PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
2512987-0	1989	Release of diamine oxidase into plasma by glycosaminoglycans in rats.	Glycosaminoglycans	42-60	amine oxidase, copper containing 1	Rattus norvegicus	11-26
2512987-2	1989	Intestinal DAO, in analogy with lipoprotein lipase (another heparin-released enzyme), is believed to be electrostatically linked to endothelial binding sites composed of a glycosaminoglycan (GAG) which is presumably heparan sulphate, but the complete mechanism of enzyme release is not known.	Glycosaminoglycans	172-189	amine oxidase, copper containing 1	Rattus norvegicus	11-14
2512987-2	1989	Intestinal DAO, in analogy with lipoprotein lipase (another heparin-released enzyme), is believed to be electrostatically linked to endothelial binding sites composed of a glycosaminoglycan (GAG) which is presumably heparan sulphate, but the complete mechanism of enzyme release is not known.	Glycosaminoglycans	172-189	lipoprotein lipase	Rattus norvegicus	32-50
2512987-2	1989	Intestinal DAO, in analogy with lipoprotein lipase (another heparin-released enzyme), is believed to be electrostatically linked to endothelial binding sites composed of a glycosaminoglycan (GAG) which is presumably heparan sulphate, but the complete mechanism of enzyme release is not known.	Glycosaminoglycans	191-194	amine oxidase, copper containing 1	Rattus norvegicus	11-14
2512987-2	1989	Intestinal DAO, in analogy with lipoprotein lipase (another heparin-released enzyme), is believed to be electrostatically linked to endothelial binding sites composed of a glycosaminoglycan (GAG) which is presumably heparan sulphate, but the complete mechanism of enzyme release is not known.	Glycosaminoglycans	191-194	lipoprotein lipase	Rattus norvegicus	32-50
2559786-4	1989	Dibutyryl cAMP (dbcAMP) elicits a striking increase in the accumulation of Alcian blue, pH 1.0-positive cartilage matrix, and a corresponding three- to fourfold increase in the accumulation of 35S-labeled glycosaminoglycans (GAG) by limb mesenchymal cells cultured in low serum medium at densities greater than confluence (i.e. micromass cultures established with 1-2 x 10(5) cells in 10 microliters of medium).	Glycosaminoglycans	205-223	cathelicidin antimicrobial peptide	Homo sapiens	10-14
2559786-4	1989	Dibutyryl cAMP (dbcAMP) elicits a striking increase in the accumulation of Alcian blue, pH 1.0-positive cartilage matrix, and a corresponding three- to fourfold increase in the accumulation of 35S-labeled glycosaminoglycans (GAG) by limb mesenchymal cells cultured in low serum medium at densities greater than confluence (i.e. micromass cultures established with 1-2 x 10(5) cells in 10 microliters of medium).	Glycosaminoglycans	225-228	cathelicidin antimicrobial peptide	Homo sapiens	10-14
2809592-6	1989	Binding of N-CAM 110 to collagens could be prevented in a concentration-dependent manner by the glycosaminoglycans heparin and chondroitin sulfate.	Glycosaminoglycans	96-114	neural cell adhesion molecule 1	Homo sapiens	11-16
2592817-1	1989	To investigate the correlation between chorioamnionitis and premature rupture of membranes (PROM), the influence of human recombinant interleukin-1 alpha (hrIL-1) on the metabolism of glycosaminoglycans (GAGs) and collagen in cultured human chorionic cells was examined and the following results were obtained.	Glycosaminoglycans	184-202	interleukin 1 alpha	Homo sapiens	134-153
2478195-5	1989	The inhibitory activity of glycosaminoglycans is accordant to their binding affinity for SAP, which was reported previously (Hamazaki, H. (1987) J. Biol.	Glycosaminoglycans	27-45	amyloid P component, serum	Homo sapiens	89-92
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
2509487-1	1989	Cultured monolayers of NMuMG mouse mammary epithelial cells have augmented amounts of cell surface chondroitin sulfate glycosaminoglycan (GAG) when cultured in transforming growth factor-beta (TGF-beta), presumably because of increased synthesis on their cell surface proteoglycan (named syndecan), previously shown to contain chondroitin sulfate and heparan sulfate GAG.	Glycosaminoglycans	138-141	transforming growth factor, beta 1	Mus musculus	193-201
2509487-1	1989	Cultured monolayers of NMuMG mouse mammary epithelial cells have augmented amounts of cell surface chondroitin sulfate glycosaminoglycan (GAG) when cultured in transforming growth factor-beta (TGF-beta), presumably because of increased synthesis on their cell surface proteoglycan (named syndecan), previously shown to contain chondroitin sulfate and heparan sulfate GAG.	Glycosaminoglycans	367-370	transforming growth factor, beta 1	Mus musculus	193-201
2780312-6	1989	From the deduced amino acid sequence of HRES-1/1 p25, residues 6-36 show a sequence homology of 32% and 39% to gag region segments of HTLV-I and HTLV-II, while residues 104-139 display a sequence homology of 33% and 28% to the gag regions of human immunodeficiency virus type 2 (HIV-2) and feline sarcoma virus (FSV), respectively.	Glycosaminoglycans	111-114	HTLV-1 related endogenous sequence	Homo sapiens	40-48
2806544-4	1989	Of interest is the presence of a characteristic decanucleotide AGGTGGT(T)GAG in the promoter regions of both the TRDV2 and TRGV9 genes.	Glycosaminoglycans	73-76	T cell receptor delta variable 2	Homo sapiens	113-118
2806544-4	1989	Of interest is the presence of a characteristic decanucleotide AGGTGGT(T)GAG in the promoter regions of both the TRDV2 and TRGV9 genes.	Glycosaminoglycans	73-76	T cell receptor gamma variable 9	Homo sapiens	123-128
2776976-2	1989	TGF-beta 1 and 2 (1-10 ng/ml) elicit a striking increase in the accumulation of Alcian blue, pH 1-positive cartilage matrix, and a corresponding twofold to threefold increase in the accumulation of 35S-sulfate- or 3H-glucosamine-labeled sulfated glycosaminoglycans (GAG) by high density micromass cultures prepared from the cells of whole stage 23/24 limb buds or the homogeneous population of chondrogenic precursor cells comprising the distal subridge mesenchyme of stage 25 wing buds.	Glycosaminoglycans	266-269	transforming growth factor beta 1	Gallus gallus	0-16
2783111-4	1989	CTAP-III (des 1-13) has a pI of 8.6 and is a relatively stable proteolytic cleavage product that retains the capacity to stimulate [14C]GAG synthesis in human synovial cell cultures.	Glycosaminoglycans	136-139	pro-platelet basic protein	Homo sapiens	0-8
2509244-1	1989	The synthesis of total sulfated glycosaminoglycans (GAG) was stimulated by transforming growth factors (TGF alpha 1.4-fold at 5 ng/ml, and TGF beta 1 2.05-fold at 2.5 ng/ml) in primary cultures of rat liver fat storing cells (FSC).	Glycosaminoglycans	32-50	transforming growth factor alpha	Rattus norvegicus	104-113
2509244-1	1989	The synthesis of total sulfated glycosaminoglycans (GAG) was stimulated by transforming growth factors (TGF alpha 1.4-fold at 5 ng/ml, and TGF beta 1 2.05-fold at 2.5 ng/ml) in primary cultures of rat liver fat storing cells (FSC).	Glycosaminoglycans	32-50	transforming growth factor, beta 1	Rattus norvegicus	139-149
2509244-1	1989	The synthesis of total sulfated glycosaminoglycans (GAG) was stimulated by transforming growth factors (TGF alpha 1.4-fold at 5 ng/ml, and TGF beta 1 2.05-fold at 2.5 ng/ml) in primary cultures of rat liver fat storing cells (FSC).	Glycosaminoglycans	52-55	transforming growth factor alpha	Rattus norvegicus	104-113
2509244-1	1989	The synthesis of total sulfated glycosaminoglycans (GAG) was stimulated by transforming growth factors (TGF alpha 1.4-fold at 5 ng/ml, and TGF beta 1 2.05-fold at 2.5 ng/ml) in primary cultures of rat liver fat storing cells (FSC).	Glycosaminoglycans	52-55	transforming growth factor, beta 1	Rattus norvegicus	139-149
2818645-6	1989	The catabolism of glycosaminoglycans was followed by estimating the activities of lysosomal glycohydrolases, namely beta-glucuronidase, beta-N-acetylglucosaminidase, cathepsin B1, cathepsin B2 and cathepsin D, in tissues and by estimating the urinary excretion and hexosamine and uronic acid.	Glycosaminoglycans	18-36	glucuronidase, beta	Rattus norvegicus	116-134
2818645-6	1989	The catabolism of glycosaminoglycans was followed by estimating the activities of lysosomal glycohydrolases, namely beta-glucuronidase, beta-N-acetylglucosaminidase, cathepsin B1, cathepsin B2 and cathepsin D, in tissues and by estimating the urinary excretion and hexosamine and uronic acid.	Glycosaminoglycans	18-36	cathepsin B	Rattus norvegicus	166-178
2818645-6	1989	The catabolism of glycosaminoglycans was followed by estimating the activities of lysosomal glycohydrolases, namely beta-glucuronidase, beta-N-acetylglucosaminidase, cathepsin B1, cathepsin B2 and cathepsin D, in tissues and by estimating the urinary excretion and hexosamine and uronic acid.	Glycosaminoglycans	18-36	cathepsin D	Rattus norvegicus	197-208
2670928-3	1989	In further experiments, the ability of both HIV-1 and HIV-2 proteases to release in vivo gag p24 from an in-frame fusion of the full length gag and protease precursors was analyzed.	Glycosaminoglycans	89-92	transmembrane p24 trafficking protein 2	Homo sapiens	93-96
2780312-6	1989	From the deduced amino acid sequence of HRES-1/1 p25, residues 6-36 show a sequence homology of 32% and 39% to gag region segments of HTLV-I and HTLV-II, while residues 104-139 display a sequence homology of 33% and 28% to the gag regions of human immunodeficiency virus type 2 (HIV-2) and feline sarcoma virus (FSV), respectively.	Glycosaminoglycans	111-114	tubulin polymerization promoting protein	Homo sapiens	49-52
2780312-6	1989	From the deduced amino acid sequence of HRES-1/1 p25, residues 6-36 show a sequence homology of 32% and 39% to gag region segments of HTLV-I and HTLV-II, while residues 104-139 display a sequence homology of 33% and 28% to the gag regions of human immunodeficiency virus type 2 (HIV-2) and feline sarcoma virus (FSV), respectively.	Glycosaminoglycans	227-230	HTLV-1 related endogenous sequence	Homo sapiens	40-48
2780312-6	1989	From the deduced amino acid sequence of HRES-1/1 p25, residues 6-36 show a sequence homology of 32% and 39% to gag region segments of HTLV-I and HTLV-II, while residues 104-139 display a sequence homology of 33% and 28% to the gag regions of human immunodeficiency virus type 2 (HIV-2) and feline sarcoma virus (FSV), respectively.	Glycosaminoglycans	227-230	tubulin polymerization promoting protein	Homo sapiens	49-52
2632462-0	1989	Biosynthesis of glycosaminoglycan precursors: evidences for different tissue specific forms of UDP-glucose dehydrogenase.	Glycosaminoglycans	16-33	UDP-glucose 6-dehydrogenase	Rattus norvegicus	95-120
2571350-5	1989	Western blot confirmatory tests showed that in some instances antibodies reacted with the gag proteins, in particular p19.	Glycosaminoglycans	90-93	interleukin 23 subunit alpha	Homo sapiens	118-121
2777882-1	1989	The effects of heparin and other glycosaminoglycans (GAGs) on the mitogenicity and stability of acidic fibroblast growth factor (aFGF) were studied.	Glycosaminoglycans	53-57	fibroblast growth factor 1	Homo sapiens	96-127
2607320-9	1989	Transforming growth factor beta (greater than 10 pmol/l) inhibited foetal calf serum (Dulbecco"s modification of Eagle"s medium with a fraction of foetal calf serum of 0.1) and epidermal growth factor stimulated proliferation but enhanced the synthesis of sulphated glycosaminoglycans about 2-fold.	Glycosaminoglycans	266-284	myotrophin	Rattus norvegicus	13-26
2528552-8	1989	The majority of the biological activity of both aFGF-potentiating HSPGP and aFGF-inhibitory HSPG1 was contained in the glycosaminoglycan chains released by alkaline borohydride treatment of intact HSPGP or HSPG1, respectively.	Glycosaminoglycans	119-136	fibroblast growth factor 1	Homo sapiens	48-52
2528552-8	1989	The majority of the biological activity of both aFGF-potentiating HSPGP and aFGF-inhibitory HSPG1 was contained in the glycosaminoglycan chains released by alkaline borohydride treatment of intact HSPGP or HSPG1, respectively.	Glycosaminoglycans	119-136	fibroblast growth factor 1	Homo sapiens	76-80
2777882-1	1989	The effects of heparin and other glycosaminoglycans (GAGs) on the mitogenicity and stability of acidic fibroblast growth factor (aFGF) were studied.	Glycosaminoglycans	53-57	fibroblast growth factor 1	Bos taurus	129-133
2528552-8	1989	The majority of the biological activity of both aFGF-potentiating HSPGP and aFGF-inhibitory HSPG1 was contained in the glycosaminoglycan chains released by alkaline borohydride treatment of intact HSPGP or HSPG1, respectively.	Glycosaminoglycans	119-136	syndecan 2	Homo sapiens	92-97
2607320-9	1989	Transforming growth factor beta (greater than 10 pmol/l) inhibited foetal calf serum (Dulbecco"s modification of Eagle"s medium with a fraction of foetal calf serum of 0.1) and epidermal growth factor stimulated proliferation but enhanced the synthesis of sulphated glycosaminoglycans about 2-fold.	Glycosaminoglycans	266-284	myotrophin	Rattus norvegicus	187-200
2528552-8	1989	The majority of the biological activity of both aFGF-potentiating HSPGP and aFGF-inhibitory HSPG1 was contained in the glycosaminoglycan chains released by alkaline borohydride treatment of intact HSPGP or HSPG1, respectively.	Glycosaminoglycans	119-136	syndecan 2	Homo sapiens	206-211
2765297-5	1989	D10 and F12 clones substantially differ in terms of protein pattern; that is, D10 is super-imposable to infected HUT-78 cells, whereas F12 exhibits a decreased uncleaved p55 gag precursor and the presence of uncleaved gp160 and of a unique p19, although they do not show qualitative or quantitative differences in viral RNA synthesis.	Glycosaminoglycans	174-177	CHRNA7 (exons 5-10) and FAM7A (exons A-E) fusion	Homo sapiens	0-3
2621717-0	1989	Binding of bovine follicular fluid glycosaminoglycans to fibronectin, laminin and low-density lipoproteins.	Glycosaminoglycans	35-53	fibronectin 1	Bos taurus	57-68
2621717-1	1989	Interactions of bovine follicular fluid glycosaminoglycans (GAGs) with extracellular matrix (ECM) components fibronectin and laminin and with low-density lipoproteins (LDL) were examined using affinity chromatography.	Glycosaminoglycans	40-58	fibronectin 1	Bos taurus	109-120
2500974-5	1989	Thus, IFN-gamma opposes the stimulatory effect of IL-1 on caseinase production and decreases IL-1-stimulated cartilage degradation, as measured by glycosaminoglycan release.	Glycosaminoglycans	147-164	interferon gamma	Homo sapiens	6-15
2503461-2	1989	Corneal opacification associated with glycosaminoglycan (GAG) deposition occurs in canine mucopolysaccharidosis I (MPS I), a deficiency of the lysosomal enzyme alpha-L-iduronidase.	Glycosaminoglycans	38-55	alpha-L-iduronidase	Canis lupus familiaris	160-179
2503461-2	1989	Corneal opacification associated with glycosaminoglycan (GAG) deposition occurs in canine mucopolysaccharidosis I (MPS I), a deficiency of the lysosomal enzyme alpha-L-iduronidase.	Glycosaminoglycans	57-60	alpha-L-iduronidase	Canis lupus familiaris	160-179
2668162-1	1989	Recombinant human interleukin-1 alpha (rhIL-1 alpha) and recombinant human interleukin 1 beta (rhIL-1 beta) stimulated the time- and concentration-dependent release of glycosaminoglycan (GAG) from bovine nasal cartilage explants.	Glycosaminoglycans	168-185	interleukin 1 alpha	Homo sapiens	18-37
2668162-1	1989	Recombinant human interleukin-1 alpha (rhIL-1 alpha) and recombinant human interleukin 1 beta (rhIL-1 beta) stimulated the time- and concentration-dependent release of glycosaminoglycan (GAG) from bovine nasal cartilage explants.	Glycosaminoglycans	168-185	interleukin 1 beta	Homo sapiens	75-93
2668162-1	1989	Recombinant human interleukin-1 alpha (rhIL-1 alpha) and recombinant human interleukin 1 beta (rhIL-1 beta) stimulated the time- and concentration-dependent release of glycosaminoglycan (GAG) from bovine nasal cartilage explants.	Glycosaminoglycans	187-190	interleukin 1 alpha	Homo sapiens	18-37
2668162-1	1989	Recombinant human interleukin-1 alpha (rhIL-1 alpha) and recombinant human interleukin 1 beta (rhIL-1 beta) stimulated the time- and concentration-dependent release of glycosaminoglycan (GAG) from bovine nasal cartilage explants.	Glycosaminoglycans	187-190	interleukin 1 beta	Homo sapiens	75-93
2500974-5	1989	Thus, IFN-gamma opposes the stimulatory effect of IL-1 on caseinase production and decreases IL-1-stimulated cartilage degradation, as measured by glycosaminoglycan release.	Glycosaminoglycans	147-164	interleukin 1 alpha	Homo sapiens	50-54
2500974-5	1989	Thus, IFN-gamma opposes the stimulatory effect of IL-1 on caseinase production and decreases IL-1-stimulated cartilage degradation, as measured by glycosaminoglycan release.	Glycosaminoglycans	147-164	interleukin 1 alpha	Homo sapiens	93-97
2570864-0	1989	Studies on interleukin-1 beta induced glycosaminoglycan release from rat femoral head cartilage in-vitro.	Glycosaminoglycans	38-55	interleukin 1 beta	Rattus norvegicus	11-29
2478117-3	1989	Due to its unique character C1q is able to interact directly with highly negatively charged molecules (e.g. mucopolysaccharides, MPS.)	Glycosaminoglycans	108-127	complement C1q A chain	Homo sapiens	28-31
2737267-4	1989	These results suggest that membrane-bound PKC may exert a modulatory effect on glycosaminoglycan sulfation, and this effect is gradually attenuated as Caco-2 cell differentiation progresses.	Glycosaminoglycans	79-96	proline rich transmembrane protein 2	Homo sapiens	42-45
2637354-13	1989	When the pressure was applied on these cells 2 min before addition of parathyroid hormone (PTH; 10(-7) M), this mechanical stimulation potentiated the increase by PTH of GAG synthesis in MCC (130% of control), but not so much that in SOS, and little that in NSC.	Glycosaminoglycans	170-173	parathyroid hormone	Oryctolagus cuniculus	70-89
2542313-3	1989	In addition to releasing H-TGL, heparin-like glycosaminoglycans have also been shown to suppress hepatocyte proliferation and to alter tissue-specific gene expression.	Glycosaminoglycans	45-63	lipase C, hepatic type	Homo sapiens	25-30
2801341-2	1989	Net GAG loss was observed from cartilage cultured in the presence of indomethacin plus rIL-1 alpha.	Glycosaminoglycans	4-7	interleukin 1 alpha	Rattus norvegicus	87-98
2637354-13	1989	When the pressure was applied on these cells 2 min before addition of parathyroid hormone (PTH; 10(-7) M), this mechanical stimulation potentiated the increase by PTH of GAG synthesis in MCC (130% of control), but not so much that in SOS, and little that in NSC.	Glycosaminoglycans	170-173	parathyroid hormone	Oryctolagus cuniculus	91-94
2637354-13	1989	When the pressure was applied on these cells 2 min before addition of parathyroid hormone (PTH; 10(-7) M), this mechanical stimulation potentiated the increase by PTH of GAG synthesis in MCC (130% of control), but not so much that in SOS, and little that in NSC.	Glycosaminoglycans	170-173	parathyroid hormone	Oryctolagus cuniculus	163-166
2785991-0	1989	Identification of protein intermediates in the processing of the p55 HIV-1 gag precursor in cells infected with recombinant vaccinia virus.	Glycosaminoglycans	75-78	H3 histone pseudogene 44	Homo sapiens	65-68
2656687-12	1989	Neither of these sites is substituted to 100% with glycosaminoglycan in native PG I.	Glycosaminoglycans	51-68	glucose-6-phosphate isomerase	Bos taurus	79-83
2785991-7	1989	We conclude that the myristylated HIV-1 gag p55 precursor is initially cleaved at random either at the p17/p24 junction or at two sites between p24 and p15 proteins, resulting in three intermediates (p41a, p41b, and p39) which are subsequently cleaved to yield mature gag proteins.	Glycosaminoglycans	40-43	family with sequence similarity 72 member B	Homo sapiens	103-106
2785991-7	1989	We conclude that the myristylated HIV-1 gag p55 precursor is initially cleaved at random either at the p17/p24 junction or at two sites between p24 and p15 proteins, resulting in three intermediates (p41a, p41b, and p39) which are subsequently cleaved to yield mature gag proteins.	Glycosaminoglycans	40-43	H3 histone pseudogene 44	Homo sapiens	44-47
2785991-7	1989	We conclude that the myristylated HIV-1 gag p55 precursor is initially cleaved at random either at the p17/p24 junction or at two sites between p24 and p15 proteins, resulting in three intermediates (p41a, p41b, and p39) which are subsequently cleaved to yield mature gag proteins.	Glycosaminoglycans	40-43	transmembrane p24 trafficking protein 2	Homo sapiens	107-110
2785991-7	1989	We conclude that the myristylated HIV-1 gag p55 precursor is initially cleaved at random either at the p17/p24 junction or at two sites between p24 and p15 proteins, resulting in three intermediates (p41a, p41b, and p39) which are subsequently cleaved to yield mature gag proteins.	Glycosaminoglycans	40-43	transmembrane p24 trafficking protein 2	Homo sapiens	144-147
2763268-5	1989	The purified protein is used to study in vitro the affinity of PF4 for several glycosaminoglycans (GAGs), by measuring the fluorescence of each PF4-GAG complex bound to fluorescamine.	Glycosaminoglycans	79-97	platelet factor 4	Homo sapiens	63-66
2785991-7	1989	We conclude that the myristylated HIV-1 gag p55 precursor is initially cleaved at random either at the p17/p24 junction or at two sites between p24 and p15 proteins, resulting in three intermediates (p41a, p41b, and p39) which are subsequently cleaved to yield mature gag proteins.	Glycosaminoglycans	40-43	Vpr	Human immunodeficiency virus 1	152-155
