PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10570220-1 2000 We show here that cell surface glycosaminoglycans (GAGs) are involved in the binding of stromal cell-derived factor (SDF)-1alpha to CD4(+)lymphoid CEM or monocytic U937 cells, inasmuch as pretreating the cells with heparitinase or chondroitinase inhibits SDF-1alpha binding by 40-41% and 31-35%, respectively. Glycosaminoglycans 31-49 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 231-245 12442278-2 2002 The deficiency of N-acetylgalactosamine-6-sulfate sulfatase leads to lysosomal accumulation of undegraded glycosaminoglycans, keratan sulfate and chondroitin-6-sulfate. Glycosaminoglycans 106-124 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 18-59 16378744-1 2006 Mucopolysaccharidosis type IVA (MPS IVA; OMIM #253000) or Morquio A syndrome is an autosomal recessive inborn error resulting from the deficient activity of the lysosomal enzyme, N-acetylgalactosamine-6-sulfatase (GALNS), and the progressive lysosomal accumulation of sulfated glycosaminoglycans. Glycosaminoglycans 277-295 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 179-212 16287098-2 2005 GALNS is required to degrade glycosaminoglycans, keratan sulfate (KS), and chondroitin-6-sulfate. Glycosaminoglycans 29-47 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 0-5 14585696-5 2004 Chondroitinase degradation of GAG resulted in swelling of the struts, causing the pores to become smaller and rounder. Glycosaminoglycans 30-33 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 0-14 14585696-6 2004 The compressive modulus of the collagen-GAG matrix decreased when degraded by collagenase, but remained unchanged when degraded by chondroitinase. Glycosaminoglycans 40-43 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 131-145 14585696-8 2004 This investigation provides information that can be used to design collagen-GAG scaffolds with desired compressive stiffness and degradation rate to collagenase and chondroitinase. Glycosaminoglycans 76-79 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 165-179 10570220-1 2000 We show here that cell surface glycosaminoglycans (GAGs) are involved in the binding of stromal cell-derived factor (SDF)-1alpha to CD4(+)lymphoid CEM or monocytic U937 cells, inasmuch as pretreating the cells with heparitinase or chondroitinase inhibits SDF-1alpha binding by 40-41% and 31-35%, respectively. Glycosaminoglycans 51-55 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 231-245 8174650-2 1994 Enzyme digestion methods with streptomyces hyaluronidase, chondroitinase and keratanase showed that the main component of glycosaminoglycans in the cornea was hyaluronic acid at the early stage and chondroitin sulfate from the middle stage to the neonatal stage. Glycosaminoglycans 122-140 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 58-72 10650714-6 1999 Chondroitinase has been used in this study to probe the influence of GAG on the physico-chemical characteristic of keloid collagen. Glycosaminoglycans 69-72 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 0-14 8001980-1 1994 Deficiency of the lysosomal enzyme, N-acetylgalactosamine 6-sulfatase (GALNS;EC 3.1.6.4), results in the storage of the glycosaminoglycans, keratan sulfate and chondroitin 6-sulfate, which leads to the lysosomal storage disorder Morquio A syndrome. Glycosaminoglycans 120-138 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 36-69 7915457-1 1994 The disaccharide contents of chondroitinase-digestible glycosaminoglycans extracted from a 6-mm punch biopsy of the forearm skin were determined using high-performance liquid chromatography after 1-phenyl-3-methyl-5-pyrasolone labelling. Glycosaminoglycans 55-73 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 29-43 8001980-1 1994 Deficiency of the lysosomal enzyme, N-acetylgalactosamine 6-sulfatase (GALNS;EC 3.1.6.4), results in the storage of the glycosaminoglycans, keratan sulfate and chondroitin 6-sulfate, which leads to the lysosomal storage disorder Morquio A syndrome. Glycosaminoglycans 120-138 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 71-76 6209270-3 1984 The glycosaminoglycan side chains (Mr = 55,000) were found to be composed of 75% chondroitin sulfate and 23% dermatan sulfate as determined by chondroitinase ABC or AC II digestion. Glycosaminoglycans 4-21 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 143-157 8240239-4 1993 The largest form was detected only after chondroitinase treatment and represents the proteoglycan form of the molecule from which the glycosaminoglycan chains have been removed. Glycosaminoglycans 134-151 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 41-55 33304816-1 2020 Introduction: Mucopolysaccharidosis type IV A (MPS IVA) or Morquio A syndrome is an autosomal recessive lysosomal storage disease caused by GALNS gene mutations that lead to a deficiency of the N-acetylgalactosamine-6-sulfate sulfatase enzyme and the accumulation of two glycosaminoglycans in cell lysosomes, namely, chondroitin and keratan sulfate. Glycosaminoglycans 271-289 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 140-145 6195665-3 1983 Separation of the various labeled glycosaminoglycans by chondroitinase digestion and chromatography revealed a transient rise from controls (P less than or equal to 0.05) in the proportion of labeled chondroitin 4-sulfate at 5 days, followed by an increase from controls (P less than or equal to 0.05) in proportionate labeling of dermatan sulfate at 15 and 45 days postbleomycin. Glycosaminoglycans 34-52 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 56-70 6195665-5 1983 Grain formation was greatly reduced by pretreatment of the slide sections with hyaluronidase and chondroitinase, demonstrating the specificity of the label for glycosaminoglycans. Glycosaminoglycans 160-178 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 97-111 6809361-3 1982 Our results could be explained by the hypothesis that accumulation of keratan sulfate and chondroitin 6-sulfate in Morquio syndrome is due to a deficiency of galactose 6-sulfate sulfatase and N-acetylgalactosamine 6-sulfate sulfatase activity, which are necessary for the degradation of these two mucopolysaccharides. Glycosaminoglycans 