77% decrease in the GAG content; more remarkably, an expression of 0.16% normal activity in lung was capable of decreasing the GAG level by 29%.	Glycosaminoglycans	189-192	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	24-29
15308126-8	2004	A low level of alpha-N-acetylglucosaminidase activity, as little as provided by transplantation of unmodified Naglu +/+ bone marrow, could normalize biochemical defects (glycosaminoglycan storage and beta-hexosaminidase elevation) in liver and spleen, but a very high level was required for an effect on kidney.	Glycosaminoglycans	170-187	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	15-44
14727810-2	2003	It is characterized by systemic heparan sulfate accumulation in lysosomes due to deficiency of the enzyme alpha-N-acetylglucosaminidase (Naglu).	Heparitin Sulfate	32-47	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	106-135
14727810-2	2003	It is characterized by systemic heparan sulfate accumulation in lysosomes due to deficiency of the enzyme alpha-N-acetylglucosaminidase (Naglu).	Heparitin Sulfate	32-47	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	137-142
10588735-1	1999	The Sanfilippo syndrome type B is an autosomal recessive disorder caused by mutation in the gene (NAGLU) encoding alpha-N-acetylglucosaminidase, a lysosomal enzyme required for the stepwise degradation of heparan sulfate.	Heparitin Sulfate	205-220	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	98-103
10588735-1	1999	The Sanfilippo syndrome type B is an autosomal recessive disorder caused by mutation in the gene (NAGLU) encoding alpha-N-acetylglucosaminidase, a lysosomal enzyme required for the stepwise degradation of heparan sulfate.	Heparitin Sulfate	205-220	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	114-143
1462869-3	1992	The development of inflammation induced by zymosan was followed by increase activity of macrophage activation markers - beta-N-acetylglucosaminidase (NAGlu) and beta-N-acetylgalactosaminidase (NAGal) in liver and serum.	Zymosan	43-50	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	120-148
1462869-3	1992	The development of inflammation induced by zymosan was followed by increase activity of macrophage activation markers - beta-N-acetylglucosaminidase (NAGlu) and beta-N-acetylgalactosaminidase (NAGal) in liver and serum.	Zymosan	43-50	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	150-155
2165995-3	1990	The co-administration of Se, especially at doses of 20 mumols/kg/day, inhibited the increase of BUN and urinary NAG and depressed the degeneration of proximal tubule cells.	Selenious Acid	25-27	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	112-115
2165995-2	1990	The administration of CDDP alone at doses of 50 mumols/kg caused the increase of blood urea nitrogen (BUN) and urinary N-acetylglucosaminidase (NAG) and the degeneration of proximal tubule cells pathologically.	Cisplatin	22-26	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	144-147
35155448-10	2021	However, the application of selective VEGFR2 and ERKs inhibitors, SU5614 and PD98059, respectively, could reverse the abnormal lysosomal storage caused by NAGLU knockdown.	SU 5614	66-72	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	155-160
35155448-10	2021	However, the application of selective VEGFR2 and ERKs inhibitors, SU5614 and PD98059, respectively, could reverse the abnormal lysosomal storage caused by NAGLU knockdown.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	77-84	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	155-160
35155448-11	2021	These results indicated that downregulation of NAGLU in HUVEC increases the abnormal accumulation of lysosomes and may be a potential biomarker for the diagnosis of EAS.	CHEMBL4167713	165-168	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	47-52