2785991-7	1989	We conclude that the myristylated HIV-1 gag p55 precursor is initially cleaved at random either at the p17/p24 junction or at two sites between p24 and p15 proteins, resulting in three intermediates (p41a, p41b, and p39) which are subsequently cleaved to yield mature gag proteins.	Glycosaminoglycans	40-43	cyclin dependent kinase 5 regulatory subunit 2	Homo sapiens	216-219
2785991-7	1989	We conclude that the myristylated HIV-1 gag p55 precursor is initially cleaved at random either at the p17/p24 junction or at two sites between p24 and p15 proteins, resulting in three intermediates (p41a, p41b, and p39) which are subsequently cleaved to yield mature gag proteins.	Glycosaminoglycans	268-271	H3 histone pseudogene 44	Homo sapiens	44-47
2763268-5	1989	The purified protein is used to study in vitro the affinity of PF4 for several glycosaminoglycans (GAGs), by measuring the fluorescence of each PF4-GAG complex bound to fluorescamine.	Glycosaminoglycans	99-102	platelet factor 4	Homo sapiens	63-66
2503275-5	1989	In contrast IgG3 antibodies, which were found to be predominantly directed against gag proteins, and which could be detected in almost all patients, remained in the circulation during disease progression.	Glycosaminoglycans	83-86	immunoglobulin heavy constant gamma 3 (G3m marker)	Homo sapiens	12-16
2713492-1	1989	Platelets secrete a low-molecular-weight protein, platelet factor four (PF-4), which binds to and neutralizes heparin and related sulfated glycosaminoglycans (GAGs).	Glycosaminoglycans	139-157	platelet factor 4	Bos taurus	72-76
2713501-2	1989	An in vivo role for thrombin (IIa) inhibition by HCII in the presence of certain glycosaminoglycans (dermatan sulfate and heparin) can be proposed.	Glycosaminoglycans	81-99	coagulation factor II, thrombin	Homo sapiens	20-28
2471571-2	1989	Mucin histochemistry indicated the presence of neutral and acid mucopolysaccharides and absence of sulphomucin.	Glycosaminoglycans	64-83	LOC100508689	Homo sapiens	0-5
2713501-2	1989	An in vivo role for thrombin (IIa) inhibition by HCII in the presence of certain glycosaminoglycans (dermatan sulfate and heparin) can be proposed.	Glycosaminoglycans	81-99	serpin family D member 1	Homo sapiens	49-53
2503275-9	1989	The difference between IgG1 and IgG3 anti-gag antibodies in relation to clearance during disease progression may depend on different properties of immune complexes formed by these two IgG subclasses.	Glycosaminoglycans	42-45	immunoglobulin heavy constant gamma 3 (G3m marker)	Homo sapiens	32-36
2538760-6	1989	Molecular cloning and sequencing of this DNA showed that the pol and env genes have been deleted, but that the complete gag region has been conserved and has a novel sequence encoding the p12 protein.	Glycosaminoglycans	120-123	polymerase (DNA-directed), delta 4	Mus musculus	188-191
2541703-3	1989	The major protein components are the gag-encoded p11 nucleocapsid protein and p26 capsid protein, which are present in equimolar amounts.	Glycosaminoglycans	37-40	endonuclease, poly(U) specific	Homo sapiens	49-52
2725492-7	1989	We have previously observed binding of C/EBP to an enhancer in the gag gene of avian retroviruses.	Glycosaminoglycans	67-70	CCAAT/enhancer binding protein gamma	Rattus norvegicus	39-44
2538650-5	1989	Cell cultures transfected with a clone deleted in 80% of the src intron (nucleotide 1149 to nucleotide 6574) demonstrated only a 2-fold reduction in the ratio of unspliced to spliced RNA relative to the wild-type clone, whereas cultures transfected with clones which were further deleted in the gag gene region (between nucleotide 630 and nucleotide 5258) demonstrated an approximate 20-fold reduction.	Glycosaminoglycans	295-298	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	61-64
2647739-7	1989	PG II (decorin) contains one attached glycosaminoglycan chain, while PG I probably contains two chains.	Glycosaminoglycans	38-55	decorin	Homo sapiens	0-5
2647739-7	1989	PG II (decorin) contains one attached glycosaminoglycan chain, while PG I probably contains two chains.	Glycosaminoglycans	38-55	biglycan	Homo sapiens	0-4
2537757-1	1989	The influence of human recombinant interleukin-1 alpha (hrIL-1) on biosynthesis of collagenase and glycosaminoglycans was investigated with fibroblast-like cells of human chorionic membrane.	Glycosaminoglycans	99-117	interleukin 1 alpha	Homo sapiens	35-54
2493252-2	1989	In fibroblast cultures, recombinant human interleukin-1 alpha (rHuIL-1 alpha), rHuIL-1 beta, and recombinant human tumor necrosis factor alpha (rHuTNF alpha) stimulated hyaluronic acid (HA) production and, to a lesser extent, sulfated GAG production, while recombinant human gamma-interferon did not have a significant effect.	Glycosaminoglycans	235-238	tumor necrosis factor	Homo sapiens	115-142
2914936-6	1989	In DS-PGI from bovine fetal skin, 81-84% of the glycosaminoglycan was composed of IdoA-GalNAc(SO4) disaccharide repeating units.	Glycosaminoglycans	48-65	glucose-6-phosphate isomerase	Bos taurus	6-9
2914936-9	1989	Thus, analogous proteoglycans from two different tissues, such as DS-PGI from skin and cartilage, possess a core protein with the same primary structure, yet contain glycosaminoglycan chains which differ greatly in iduronic acid content.	Glycosaminoglycans	166-183	glucose-6-phosphate isomerase	Bos taurus	69-72
2735658-3	1989	The purpose of this study was to identify the GAG-binding domains in apoB and E. By a combination of fragmentation of the intact proteins, peptide synthesis and quantitative GAG-binding, domains in apoB and apoE were identified and are shown below.	Glycosaminoglycans	46-49	apolipoprotein B	Homo sapiens	69-73
2783590-0	1989	Stimulation of glycosaminoglycan synthesis in cultured human dermal fibroblasts by interleukin 1.	Glycosaminoglycans	15-32	interleukin 1 alpha	Homo sapiens	83-96
2471467-2	1989	Our results show that short-term (48 h) treatment of confluent fibroblast cultures with hu-r-IFN-alpha 2 and hu-r-IFN-beta-ser17 causes a concentration (1 to 1 x 10(5) U/ml)-dependent inhibition of glycosaminoglycan production, has no effect on fibronectin production, and markedly increases collagenase production.	Glycosaminoglycans	198-215	interferon alpha 1	Homo sapiens	93-102
2913951-6	1989	beta-Glucuronidase internalized by either system is targeted to secondary lysosomes of human beta-glucuronidase-deficient fibroblasts, where it is able to degrade accumulated glycosaminoglycans.	Glycosaminoglycans	175-193	beta-glucuronidase	Bos taurus	0-18
2913951-6	1989	beta-Glucuronidase internalized by either system is targeted to secondary lysosomes of human beta-glucuronidase-deficient fibroblasts, where it is able to degrade accumulated glycosaminoglycans.	Glycosaminoglycans	175-193	glucuronidase beta	Homo sapiens	93-111
2497067-4	1989	Retrospective studies of the HIV(-) subjects" sequentially stored serum samples demonstrated an early transient appearance of gag encoded p24 antigen (Ag) which preceded their production of NA and specific anti-p24 Ab.	Glycosaminoglycans	126-129	transmembrane p24 trafficking protein 2	Homo sapiens	138-141
2497067-4	1989	Retrospective studies of the HIV(-) subjects" sequentially stored serum samples demonstrated an early transient appearance of gag encoded p24 antigen (Ag) which preceded their production of NA and specific anti-p24 Ab.	Glycosaminoglycans	126-129	transmembrane p24 trafficking protein 2	Homo sapiens	211-214
2786727-2	1989	In the brain, both gag- and env-coded antigens were confined to cells of micronodular lesions with immunophenotype of monocyte/macrophages (KiM6+, 9.4+, CD4+/-).	Glycosaminoglycans	19-22	CD4 molecule	Homo sapiens	153-156
2735658-3	1989	The purpose of this study was to identify the GAG-binding domains in apoB and E. By a combination of fragmentation of the intact proteins, peptide synthesis and quantitative GAG-binding, domains in apoB and apoE were identified and are shown below.	Glycosaminoglycans	46-49	apolipoprotein B	Homo sapiens	198-202
2735658-3	1989	The purpose of this study was to identify the GAG-binding domains in apoB and E. By a combination of fragmentation of the intact proteins, peptide synthesis and quantitative GAG-binding, domains in apoB and apoE were identified and are shown below.	Glycosaminoglycans	46-49	apolipoprotein E	Homo sapiens	207-211
2735658-3	1989	The purpose of this study was to identify the GAG-binding domains in apoB and E. By a combination of fragmentation of the intact proteins, peptide synthesis and quantitative GAG-binding, domains in apoB and apoE were identified and are shown below.	Glycosaminoglycans	174-177	apolipoprotein B	Homo sapiens	69-73
2735658-3	1989	The purpose of this study was to identify the GAG-binding domains in apoB and E. By a combination of fragmentation of the intact proteins, peptide synthesis and quantitative GAG-binding, domains in apoB and apoE were identified and are shown below.	Glycosaminoglycans	174-177	apolipoprotein B	Homo sapiens	198-202
2735658-3	1989	The purpose of this study was to identify the GAG-binding domains in apoB and E. By a combination of fragmentation of the intact proteins, peptide synthesis and quantitative GAG-binding, domains in apoB and apoE were identified and are shown below.	Glycosaminoglycans	174-177	apolipoprotein E	Homo sapiens	207-211
2976993-6	1988	Exposure of the glycosaminoglycan-binding region of S protein by reduction and carboxymethylation of the protein increased the neutralizing activity of S protein towards heparin and pentosan polysulfate.	Glycosaminoglycans	16-33	vitronectin	Homo sapiens	52-61
2483538-2	1989	3H-FN binds to Dowex beads coated with chondroitin sulfate GAG chains (CS) but not to beads coated with hyaluronic acid (HA).	Glycosaminoglycans	59-62	fibronectin 1	Homo sapiens	3-5
2319954-4	1989	Because of the higher frequency of reactivity to the gag p24 in AIDS patients, the patterns of anti-HIV IgG responses are similar to those observed in their African counterparts.	Glycosaminoglycans	53-56	transmembrane p24 trafficking protein 2	Homo sapiens	57-60
2500770-13	1989	These findings suggest that proteinuria might be caused by the structural alteration in the glycosaminoglycan portion of HSPG, changes in any anionic material other than HSPG, or both, and also indicate that the glomerular mesangial sclerosis is closely related to the increase of type V and VI collagens.	Glycosaminoglycans	92-109	CD44 molecule (Indian blood group)	Homo sapiens	121-125
2787228-5	1989	Killing of the cartilage cells abolished induced GAG release by all forms of IL-1.	Glycosaminoglycans	49-52	interleukin 1 beta	Homo sapiens	77-81
2787228-7	1989	Both forms of recombinant IL-1 inhibited GAG synthesis when continually present in the culture medium.	Glycosaminoglycans	41-44	interleukin 1 beta	Homo sapiens	26-30
2976993-6	1988	Exposure of the glycosaminoglycan-binding region of S protein by reduction and carboxymethylation of the protein increased the neutralizing activity of S protein towards heparin and pentosan polysulfate.	Glycosaminoglycans	16-33	vitronectin	Homo sapiens	152-161
2903227-7	1988	However, the conductance increased by the agonists (Gag) was not well expressed by simply increasing the values of G1 and Gir,max.	Glycosaminoglycans	52-55	G protein-coupled receptor 83	Rattus norvegicus	122-125
3058540-12	1988	Measurable increases in uptake of [35S]sulfate into GAG occurred with IL-1, baFGF, TGF-beta, h-EGF, IGF-1, bbFGF, NGF, and Forskolin.	Glycosaminoglycans	52-55	interleukin 1 alpha	Homo sapiens	70-74
3058540-12	1988	Measurable increases in uptake of [35S]sulfate into GAG occurred with IL-1, baFGF, TGF-beta, h-EGF, IGF-1, bbFGF, NGF, and Forskolin.	Glycosaminoglycans	52-55	insulin like growth factor 1	Homo sapiens	100-105
3058540-12	1988	Measurable increases in uptake of [35S]sulfate into GAG occurred with IL-1, baFGF, TGF-beta, h-EGF, IGF-1, bbFGF, NGF, and Forskolin.	Glycosaminoglycans	52-55	nerve growth factor	Homo sapiens	114-117
3196333-1	1988	Glucosamine-6-sulfatase is a lysosomal enzyme which degrades glycosaminoglycans and is deficient in mucopolysaccharidosis type IIID.	Glycosaminoglycans	61-79	glucosamine (N-acetyl)-6-sulfatase	Homo sapiens	0-23
2973783-1	1988	The lipoprotein complexing activity of glycosaminoglycans (GAG) prepared from human aortas with lipoprotein Lp(a) in comparison to low density lipoproteins (LDL) was determined tubidimetrically in the presence of Ca++.	Glycosaminoglycans	39-57	lipoprotein(a)	Homo sapiens	108-113
2973783-1	1988	The lipoprotein complexing activity of glycosaminoglycans (GAG) prepared from human aortas with lipoprotein Lp(a) in comparison to low density lipoproteins (LDL) was determined tubidimetrically in the presence of Ca++.	Glycosaminoglycans	59-62	lipoprotein(a)	Homo sapiens	108-113
2973783-4	1988	Analyzing the chemical composition of the complexes, we found that Lp(a) had greater than fourfold higher binding capacity for GAG.	Glycosaminoglycans	127-130	lipoprotein(a)	Homo sapiens	67-72
2973783-8	1988	If, on the other hand, Lp(a) was treated with dithiothreitol and the Lp(a)-specific protein (apoprotein [apo] a) was removed, the GAG binding was reduced by about 45%.	Glycosaminoglycans	130-133	lipoprotein(a)	Homo sapiens	23-28
2973783-8	1988	If, on the other hand, Lp(a) was treated with dithiothreitol and the Lp(a)-specific protein (apoprotein [apo] a) was removed, the GAG binding was reduced by about 45%.	Glycosaminoglycans	130-133	lipoprotein(a)	Homo sapiens	69-74
2973783-10	1988	LDL and Lp(a)-s GAG and -LP(a)-PG complexes were incubated with mouse peritoneal macrophages (MPM), and the stimulation of cholesteryl ester formation was studied.	Glycosaminoglycans	16-19	lipoprotein(a)	Homo sapiens	8-13
2973783-11	1988	At identical lipoprotein cholesterol concentrations, Lp(a)-GAG complexes exhibited a 1.3-fold higher stimulation of cholesterol esterification as compared to LDL-GAG.	Glycosaminoglycans	59-62	lipoprotein(a)	Homo sapiens	53-58
2905842-3	1988	1987; 57: 286-93) demonstrated that when rabbits were injected with the minimum weight of a variety of glycosaminoglycans required to inhibit tissue factor-induced thrombus formation by approximately 80%, exogenous thrombin was inactivated approximately twice as fast in the post-treatment plasmas as the pre-treatment plasmas.	Glycosaminoglycans	103-121	prothrombin	Oryctolagus cuniculus	215-223
2851191-6	1988	This concentration of each glycosaminoglycan completely inhibited prothrombin activation for 45 s after CaCl2 was added to contact-activated plasma; accelerated thrombin inhibition by purified antithrombin III by approximately 50-fold; and accelerated thrombin inhibition equally by antithrombin III in undiluted plasma.	Glycosaminoglycans	27-44	coagulation factor II, thrombin	Homo sapiens	69-77
2851191-6	1988	This concentration of each glycosaminoglycan completely inhibited prothrombin activation for 45 s after CaCl2 was added to contact-activated plasma; accelerated thrombin inhibition by purified antithrombin III by approximately 50-fold; and accelerated thrombin inhibition equally by antithrombin III in undiluted plasma.	Glycosaminoglycans	27-44	serpin family C member 1	Homo sapiens	193-209
2905842-12	1988	These observations confirm the utility of catalysis of thrombin inhibition as an index for assessing antithrombotic potential of glycosaminoglycans and other sulfated polysaccharides in rabbits.	Glycosaminoglycans	129-147	prothrombin	Oryctolagus cuniculus	55-63
2851191-6	1988	This concentration of each glycosaminoglycan completely inhibited prothrombin activation for 45 s after CaCl2 was added to contact-activated plasma; accelerated thrombin inhibition by purified antithrombin III by approximately 50-fold; and accelerated thrombin inhibition equally by antithrombin III in undiluted plasma.	Glycosaminoglycans	27-44	coagulation factor II, thrombin	Homo sapiens	161-169
2851191-6	1988	This concentration of each glycosaminoglycan completely inhibited prothrombin activation for 45 s after CaCl2 was added to contact-activated plasma; accelerated thrombin inhibition by purified antithrombin III by approximately 50-fold; and accelerated thrombin inhibition equally by antithrombin III in undiluted plasma.	Glycosaminoglycans	27-44	serpin family C member 1	Homo sapiens	283-299
2970980-1	1988	In this study we examined the effect of experimental diabetes and of treatment with an aldose reductase inhibitor on the level of sulfation of glomerular basement membrane (GBM) heparan sulfate, the principal glycosaminoglycan in this extracellular matrix.	Glycosaminoglycans	209-226	aldo-keto reductase family 1 member B1	Rattus norvegicus	87-103
3218731-0	1988	Measurement of the affinities of heparins, naturally occurring glycosaminoglycans, and other sulfated polymers for antithrombin III and thrombin.	Glycosaminoglycans	63-81	serpin family C member 1	Homo sapiens	115-131
3218731-0	1988	Measurement of the affinities of heparins, naturally occurring glycosaminoglycans, and other sulfated polymers for antithrombin III and thrombin.	Glycosaminoglycans	63-81	coagulation factor II, thrombin	Homo sapiens	119-127
3218731-3	1988	This has been used to compare the binding of a range of glycosaminoglycans and other sulfated polymers to antithrombin III and thrombin, a major inhibitor of and a central protease in the coagulation system, respectively.	Glycosaminoglycans	56-74	serpin family C member 1	Homo sapiens	106-122
3218731-3	1988	This has been used to compare the binding of a range of glycosaminoglycans and other sulfated polymers to antithrombin III and thrombin, a major inhibitor of and a central protease in the coagulation system, respectively.	Glycosaminoglycans	56-74	coagulation factor II, thrombin	Homo sapiens	110-118
3218731-4	1988	The results are consistent with the binding of naturally occurring glycosaminoglycans to antithrombin III solely through the well-defined antithrombin III-binding pentasaccharide found in heparin, the apparent affinity of a preparation depending upon its content of this pentasaccharide.	Glycosaminoglycans	67-85	serpin family C member 1	Homo sapiens	89-105
3218731-4	1988	The results are consistent with the binding of naturally occurring glycosaminoglycans to antithrombin III solely through the well-defined antithrombin III-binding pentasaccharide found in heparin, the apparent affinity of a preparation depending upon its content of this pentasaccharide.	Glycosaminoglycans	67-85	serpin family C member 1	Homo sapiens	138-154
3137232-2	1988	Ornithine decarboxylase (ODC), the rate-limiting enzyme in the polyamine biosynthetic pathway, has been shown to be causally related to an increase in glycosaminoglycan synthesis in murine embryonic palatal mesenchyme cells (MEPM).	Glycosaminoglycans	151-168	ornithine decarboxylase, structural 1	Mus musculus	0-23
2459842-2	1988	In mammalian cells infected with the recombinant vaccinia virus containing the gag/pol gene, major and minor polypeptides of 55 and 41 kDa were made, but processed gag products (p24/p17/p15) were not detected.	Glycosaminoglycans	79-82	endogenous retrovirus group W member 4	Homo sapiens	83-86
2902851-7	1988	The findings suggest more stringent structural requirements for GAG stimulation of antithrombin-thrombin interaction than for antithrombin-Factor Xa or heparin cofactor-thrombin interaction, which may also be of significance in physiological control of haemostasis.	Glycosaminoglycans	64-67	coagulation factor II, thrombin	Homo sapiens	87-95
2902851-7	1988	The findings suggest more stringent structural requirements for GAG stimulation of antithrombin-thrombin interaction than for antithrombin-Factor Xa or heparin cofactor-thrombin interaction, which may also be of significance in physiological control of haemostasis.	Glycosaminoglycans	64-67	coagulation factor II, thrombin	Homo sapiens	96-104
3417782-5	1988	The binding of [3H]heparin to peptide F-9 was dramatically reduced when heparin but not other glycosaminoglycans other than heparin (dextran sulfate, dermatan sulfate) were used in competition assays.	Glycosaminoglycans	94-112	coagulation factor IX	Homo sapiens	38-41
2458354-4	1988	When eosinophils were cultured for 1 day or longer in the presence of 10 pM IL 3, 1 pM IL 5, or 10 pM GM-CSF, the rates of [35S]sulfate incorporation were increased approximately 2-fold, and the cells synthesized Mr approximately 300,000 Pronase-resistant 35S-labeled proteoglycans which contained Mr approximately 30,000 35S-labeled glycosaminoglycans.	Glycosaminoglycans	334-352	interleukin 3	Homo sapiens	76-80
2458354-4	1988	When eosinophils were cultured for 1 day or longer in the presence of 10 pM IL 3, 1 pM IL 5, or 10 pM GM-CSF, the rates of [35S]sulfate incorporation were increased approximately 2-fold, and the cells synthesized Mr approximately 300,000 Pronase-resistant 35S-labeled proteoglycans which contained Mr approximately 30,000 35S-labeled glycosaminoglycans.	Glycosaminoglycans	334-352	colony stimulating factor 2	Homo sapiens	102-108
3171269-2	1988	N-acetyl-beta-glucosaminidase (NAG; EC3.2.1.30), one of marker enzymes of lysosome, may also degrade extracellular GAG in the uterine cervix.	Glycosaminoglycans	115-118	O-GlcNAcase	Homo sapiens	0-29
3171269-2	1988	N-acetyl-beta-glucosaminidase (NAG; EC3.2.1.30), one of marker enzymes of lysosome, may also degrade extracellular GAG in the uterine cervix.	Glycosaminoglycans	115-118	O-GlcNAcase	Homo sapiens	31-34