297-316 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 158-187 6809361-3 1982 Our results could be explained by the hypothesis that accumulation of keratan sulfate and chondroitin 6-sulfate in Morquio syndrome is due to a deficiency of galactose 6-sulfate sulfatase and N-acetylgalactosamine 6-sulfate sulfatase activity, which are necessary for the degradation of these two mucopolysaccharides. Glycosaminoglycans 297-316 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 192-233 798737-0 1976 The exzymatic determination of acidic glycosaminoglycans in scar and keloid wtih chondroitinase. Glycosaminoglycans 38-56 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 81-95 204626-3 1978 The determination is based on the color production of D-gluco-4-enepyranosyluronic acid-containing disaccharides produced by the action of chondroitinase-ABC and -AC (acidic glycosaminoglycans-endoeliminase) when the periodate-thiobarbituric acid method is applied to the alpha,beta-unsaturated disaccharides. Glycosaminoglycans 174-192 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 139-153 33636292-1 2021 Mucopolysaccharidosis type IVA (MPS IVA) is a lysosomal storage disease produced by the deficiency of the N-acetylgalactosamine-6-sulfate sulfatase (GALNS) enzyme, leading to glycosaminoglycans (GAGs) accumulation. Glycosaminoglycans 175-193 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 149-154 33957983-1 2021 BACKGROUND: Mucopolysaccharidosis IVA (Morquio A syndrome) is a lysosomal storage disease caused by the deficiency of enzyme N-acetylgalactosamine-6-sulfate sulfatase (GALNS), which results in the accumulation of the glycosaminoglycans (GAGs), keratan sulfate, and chondroitin-6-sulfate in the lysosomes of all tissues causing systemic dysfunction. Glycosaminoglycans 217-235 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 168-173 32905071-1 2020 Mucopolysaccharidosis type IVA (MPS IVA) is an inborn error of glycosaminoglycan (GAG) catabolism characterized by a deficiency of the lysosomal enzyme, N-acetylgalactosamine 6-sulphatase (GALNS). Glycosaminoglycans 82-85 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 189-194 33390680-1 2020 Morquio syndrome is caused by the deficiency of N-acetylgalactosamine-6-sulfate sulfatase (GALNS) enzyme, which is required for the catabolism of glycosaminoglycans (namely, chondroitin-6-sulfate and keratan sulfate). Glycosaminoglycans 146-164 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 91-96 28904929-2 2017 The loss of GALNS activity leads to the impaired breakdown of glycosaminoglycans (GAGs) keratan sulfate and chondroitin-6-sulfate. Glycosaminoglycans 62-80 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 12-17 30797135-2 2019 GALNS encodes N-acetylgalactosamine-6-sulfatase that breaks down certain complex carbohydrates known as glycosaminoglycans (GAGs). Glycosaminoglycans 104-122 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 0-5 30797135-2 2019 GALNS encodes N-acetylgalactosamine-6-sulfatase that breaks down certain complex carbohydrates known as glycosaminoglycans (GAGs). Glycosaminoglycans 124-128 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 0-5 25209263-9 2015 Enzymatic treatments indicate that this barrier likely includes glycosaminoglycans, as it was disrupted by chondroitinase but, less effectively, by proteases. Glycosaminoglycans 64-82 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 107-121 26172013-1 2015 Mucopolysaccharidosis type IV-A (Morquio A disease) is an autosomal recessive lysosomal storage disease caused by mutations in the gene encoding the N-acetylgalactosamine-6-sulfate sulfatase, that results in impaired catabolism of two glycosaminoglycans, chondroitin-6-sulfate and keratan sulfate. Glycosaminoglycans 235-253 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 149-190 25101330-2 2014 GALNS is essential for breakdown of glycosaminoglycans. Glycosaminoglycans 36-54 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 0-5 18373483-0 2008 Single, high-dose intraspinal injection of chondroitinase reduces glycosaminoglycans in injured spinal cord and promotes corticospinal axonal regrowth after hemisection but not contusion. Glycosaminoglycans 66-84 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 43-57 24726177-2 2014 Patients who inherit two mutated GALNS gene alleles have a decreased ability to degrade the glycosaminoglycans (GAGs) keratan sulfate and chondroitin 6-sulfate, thereby causing GAG accumulation within lysosomes and consequently pleiotropic disease. Glycosaminoglycans 92-110 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 33-38 24726177-2 2014 Patients who inherit two mutated GALNS gene alleles have a decreased ability to degrade the glycosaminoglycans (GAGs) keratan sulfate and chondroitin 6-sulfate, thereby causing GAG accumulation within lysosomes and consequently pleiotropic disease. Glycosaminoglycans 112-116 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 33-38 24726177-2 2014 Patients who inherit two mutated GALNS gene alleles have a decreased ability to degrade the glycosaminoglycans (GAGs) keratan sulfate and chondroitin 6-sulfate, thereby causing GAG accumulation within lysosomes and consequently pleiotropic disease. Glycosaminoglycans 112-115 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 33-38 17885814-1 2007 Several methods to alter cell surface glycosaminoglycan (GAG) expression have previously been described, including treatments with chlorate to reduce the addition of charged sulfate groups, xyloside compounds to displace GAGs from their core proteins, and GAG lyases, such as heparinase and chondroitinase, to release GAG fragments from the cell layer. Glycosaminoglycans 38-55 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 291-305 17885814-1 2007 Several methods to alter cell surface glycosaminoglycan (GAG) expression have previously been described, including treatments with chlorate to reduce the addition of charged sulfate groups, xyloside compounds to displace GAGs from their core proteins, and GAG lyases, such as heparinase and chondroitinase, to release GAG fragments from the cell layer. Glycosaminoglycans 57-60 galactosamine (N-acetyl)-6-sulfatase Homo sapiens 291-305