3171269-8	1988	It is concluded that NAG is released into the maternal circulation from lysosomes in amnion and decidua, and it is also estimated that NAG plays a role in the ripening of the uterine cervix during parturition by degrading GAG in the cervical extracellular matrix.	Glycosaminoglycans	222-225	O-GlcNAcase	Homo sapiens	21-24
3171269-8	1988	It is concluded that NAG is released into the maternal circulation from lysosomes in amnion and decidua, and it is also estimated that NAG plays a role in the ripening of the uterine cervix during parturition by degrading GAG in the cervical extracellular matrix.	Glycosaminoglycans	222-225	O-GlcNAcase	Homo sapiens	135-138
2971068-1	1988	Cultured bovine capillary endothelial (BCE) cells were found to synthesize and secrete high molecular mass heparan sulfate proteoglycans and glycosaminoglycans, which bound basic fibroblast growth factor (bFGF).	Glycosaminoglycans	141-159	fibroblast growth factor 2	Bos taurus	173-203
2971068-1	1988	Cultured bovine capillary endothelial (BCE) cells were found to synthesize and secrete high molecular mass heparan sulfate proteoglycans and glycosaminoglycans, which bound basic fibroblast growth factor (bFGF).	Glycosaminoglycans	141-159	fibroblast growth factor 2	Bos taurus	205-209
3137232-2	1988	Ornithine decarboxylase (ODC), the rate-limiting enzyme in the polyamine biosynthetic pathway, has been shown to be causally related to an increase in glycosaminoglycan synthesis in murine embryonic palatal mesenchyme cells (MEPM).	Glycosaminoglycans	151-168	ornithine decarboxylase, structural 1	Mus musculus	25-28
2839604-0	1988	Identification of gag precursor of equine infectious anaemia virus with monoclonal antibodies to the major viral core protein, p26.	Glycosaminoglycans	18-21	transmembrane p24 trafficking protein 3	Homo sapiens	127-130
3260902-12	1988	In summary, heparin reduces the number of EGF receptors on both explant and enzyme dispersed SMC by a mechanism which closely parallels the antiproliferative effects of this glycosaminoglycan.	Glycosaminoglycans	174-191	LOC521832	Bos taurus	42-45
3290901-3	1988	The HIV protease gene product was expressed in Escherichia coli and observed to cleave HIV gag p55 to gag p24 and gag p17 in vitro.	Glycosaminoglycans	91-94	H3 histone pseudogene 44	Homo sapiens	95-98
3290901-3	1988	The HIV protease gene product was expressed in Escherichia coli and observed to cleave HIV gag p55 to gag p24 and gag p17 in vitro.	Glycosaminoglycans	91-94	transmembrane p24 trafficking protein 2	Homo sapiens	106-109
3290901-3	1988	The HIV protease gene product was expressed in Escherichia coli and observed to cleave HIV gag p55 to gag p24 and gag p17 in vitro.	Glycosaminoglycans	102-105	H3 histone pseudogene 44	Homo sapiens	95-98
3290901-3	1988	The HIV protease gene product was expressed in Escherichia coli and observed to cleave HIV gag p55 to gag p24 and gag p17 in vitro.	Glycosaminoglycans	102-105	transmembrane p24 trafficking protein 2	Homo sapiens	106-109
3049075-12	1988	Cleavage of the gag precursor results in the mature capsid protein, p17.	Glycosaminoglycans	16-19	family with sequence similarity 72 member B	Homo sapiens	68-71
2897367-4	1988	Cell monolayers that had been predigested with GAG-specific degradative enzymes were capable of binding high levels of TGF-beta 1, but the size of the binding components was shifted from the high molecular weight species to the lower molecular weight core proteins, indicating that GAG chains are not necessary for TGF-beta 1 binding to the cell.	Glycosaminoglycans	47-50	transforming growth factor beta 1	Homo sapiens	119-129
2897367-4	1988	Cell monolayers that had been predigested with GAG-specific degradative enzymes were capable of binding high levels of TGF-beta 1, but the size of the binding components was shifted from the high molecular weight species to the lower molecular weight core proteins, indicating that GAG chains are not necessary for TGF-beta 1 binding to the cell.	Glycosaminoglycans	47-50	transforming growth factor beta 1	Homo sapiens	315-325
2836408-5	1988	The heparin-neutralizing proteins all inhibited the two latter activities, albeit to a varying extent, but did not appreciably affect the activation of protein C. These results are interpreted in relation to our previous finding that rabbit thrombomodulin contains an acidic domain, tentatively identified as a sulfated glycosaminoglycan (Bourin, M.-C., Boffa, M.-C., Bjork, I., and Lindahl, U.	Glycosaminoglycans	320-337	thrombomodulin	Oryctolagus cuniculus	241-255
3165003-3	1988	The development of AIDS was preceded 1-4 years by loss or lack of antibody to gag (p15, 24, or 55) and/or to pol (p31, 53, or 64), each p less than 0.001, compared with non-AIDS patients.	Glycosaminoglycans	78-81	cyclin dependent kinase inhibitor 2B	Homo sapiens	83-86
3165484-3	1988	This antibody response is mainly directed against the env-encoded envelope proteins gp160, gp120 and gp41, against the gag-encoded core proteins p55, p24 and p17 as well as against the pol-encoded enzymatic proteins p66, p51 and p31.	Glycosaminoglycans	119-122	H3 histone pseudogene 44	Homo sapiens	145-148
2908504-8	1988	These data indicate that the antigen recognized by FH6 in the culture supernatant of PC-9 is not a glycolipid, but a high molecular weight glycoprotein which could be referred to as a mucin, or a proteoglycan, which contains keratan-sulfate like glycosaminoglycan chains, as judged from the results of the glycosidase treatments.	Glycosaminoglycans	246-263	proprotein convertase subtilisin/kexin type 9	Homo sapiens	85-89
3378053-1	1988	A form of protease nexin 1 (PN-1) that binds heparin with a low affinity (L-PN-1) was purified and studies since altered interactions with glycosaminoglycans could affect its inhibition of certain serine proteases.	Glycosaminoglycans	139-157	serpin family E member 2	Homo sapiens	10-26
2967302-2	1988	Recent studies have shown that heparin, a GAG found in mast cells, potentiates the ability of acidic fibroblast growth factor (aFGF) to induce neurite outgrowth in pheochromocytoma (PC12) cells.	Glycosaminoglycans	42-45	fibroblast growth factor 1	Rattus norvegicus	94-125
2967302-2	1988	Recent studies have shown that heparin, a GAG found in mast cells, potentiates the ability of acidic fibroblast growth factor (aFGF) to induce neurite outgrowth in pheochromocytoma (PC12) cells.	Glycosaminoglycans	42-45	fibroblast growth factor 1	Rattus norvegicus	127-131
3420027-4	1988	The positivity of S-100 immunoreaction was found to be related to the presence of stromal glycosaminoglycans of the chondroitine sulfate A and C type.	Glycosaminoglycans	90-108	S100 calcium binding protein A1	Homo sapiens	18-23
3366780-5	1988	Since the RBL-1 cell and the rat L2 cell proteoglycans have different types of glycosaminoglycans bound to them, it can also be concluded that the selection of the type of glycosaminoglycan that will be synthesized onto a peptide core is a cell-specific event which is not exclusively dependent on the translated peptide core.	Glycosaminoglycans	79-97	RB transcriptional corepressor like 1	Rattus norvegicus	10-15
2835311-8	1988	Further analysis of the bovine IL-2R sequence also revealed the following: (i) the hydrophobic domains of the IL-2R protein were more conserved between species than the hydrophilic domains, (ii) the predominant site of intracellular IL-2R phosphorylation in mouse and human was a conserved Ser which was not conserved in the bovine sequence, and (iii) there exists a statistically significant amino acid homology with the AIDS gag protein.	Glycosaminoglycans	427-430	interleukin 2 receptor subunit alpha	Homo sapiens	31-36
2835311-8	1988	Further analysis of the bovine IL-2R sequence also revealed the following: (i) the hydrophobic domains of the IL-2R protein were more conserved between species than the hydrophilic domains, (ii) the predominant site of intracellular IL-2R phosphorylation in mouse and human was a conserved Ser which was not conserved in the bovine sequence, and (iii) there exists a statistically significant amino acid homology with the AIDS gag protein.	Glycosaminoglycans	427-430	interleukin 2 receptor subunit alpha	Homo sapiens	110-115
2835311-8	1988	Further analysis of the bovine IL-2R sequence also revealed the following: (i) the hydrophobic domains of the IL-2R protein were more conserved between species than the hydrophilic domains, (ii) the predominant site of intracellular IL-2R phosphorylation in mouse and human was a conserved Ser which was not conserved in the bovine sequence, and (iii) there exists a statistically significant amino acid homology with the AIDS gag protein.	Glycosaminoglycans	427-430	interleukin 2 receptor subunit alpha	Homo sapiens	110-115
3400080-4	1988	Our results suggested that heparin-like glycosaminoglycans on endothelial cells play as important a role as heparin does in the regulation of antithrombin activity.	Glycosaminoglycans	40-58	serpin family C member 1	Homo sapiens	142-154
3378053-1	1988	A form of protease nexin 1 (PN-1) that binds heparin with a low affinity (L-PN-1) was purified and studies since altered interactions with glycosaminoglycans could affect its inhibition of certain serine proteases.	Glycosaminoglycans	139-157	serpin family E member 2	Homo sapiens	28-32
3422640-2	1988	TGF-beta regulates the level and molecular size of these proteoglycans by acting simultaneously at two levels: it elevates the biosynthetic rate of the 45-kDa proteoglycan core protein in a cycloheximide- and actinomycin D-sensitive manner, and it induces an increase in the molecular mass of the glycosaminoglycan chains.	Glycosaminoglycans	297-314	transforming growth factor beta 1	Homo sapiens	0-8
3351481-3	1988	Results indicated that the gag gene-encoded p28, p19 and p16 virion core proteins were formed by cleavage processing of a 55K Mr precursor with several intermediate polypeptides.	Glycosaminoglycans	27-30	golgi SNAP receptor complex member 1	Homo sapiens	44-47
3351481-3	1988	Results indicated that the gag gene-encoded p28, p19 and p16 virion core proteins were formed by cleavage processing of a 55K Mr precursor with several intermediate polypeptides.	Glycosaminoglycans	27-30	cyclin dependent kinase inhibitor 2A	Homo sapiens	49-52
3351481-3	1988	Results indicated that the gag gene-encoded p28, p19 and p16 virion core proteins were formed by cleavage processing of a 55K Mr precursor with several intermediate polypeptides.	Glycosaminoglycans	27-30	cyclin dependent kinase inhibitor 2A	Homo sapiens	57-60
3342932-6	1988	Finally, we provide evidence indicating that FGF can combine with endogenously occurring heparin-like components: immobilized FGF binds sodium-[35S]sulfate labeled components secreted in muscle culture conditioned medium, an interaction inhibited by anti-HeSPG antibodies or heparin, but not by other sulfated glycosaminoglycans.	Glycosaminoglycans	310-328	fibroblast growth factor 10	Gallus gallus	45-48
3342932-6	1988	Finally, we provide evidence indicating that FGF can combine with endogenously occurring heparin-like components: immobilized FGF binds sodium-[35S]sulfate labeled components secreted in muscle culture conditioned medium, an interaction inhibited by anti-HeSPG antibodies or heparin, but not by other sulfated glycosaminoglycans.	Glycosaminoglycans	310-328	fibroblast growth factor 10	Gallus gallus	126-129
2448341-5	1988	In addition, rIFN-gamma synergized with rTNF and rLT to further augment GAG biosynthesis.	Glycosaminoglycans	72-75	interferon gamma	Rattus norvegicus	13-23
2448341-5	1988	In addition, rIFN-gamma synergized with rTNF and rLT to further augment GAG biosynthesis.	Glycosaminoglycans	72-75	tumor necrosis factor	Rattus norvegicus	40-44
2448341-13	1988	These studies demonstrate that IFN-gamma, TNF, and LT are important stimulators of fibroblast GAG biosynthesis, that interactions between these cytokines may be important in this regulatory process, that these cytokines predominantly stimulate hyaluronic acid production and that this effect may be mediated by stimulation of fibroblast hyaluronate synthetase activity.	Glycosaminoglycans	94-97	interferon gamma	Homo sapiens	31-40
2448341-13	1988	These studies demonstrate that IFN-gamma, TNF, and LT are important stimulators of fibroblast GAG biosynthesis, that interactions between these cytokines may be important in this regulatory process, that these cytokines predominantly stimulate hyaluronic acid production and that this effect may be mediated by stimulation of fibroblast hyaluronate synthetase activity.	Glycosaminoglycans	94-97	tumor necrosis factor	Homo sapiens	42-45
3043717-3	1988	At the dose equivalent to that of chymopapain used in human chemonucleolysis, two human serine proteinases, cathepsin G and chymotrypsin, were as effective as chymopapain in removing up to 80% of the glycosaminoglycan from the disc.	Glycosaminoglycans	200-217	cathepsin G	Homo sapiens	108-119
3257505-3	1988	rTNF alpha, as well as rIL-1 alpha and rIL-1 beta, decreased the incorporation of [35S]sulfate into glycosaminoglycan to about 10% of the levels in the control.	Glycosaminoglycans	100-117	tumor necrosis factor	Rattus norvegicus	0-10
3257505-3	1988	rTNF alpha, as well as rIL-1 alpha and rIL-1 beta, decreased the incorporation of [35S]sulfate into glycosaminoglycan to about 10% of the levels in the control.	Glycosaminoglycans	100-117	interleukin 1 alpha	Rattus norvegicus	23-34
3257505-3	1988	rTNF alpha, as well as rIL-1 alpha and rIL-1 beta, decreased the incorporation of [35S]sulfate into glycosaminoglycan to about 10% of the levels in the control.	Glycosaminoglycans	100-117	interleukin 1 beta	Rattus norvegicus	39-49
3257505-4	1988	The half-maximal doses of rTNF alpha, rIL-1 alpha or rIL-1 beta required for the suppression of glycosaminoglycan synthesis (by rTNF alpha, rIL-1 alpha, and rIL-1 beta) were 2 ng/ml, 30 ng/ml, or 5 ng/ml, respectively.	Glycosaminoglycans	96-113	tumor necrosis factor	Rattus norvegicus	26-36
3257505-4	1988	The half-maximal doses of rTNF alpha, rIL-1 alpha or rIL-1 beta required for the suppression of glycosaminoglycan synthesis (by rTNF alpha, rIL-1 alpha, and rIL-1 beta) were 2 ng/ml, 30 ng/ml, or 5 ng/ml, respectively.	Glycosaminoglycans	96-113	interleukin 1 alpha	Rattus norvegicus	38-49
3257505-4	1988	The half-maximal doses of rTNF alpha, rIL-1 alpha or rIL-1 beta required for the suppression of glycosaminoglycan synthesis (by rTNF alpha, rIL-1 alpha, and rIL-1 beta) were 2 ng/ml, 30 ng/ml, or 5 ng/ml, respectively.	Glycosaminoglycans	96-113	interleukin 1 beta	Rattus norvegicus	53-63
3257505-4	1988	The half-maximal doses of rTNF alpha, rIL-1 alpha or rIL-1 beta required for the suppression of glycosaminoglycan synthesis (by rTNF alpha, rIL-1 alpha, and rIL-1 beta) were 2 ng/ml, 30 ng/ml, or 5 ng/ml, respectively.	Glycosaminoglycans	96-113	tumor necrosis factor	Rattus norvegicus	128-138
3257505-4	1988	The half-maximal doses of rTNF alpha, rIL-1 alpha or rIL-1 beta required for the suppression of glycosaminoglycan synthesis (by rTNF alpha, rIL-1 alpha, and rIL-1 beta) were 2 ng/ml, 30 ng/ml, or 5 ng/ml, respectively.	Glycosaminoglycans	96-113	interleukin 1 alpha	Rattus norvegicus	140-151
3257505-4	1988	The half-maximal doses of rTNF alpha, rIL-1 alpha or rIL-1 beta required for the suppression of glycosaminoglycan synthesis (by rTNF alpha, rIL-1 alpha, and rIL-1 beta) were 2 ng/ml, 30 ng/ml, or 5 ng/ml, respectively.	Glycosaminoglycans	96-113	interleukin 1 beta	Rattus norvegicus	157-167
3043717-4	1988	A cysteine proteinase, cathepsin B released no more than 45% of glycosaminoglycan.	Glycosaminoglycans	64-81	cathepsin B	Homo sapiens	23-34
2963622-3	1987	Antithrombotic and anticoagulant effects of glycosaminoglycans depend on their ability to catalyse the inhibition of thrombin and/or to inhibit the activation of prothrombin.	Glycosaminoglycans	44-62	coagulation factor II, thrombin	Sus scrofa	117-125
3276308-3	1988	A specific binding of SAP to hyaluronic acid, heparan sulfate, and dermatan sulfate was also confirmed by the fact that these glycosaminoglycans blocked the binding of SAP to agarose, a specific ligand of SAP.	Glycosaminoglycans	126-144	amyloid P component, serum	Homo sapiens	22-25
3276308-3	1988	A specific binding of SAP to hyaluronic acid, heparan sulfate, and dermatan sulfate was also confirmed by the fact that these glycosaminoglycans blocked the binding of SAP to agarose, a specific ligand of SAP.	Glycosaminoglycans	126-144	amyloid P component, serum	Homo sapiens	168-171
3276308-3	1988	A specific binding of SAP to hyaluronic acid, heparan sulfate, and dermatan sulfate was also confirmed by the fact that these glycosaminoglycans blocked the binding of SAP to agarose, a specific ligand of SAP.	Glycosaminoglycans	126-144	amyloid P component, serum	Homo sapiens	168-171
2449172-12	1987	The mast cell proteoglycans heparin and chondroitin sulphate E, by virtue of containing the naturally occurring glycosaminoglycans of highest negative charge density, may play a major role in the regulation of mast cell tryptase activity in vivo.	Glycosaminoglycans	112-130	tryptase delta 1	Homo sapiens	210-228
2447023-5	1988	Putative gag proteins of p55, p24 and p17 were recognized by sera of human AIDS patients, but the corresponding env proteins of 32-40 and 120 kDa showed only weak cross-reactivity with those of HIV.	Glycosaminoglycans	9-12	H3 histone pseudogene 44	Homo sapiens	25-28
2447023-5	1988	Putative gag proteins of p55, p24 and p17 were recognized by sera of human AIDS patients, but the corresponding env proteins of 32-40 and 120 kDa showed only weak cross-reactivity with those of HIV.	Glycosaminoglycans	9-12	transmembrane p24 trafficking protein 2	Homo sapiens	30-33
2447023-5	1988	Putative gag proteins of p55, p24 and p17 were recognized by sera of human AIDS patients, but the corresponding env proteins of 32-40 and 120 kDa showed only weak cross-reactivity with those of HIV.	Glycosaminoglycans	9-12	family with sequence similarity 72 member B	Homo sapiens	38-41
2963622-8	1987	The least sulphated glycosaminoglycans were least able to catalyse the inhibition of thrombin added to plasma and to inhibit the activation of prothrombin.	Glycosaminoglycans	20-38	coagulation factor II, thrombin	Sus scrofa	85-93
3126770-5	1987	Extracted, infected glial cells revealed bands for three major gag proteins, p18, p24 and p55, in Western blotting.	Glycosaminoglycans	63-66	H3 histone pseudogene 12	Homo sapiens	77-80
3126770-5	1987	Extracted, infected glial cells revealed bands for three major gag proteins, p18, p24 and p55, in Western blotting.	Glycosaminoglycans	63-66	transmembrane p24 trafficking protein 2	Homo sapiens	82-85
3126770-5	1987	Extracted, infected glial cells revealed bands for three major gag proteins, p18, p24 and p55, in Western blotting.	Glycosaminoglycans	63-66	H3 histone pseudogene 44	Homo sapiens	90-93
3125138-2	1987	We examined the effect of three different subcellular matrices, plastic, type I collagen, and reconstituted basement membrane-like material (RBM), on the synthesis of sulfated glycosaminoglycans by cultured IMR-90 human lung fibroblasts.	Glycosaminoglycans	176-194	RNA binding motif protein Y-linked family 1 member A1	Homo sapiens	141-144
3125138-5	1987	Cells grown on the RBM synthesized significantly more glycosaminoglycans than cells on plastic or collagen and also had 260% more labeled glycosaminoglycans present in the cell-matrix layer than cells on plastic.	Glycosaminoglycans	54-72	RNA binding motif protein Y-linked family 1 member A1	Homo sapiens	19-22
3125138-5	1987	Cells grown on the RBM synthesized significantly more glycosaminoglycans than cells on plastic or collagen and also had 260% more labeled glycosaminoglycans present in the cell-matrix layer than cells on plastic.	Glycosaminoglycans	138-156	RNA binding motif protein Y-linked family 1 member A1	Homo sapiens	19-22
2446010-4	1987	In the gag region of RTVL-H2, there is a segment with significant homology to a region of the gag protein p30 of type C baboon endogenous virus.	Glycosaminoglycans	7-10	centromere protein V	Homo sapiens	106-109
2821689-2	1987	In this procedure, a resin with a covalently attached monoclonal antibody to the gag protein p19 is used to bind gag-containing proteins from crude extracts.	Glycosaminoglycans	81-84	interleukin 23 subunit alpha	Homo sapiens	93-96
2958485-8	1987	All evidence indicated that the mechanism using the intact pFN molecule involved the binding of the DS-PGs to the glycosaminoglycan (GAG)-binding sites of substratum-bound pFN, thereby inhibiting the interaction of the fibronectin with receptors on the cell surface.	Glycosaminoglycans	114-131	fibronectin 1	Mus musculus	219-230
2958485-8	1987	All evidence indicated that the mechanism using the intact pFN molecule involved the binding of the DS-PGs to the glycosaminoglycan (GAG)-binding sites of substratum-bound pFN, thereby inhibiting the interaction of the fibronectin with receptors on the cell surface.	Glycosaminoglycans	133-136	fibronectin 1	Mus musculus	219-230
3111454-4	1987	Apo B and apo A-I had significant positive correlations with the content of chondroitin sulphates A + C (CS A + C), which comprised 35% to 47% of the aortic GAG.	Glycosaminoglycans	157-160	apolipoprotein B	Homo sapiens	0-5
3111454-4	1987	Apo B and apo A-I had significant positive correlations with the content of chondroitin sulphates A + C (CS A + C), which comprised 35% to 47% of the aortic GAG.	Glycosaminoglycans	157-160	apolipoprotein A1	Homo sapiens	10-17
3111454-4	1987	Apo B and apo A-I had significant positive correlations with the content of chondroitin sulphates A + C (CS A + C), which comprised 35% to 47% of the aortic GAG.	Glycosaminoglycans	157-160	chorionic somatomammotropin hormone 1	Homo sapiens	105-109
3334100-3	1987	A fusion protein connected through a tetradecapeptide (Asp-Asp-Pro-Pro-Thr-Val-Glu-Leu-Gln-Gly-Leu-Val-Pro-Arg) was efficiently and correctly cleaved by alpha-thrombin, and the purified IGF-I possessed somatomedin-like activity, as determined by the enhancement of sulfation of glycosaminoglycans in cultured costal chondrocytes from rabbits.	Glycosaminoglycans	278-296	prothrombin	Oryctolagus cuniculus	159-167
3334100-3	1987	A fusion protein connected through a tetradecapeptide (Asp-Asp-Pro-Pro-Thr-Val-Glu-Leu-Gln-Gly-Leu-Val-Pro-Arg) was efficiently and correctly cleaved by alpha-thrombin, and the purified IGF-I possessed somatomedin-like activity, as determined by the enhancement of sulfation of glycosaminoglycans in cultured costal chondrocytes from rabbits.	Glycosaminoglycans	278-296	insulin-like growth factor I	Oryctolagus cuniculus	186-191
2851342-6	1987	The increase in GAG synthesis and intracellular cyclic AMP induced by PTH also became smaller and were lost in the 4th passage.	Glycosaminoglycans	16-19	parathyroid hormone	Mus musculus	70-73
2888772-6	1987	Data are presented suggesting that matrix glycosaminoglycans (GAGs) prevent spontaneous tropoelastin aggregation in vivo, at least up to the deamination of lysine residues on tropoelastin by matrix lysyl oxidase.	Glycosaminoglycans	42-60	lysyl oxidase	Gallus gallus	198-211
3109985-0	1987	Epidermal growth factor potentiates the induction of ornithine decarboxylase activity by prostaglandins in embryonic palate mesenchymal cells: effects on cell proliferation and glycosaminoglycan synthesis.	Glycosaminoglycans	177-194	epidermal growth factor	Homo sapiens	0-23
3109985-8	1987	Stimulation of ODC activity by EGF and PGE2 in these cells was not positively correlated with the level of cellular DNA synthesis but did result in a ninefold increase in the synthesis of extracellular glycosaminoglycans (GAGs), a key macromolecular family implicated in palatal morphogenesis.	Glycosaminoglycans	202-220	ornithine decarboxylase, structural 1	Mus musculus	15-18
3109985-8	1987	Stimulation of ODC activity by EGF and PGE2 in these cells was not positively correlated with the level of cellular DNA synthesis but did result in a ninefold increase in the synthesis of extracellular glycosaminoglycans (GAGs), a key macromolecular family implicated in palatal morphogenesis.	Glycosaminoglycans	202-220	epidermal growth factor	Mus musculus	31-34
3109985-9	1987	Stimulation of GAG synthesis was significantly inhibited by the administration of 5 mM DFMO (an irreversible inhibitor of ODC), indicating that the marked increase in GAG production was dependent, in part, on the induction of ODC activity by EGF and PGE2.	Glycosaminoglycans	15-18	ornithine decarboxylase, structural 1	Mus musculus	122-125
3109985-9	1987	Stimulation of GAG synthesis was significantly inhibited by the administration of 5 mM DFMO (an irreversible inhibitor of ODC), indicating that the marked increase in GAG production was dependent, in part, on the induction of ODC activity by EGF and PGE2.	Glycosaminoglycans	15-18	ornithine decarboxylase, structural 1	Mus musculus	226-229
3109985-9	1987	Stimulation of GAG synthesis was significantly inhibited by the administration of 5 mM DFMO (an irreversible inhibitor of ODC), indicating that the marked increase in GAG production was dependent, in part, on the induction of ODC activity by EGF and PGE2.	Glycosaminoglycans	15-18	epidermal growth factor	Mus musculus	242-245
3109985-9	1987	Stimulation of GAG synthesis was significantly inhibited by the administration of 5 mM DFMO (an irreversible inhibitor of ODC), indicating that the marked increase in GAG production was dependent, in part, on the induction of ODC activity by EGF and PGE2.	Glycosaminoglycans	167-170	ornithine decarboxylase, structural 1	Mus musculus	122-125
3109985-9	1987	Stimulation of GAG synthesis was significantly inhibited by the administration of 5 mM DFMO (an irreversible inhibitor of ODC), indicating that the marked increase in GAG production was dependent, in part, on the induction of ODC activity by EGF and PGE2.	Glycosaminoglycans	167-170	ornithine decarboxylase, structural 1	Mus musculus	226-229
3109985-9	1987	Stimulation of GAG synthesis was significantly inhibited by the administration of 5 mM DFMO (an irreversible inhibitor of ODC), indicating that the marked increase in GAG production was dependent, in part, on the induction of ODC activity by EGF and PGE2.	Glycosaminoglycans	167-170	epidermal growth factor	Mus musculus	242-245
2440107-6	1987	During the course of these experiments, a transforming recombinant of bcr/abl was isolated which fuses gag determinants derived from helper virus to the NH2-terminus of the bcr/abl protein.	Glycosaminoglycans	103-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
2440107-6	1987	During the course of these experiments, a transforming recombinant of bcr/abl was isolated which fuses gag determinants derived from helper virus to the NH2-terminus of the bcr/abl protein.	Glycosaminoglycans	103-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
2440107-7	1987	This suggests that a property of viral gag sequences, probably myristylation-dependent membrane localization, must be provided to bcr/abl for it to transform fibroblasts.	Glycosaminoglycans	39-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
2444468-4	1987	The activation and redistribution of the GH under the ADH influence and the role of GAG and GH in the mechanism of ADH action, were discussed.	Glycosaminoglycans	84-87	alcohol dehydrogenase 1C (class I), gamma polypeptide	Rattus norvegicus	115-118
3496398-0	1987	Transforming growth factor-beta: selective increase in glycosaminoglycan synthesis by cultures of fibroblasts from patients with progressive systemic sclerosis.	Glycosaminoglycans	55-72	transforming growth factor beta 1	Homo sapiens	0-31
3496398-2	1987	We now report that TGF-beta, alone or in combination with epidermal growth factor (EGF), led to a preferential increase in glycosaminoglycan synthesis by cultures of dermal fibroblasts from patients with progressive systemic sclerosis (PSS) when compared with normal fibroblasts (p less than 0.001).	Glycosaminoglycans	123-140	transforming growth factor beta 1	Homo sapiens	19-27
3496398-2	1987	We now report that TGF-beta, alone or in combination with epidermal growth factor (EGF), led to a preferential increase in glycosaminoglycan synthesis by cultures of dermal fibroblasts from patients with progressive systemic sclerosis (PSS) when compared with normal fibroblasts (p less than 0.001).	Glycosaminoglycans	123-140	epidermal growth factor	Homo sapiens	58-81
3496398-2	1987	We now report that TGF-beta, alone or in combination with epidermal growth factor (EGF), led to a preferential increase in glycosaminoglycan synthesis by cultures of dermal fibroblasts from patients with progressive systemic sclerosis (PSS) when compared with normal fibroblasts (p less than 0.001).	Glycosaminoglycans	123-140	epidermal growth factor	Homo sapiens	83-86
3584978-7	1987	NAGA is one of the components from which HA is built up; the other component glucuronic acid was without effect, and so were the other glycosaminoglycans, N-acetyl-D-mannosamine, N-acetyl-D-galactosamine, and D-glucosamine.	Glycosaminoglycans	135-153	alpha-N-acetylgalactosaminidase	Homo sapiens	0-4
3114193-3	1987	SDS-PAGE analysis also showed a similar difference in the amounts of major gag protein p24.	Glycosaminoglycans	75-78	transmembrane p24 trafficking protein 2	Homo sapiens	87-90
2955079-9	1987	The large-sized HSPG, which is concentrated in synaptic regions, contains only GAG chains of Mr 20,000, suggesting that each HSPG contains only one kind of heparan sulfate chain in its structure.	Glycosaminoglycans	79-82	syndecan 2	Rattus norvegicus	16-20
3112309-6	1987	The phenotypic variation and the fact that increased levels of glycosaminoglycans were not found in the urine of the two patients lead to the suggestion that in certain cases a correct diagnosis may be missed if the beta-glucuronidase activity in plasma and leucocytes is not determined and only routine urine investigation is performed as a screening for a mucopolysaccharidosis.	Glycosaminoglycans	63-81	glucuronidase beta	Homo sapiens	216-234
3681068-4	1987	It is noteworthy that the PG of small molecular size shows a shortening of the glycosaminoglycan link and core protein on undersulfation.	Glycosaminoglycans	79-96	versican	Gallus gallus	26-28
3116701-0	1987	Catalysis of thrombin inhibition provides an index for estimating the antithrombotic potential of glycosaminoglycans in rabbits.	Glycosaminoglycans	98-116	prothrombin	Oryctolagus cuniculus	13-21
3116701-1	1987	Previous studies have demonstrated that standard anticoagulant tests are poor indices of the antithrombotic potential of glycosaminoglycans which are weak catalysts of the thrombin-antithrombin III reaction.	Glycosaminoglycans	121-139	prothrombin	Oryctolagus cuniculus	172-180
3116701-2	1987	In this study we investigated whether the catalysis of thrombin inhibition by plasma could serve as a reliable index for assessing the antithrombotic effectiveness of glycosaminoglycans.	Glycosaminoglycans	167-185	prothrombin	Oryctolagus cuniculus	55-63
3116701-6	1987	When ex vivo plasmas obtained from rabbits that had been injected with the minimum dose of any one of seven glycosaminoglycans required to achieve their optimal antithrombotic effect were assessed for their ability to catalyse thrombin inhibition, there was approximately a 2-fold increase in the amount of thrombin inactivated 30 s after the thrombin had been added to the plasma.	Glycosaminoglycans	108-126	prothrombin	Oryctolagus cuniculus	227-235
3116701-6	1987	When ex vivo plasmas obtained from rabbits that had been injected with the minimum dose of any one of seven glycosaminoglycans required to achieve their optimal antithrombotic effect were assessed for their ability to catalyse thrombin inhibition, there was approximately a 2-fold increase in the amount of thrombin inactivated 30 s after the thrombin had been added to the plasma.	Glycosaminoglycans	108-126	prothrombin	Oryctolagus cuniculus	307-315
3116701-6	1987	When ex vivo plasmas obtained from rabbits that had been injected with the minimum dose of any one of seven glycosaminoglycans required to achieve their optimal antithrombotic effect were assessed for their ability to catalyse thrombin inhibition, there was approximately a 2-fold increase in the amount of thrombin inactivated 30 s after the thrombin had been added to the plasma.	Glycosaminoglycans	108-126	prothrombin	Oryctolagus cuniculus	307-315
3116701-8	1987	These results suggest that measurement of the catalysis of thrombin inactivation in undiluted plasma is a sensitive and reliable index for estimating the antithrombotic potential of glycosaminoglycans in rabbits.	Glycosaminoglycans	182-200	prothrombin	Oryctolagus cuniculus	59-67
3603428-6	1987	In consumption coagulopathy, the HC II levels are as low as AT, possibly reflecting intravascular consumption accelerated by vascular glycosaminoglycans.	Glycosaminoglycans	134-152	serpin family D member 1	Homo sapiens	33-38
3574136-3	1987	Since the glycosaminoglycan, heparan sulfate, was found to stimulate the lipoprotein lipase reaction in vitro, we investigated the plasma heparan sulfate content and measured the urinary excretion of heparan sulfate in control rats and rats with experimentally induced nephrotic syndrome.	Glycosaminoglycans	10-27	lipoprotein lipase	Rattus norvegicus	73-91
2948956-4	1987	Both the binding affinity of SAP for these glycosaminoglycans and the numbers of binding sites of SAP depended on calcium concentration.	Glycosaminoglycans	43-61	amyloid P component, serum	Homo sapiens	29-32
3034296-1	1987	Human recombinant interleukin-1 beta (rIL-1 beta) stimulated glycosaminoglycan (GAG) production in human synovial fibroblast cultures.	Glycosaminoglycans	61-78	interleukin 1 beta	Homo sapiens	18-36
3034296-1	1987	Human recombinant interleukin-1 beta (rIL-1 beta) stimulated glycosaminoglycan (GAG) production in human synovial fibroblast cultures.	Glycosaminoglycans	61-78	interleukin 1 beta	Rattus norvegicus	38-48
3549363-7	1987	Thus, interleukin 3-dependent mouse BMMC can be induced to undergo phenotypic changes in staining characteristics, histamine content, glycosaminoglycan structure, and metabolism of arachidonic acid to resemble heparin-containing CTMC.	Glycosaminoglycans	134-151	interleukin 3	Mus musculus	6-19
3298650-0	1987	Glycosaminoglycan composition of tight skin and control mouse skins.	Glycosaminoglycans	0-17	fibrillin 1	Mus musculus	33-43
3298650-1	1987	Tight skin (TSK) mouse skin has previously been shown to contain increased amounts of collagen and glycosaminoglycans (GAG).	Glycosaminoglycans	99-117	fibrillin 1	Mus musculus	0-10
3298650-1	1987	Tight skin (TSK) mouse skin has previously been shown to contain increased amounts of collagen and glycosaminoglycans (GAG).	Glycosaminoglycans	99-117	fibrillin 1	Mus musculus	12-15
3298650-1	1987	Tight skin (TSK) mouse skin has previously been shown to contain increased amounts of collagen and glycosaminoglycans (GAG).	Glycosaminoglycans	119-122	fibrillin 1	Mus musculus	0-10
3298650-1	1987	Tight skin (TSK) mouse skin has previously been shown to contain increased amounts of collagen and glycosaminoglycans (GAG).	Glycosaminoglycans	119-122	fibrillin 1	Mus musculus	12-15
3298650-2	1987	We now report on the GAG composition of TSK mouse skin.	Glycosaminoglycans	21-24	fibrillin 1	Mus musculus	40-43
3495201-6	1987	The final preparation of gag and gag/env proteins in 8 M urea reacted with sheep anti-HTLV-III p24 gag antibodies and acquired immune deficiency syndrome (AIDS) patient sera.	Glycosaminoglycans	25-28	transmembrane p24 trafficking protein 2	Homo sapiens	95-98
3495201-6	1987	The final preparation of gag and gag/env proteins in 8 M urea reacted with sheep anti-HTLV-III p24 gag antibodies and acquired immune deficiency syndrome (AIDS) patient sera.	Glycosaminoglycans	33-36	endogenous retrovirus group K member 20	Homo sapiens	37-40
3495201-6	1987	The final preparation of gag and gag/env proteins in 8 M urea reacted with sheep anti-HTLV-III p24 gag antibodies and acquired immune deficiency syndrome (AIDS) patient sera.	Glycosaminoglycans	33-36	transmembrane p24 trafficking protein 2	Homo sapiens	95-98
3495201-6	1987	The final preparation of gag and gag/env proteins in 8 M urea reacted with sheep anti-HTLV-III p24 gag antibodies and acquired immune deficiency syndrome (AIDS) patient sera.	Glycosaminoglycans	33-36	endogenous retrovirus group K member 20	Homo sapiens	37-40
3495201-6	1987	The final preparation of gag and gag/env proteins in 8 M urea reacted with sheep anti-HTLV-III p24 gag antibodies and acquired immune deficiency syndrome (AIDS) patient sera.	Glycosaminoglycans	33-36	transmembrane p24 trafficking protein 2	Homo sapiens	95-98
3304356-6	1987	The quantitative analysis of sera with env and gag antigens by ELISA showed AIDS patients had very low gag reactivity while retaining high env reactivity.	Glycosaminoglycans	103-106	endogenous retrovirus group K member 20	Homo sapiens	39-42
3304356-8	1987	This correlation and the analysis of sera with both the ENV and GAG ELISAs indicate that the antibodies reactive to gag are specifically affected relative to env reactivity and that different levels of antibodies to separate viral components in these sera may correlate with disease state.	Glycosaminoglycans	116-119	endogenous retrovirus group K member 20	Homo sapiens	56-59
3581111-2	1987	experiments conducted on synthetic fragments of glycosaminoglycans, one of them representing the pentasaccharidic sequence present in heparin and responsible for the binding to antithrombin III, and the others being related to this sequence.	Glycosaminoglycans	48-66	serpin family C member 1	Homo sapiens	177-193
3118854-9	1987	Though the percentage of heparan sulfate on total glycosaminoglycans (GAGs) of the C-6-S group was lower than in the cholesterol-diet group, there were no significant differences in the percentages of dermatan sulfate and chondroitin-4/6-sulfate in total GAGs between the cholesterol-diet and C-6-S groups.	Glycosaminoglycans	70-74	LOW QUALITY PROTEIN: complement component C6	Oryctolagus cuniculus	83-86
3332689-5	1987	Glycosaminoglycans (heparin) inhibit nerve fiber growth on fibronectin substrata.	Glycosaminoglycans	0-18	fibronectin 1	Rattus norvegicus	59-70
3119427-4	1987	The sequences for the pol, env and the 3" two-thirds of the gag region were conserved among the IAP elements.	Glycosaminoglycans	60-63	intracisternal A particle, Eya1 linked	Mus musculus	96-99
3040821-3	1987	PTH stimulated glycosaminoglycan (GAG) synthesis, a characteristic of the cartilage phenotype in cultured chondrocytes isolated from mandibular condylar cartilage (MCC), nasal septal cartilage (NSC), and spheno-occipital synchondrosis (SOS).	Glycosaminoglycans	15-32	parathyroid hormone	Bos taurus	0-3
3040821-3	1987	PTH stimulated glycosaminoglycan (GAG) synthesis, a characteristic of the cartilage phenotype in cultured chondrocytes isolated from mandibular condylar cartilage (MCC), nasal septal cartilage (NSC), and spheno-occipital synchondrosis (SOS).	Glycosaminoglycans	34-37	parathyroid hormone	Bos taurus	0-3
3040821-4	1987	These stimulations of GAG synthesis by PTH were dose-dependent.	Glycosaminoglycans	22-25	parathyroid hormone	Bos taurus	39-42
3040821-7	1987	The increases in the cAMP level, ODC activity, and GAG synthesis after addition of PTH (10(-7) mol/L) were greatest in MCC-chondrocytes and least in NSC-chondrocytes.	Glycosaminoglycans	51-54	parathyroid hormone	Bos taurus	83-86
2893245-4	1987	The data indicate polymorphism in the apparent size of gag gene-encoded p55 and env gene-encoded p41 proteins.	Glycosaminoglycans	55-58	H3 histone pseudogene 44	Homo sapiens	72-75
2439872-0	1987	Detection of glycosaminoglycans with 125I-labeled cytochrome c.	Glycosaminoglycans	13-31	cytochrome c, somatic	Homo sapiens	50-62
3659055-3	1987	From sequence analysis of the cloned provirus, the p135 transforming protein was found to be tripartite, with gag, myb and ets sequences.	Glycosaminoglycans	110-113	dynactin subunit 1	Homo sapiens	51-55
3099305-0	1987	Effects of human carbonic anhydrase III (CA III) on synovial and muscle fibroblast glycosaminoglycan metabolism.	Glycosaminoglycans	83-100	carbonic anhydrase 3	Homo sapiens	17-39
3099305-0	1987	Effects of human carbonic anhydrase III (CA III) on synovial and muscle fibroblast glycosaminoglycan metabolism.	Glycosaminoglycans	83-100	carbonic anhydrase 3	Homo sapiens	41-47
3099305-1	1987	We investigated the ability of CA III, isolated from adult human skeletal muscle, to regulate cell growth and glycosaminoglycan (GAG) formation in connective tissue cells derived from various human tissues.	Glycosaminoglycans	110-127	carbonic anhydrase 3	Homo sapiens	31-37
3099305-1	1987	We investigated the ability of CA III, isolated from adult human skeletal muscle, to regulate cell growth and glycosaminoglycan (GAG) formation in connective tissue cells derived from various human tissues.	Glycosaminoglycans	129-132	carbonic anhydrase 3	Homo sapiens	31-37
2431720-7	1986	Short incubations with heparin (5 min) caused a release of the enzyme into the media, while longer incubations caused a 2-8-fold increase in net lipoprotein lipase secretion which was maximal after 2-16 h depending on cell type, and persisted for 24 h. The effect of heparin was dose-dependent and specific (it was not duplicated by other glycosaminoglycans).	Glycosaminoglycans	339-357	lipoprotein lipase	Mus musculus	145-163
3491459-2	1986	While the product of the viral src gene could be readily labeled biosynthetically with [3H]myristic acid, the gag-onc transforming proteins of Fujinami sarcoma virus, PRCII, PRCIIp, and Y73 avian sarcoma viruses were not readily labeled with either [3H]myristate or [3H]palmitate.	Glycosaminoglycans	110-113	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	31-34
3536222-3	1986	Human IL-1 and the P388D1 supernatants enhanced glycosaminoglycan (GAG) release from bovine nasal cartilage explants.	Glycosaminoglycans	48-65	interleukin 1 alpha	Homo sapiens	6-10
3536222-3	1986	Human IL-1 and the P388D1 supernatants enhanced glycosaminoglycan (GAG) release from bovine nasal cartilage explants.	Glycosaminoglycans	67-70	interleukin 1 alpha	Homo sapiens	6-10
3816142-5	1986	On the contrary, in the aortas of both patients collagen fibrils were significantly smaller than in the controls; moreover, elastin lamellae were deeply altered and consisted of roundish aggregates of elastin, massively permeated by cytochemically recognizable glycosaminoglycans.	Glycosaminoglycans	261-279	elastin	Homo sapiens	124-131
3490846-1	1986	Effects of human recombinant interleukin 1 (IL-1) on the synthesis of glycosaminoglycan were examined with cultured rat costal chondrocytes.	Glycosaminoglycans	70-87	interleukin 1 alpha	Homo sapiens	29-48
2948501-1	1986	The binding of Apolipoprotein E supplemented triglyceride emulsions to sulfated glycosaminoglycans demonstrated specificity for the carbohydrate polymers.	Glycosaminoglycans	80-98	apolipoprotein E	Homo sapiens	15-31
2948501-4	1986	The Apo E induced uptake of triglyceride emulsions by hepatocytes was inhibited by highly sulfated polysaccharides (i.e. heparin, dextran sulfate) but other glycosaminoglycans which did not bind the emulsion were ineffective in this inhibition.	Glycosaminoglycans	157-175	apolipoprotein E	Homo sapiens	4-9
2432769-1	1986	This study uses histochemical methods to determine the ultrastructural distribution of specific glycosaminoglycans (GAGs) during the development of blood vessels in the chick chorioallantoic membrane (CAM) and to correlate changes in GAG composition with the significant structural events in the development of these vessels.	Glycosaminoglycans	96-114	uncharacterized LOC107052719	Gallus gallus	116-119
2434472-0	1986	Immunological characterization of human vitronectin and its binding to glycosaminoglycans.	Glycosaminoglycans	71-89	vitronectin	Homo sapiens	40-51
3490846-2	1986	Incorporation of [35S]sulfate into glycosaminoglycan was strikingly diminished by the addition of IL-1 in a dose- and time- dependent manner.	Glycosaminoglycans	35-52	interleukin 1 alpha	Homo sapiens	98-102
3490846-3	1986	When the cells were cultured with 340 micrograms/ml of IL-1 for 72 hr, the synthesis of glycosaminoglycan was inhibited to 10% of the control.	Glycosaminoglycans	88-105	interleukin 1 alpha	Homo sapiens	55-59
3800671-1	1986	Distribution of beta-glucuronidase, one of three enzymes of hyaluronate hydrolases (HH) that hydrolyze extracellular glycosamine glycans (GAG), has been studied in the intact white rat kidney and under effect of antidiuretic hormone (ADH).	Glycosaminoglycans	138-141	glucuronidase, beta	Rattus norvegicus	16-34
3018286-7	1986	In the HZ5-FeSV and the SM-FeSV, identical c-fms and feline leukemia virus p10 sequences form the 5" gag-fms junction.	Glycosaminoglycans	101-104	colony stimulating factor 1 receptor	Homo sapiens	43-48
3094551-4	1986	GAG changes were correlated with tissue LDL accumulation estimated by quantification of immunochemically-identifiable apolipoprotein B (apoB).	Glycosaminoglycans	0-3	apolipoprotein B	Sus scrofa	118-134
3094551-4	1986	GAG changes were correlated with tissue LDL accumulation estimated by quantification of immunochemically-identifiable apolipoprotein B (apoB).	Glycosaminoglycans	0-3	apolipoprotein B	Sus scrofa	136-140
3094551-6	1986	Although total GAG concentrations did not differ between a normolipemic control and the two diet groups, apoB showed a significantly positive correlation with the percent of total GAG that was chondroitin sulfate and a significantly negative correlation with the percent of total GAG that was dermatan sulfate.	Glycosaminoglycans	180-183	apolipoprotein B	Sus scrofa	105-109
3094551-6	1986	Although total GAG concentrations did not differ between a normolipemic control and the two diet groups, apoB showed a significantly positive correlation with the percent of total GAG that was chondroitin sulfate and a significantly negative correlation with the percent of total GAG that was dermatan sulfate.	Glycosaminoglycans	180-183	apolipoprotein B	Sus scrofa	105-109
3023963-12	1986	Additionally, we demonstrate that activated c-erbB mRNA precursors can be processed by alternative splicing to yield mRNAs with viral gag sequences fused directly to c-erbB sequences.	Glycosaminoglycans	134-137	epidermal growth factor receptor	Homo sapiens	46-50
3740547-5	1986	The correlation coefficients of serum beta-glucuronidase activity with high-sulfated and total plasma glycosaminoglycans were 0.794 and 0.809, respectively (p less than 0.01 and p less than 0.005, respectively).	Glycosaminoglycans	102-120	glucuronidase beta	Homo sapiens	38-56
3740547-6	1986	The results suggest that the decreased plasma high-sulfated glycosaminoglycan levels in Marfan syndrome are due to the reduction of serum beta-glucuronidase, which leads to the decreased degradation of macromolecules and, subsequently, the accumulation of the glycosaminoglycans in the tissues.	Glycosaminoglycans	60-77	glucuronidase beta	Homo sapiens	138-156
3740547-6	1986	The results suggest that the decreased plasma high-sulfated glycosaminoglycan levels in Marfan syndrome are due to the reduction of serum beta-glucuronidase, which leads to the decreased degradation of macromolecules and, subsequently, the accumulation of the glycosaminoglycans in the tissues.	Glycosaminoglycans	260-278	glucuronidase beta	Homo sapiens	138-156
3488088-3	1986	There was a positive correlation between osteocalcin and fasting mucopolysaccharide/creatinine ratio in both sexes, and between osteocalcin and fasting hydroxyproline/creatinine ratio in women.	Glycosaminoglycans	65-83	bone gamma-carboxyglutamate protein	Homo sapiens	41-52
3011858-5	1986	The M-protein bound to a single GAG band with intermediate mobility which eluted with 1.25 N NaCl on ion-exchange chromatography and was chondroitinase sensitive.	Glycosaminoglycans	32-35	myomesin 2	Homo sapiens	4-13
3796630-11	1986	A theory is developed that the binding of polyionic GAG to C1 and to C1 INH may provide a charged local environment which simulates a relatively higher ionic strength.	Glycosaminoglycans	52-55	serpin family G member 1	Homo sapiens	69-75
3755134-2	1986	To determine the minimum structure of dermatan sulfate required to activate HCII, the glycosaminoglycan was partially degraded by sequential treatment with periodate, [3H]borohydride, and sulfuric acid.	Glycosaminoglycans	86-103	serpin family D member 1	Homo sapiens	76-80
3089205-5	1986	All glycosaminoglycans were identified as chondroitin sulfate sulfated at the C-6 position.	Glycosaminoglycans	4-22	complement C6	Homo sapiens	78-81
2439645-0	1987	Pathobiochemical significance of granulocyte elastase complexed with proteinase inhibitors: effect on glycosaminoglycan metabolism in cultured synovial cells.	Glycosaminoglycans	102-119	endogenous retrovirus group K member 18	Homo sapiens	69-79
2439645-2	1987	To study the effect of elastase-alpha 2-macroglobulin and elastase-alpha 1-proteinase inhibitor complexes on the glycosaminoglycan metabolism of cultured synovial cells, we determined the distribution of [3H]glucosamine-labelled hyaluronate, which represents the main synthesized glycosaminoglycan, and of 35SO4(2-)-labelled chondroitin sulphate into the intracellular, pericellular and extracellular compartments of the cell culture.	Glycosaminoglycans	113-130	endogenous retrovirus group K member 18	Homo sapiens	75-85
3720090-10	1986	Repeated doses of BMP/iNCP with each change of culture medium produced a greater incidence and quantity of cartilage than a single dose, but the 35S incorporation into GAG always reached peak levels, in the interval between four and ten days, irrespective of the schedule of administration or dosage.	Glycosaminoglycans	168-171	bone morphogenetic protein 1	Homo sapiens	18-21
3706560-5	1986	The acceleration of thrombin-antithrombin interactions in the presence of endothelial cell-derived glycosaminoglycans was similar for W/Wv and +/+ mice, was abolished with purified bacterial heparinase, and was expressed to only a minor extent when utilizing modified antithrombin.	Glycosaminoglycans	99-117	coagulation factor II	Mus musculus	20-28
3084487-7	1986	Alkaline borohydride treatment released glycosaminoglycan chains with Mr of 2.0 X 10(4) which were susceptible to chondroitinase AC II and chondroitinase ABC digestion.	Glycosaminoglycans	40-57	galactosamine (N-acetyl)-6-sulfatase	Rattus norvegicus	114-153
3706560-5	1986	The acceleration of thrombin-antithrombin interactions in the presence of endothelial cell-derived glycosaminoglycans was similar for W/Wv and +/+ mice, was abolished with purified bacterial heparinase, and was expressed to only a minor extent when utilizing modified antithrombin.	Glycosaminoglycans	99-117	serine (or cysteine) peptidase inhibitor, clade C (antithrombin), member 1	Mus musculus	29-41
3706560-5	1986	The acceleration of thrombin-antithrombin interactions in the presence of endothelial cell-derived glycosaminoglycans was similar for W/Wv and +/+ mice, was abolished with purified bacterial heparinase, and was expressed to only a minor extent when utilizing modified antithrombin.	Glycosaminoglycans	99-117	serine (or cysteine) peptidase inhibitor, clade C (antithrombin), member 1	Mus musculus	268-280
2421806-9	1986	The included peaks on Sepharose CL-6B (MIIb, CIIb) from both medium and cell layer compartments resisted digestion with papain, indicating the presence of glycosaminoglycan chains of mol wt approximately 38,000 either free or attached to a small peptide.	Glycosaminoglycans	155-172	secretoglobin family 2B member 3, pseudogene	Homo sapiens	45-49
2419018-1	1986	Repeated intravenous injections of bovine serum albumin in rabbits caused a significant reduction in the aortic in vivo biosynthesis of chondroitin-4,6-sulfate, whereas no changes were observed in the synthesis of other glycosaminoglycans nor in the content of collagen.	Glycosaminoglycans	220-238	albumin	Oryctolagus cuniculus	42-55
3517485-13	1986	The defects in lipoprotein metabolism may in part be the end result of the urinary loss of highly negative-charged macromolecules of the mucopolysaccharide called orosomucoid, which carries with it heparan sulfate, and important cofactor for LPL.	Glycosaminoglycans	137-155	lipoprotein lipase	Homo sapiens	242-245
2419433-3	1986	Polyclonal rabbit antisera to N- and C-terminal peptides reacted with a native viral protein of 19,000 daltons and with gag-encoded precursors of p19.	Glycosaminoglycans	120-123	interleukin 23 subunit alpha	Homo sapiens	146-149
3484980-6	1986	A minority of those patients positive for salivary antibodies to env gene-encoded gp160 and gp120 also had salivary antibodies to gag gene-encoded proteins of 55,000, 24,000, and/or 17,000 daltons.	Glycosaminoglycans	130-133	endogenous retrovirus group K member 20	Homo sapiens	65-68
3484980-6	1986	A minority of those patients positive for salivary antibodies to env gene-encoded gp160 and gp120 also had salivary antibodies to gag gene-encoded proteins of 55,000, 24,000, and/or 17,000 daltons.	Glycosaminoglycans	130-133	glutamyl aminopeptidase	Homo sapiens	82-87
3484980-6	1986	A minority of those patients positive for salivary antibodies to env gene-encoded gp160 and gp120 also had salivary antibodies to gag gene-encoded proteins of 55,000, 24,000, and/or 17,000 daltons.	Glycosaminoglycans	130-133	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	92-97
3512096-3	1986	One of the four cDNAs has a predicted N-terminal sequence of met-gly-gln in common with the gag N terminus of v-abl.	Glycosaminoglycans	92-95	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	112-115
3525295-2	1986	The relationship between the presence of glycosaminoglycans (GAGs) and the morphology of the middle layer or mesoblast was examined by performing transmission electron microscopy of chicken blastoderms microinjected with GAG-degrading enzymes.	Glycosaminoglycans	41-59	uncharacterized LOC107052719	Gallus gallus	61-64
3004634-3	1986	These were soon followed by antibodies to pr55 and more gradually by antibodies to the other gag gene encoded cleavage product p18, the env gene encoded transmembrane glycoprotein gp41, the env gene encoded glycoproteins gp65 and gp110, and the putative pol gene product p33.	Glycosaminoglycans	93-96	H3 histone pseudogene 12	Homo sapiens	127-130
3718422-1	1986	The effect of modifications of the extracellular matrix on the biosynthesis of glycosaminoglycans was investigated in human skin fibroblast cultures by studying UDPGDH activity in order to evaluate: a), the histoenzymological and biochemical modifications induced by chondroitinase ABC treatment (new experimental conditions were developed in order to obtain minimum cell damage); b), the reversibility of these modifications; c), the effect of growing the cells in the presence of chondroitinsulfate; d), the specificity of the modifications induced.	Glycosaminoglycans	79-97	UDP-glucose 6-dehydrogenase	Homo sapiens	161-167
3771628-1	1986	The p110gag-myc protein coded for by the retrovirus MC29 was purified 3,000-fold from MC29-Q8 transformed cells by immuno-affinity chromatography using IgG specific for the N-terminal region of the gag protein.	Glycosaminoglycans	8-11	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	12-15
2417857-8	1986	Similarly, on days 4 and 10, the amounts of uronic acids were higher in the Hex-Cer group than in the controls, reflecting an enhanced accumulation of glycosaminoglycans.	Glycosaminoglycans	151-169	hematopoietically expressed homeobox	Rattus norvegicus	76-79
4092860-7	1985	Incorporation of glycosaminoglycans as evaluated by [35SO4]-labelling was reduced by 8% when cells were exposed to growth hormone (2p less than 0.01).	Glycosaminoglycans	17-35	somatotropin	Oryctolagus cuniculus	115-129
3006536-0	1985	Detection of glycosaminoglycans at the one-nanogram level by 125I-cytochrome c.	Glycosaminoglycans	13-31	cytochrome c, somatic	Homo sapiens	66-78
3006536-1	1985	The basic protein cytochrome c forms stable ionic complexes with all known glycosaminoglycans.	Glycosaminoglycans	75-93	cytochrome c, somatic	Homo sapiens	18-30
4056061-11	1985	Because glycosaminoglycans have been implicated in lipid metabolism and atherosclerosis, we tested all of these compounds, isolated in free form, on the in vitro hydrolysis of triglycerides by lipoprotein lipase.	Glycosaminoglycans	8-26	lipoprotein lipase	Homo sapiens	193-211
3877932-4	1985	Thus, we have expressed the p24 gag antigen in Escherichia coli in order to produce a diagnostic reagent for the detection of virus exposure.	Glycosaminoglycans	32-35	transmembrane p24 trafficking protein 2	Homo sapiens	28-31
3878251-7	1985	Conversely to hydrocortisone, EGF increases the proliferation of the 9-4/0 line and also increases the label in sulphated cell surface glycosaminoglycans.	Glycosaminoglycans	135-153	epidermal growth factor	Rattus norvegicus	30-33
2993659-5	1985	This implies the existence of a sixth gag protein 22 amino acids in length and located between p19 and p10 on the gag precursor.	Glycosaminoglycans	38-41	S100 calcium binding protein A10	Homo sapiens	103-106
2993659-7	1985	We have elucidated the structure of these forms, called p19 beta, by analysis of the proteins and determination of the DNA sequence of the p19 region of the gag gene from ev-1 and ev-2.	Glycosaminoglycans	157-160	S-phase kinase associated protein 1 pseudogene 2	Homo sapiens	56-64
2993659-7	1985	We have elucidated the structure of these forms, called p19 beta, by analysis of the proteins and determination of the DNA sequence of the p19 region of the gag gene from ev-1 and ev-2.	Glycosaminoglycans	157-160	interleukin 23 subunit alpha	Homo sapiens	56-59
2993659-7	1985	We have elucidated the structure of these forms, called p19 beta, by analysis of the proteins and determination of the DNA sequence of the p19 region of the gag gene from ev-1 and ev-2.	Glycosaminoglycans	157-160	transmembrane channel like 6	Homo sapiens	171-184
2992779-7	1985	In contrast, either transforming growth factor beta or epidermal growth factor alone was able to decrease synthesis of glycosaminoglycans and collagen.	Glycosaminoglycans	119-137	pro-epidermal growth factor	Oryctolagus cuniculus	55-78
2931856-3	1985	Thrombin at more than one unit/ml accelerated the release of [35S] sulfate-labeled glycosaminoglycans from cultured porcine aortic endothelial cells.	Glycosaminoglycans	83-101	coagulation factor II, thrombin	Homo sapiens	0-8
4019466-0	1985	A sulfatase specific for glucuronic acid 2-sulfate residues in glycosaminoglycans.	Glycosaminoglycans	63-81	arylsulfatase family member H	Homo sapiens	2-11
4019466-12	1985	The results indicate that there exists a separate sulfatase for the removal of sulfate substituents from C-2 of GlcA residues in glycosaminoglycans.	Glycosaminoglycans	129-147	arylsulfatase family member H	Homo sapiens	50-59
2989561-4	1985	This resulted in the junction of gag sequences in p12 to env sequences in gp37, and in the loss of the src gene.	Glycosaminoglycans	33-36	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	50-53
2989561-7	1985	Although the gag-env deletion endpoints were identical in the two subclones, heterogeneity was observed across the src deletion in that both mutants analyzed had the same 5" endpoint but slightly different 3" endpoints.	Glycosaminoglycans	13-16	endogenous retrovirus group K member 20	Homo sapiens	17-20
2989562-2	1985	One of these joins gag sequences in the p12 coding region to env sequences in region encoding gp37; the other deletion spans the src region.	Glycosaminoglycans	19-22	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	40-43
2581830-15	1985	Conversely, the GAG increase the retention of 3H-FN in the gels.	Glycosaminoglycans	16-19	fibronectin 1	Homo sapiens	49-51
2581830-17	1985	The increased retention of GAG and CSPG by the addition of FN may be due to both stabilization of binding to the collagen and trapping of matrix complexes within the gel.	Glycosaminoglycans	27-30	fibronectin 1	Homo sapiens	59-61
4024085-6	1985	Therefore, it is highly likely that endo-beta-glucuronidase(s) and endo-alpha-iduronidase(s) which belong to the glycosidase of endo type such as hyaluronidase are involved in the catabolic degradation of glycosaminoglycans in tissues.	Glycosaminoglycans	205-223	glucuronidase beta	Homo sapiens	41-59
3988937-1	1985	Clinical grade heparin is a very heterogeneous mucopolysaccharide, containing molecules with Mr ranging from 6,000 to 30,000 that have either a high affinity or a low affinity for antithrombin III (AT).	Glycosaminoglycans	47-65	serpin family C member 1	Homo sapiens	180-196
2983109-3	1985	Smaller deletions in gag reveal that p15 gag sequences are responsible for this effect, whereas deletion of p12 sequences had no effect on lymphoid transformation.	Glycosaminoglycans	21-24	cyclin dependent kinase inhibitor 2B	Homo sapiens	37-40
2983109-3	1985	Smaller deletions in gag reveal that p15 gag sequences are responsible for this effect, whereas deletion of p12 sequences had no effect on lymphoid transformation.	Glycosaminoglycans	41-44	cyclin dependent kinase inhibitor 2B	Homo sapiens	37-40
2982497-3	1985	We map the activity to an alternate reading frame in the p19-p10 region of the gag gene and identify a mRNA whose spliced structure would direct translation of this reading frame from the Pr76gag initiation codon.	Glycosaminoglycans	79-82	interleukin 23 subunit alpha	Homo sapiens	57-60
2982497-3	1985	We map the activity to an alternate reading frame in the p19-p10 region of the gag gene and identify a mRNA whose spliced structure would direct translation of this reading frame from the Pr76gag initiation codon.	Glycosaminoglycans	79-82	S100 calcium binding protein A10	Homo sapiens	61-64
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
6092677-1	1984	Fujinami sarcoma virus (FSV) encodes a 140,000-dalton transforming protein, P140, which contains gag- and fps-specific sequences.	Glycosaminoglycans	97-100	SRC kinase signaling inhibitor 1	Homo sapiens	76-80
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
28305109-1	1984	A method utilizing microinjection of glycosaminoglycan-degrading enzymes in the chicken blastoderm prior to embryo culture and immunostaining for fibronectin have been applied to demonstrate an interaction between glycosaminoglycans and fibronectin in the basement membrane of the epiblast.	Glycosaminoglycans	37-54	fibronectin 1	Gallus gallus	237-248
28305109-1	1984	A method utilizing microinjection of glycosaminoglycan-degrading enzymes in the chicken blastoderm prior to embryo culture and immunostaining for fibronectin have been applied to demonstrate an interaction between glycosaminoglycans and fibronectin in the basement membrane of the epiblast.	Glycosaminoglycans	214-232	fibronectin 1	Gallus gallus	146-157
28305109-1	1984	A method utilizing microinjection of glycosaminoglycan-degrading enzymes in the chicken blastoderm prior to embryo culture and immunostaining for fibronectin have been applied to demonstrate an interaction between glycosaminoglycans and fibronectin in the basement membrane of the epiblast.	Glycosaminoglycans	214-232	fibronectin 1	Gallus gallus	237-248
28305109-4	1984	After degradation of glycosaminoglycans in the living organism, it is shown that this particular site, in fact, also contains fibronectin that is masked in vivo by, at least, hyaluronate.	Glycosaminoglycans	21-39	fibronectin 1	Gallus gallus	126-137
6093355-2	1984	Immunoprecipitation and removal of P85gag-mos from the reaction mixture by either an anti-mos or anti-gag serum resulted in a subsequent elimination of in vitro P85gag-mos and P58gag phosphorylation.	Glycosaminoglycans	38-41	MOS proto-oncogene, serine/threonine kinase	Homo sapiens	42-45
6093355-2	1984	Immunoprecipitation and removal of P85gag-mos from the reaction mixture by either an anti-mos or anti-gag serum resulted in a subsequent elimination of in vitro P85gag-mos and P58gag phosphorylation.	Glycosaminoglycans	38-41	MOS proto-oncogene, serine/threonine kinase	Homo sapiens	90-93
6093355-2	1984	Immunoprecipitation and removal of P85gag-mos from the reaction mixture by either an anti-mos or anti-gag serum resulted in a subsequent elimination of in vitro P85gag-mos and P58gag phosphorylation.	Glycosaminoglycans	38-41	MOS proto-oncogene, serine/threonine kinase	Homo sapiens	90-93
6093355-5	1984	Viral gag antisera were also used to show immune complex phosphorylation of another gag-mos hybrid protein termed P100gag-mos, derived from a revertant of ts110.	Glycosaminoglycans	6-9	MOS proto-oncogene, serine/threonine kinase	Homo sapiens	88-91
6094844-6	1984	Histochemically, this mucin was composed of a mixture of neutral and acidic mucopolysaccharide, the latter being predominantly sialomucin.	Glycosaminoglycans	76-94	solute carrier family 13 member 2	Rattus norvegicus	22-27
6486808-2	1984	This alteration led to a 500-fold reduction in the heparin-dependent acceleration of thrombin-modified antithrombin interactions, as well as a 10-fold decrease in the avidity of the modified protease inhibitor for mucopolysaccharide.	Glycosaminoglycans	214-232	coagulation factor II, thrombin	Homo sapiens	85-93
6486808-2	1984	This alteration led to a 500-fold reduction in the heparin-dependent acceleration of thrombin-modified antithrombin interactions, as well as a 10-fold decrease in the avidity of the modified protease inhibitor for mucopolysaccharide.	Glycosaminoglycans	214-232	serpin family C member 1	Homo sapiens	103-115
6486808-5	1984	Based upon these data, it was proposed that the loss of "heparin cofactor" activity of antithrombin must be predominantly due to an inability of the modified protease inhibitor to undergo a conformational transition required for mucopolysaccharide-dependent "activation" of the macromolecule.	Glycosaminoglycans	229-247	serpin family C member 1	Homo sapiens	87-99
6746897-6	1984	The above mucopolysaccharides function in a manner similar to commercial heparin, since modification of antithrombin at a site critical for heparin-dependent acceleration of the protease inhibitor resulted in a level of interaction product identical to the uncatalyzed amount.	Glycosaminoglycans	10-29	serpin family C member 1	Homo sapiens	104-116
6384678-2	1984	The glycosaminoglycans found in the incubation medium were mainly intact carbohydrate moieties of partially degraded proteoglycan molecules, whereas the tissue-bound glycosaminoglycans were of intact proteoglycan molecules.	Glycosaminoglycans	4-22	versican	Gallus gallus	117-129
6384678-8	1984	These findings suggest that the synthesis and/or degradation of the various types of glycosaminoglycan chains (chondroitin sulfate and keratan sulfate) of cartilage proteoglycan can be regulated differentially by serum growth factors.	Glycosaminoglycans	85-102	versican	Gallus gallus	165-177
6586291-0	1984	Glycosaminoglycan synthesis during differentiation of HL60/HGPRT-leukemia cells induced by dimethyl sulfoxide and 12-O-tetradecanoylphorbol-13-acetate.	Glycosaminoglycans	0-17	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	59-64
6586291-2	1984	For this reason, the production of GAGs during the induction of myelocytic and macrophage-like differentiation of the human promyelocytic leukemia cloned cell line HL60/HGPRT- was studied.	Glycosaminoglycans	35-39	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	169-174
6586291-3	1984	The major GAG component of HL60/HGPRT- was chondroitin 4-sulfate.	Glycosaminoglycans	10-13	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	32-37
6094162-2	1984	We confirmed that somatomedin and insulin stimulate GAG synthesis in normal rat chondrocytes.	Glycosaminoglycans	52-55	insulin-like growth factor 1	Rattus norvegicus	18-29
6094162-2	1984	We confirmed that somatomedin and insulin stimulate GAG synthesis in normal rat chondrocytes.	Glycosaminoglycans	52-55	insulin	Homo sapiens	34-41
6094162-3	1984	The maximal responses of somatomedin and insulin in GAG synthesis were the same, but the stimulation of GAG synthesis by maximally effective concentrations of insulin plus somatomedin was not cumulative.	Glycosaminoglycans	52-55	insulin-like growth factor 1	Rattus norvegicus	25-36
6094162-3	1984	The maximal responses of somatomedin and insulin in GAG synthesis were the same, but the stimulation of GAG synthesis by maximally effective concentrations of insulin plus somatomedin was not cumulative.	Glycosaminoglycans	52-55	insulin	Homo sapiens	41-48
6328019-5	1984	The nucleotide sequence predicts the order of amino acids in each of the individual gag-coded proteins (p15, p12, p30, p10), all of which derive from the gag gene precursor.	Glycosaminoglycans	84-87	cyclin dependent kinase inhibitor 2B	Homo sapiens	104-107
6328019-5	1984	The nucleotide sequence predicts the order of amino acids in each of the individual gag-coded proteins (p15, p12, p30, p10), all of which derive from the gag gene precursor.	Glycosaminoglycans	84-87	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	109-112
6328019-5	1984	The nucleotide sequence predicts the order of amino acids in each of the individual gag-coded proteins (p15, p12, p30, p10), all of which derive from the gag gene precursor.	Glycosaminoglycans	84-87	centromere protein V	Homo sapiens	114-117
6328019-5	1984	The nucleotide sequence predicts the order of amino acids in each of the individual gag-coded proteins (p15, p12, p30, p10), all of which derive from the gag gene precursor.	Glycosaminoglycans	84-87	S100 calcium binding protein A10	Homo sapiens	119-122
6328019-5	1984	The nucleotide sequence predicts the order of amino acids in each of the individual gag-coded proteins (p15, p12, p30, p10), all of which derive from the gag gene precursor.	Glycosaminoglycans	154-157	cyclin dependent kinase inhibitor 2B	Homo sapiens	104-107
6328019-5	1984	The nucleotide sequence predicts the order of amino acids in each of the individual gag-coded proteins (p15, p12, p30, p10), all of which derive from the gag gene precursor.	Glycosaminoglycans	154-157	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	109-112
6328019-5	1984	The nucleotide sequence predicts the order of amino acids in each of the individual gag-coded proteins (p15, p12, p30, p10), all of which derive from the gag gene precursor.	Glycosaminoglycans	154-157	centromere protein V	Homo sapiens	114-117
6328019-5	1984	The nucleotide sequence predicts the order of amino acids in each of the individual gag-coded proteins (p15, p12, p30, p10), all of which derive from the gag gene precursor.	Glycosaminoglycans	154-157	S100 calcium binding protein A10	Homo sapiens	119-122
6425097-1	1984	Our recent studies have shown that chick embryo epiphyseal cartilage synthesizes three distinct species of proteoglycan (PG-H, PG-Lb, and PG-Lt) which are analogous in having glycosaminoglycan side chains of the chondroitin (dermatan) sulfate type but different from one another in regard to the structure of core protein.	Glycosaminoglycans	175-192	versican	Gallus gallus	107-119
6705893-0	1984	Elastin fiber-associated glycosaminoglycans in beta-aminopropionitrile-induced lathyrism.	Glycosaminoglycans	25-43	elastin	Gallus gallus	0-7
6705893-10	1984	The conclusion is reached that glycosaminoglycans associated with beta-aminopropionitrile-induced lathyritic elastin (i) are different from those of the matrix or associated with collagen, and (ii) include mainly dermatan and heparan sulfates.	Glycosaminoglycans	31-49	elastin	Gallus gallus	109-116
3006536-2	1985	When labeled with 125I, cytochrome c is capable of detecting exceptionally small quantities of glycosaminoglycans.	Glycosaminoglycans	95-113	cytochrome c, somatic	Homo sapiens	24-36
3006536-3	1985	Subsequent to electrophoresis on cellulose acetate strips using pyridine formate buffer at pH 3, followed by ethanol fixation, and treatment with 125I-cytochrome c, all the known glycosaminoglycans are detected at minimum levels of 1 ng/0.25-microliter application.	Glycosaminoglycans	179-197	cytochrome c, somatic	Homo sapiens	151-163
4055755-3	1985	The glycosaminoglycan chains carry sulfate residues predominantly attached to C-4 of the galactosamine unit; less than 10% of the sulfate groups occur as 6-sulfated galactosamine units.	Glycosaminoglycans	4-21	complement component 4B (Chido blood group)	Mus musculus	78-81
2994296-7	1985	The gP90gag-raf thus appears to be a glycosylated form of P75gag-raf specified by the gag sequences of the fusion protein, in analogy with Pr65gag and gPr80gag of murine leukemia viruses.	Glycosaminoglycans	8-11	zinc fingers and homeoboxes 2	Homo sapiens	12-15
2994296-7	1985	The gP90gag-raf thus appears to be a glycosylated form of P75gag-raf specified by the gag sequences of the fusion protein, in analogy with Pr65gag and gPr80gag of murine leukemia viruses.	Glycosaminoglycans	8-11	zinc fingers and homeoboxes 2	Homo sapiens	65-68
2995409-4	1985	Furthermore, the biological activity of ECGF, acidic FGF, and EDGF-II is potentiated by the glycosaminoglycan, heparin.	Glycosaminoglycans	92-109	fibroblast growth factor 1	Bos taurus	40-44
2995409-4	1985	Furthermore, the biological activity of ECGF, acidic FGF, and EDGF-II is potentiated by the glycosaminoglycan, heparin.	Glycosaminoglycans	92-109	fibroblast growth factor 1	Bos taurus	62-69
2993659-5	1985	This implies the existence of a sixth gag protein 22 amino acids in length and located between p19 and p10 on the gag precursor.	Glycosaminoglycans	38-41	interleukin 23 subunit alpha	Homo sapiens	95-98
3863104-2	1985	The rate of thrombin inhibition by heparin cofactor II is accelerated (greater than or equal to 1000-fold) in the presence of the glycosaminoglycans, heparin and dermatan sulfate.	Glycosaminoglycans	130-148	coagulation factor II, thrombin	Homo sapiens	12-20
2411730-5	1985	Approximately 70% of the glycosaminoglycan side chains of RBL-1 proteoglycans were digested by chondroitinase ABC and 27% were hydrolyzed by treatment with nitrous acid.	Glycosaminoglycans	25-42	RB transcriptional corepressor like 1	Rattus norvegicus	58-63
4022379-6	1985	The data suggest that the M-protein bound to mucopolysaccharides in nerve endoneurium and connective tissue.	Glycosaminoglycans	45-64	myomesin 2	Homo sapiens	26-35
4005430-0	1985	Ultrastructural and biochemical characterization of glycosaminoglycans in HNK-1-positive large granular lymphocytes.	Glycosaminoglycans	52-70	beta-1,3-glucuronyltransferase 1	Homo sapiens	74-79
2992940-3	1985	A-MuLV-derived gag sequences could, however, functionally replace the 5" end of src and restore the transformation potential of a 5"-truncated src gene.	Glycosaminoglycans	15-18	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	80-83
2992940-3	1985	A-MuLV-derived gag sequences could, however, functionally replace the 5" end of src and restore the transformation potential of a 5"-truncated src gene.	Glycosaminoglycans	15-18	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	143-146
2992940-7	1985	Furthermore, it shows that a functional homology exists between the gag sequence of A-MuLV and the 5" end of src.	Glycosaminoglycans	68-71	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	109-112
4010229-4	1985	Selective and partial inhibition of cell attachment to type I collagen, and, to a lesser extent, fibronectin, occurred upon preincubating these substrates with the sulfated glycosaminoglycans, heparin and heparan sulfate, at concentrations of 1 to 100 micrograms/ml; for 3T3 cells heparin was significantly more inhibitory (mean maximal inhibition of approximately 40%) than were two heparan sulfate fractions.	Glycosaminoglycans	173-191	fibronectin 1	Mus musculus	97-108
3891641-5	1985	Five out of 7 SCC lines showed a shift in GAG production compared with normal keratinocytes, so that in these lines heparan sulphate was the major GAG as opposed to hyaluronic acid in the normal keratinocytes.	Glycosaminoglycans	42-45	serpin family B member 3	Homo sapiens	14-17
3891641-5	1985	Five out of 7 SCC lines showed a shift in GAG production compared with normal keratinocytes, so that in these lines heparan sulphate was the major GAG as opposed to hyaluronic acid in the normal keratinocytes.	Glycosaminoglycans	147-150	serpin family B member 3	Homo sapiens	14-17
2986953-1	1985	Previously, we demonstrated that PTH increases the level of cAMP, the activity of ornithine decarboxylase (ODC; EC 4.1.1.17; which is a rate-limiting enzyme in polyamine biosynthesis), and glycosaminoglycan (GAG) synthesis (which is characteristic of the chondrocyte phenotype) in rabbit costal chondrocytes in culture.	Glycosaminoglycans	189-206	parathyroid hormone	Oryctolagus cuniculus	33-36
2986953-1	1985	Previously, we demonstrated that PTH increases the level of cAMP, the activity of ornithine decarboxylase (ODC; EC 4.1.1.17; which is a rate-limiting enzyme in polyamine biosynthesis), and glycosaminoglycan (GAG) synthesis (which is characteristic of the chondrocyte phenotype) in rabbit costal chondrocytes in culture.	Glycosaminoglycans	208-211	parathyroid hormone	Oryctolagus cuniculus	33-36
2582414-0	1985	Immunological properties of the Gag protein p24 of the acquired immunodeficiency syndrome retrovirus (human T-cell leukemia virus type III).	Glycosaminoglycans	32-35	transmembrane p24 trafficking protein 2	Homo sapiens	44-47
3157703-1	1985	It has been postulated that thrombin binds to endothelial cells through, at least in part, cell surface glycosaminoglycans such as heparan sulfate, which could serve as antithrombin cofactor on the endothelium.	Glycosaminoglycans	104-122	coagulation factor II, thrombin	Bos taurus	28-36
3989479-1	1985	In high performance liquid chromatographic procedures hitherto described, SiO2, NH2 and RP columns have been used for the analysis of disaccharides produced by the digestion of glycosaminoglycans with the chondroitin sulphate lyases AC and ABC.	Glycosaminoglycans	177-195	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	240-243
3919220-5	1985	In contrast, full-thickness skin fibroblasts from an elderly patient (AG2261) generate GAG distributions in their L-SAMs (with greatly elevated levels of hyaluronate and chondroitin sulfate) that are very different from those of the cell fractions and from those of AG4449; furthermore, these distributions in AG2261 fractions do not change when shifted from asc- to asc+ medium.	Glycosaminoglycans	87-90	methionine adenosyltransferase 1A	Homo sapiens	116-120
3968986-7	1985	LDL isolated from plasma incubated in the presence of LCAT, on the other hand, showed a significant reduction in GAG binding.	Glycosaminoglycans	113-116	lecithin-cholesterol acyltransferase	Homo sapiens	54-58
3968986-8	1985	The ratio of free cholesterol:GAG in the complex was most significantly reduced in LCAT-modified LDL.	Glycosaminoglycans	30-33	lecithin-cholesterol acyltransferase	Homo sapiens	83-87
6084876-0	1984	Purification and biological property of heparin cofactor II: activation of heparin cofactor II and antithrombin III by dextran sulfate and various glycosaminoglycans.	Glycosaminoglycans	147-165	serpin family D member 1	Homo sapiens	40-59
6084876-0	1984	Purification and biological property of heparin cofactor II: activation of heparin cofactor II and antithrombin III by dextran sulfate and various glycosaminoglycans.	Glycosaminoglycans	147-165	serpin family D member 1	Homo sapiens	75-94
6084876-0	1984	Purification and biological property of heparin cofactor II: activation of heparin cofactor II and antithrombin III by dextran sulfate and various glycosaminoglycans.	Glycosaminoglycans	147-165	serpin family C member 1	Homo sapiens	99-115
6084876-3	1984	Chem., 257, 2162, 1982) and abilities of dextran sulfate and various glycosaminoglycans to activate the antithrombin activities of HC II and antithrombin III (AT III) were studied.	Glycosaminoglycans	69-87	serpin family C member 1	Homo sapiens	104-116
6084876-3	1984	Chem., 257, 2162, 1982) and abilities of dextran sulfate and various glycosaminoglycans to activate the antithrombin activities of HC II and antithrombin III (AT III) were studied.	Glycosaminoglycans	69-87	serpin family D member 1	Homo sapiens	131-136
6240765-1	1984	Urinary mucopolysaccharides (u MPZ) were determined in 114 patients with thyroid diseases.	Glycosaminoglycans	8-27	myelin protein zero	Homo sapiens	31-34
6381881-7	1984	Apo B in these areas was associated with Alcian blue-positive areas suggested to contain sulfated glycosaminoglycans, which may be responsible for the preferential LDL accumulation.	Glycosaminoglycans	98-116	apolipoprotein B	Sus scrofa	0-5
6087548-8	1984	The precursor of gag products was a protein with an apparent molecular weight of 53,000 (Pr53), and was shown to be processed into three mature gag proteins, p19, p24, and p15, in this order, from the 5" end of the gag gene.	Glycosaminoglycans	17-20	protein phosphatase 2 phosphatase activator	Homo sapiens	89-93
6087548-8	1984	The precursor of gag products was a protein with an apparent molecular weight of 53,000 (Pr53), and was shown to be processed into three mature gag proteins, p19, p24, and p15, in this order, from the 5" end of the gag gene.	Glycosaminoglycans	17-20	interleukin 23 subunit alpha	Homo sapiens	158-161
6087548-8	1984	The precursor of gag products was a protein with an apparent molecular weight of 53,000 (Pr53), and was shown to be processed into three mature gag proteins, p19, p24, and p15, in this order, from the 5" end of the gag gene.	Glycosaminoglycans	17-20	transmembrane p24 trafficking protein 2	Homo sapiens	163-166
6087548-8	1984	The precursor of gag products was a protein with an apparent molecular weight of 53,000 (Pr53), and was shown to be processed into three mature gag proteins, p19, p24, and p15, in this order, from the 5" end of the gag gene.	Glycosaminoglycans	17-20	cyclin dependent kinase inhibitor 2B	Homo sapiens	172-175
6087548-8	1984	The precursor of gag products was a protein with an apparent molecular weight of 53,000 (Pr53), and was shown to be processed into three mature gag proteins, p19, p24, and p15, in this order, from the 5" end of the gag gene.	Glycosaminoglycans	144-147	protein phosphatase 2 phosphatase activator	Homo sapiens	89-93
6087548-8	1984	The precursor of gag products was a protein with an apparent molecular weight of 53,000 (Pr53), and was shown to be processed into three mature gag proteins, p19, p24, and p15, in this order, from the 5" end of the gag gene.	Glycosaminoglycans	144-147	interleukin 23 subunit alpha	Homo sapiens	158-161
6087548-8	1984	The precursor of gag products was a protein with an apparent molecular weight of 53,000 (Pr53), and was shown to be processed into three mature gag proteins, p19, p24, and p15, in this order, from the 5" end of the gag gene.	Glycosaminoglycans	144-147	cyclin dependent kinase inhibitor 2B	Homo sapiens	172-175
6087548-8	1984	The precursor of gag products was a protein with an apparent molecular weight of 53,000 (Pr53), and was shown to be processed into three mature gag proteins, p19, p24, and p15, in this order, from the 5" end of the gag gene.	Glycosaminoglycans	144-147	protein phosphatase 2 phosphatase activator	Homo sapiens	89-93
6087548-8	1984	The precursor of gag products was a protein with an apparent molecular weight of 53,000 (Pr53), and was shown to be processed into three mature gag proteins, p19, p24, and p15, in this order, from the 5" end of the gag gene.	Glycosaminoglycans	144-147	interleukin 23 subunit alpha	Homo sapiens	158-161
6087548-8	1984	The precursor of gag products was a protein with an apparent molecular weight of 53,000 (Pr53), and was shown to be processed into three mature gag proteins, p19, p24, and p15, in this order, from the 5" end of the gag gene.	Glycosaminoglycans	144-147	cyclin dependent kinase inhibitor 2B	Homo sapiens	172-175
6094162-3	1984	The maximal responses of somatomedin and insulin in GAG synthesis were the same, but the stimulation of GAG synthesis by maximally effective concentrations of insulin plus somatomedin was not cumulative.	Glycosaminoglycans	104-107	insulin	Homo sapiens	159-166
6094162-3	1984	The maximal responses of somatomedin and insulin in GAG synthesis were the same, but the stimulation of GAG synthesis by maximally effective concentrations of insulin plus somatomedin was not cumulative.	Glycosaminoglycans	104-107	insulin-like growth factor 1	Rattus norvegicus	172-183
6094162-7	1984	Somatomedin used for GAG synthesis and displacement was the partially purified somatomedin A with a biological activity of 80 U/mg.	Glycosaminoglycans	21-24	insulin-like growth factor 1	Rattus norvegicus	0-11
6094162-7	1984	Somatomedin used for GAG synthesis and displacement was the partially purified somatomedin A with a biological activity of 80 U/mg.	Glycosaminoglycans	21-24	insulin-like growth factor 1	Rattus norvegicus	79-90
6429328-0	1984	Glycosaminoglycan content in the lung of the tight-skin mouse.	Glycosaminoglycans	0-17	fibrillin 1	Mus musculus	45-55
6429328-2	1984	We performed qualitative and quantitative analyses of glycosaminoglycans (GAG) on lungs of the TSK mouse.	Glycosaminoglycans	54-72	fibrillin 1	Mus musculus	95-98
6429328-2	1984	We performed qualitative and quantitative analyses of glycosaminoglycans (GAG) on lungs of the TSK mouse.	Glycosaminoglycans	74-77	fibrillin 1	Mus musculus	95-98
6722318-3	1984	The data obtained suggest that GAG contained by the choroid plexus are involved in the mechanism by which the rate of CSF formation is regulated.	Glycosaminoglycans	31-34	colony stimulating factor 2	Canis lupus familiaris	118-121
6746772-0	1984	Role of glycosaminoglycans and collagen in the development of a fibronectin-rich extracellular matrix in cultured embryonic corneal epithelial cells.	Glycosaminoglycans	8-26	fibronectin 1	Gallus gallus	64-75
6203318-2	1984	Mucopolysaccharide containing structures (e.g. mucin) were found stained in orange, meanwhile the chromatin and remaining tissue components appeared in a bright pink-red color.	Glycosaminoglycans	0-18	LOC100508689	Homo sapiens	47-52
6242442-1	1984	The control of glycosaminoglycan biosynthesis was investigated by studying the kinetic and regulatory properties of some enzymes involved in the formation of UDP-sugar precursors: UDP-N-acetylglucosamine 4"-epimerase, catalyzing the interconversion of hexosamine precursors and UDP-glucose dehydrogenase and UDP-glucose 4"-epimerase, utilizing UDP-glucose for the formation of uronic acid and galactose precursors.	Glycosaminoglycans	15-32	UDP-galactose-4-epimerase	Bos taurus	180-216
6242442-1	1984	The control of glycosaminoglycan biosynthesis was investigated by studying the kinetic and regulatory properties of some enzymes involved in the formation of UDP-sugar precursors: UDP-N-acetylglucosamine 4"-epimerase, catalyzing the interconversion of hexosamine precursors and UDP-glucose dehydrogenase and UDP-glucose 4"-epimerase, utilizing UDP-glucose for the formation of uronic acid and galactose precursors.	Glycosaminoglycans	15-32	UDP-glucose 6-dehydrogenase	Bos taurus	278-303
6242442-1	1984	The control of glycosaminoglycan biosynthesis was investigated by studying the kinetic and regulatory properties of some enzymes involved in the formation of UDP-sugar precursors: UDP-N-acetylglucosamine 4"-epimerase, catalyzing the interconversion of hexosamine precursors and UDP-glucose dehydrogenase and UDP-glucose 4"-epimerase, utilizing UDP-glucose for the formation of uronic acid and galactose precursors.	Glycosaminoglycans	15-32	UDP-galactose-4-epimerase	Bos taurus	308-332
6242442-4	1984	This control mechanism regulated also the activities of both UDP-glucose dehydrogenase and UDP-glucose 4"-epimerase and, therefore, it could correlate the biosynthesis of glycosaminoglycan precursors with the redox activity of the cell.	Glycosaminoglycans	171-188	UDP-glucose 6-dehydrogenase	Bos taurus	61-86
6202020-0	1984	Selective PF4 release in vitro induced by heparin and related glycosaminoglycans (GAGs)--correlation with beta-TG release and platelet aggregation.	Glycosaminoglycans	62-80	platelet factor 4	Homo sapiens	10-13
6202020-0	1984	Selective PF4 release in vitro induced by heparin and related glycosaminoglycans (GAGs)--correlation with beta-TG release and platelet aggregation.	Glycosaminoglycans	62-80	pro-platelet basic protein	Homo sapiens	106-113
6202020-0	1984	Selective PF4 release in vitro induced by heparin and related glycosaminoglycans (GAGs)--correlation with beta-TG release and platelet aggregation.	Glycosaminoglycans	82-86	platelet factor 4	Homo sapiens	10-13
6202020-0	1984	Selective PF4 release in vitro induced by heparin and related glycosaminoglycans (GAGs)--correlation with beta-TG release and platelet aggregation.	Glycosaminoglycans	82-86	pro-platelet basic protein	Homo sapiens	106-113
6202020-1	1984	We studied human platelet aggregation and beta-TG/PF4 release induced by heparin and related GAGs in vitro both in normal PRP and in PRP after aspirin.	Glycosaminoglycans	93-97	platelet factor 4	Homo sapiens	50-53
6202020-2	1984	In our experimental conditions, heparin and related GAGs always caused PF4 release in vitro from normal platelets, whether or not there was measurable platelet aggregation in the aggregometer.	Glycosaminoglycans	52-56	platelet factor 4	Homo sapiens	71-74
6202020-4	1984	Therefore, while beta-TG release in vitro seems to correlate with platelet aggregating activity of heparin, the selective PF4 release, caused by heparin and related GAGs also in conditions in which neither platelet aggregation nor beta-TG are measurable, is probably associated with the high affinity of PF4 for heparin.	Glycosaminoglycans	165-169	platelet factor 4	Homo sapiens	122-125
6202020-5	1984	The degree of affinity of GAGs for PF4 (heparin greater than DeS greater than HS) seems to correlate with PF4 release.	Glycosaminoglycans	26-30	platelet factor 4	Homo sapiens	35-38
6202020-5	1984	The degree of affinity of GAGs for PF4 (heparin greater than DeS greater than HS) seems to correlate with PF4 release.	Glycosaminoglycans	26-30	platelet factor 4	Homo sapiens	106-109
6202020-6	1984	Moreover, the significant reduction in PF4 release in vitro after aspirin suggests that GAGs-induced PF4 release is related to a cyclooxygenase-dependent activation process.	Glycosaminoglycans	88-92	platelet factor 4	Homo sapiens	39-42
6202020-6	1984	Moreover, the significant reduction in PF4 release in vitro after aspirin suggests that GAGs-induced PF4 release is related to a cyclooxygenase-dependent activation process.	Glycosaminoglycans	88-92	platelet factor 4	Homo sapiens	101-104
6242442-4	1984	This control mechanism regulated also the activities of both UDP-glucose dehydrogenase and UDP-glucose 4"-epimerase and, therefore, it could correlate the biosynthesis of glycosaminoglycan precursors with the redox activity of the cell.	Glycosaminoglycans	171-188	UDP-galactose-4-epimerase	Bos taurus	91-115
6242442-5	1984	At the level of UDP-glucose utilization two other control mechanisms were demonstrated: the different affinities of UDP-glucose dehydrogenase and UDP-glucose 4"-epimerase for UDP-glucose in tissues with different glycosaminoglycan production and the cellular concentration of UDP-xylose.	Glycosaminoglycans	213-230	UDP-glucose 6-dehydrogenase	Bos taurus	116-141
6242442-5	1984	At the level of UDP-glucose utilization two other control mechanisms were demonstrated: the different affinities of UDP-glucose dehydrogenase and UDP-glucose 4"-epimerase for UDP-glucose in tissues with different glycosaminoglycan production and the cellular concentration of UDP-xylose.	Glycosaminoglycans	213-230	UDP-galactose-4-epimerase	Bos taurus	146-170
6643486-2	1983	Binding of intact plasma fibronectin and its proteolytic fragments to glycosaminoglycans immobilized on agarose beads was systematically compared at different ionic strengths.	Glycosaminoglycans	70-88	fibronectin 1	Homo sapiens	25-36
6538394-2	1984	S pneumoniae neuraminidase exhibits optimum activity near neutral pH (6.0 to 6.5), and catalyzes the cleavage of sialic acid residues from glycoproteins, gangliosides and mucopolysaccharides.	Glycosaminoglycans	171-190	neuraminidase 1	Homo sapiens	13-26
6705972-2	1984	When the rates of triglyceride hydrolysis catalysed by lipoprotein lipase were compared for the subfractions the results were consistent with the view that apolipoprotein E may play a role in facilitating the catabolism of very low density lipoprotein triglyceride in the presence of glycosaminoglycan.	Glycosaminoglycans	284-301	apolipoprotein E	Homo sapiens	156-172
6100640-9	1984	By the sequence analysis of the amplified gag-pXs fused genes, we found that a carboxy terminal portion of p28 is translated from a pX-0 region.	Glycosaminoglycans	42-45	golgi SNAP receptor complex member 1	Homo sapiens	107-110
6418214-5	1983	Experiments in vitro revealed the sulfated glycosaminoglycans chondroitin 4-sulfate and heparin, the polysaccharide dextran sulfate, and the trypanocidal drug suramin to be strongly inhibitory on the ganglioside GD1a neuraminidase activity of normal fibroblast homogenates.	Glycosaminoglycans	43-61	neuraminidase 1	Homo sapiens	217-230
6418214-9	1983	We conclude that the decreased ganglioside neuraminidase activities of mucopolysaccharidosis fibroblasts are due to an inhibition by the accumulated sulfated glycosaminoglycans and that such inhibition is responsible for the storage of certain gangliosides in the tissues of the patients.	Glycosaminoglycans	158-176	neuraminidase 1	Homo sapiens	43-56
6643486-4	1983	Fractionation of the thermolysin digest of fibronectin on the glycosaminoglycan-Sepharoses at low ionic strength revealed that three groups of fragments, i.e. Mr = 150,000-140,000, 24,000, and 16,000 (150K-140K, 24K, and 16K) fragments, were capable of binding to glycosaminoglycans with different specificities and affinities.	Glycosaminoglycans	62-79	fibronectin 1	Homo sapiens	43-54
6643486-4	1983	Fractionation of the thermolysin digest of fibronectin on the glycosaminoglycan-Sepharoses at low ionic strength revealed that three groups of fragments, i.e. Mr = 150,000-140,000, 24,000, and 16,000 (150K-140K, 24K, and 16K) fragments, were capable of binding to glycosaminoglycans with different specificities and affinities.	Glycosaminoglycans	264-282	fibronectin 1	Homo sapiens	43-54
6643486-9	1983	The binding of fibronectin and its fragments to glycosaminoglycans is dependent on the ionic strength.	Glycosaminoglycans	48-66	fibronectin 1	Homo sapiens	15-26
6315262-1	1983	Using the reagents from the CEA-Roche kit, we found that solutions containing only glycosaminoglycans (GAG) yielded false concentrations of carcinoembryonic antigen (CEA), and mixtures of CEA and GAG produced falsely high values.	Glycosaminoglycans	83-101	CEA cell adhesion molecule 3	Homo sapiens	140-164
6315262-1	1983	Using the reagents from the CEA-Roche kit, we found that solutions containing only glycosaminoglycans (GAG) yielded false concentrations of carcinoembryonic antigen (CEA), and mixtures of CEA and GAG produced falsely high values.	Glycosaminoglycans	103-106	CEA cell adhesion molecule 3	Homo sapiens	28-31
6315262-1	1983	Using the reagents from the CEA-Roche kit, we found that solutions containing only glycosaminoglycans (GAG) yielded false concentrations of carcinoembryonic antigen (CEA), and mixtures of CEA and GAG produced falsely high values.	Glycosaminoglycans	103-106	CEA cell adhesion molecule 3	Homo sapiens	140-164
6315262-1	1983	Using the reagents from the CEA-Roche kit, we found that solutions containing only glycosaminoglycans (GAG) yielded false concentrations of carcinoembryonic antigen (CEA), and mixtures of CEA and GAG produced falsely high values.	Glycosaminoglycans	103-106	CEA cell adhesion molecule 3	Homo sapiens	166-169
6315262-1	1983	Using the reagents from the CEA-Roche kit, we found that solutions containing only glycosaminoglycans (GAG) yielded false concentrations of carcinoembryonic antigen (CEA), and mixtures of CEA and GAG produced falsely high values.	Glycosaminoglycans	103-106	CEA cell adhesion molecule 3	Homo sapiens	166-169
6315262-3	1983	These effects of GAG were not ascribable to contamination, because neither gel filtration nor ion-exchange column chromatography separated the false Roche CEA content related to GAG from their peaks of uronic acid or from their anticoagulant activity.	Glycosaminoglycans	178-181	CEA cell adhesion molecule 3	Homo sapiens	155-158
6415069-1	1983	beta-galactosidase is a ubiquitous lysosomal hydrolase that specifically cleaves terminal beta-galactosyl residues from glycoproteins, glycosaminoglycans, oligosaccharides, and glycolipids.	Glycosaminoglycans	135-153	galactosidase, beta 1	Rattus norvegicus	0-18
6327248-2	1983	Somatomedin A stimulated GAG synthesis at a physiological concentration, however in the case of insulin the dose required to stimulate GAG synthesis was 500 times as great as the physiological concentration.	Glycosaminoglycans	25-28	insulin-like growth factor 1	Rattus norvegicus	0-11
6327248-2	1983	Somatomedin A stimulated GAG synthesis at a physiological concentration, however in the case of insulin the dose required to stimulate GAG synthesis was 500 times as great as the physiological concentration.	Glycosaminoglycans	135-138	insulin-like growth factor 1	Rattus norvegicus	0-11
6327248-3	1983	Parathyroid hormone also increased GAG synthesis.	Glycosaminoglycans	35-38	parathyroid hormone	Rattus norvegicus	0-19
6363084-3	1983	Lipoprotein lipase, bound to mucopolysaccharides on the outside of cells, is released during Ca2+-free perfusion.	Glycosaminoglycans	29-48	lipoprotein lipase	Homo sapiens	0-18
6658719-4	1983	Thrombin was shown to bind to vascular endothelium and artificial surfaces containing GAG:s. The binding could be inhibited on both types of surfaces by pretreating them with protamine.	Glycosaminoglycans	86-89	coagulation factor II, thrombin	Homo sapiens	0-8
6658719-6	1983	It is concluded that thrombin binds to vessel wall GAG:s and is inactivated by the endothelium.	Glycosaminoglycans	51-54	coagulation factor II, thrombin	Homo sapiens	21-29
6631483-11	1983	Our studies suggest that the growth of nerve fibers on fibronectin substrates results from direct interaction with a specific portion of the fibronectin molecule and that this interaction can be inhibited by heparin and possibly other glycosaminoglycans.	Glycosaminoglycans	235-253	fibronectin 1	Gallus gallus	55-66
6641804-5	1983	EDGF reduces radiosulfate incorporation and provides the formation of low molecular weight (LMW) proteoglycans and glycosaminoglycans.	Glycosaminoglycans	115-133	fibroblast growth factor 1	Bos taurus	0-4
6412235-4	1983	Fibroblasts cultured from the skin of the affected dogs accumulated excessive 35S-labeled mucopolysaccharide; this accumulation could be decreased to a normal level by exogenous human high-uptake alpha-L-iduronidase (Hurler corrective factor) as well as by secretions of normal human or canine fibroblasts.	Glycosaminoglycans	90-108	alpha-L-iduronidase	Homo sapiens	196-215
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
6631483-11	1983	Our studies suggest that the growth of nerve fibers on fibronectin substrates results from direct interaction with a specific portion of the fibronectin molecule and that this interaction can be inhibited by heparin and possibly other glycosaminoglycans.	Glycosaminoglycans	235-253	fibronectin 1	Gallus gallus	141-152
6687802-3	1983	Heparin and dermatan sulfate which were eluted from the affinity column catalyzed the inhibition of thrombin by heparin cofactor II to a greater degree than did the respective unfractionated mucopolysaccharides.	Glycosaminoglycans	191-210	coagulation factor II, thrombin	Homo sapiens	100-108
6847727-0	1983	Glycosaminoglycan content in skin of the tight-skin mouse.	Glycosaminoglycans	0-17	fibrillin 1	Mus musculus	41-51
6687802-5	1983	The results suggest that heparin cofactor II differs from antithrombin III with respect to the mucopolysaccharide binding site.	Glycosaminoglycans	95-113	serpin family C member 1	Homo sapiens	58-74
6308892-3	1983	Provirus present in H-12 lacks the 3" part of the gag gene sequences as well as the pol gene, therefore, it gives rise to an anomalous 1.8 Md EcoRI fragment.	Glycosaminoglycans	50-53	H1.2 linker histone, cluster member	Homo sapiens	20-24
6687888-1	1983	We have tested the ability of various glycosaminoglycans to increase the rate of inhibition of thrombin by heparin cofactor II (HCII) and by antithrombin III (ATIII) isolated from human plasma.	Glycosaminoglycans	38-56	coagulation factor II, thrombin	Homo sapiens	95-103
6687888-1	1983	We have tested the ability of various glycosaminoglycans to increase the rate of inhibition of thrombin by heparin cofactor II (HCII) and by antithrombin III (ATIII) isolated from human plasma.	Glycosaminoglycans	38-56	serpin family D member 1	Homo sapiens	107-126
6687888-1	1983	We have tested the ability of various glycosaminoglycans to increase the rate of inhibition of thrombin by heparin cofactor II (HCII) and by antithrombin III (ATIII) isolated from human plasma.	Glycosaminoglycans	38-56	serpin family D member 1	Homo sapiens	128-132
6687888-1	1983	We have tested the ability of various glycosaminoglycans to increase the rate of inhibition of thrombin by heparin cofactor II (HCII) and by antithrombin III (ATIII) isolated from human plasma.	Glycosaminoglycans	38-56	serpin family C member 1	Homo sapiens	141-157
6687888-1	1983	We have tested the ability of various glycosaminoglycans to increase the rate of inhibition of thrombin by heparin cofactor II (HCII) and by antithrombin III (ATIII) isolated from human plasma.	Glycosaminoglycans	38-56	serpin family C member 1	Homo sapiens	159-164
6305407-4	1983	The 10 glutamic acid residues that are present in the amino-terminal region of prothrombin and are converted to gamma-carboxyglutamic acid in the mature protein are coded by only the GAG codon.	Glycosaminoglycans	183-186	coagulation factor II, thrombin	Homo sapiens	79-90
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
6835010-2	1983	The GAG fractions were tested for their effects on two lipoprotein lipase (LPL) enzyme systems containing an apolipoprotein C-II activated emulsion as the triglyceride substrate and bovine serum albumin as the free fatty acid acceptor.	Glycosaminoglycans	4-7	lipoprotein lipase	Homo sapiens	75-78
6835010-4	1983	The high-charge GAG (Fraction II) stimulated the LPL reaction 100 to 300%.	Glycosaminoglycans	16-19	lipoprotein lipase	Homo sapiens	49-52
6835010-8	1983	Degradation with nitrous acid eliminated the ability of high-charge GAG to stimulate LPL.	Glycosaminoglycans	68-71	lipoprotein lipase	Homo sapiens	85-88
6835010-9	1983	This and other evidence suggests that the high-charge GAG in human plasma responsible for LPL activation is heparan sulfate (HS).	Glycosaminoglycans	54-57	lipoprotein lipase	Homo sapiens	90-93
6218163-13	1983	The ability of mucopolysaccharides to interact with purified C1q suggests a role for such molecules in the regulation of the first component of complement.	Glycosaminoglycans	15-34	complement C1q C chain	Homo sapiens	61-64
6300442-1	1983	We have identified p10 as a fifth gag protein of avian sarcoma and leukemia viruses.	Glycosaminoglycans	34-37	S100 calcium binding protein A10	Homo sapiens	19-22
6300442-2	1983	Amino-terminal protein sequencing of this polypeptide purified from the Prague C strain of Rous sarcoma virus and from avian myeloblastosis virus implies that it is encoded within a stretch of 64 amino acid residues between p19 and p27 on the gag precursor polypeptide.	Glycosaminoglycans	243-246	interleukin 23 subunit alpha	Homo sapiens	224-227
6300442-2	1983	Amino-terminal protein sequencing of this polypeptide purified from the Prague C strain of Rous sarcoma virus and from avian myeloblastosis virus implies that it is encoded within a stretch of 64 amino acid residues between p19 and p27 on the gag precursor polypeptide.	Glycosaminoglycans	243-246	interferon alpha inducible protein 27	Homo sapiens	232-235
6218163-2	1983	Quantitative measurements have been made of the interaction of human complement subcomponent C1q with mucopolysaccharides.	Glycosaminoglycans	102-121	complement C1q C chain	Homo sapiens	93-96
6218163-10	1983	A variety of mucopolysaccharides were able to inhibit interaction of C1q with 125I-LMW-Hep, the most effective being heparan sulfate and dermatan sulfate.	Glycosaminoglycans	13-32	complement C1q C chain	Homo sapiens	69-72
6572368-5	1983	CTAP-III, CTAP-III(A), and LA-PF-4 are biologically active in that they stimulate DNA and glycosaminoglycan synthesis by human synovial cells; beta-TG is inactive.	Glycosaminoglycans	90-107	pro-platelet basic protein	Homo sapiens	0-8
6572368-5	1983	CTAP-III, CTAP-III(A), and LA-PF-4 are biologically active in that they stimulate DNA and glycosaminoglycan synthesis by human synovial cells; beta-TG is inactive.	Glycosaminoglycans	90-107	pro-platelet basic protein	Homo sapiens	10-18
6572368-5	1983	CTAP-III, CTAP-III(A), and LA-PF-4 are biologically active in that they stimulate DNA and glycosaminoglycan synthesis by human synovial cells; beta-TG is inactive.	Glycosaminoglycans	90-107	pro-platelet basic protein	Homo sapiens	27-34
6194990-6	1983	Monoclonal antibodies against the N terminus of gag, p19, were used to localize the protein in MH2- and CMII-transformed non-producer fibroblasts.	Glycosaminoglycans	48-51	interleukin 23 subunit alpha	Homo sapiens	53-56
6224443-13	1983	It has been seen that, by the intermediary of a low concentration of Ca++ ions, the reactivity of Lp(a) to GAG was selective.	Glycosaminoglycans	107-110	lipoprotein(a)	Homo sapiens	98-103
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
6961402-1	1982	We have utilized circular dichroism spectroscopy to examine the interaction of antithrombin with heparin-derived oligosaccharides and mucopolysaccharides of various sizes.	Glycosaminoglycans	134-153	serpin family C member 1	Homo sapiens	79-91
6961402-15	1982	Given our method for generating the above data, these spectral alterations must be associated with the binding of a second critical domain of the mucopolysaccharide to antithrombin that is required for rapid complex formation with thrombin or the activation of the protease inhibitor with respect to the neutralization of the latter enzyme.	Glycosaminoglycans	146-164	serpin family C member 1	Homo sapiens	168-180
6961402-15	1982	Given our method for generating the above data, these spectral alterations must be associated with the binding of a second critical domain of the mucopolysaccharide to antithrombin that is required for rapid complex formation with thrombin or the activation of the protease inhibitor with respect to the neutralization of the latter enzyme.	Glycosaminoglycans	146-164	coagulation factor II, thrombin	Homo sapiens	172-180
7164033-9	1982	The antithrombin III independent effect of heparin is unlikely to be important therapeutically, however, if this property of heparin is shared by other naturally occurring glycosaminoglycans, it could be important in maintaining the fluidity of blood under physiological conditions.	Glycosaminoglycans	172-190	serpin family C member 1	Homo sapiens	4-20
7171625-0	1982	Interactions of cellular glycosaminoglycans with plasma fibronectin and collagen.	Glycosaminoglycans	25-43	fibronectin 1	Mus musculus	56-67
7171625-1	1982	The interactions of metabolically radiolabelled glycosaminoglycans, isolated from Swiss mouse 3T3 and SV3T3 cells, with plasma fibronectin and collagen were studied by affinity column chromatograph in Hepes-buffered saline (150 mM NaCl in 10 mM Hepes buffer).	Glycosaminoglycans	48-66	fibronectin 1	Mus musculus	127-138
6215925-8	1982	There was an inverse relationship between GAG and DNA synthesis when proliferation of cells was increased by EGF and platelet lysate.	Glycosaminoglycans	42-45	pro-epidermal growth factor	Oryctolagus cuniculus	109-112
7139602-0	1982	Glycosaminoglycan synthesis by a cell line (C1-S1) established from a preneoplastic mouse mammary outgrowth.	Glycosaminoglycans	0-17	complement component 1, s subcomponent 1	Mus musculus	44-49
7139602-1	1982	We have measured the synthesis of several types of glycosaminoglycans by a line of mouse mammary epithelial cells (C1-S1) established from a hyperplastic nodule outgrowth.	Glycosaminoglycans	51-69	complement component 1, s subcomponent 1	Mus musculus	115-120
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
6285638-4	1982	Preincubation with separate glycosaminoglycan fractions in concentrations 10(-3) M and 10(-4) M for 1 hr resulted in a significant activity decrease of released beta glucuronidase, neutral proteinase and myeloperoxidase.	Glycosaminoglycans	28-45	glucuronidase beta	Homo sapiens	161-179
7112518-0	1982	Demonstration of a direct anti-factor Xa activity in certain heparin-related glycosaminoglycans.	Glycosaminoglycans	77-95	coagulation factor X	Homo sapiens	31-40
6804234-0	1982	Cell-associated glycosaminoglycans of human teratocarcinoma-derived cells of line PA 1.	Glycosaminoglycans	16-34	PAXIP1 associated glutamate rich protein 1	Homo sapiens	82-86
6179951-2	1982	While it has been established that fibronectin possesses binding sites for several glycosaminoglycans, it was found that only dextran sulfate and macromolecular heparin could decrease the initial rate of cell attachment to collagen.	Glycosaminoglycans	83-101	fibronectin 1	Homo sapiens	35-46
6812235-1	1982	Chondroitin-4-sulfate (chondroitin sulfate A, CSA) is a natural glycosaminoglycan which has been shown to have antithrombotic effects in vivo.	Glycosaminoglycans	64-81	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	46-49
6210440-5	1982	Interactions between sulfated glycosaminoglycans produced by the fibroblasts and fibronectin could also be demonstrated by affinity chromatography on immobilized plasma fibronectin and by immunoprecipitation of fibronectin in conditioned culture medium, which resulted in a coprecipitation of the sulfated glycosaminoglycans.	Glycosaminoglycans	30-48	fibronectin 1	Homo sapiens	81-92
6210440-5	1982	Interactions between sulfated glycosaminoglycans produced by the fibroblasts and fibronectin could also be demonstrated by affinity chromatography on immobilized plasma fibronectin and by immunoprecipitation of fibronectin in conditioned culture medium, which resulted in a coprecipitation of the sulfated glycosaminoglycans.	Glycosaminoglycans	30-48	fibronectin 1	Homo sapiens	169-180
6210440-5	1982	Interactions between sulfated glycosaminoglycans produced by the fibroblasts and fibronectin could also be demonstrated by affinity chromatography on immobilized plasma fibronectin and by immunoprecipitation of fibronectin in conditioned culture medium, which resulted in a coprecipitation of the sulfated glycosaminoglycans.	Glycosaminoglycans	30-48	fibronectin 1	Homo sapiens	169-180
6210440-6	1982	In these two systems, the fibronectin glycosaminoglycan bonds were broken at 0.2 M salt and were apparently weaker than the bonds responsible for the structural integrity of the matrix.	Glycosaminoglycans	38-55	fibronectin 1	Homo sapiens	26-37
7053378-2	1982	This methodology is able to subdivide the active mucopolysaccharide pools of molecular weight 6,000 to 8,000 (LMW) or 18,000 to 22,000 (HMW) into various species with descending affinities for antithrombin as well as decreasing anticoagulant potencies.	Glycosaminoglycans	49-67	cilia and flagella associated protein 97	Homo sapiens	136-139
7053378-8	1982	The avidity of platelet factor 4 for HMW highly active heparin could not be quantitated but appears to be at least 10 to 100 times greater than that of antithrombin for mucopolysaccharide.	Glycosaminoglycans	169-187	serpin family C member 1	Homo sapiens	152-164
7059522-10	1982	It is concluded that this new sulphated mucopolysaccharide acts as a pure antithrombin with a potency corresponding to 40--50 iu heparin/mg S-Lim.	Glycosaminoglycans	40-58	serpin family C member 1	Homo sapiens	74-86
7059522-10	1982	It is concluded that this new sulphated mucopolysaccharide acts as a pure antithrombin with a potency corresponding to 40--50 iu heparin/mg S-Lim.	Glycosaminoglycans	40-58	PDZ and LIM domain 5	Homo sapiens	142-145
7053378-2	1982	This methodology is able to subdivide the active mucopolysaccharide pools of molecular weight 6,000 to 8,000 (LMW) or 18,000 to 22,000 (HMW) into various species with descending affinities for antithrombin as well as decreasing anticoagulant potencies.	Glycosaminoglycans	49-67	serpin family C member 1	Homo sapiens	193-205
7053378-6	1982	The stoichiometries of interaction of antithrombin and platelet factor 4 with HMW highly active heparin as determined by fluorescence spectroscopy indicated that 2 molecules of either protein are able to bind to 1 molecule of the mucopolysaccharide.	Glycosaminoglycans	230-248	serpin family C member 1	Homo sapiens	38-50
7053378-6	1982	The stoichiometries of interaction of antithrombin and platelet factor 4 with HMW highly active heparin as determined by fluorescence spectroscopy indicated that 2 molecules of either protein are able to bind to 1 molecule of the mucopolysaccharide.	Glycosaminoglycans	230-248	cilia and flagella associated protein 97	Homo sapiens	78-81
7117492-0	1982	Effect of thrombin on glycosaminoglycans in fibroblast cultures.	Glycosaminoglycans	22-40	coagulation factor II	Rattus norvegicus	10-18
6179331-6	1982	Glycosaminoglycan analysis showed a less reduced content of hexosamine and uronic acid in the atrophic area per mm2 skin, but no differences in the concentrations.	Glycosaminoglycans	0-17	PNMA family member 2	Homo sapiens	112-115
6286372-11	1982	The results hav allowed us to conclude that the arrangement of the gag proteins in the Pr76gag is N-p19-(p10?	Glycosaminoglycans	67-70	interleukin 23 subunit alpha	Homo sapiens	100-103
6172595-9	1981	F80 contained the gag determinants of P120 but did not react with Abelson-specific serum.	Glycosaminoglycans	18-21	catenin delta 1	Homo sapiens	38-42
6286372-11	1982	The results hav allowed us to conclude that the arrangement of the gag proteins in the Pr76gag is N-p19-(p10?	Glycosaminoglycans	67-70	S100 calcium binding protein A10	Homo sapiens	105-108
6459128-0	1981	Characterization of glycosaminoglycans in urine from patients with nephrotic syndrome and control subjects, and their effects on lipoprotein lipase.	Glycosaminoglycans	20-38	lipoprotein lipase	Homo sapiens	129-147
7178858-4	1982	The catabolism of glycosaminoglycans was followed by estimating the activities of lysosomal glycohydrolases, viz., beta-glucuronidase, beta-N-acetyl glucosaminidase and cathepsin D in liver, kidney and spleen and urinary excretion of hexosamine and uronic acid.	Glycosaminoglycans	18-36	glucuronidase, beta	Rattus norvegicus	115-133
7178858-4	1982	The catabolism of glycosaminoglycans was followed by estimating the activities of lysosomal glycohydrolases, viz., beta-glucuronidase, beta-N-acetyl glucosaminidase and cathepsin D in liver, kidney and spleen and urinary excretion of hexosamine and uronic acid.	Glycosaminoglycans	18-36	cathepsin D	Rattus norvegicus	169-180
6275111-1	1981	The Fujinami avian sarcoma virus (FSV) transforming gene product, P140, is a fusion protein which contains both gag-related and FSV-specific methionine-containing tryptic peptides.	Glycosaminoglycans	112-115	SRC kinase signaling inhibitor 1	Homo sapiens	66-70
6275111-2	1981	The virion protease p15 cleaved p140 into two fragments: an N-terminal 33K fragment which contained all but one of the gag-related tryptic peptides and a C-terminal 120K fragment which contained all of the FSV-specific tryptic peptides.	Glycosaminoglycans	119-122	cyclin dependent kinase inhibitor 2B	Homo sapiens	20-23
6275111-2	1981	The virion protease p15 cleaved p140 into two fragments: an N-terminal 33K fragment which contained all but one of the gag-related tryptic peptides and a C-terminal 120K fragment which contained all of the FSV-specific tryptic peptides.	Glycosaminoglycans	119-122	SRC kinase signaling inhibitor 1	Homo sapiens	32-36
6275111-3	1981	The 33K gag-related fragment from P140 phosphorylated in FSV-transformed cells contained only phosphoserine, whereas the 120K C-terminal FSV-specific fragments contained both phosphoserine and phosphotyrosine.	Glycosaminoglycans	8-11	SRC kinase signaling inhibitor 1	Homo sapiens	34-38
6275112-4	1981	The sequential appearance of these RNAs, the probable mRNA"s for the gag and env proteins, paralleled the order of appearance of the gag and env proteins, respectively, after hormone treatment.	Glycosaminoglycans	69-72	endogenous retrovirus group K member 20	Homo sapiens	141-144
6275112-4	1981	The sequential appearance of these RNAs, the probable mRNA"s for the gag and env proteins, paralleled the order of appearance of the gag and env proteins, respectively, after hormone treatment.	Glycosaminoglycans	133-136	endogenous retrovirus group K member 20	Homo sapiens	77-80
7296305-1	1981	GABA and gamma-acetylenic-GABA (GAG), a GABA-Transaminase inhibitor, were used in this study to determine the influence of GABA on the release of prolactin.	Glycosaminoglycans	32-35	4-aminobutyrate aminotransferase	Rattus norvegicus	40-57
7263639-8	1981	No dermatan sulfate was detected in PG-I, but this glycosaminoglycan was the predominant glycosaminoglycan in PG-II (50 to 70%).	Glycosaminoglycans	51-68	decorin	Homo sapiens	110-115
7298057-2	1981	Regulation of glycosaminoglycan metabolism by lymphocyte (CTAP-I) and platelet (CTAP-III) growth factors.	Glycosaminoglycans	14-31	pro-platelet basic protein	Homo sapiens	80-88
6170987-0	1981	Cleavage of four avian sarcoma virus polyproteins with virion protease p15 removes gag sequences and yields large fragments that function as tyrosine phosphoacceptors in vitro.	Glycosaminoglycans	83-86	cyclin dependent kinase inhibitor 2B	Homo sapiens	71-74
6170987-2	1981	These gag-linked proteins were cleaved with retrovirion protease p15.	Glycosaminoglycans	6-9	cyclin dependent kinase inhibitor 2B	Homo sapiens	65-68
6170987-4	1981	ESV P80 was cleaved inside the transformation-specific domain, yielding a Mr 35,000--38,000 fragment from the NH2-terminal half of the molecule consisting of the entire gag portion and some no-gag sequences and a Mr 48,000 fragment containing most of the transformation-specific sequences.	Glycosaminoglycans	169-172	coilin	Homo sapiens	4-7
6170987-4	1981	ESV P80 was cleaved inside the transformation-specific domain, yielding a Mr 35,000--38,000 fragment from the NH2-terminal half of the molecule consisting of the entire gag portion and some no-gag sequences and a Mr 48,000 fragment containing most of the transformation-specific sequences.	Glycosaminoglycans	193-196	coilin	Homo sapiens	4-7
6170987-6	1981	The major serine phosphorylation site of ESV P80 was found to reside in the Mr 35,000--38,000 gag-containing fragment, probably within the transformation-specific sequences of that cleavage product.	Glycosaminoglycans	94-97	coilin	Homo sapiens	45-48
6170987-7	1981	Removal of all of the gag domain of ESV P80 or most of the gag domain in PRCII-p P170, PRCII P105, and FSV P140 does not affect their ability to be phosphorylated by the polyprotein-associated tyrosine-specific protein kinase activities.	Glycosaminoglycans	22-25	coilin	Homo sapiens	40-43
6457061-1	1981	It has been postulated that lipoprotein lipase, an enzyme important in the uptake of fatty acids into tissues, is bound to the vascular endothelial cell surface and that this binding occurs through attachment to heparinlike glycosaminoglycans.	Glycosaminoglycans	224-242	lipoprotein lipase	Bos taurus	28-46
7263639-8	1981	No dermatan sulfate was detected in PG-I, but this glycosaminoglycan was the predominant glycosaminoglycan in PG-II (50 to 70%).	Glycosaminoglycans	89-106	decorin	Homo sapiens	110-115
6164767-4	1981	CSF mucopolysaccharides were also abnormally high.	Glycosaminoglycans	4-23	colony stimulating factor 2	Homo sapiens	0-3
6269308-1	1981	N-acetyl-beta-D-glucosaminidase is a lysosomal glycosidase, which participates in the catabolism of the mucopolysaccharides and of the glycoproteins.	Glycosaminoglycans	104-123	O-GlcNAcase	Homo sapiens	0-31
6972535-5	1981	Our results show that conversion of B-tropism to NB-tropism is associated with changes in the primary structure of three gag proteins--p15, p12, and p30.	Glycosaminoglycans	121-124	cyclin dependent kinase inhibitor 2B	Mus musculus	135-138
6972535-5	1981	Our results show that conversion of B-tropism to NB-tropism is associated with changes in the primary structure of three gag proteins--p15, p12, and p30.	Glycosaminoglycans	121-124	CDK2 (cyclin-dependent kinase 2)-associated protein 1	Mus musculus	140-143
6972535-5	1981	Our results show that conversion of B-tropism to NB-tropism is associated with changes in the primary structure of three gag proteins--p15, p12, and p30.	Glycosaminoglycans	121-124	high mobility group box 1	Mus musculus	149-152
7046349-0	1981	Glycosaminoglycan synthesis by human diabetic, normal adult, and embryonic fibroblasts in relation to insulin levels.	Glycosaminoglycans	0-17	insulin	Homo sapiens	102-109
7215332-4	1981	The low levels of hyaluronidase and cholesterol esterase in thyroidectomized rats may account for the accumulation of mucopolysaccharides in skin and for the elevation of serum cholesterol levels in hypothyroid patients.	Glycosaminoglycans	118-137	carboxyl ester lipase	Rattus norvegicus	36-56
6788768-5	1981	Additional evidence for the noncartilaginous origin of C1q inhibitor is that its glycosaminoglycan chains totally lack chondroitin 6-sulfate isomers.	Glycosaminoglycans	81-98	complement C1q A chain	Homo sapiens	55-58
6788768-6	1981	Furthermore, the glycosaminoglycan component of C1q inhibitor was eluted from Sepharose CL-6B with a Kav of 0.52, indicating that these polysaccharide chains are considerably larger than those of human articular cartilage proteoglycan.	Glycosaminoglycans	17-34	complement C1q A chain	Homo sapiens	48-51
6264151-5	1981	The ts lesions of the FSV mutants affected 90% of the phosphorylation of the nonstructural, gag-related 140,000-kilodalton phosphoprotein coded by FSV (p140), but did not affect virus replication or the synthesis of p140.	Glycosaminoglycans	92-95	SRC kinase signaling inhibitor 1	Homo sapiens	152-156
6264151-5	1981	The ts lesions of the FSV mutants affected 90% of the phosphorylation of the nonstructural, gag-related 140,000-kilodalton phosphoprotein coded by FSV (p140), but did not affect virus replication or the synthesis of p140.	Glycosaminoglycans	92-95	SRC kinase signaling inhibitor 1	Homo sapiens	216-220
6264151-13	1981	p140 of ts FSV recovered from cells maintained at 41.5 degrees C with anti-gag serum was over 10 times less phosphorylated by associated kinase than the same protein recovered from cells at 37 degrees C if assayed in vitro at 20 degrees C. This kinase activity associated with or dissociated from p140 with a half-life of less than 30 min during temperature shifts of ts FSV-infected cells.	Glycosaminoglycans	75-78	SRC kinase signaling inhibitor 1	Homo sapiens	0-4
6260820-6	1981	Glycosaminoglycan synthesis, a characteristic of the cartilage phenotype, began to increase 8 hours after addition of PTH or DBcAMP, reaching a plateau 32 hours after their addition.	Glycosaminoglycans	0-17	parathyroid hormone	Oryctolagus cuniculus	118-121
6253823-5	1980	MC29-transformed cells contain a gag gene-related protein of a 110,000 molecular weight (MW) (p110), which by tryptic peptide analysis has been shown to be a fusion product comprised of a gag gene-derived sequences and sequences which are presumed to be coded by the adjacent mac gene.	Glycosaminoglycans	33-36	spliceosome associated factor 3, U4/U6 recycling protein	Homo sapiens	94-98
6257396-2	1980	p140 is the product of a fused gene consisting of a part of the gag gene of avian retrovirus and FSV-unique sequences which are not related to the src sequences of Rous sarcoma virus.	Glycosaminoglycans	64-67	SRC kinase signaling inhibitor 1	Homo sapiens	0-4
6448845-1	1980	A low molecular weight preparation of porcine heparin (specific anticoagulation activity = 125 units/mg) was fractionated to obtain a mucopolysaccharide product of 6500 daltons (specific anticoagulant activity = 373 units/mg) that is homogeneous with respect to its interaction with antithrombin.	Glycosaminoglycans	134-152	serpin family C member 1	Homo sapiens	283-295
6448845-3	1980	Initially, we showed that the fluorescamine-heparin conjugate and the unlabeled mucopolysaccharide interacted with antithrombin in a virtually identical fashion.	Glycosaminoglycans	80-98	serpin family C member 1	Homo sapiens	115-127
6254670-6	1980	Six of ten p25 peptides and four more gag-related peptides are shared by PR78gag and gP130.	Glycosaminoglycans	38-41	Neutrophil migration (granulocyte glycoprotein)	Homo sapiens	85-90
6448845-4	1980	Subsequently, we demonstrated that labeled heparin could be utilized in conjunction with fluorescence polarization spectroscopy to monitor the binding of mucopolysaccharide to thrombin, factor IXa, factor Xa, and plasmin.	Glycosaminoglycans	154-172	coagulation factor II, thrombin	Homo sapiens	176-207
6448845-4	1980	Subsequently, we demonstrated that labeled heparin could be utilized in conjunction with fluorescence polarization spectroscopy to monitor the binding of mucopolysaccharide to thrombin, factor IXa, factor Xa, and plasmin.	Glycosaminoglycans	154-172	plasminogen	Homo sapiens	213-220
6448845-5	1980	The interaction of this complex carbohydrate with thrombin exhibited a stoichiometry of 2:1 with KH1T DISS = KH2T DISS = 8 x 10(-7) M. The formation of mucopolysaccharide .	Glycosaminoglycans	152-170	coagulation factor II, thrombin	Homo sapiens	50-58
6448846-6	1980	The second-order rate constants for the neutralization of factor Xa or plasmin by the mucopolysaccharide .	Glycosaminoglycans	86-104	coagulation factor X	Homo sapiens	58-67
6448846-6	1980	The second-order rate constants for the neutralization of factor Xa or plasmin by the mucopolysaccharide .	Glycosaminoglycans	86-104	plasminogen	Homo sapiens	71-78
6448846-17	1980	Thus, our data demonstrate that binding of heparin to antithrombin is required for the mucopolysaccharide-dependent enhancement in the rates of neutralization of thrombin, factor IXa, factor Xa, or plasmin by the protease inhibitor.	Glycosaminoglycans	87-105	serpin family C member 1	Homo sapiens	54-66
6448846-17	1980	Thus, our data demonstrate that binding of heparin to antithrombin is required for the mucopolysaccharide-dependent enhancement in the rates of neutralization of thrombin, factor IXa, factor Xa, or plasmin by the protease inhibitor.	Glycosaminoglycans	87-105	coagulation factor II, thrombin	Homo sapiens	162-193
6448846-17	1980	Thus, our data demonstrate that binding of heparin to antithrombin is required for the mucopolysaccharide-dependent enhancement in the rates of neutralization of thrombin, factor IXa, factor Xa, or plasmin by the protease inhibitor.	Glycosaminoglycans	87-105	plasminogen	Homo sapiens	198-205
6448846-18	1980	Furthermore, a careful comparison of the various constants suggests that the direct interaction between heparin and antithrombin may be largely responsible for the kinetic effect of this mucopolysaccharide.	Glycosaminoglycans	187-205	serpin family C member 1	Homo sapiens	116-128
6451055-4	1980	It appears that the glycosaminoglycans accumulating in the liver of those patients are partly bound to Hex A, and that this binding may cause some changes of its properties such as ionic charge and thermostability.	Glycosaminoglycans	20-38	hexosaminidase subunit alpha	Homo sapiens	103-108
7209966-7	1980	The present observations provided with evidence for the action of endo-beta-glucuronidase and endo-beta-N-acetylhexosaminidase on the tissue GAG, specifically on chondroitin sulfates.	Glycosaminoglycans	141-144	glucuronidase beta	Homo sapiens	71-89
6253382-2	1980	Mucin histochemistry demonstrated qualitative and quantitative differences between the mucopolysaccharides produced by these two groups of tumours.	Glycosaminoglycans	87-106	LOC100508689	Homo sapiens	0-5
6773589-4	1980	The glycosaminoglycan fraction obtained from the AB-CBF1-MCT-1 mastocytoma cultured in vitro consisted predominantly of dermatan sulfate-like material.	Glycosaminoglycans	4-21	recombination signal binding protein for immunoglobulin kappa J region	Mus musculus	52-56
6773589-4	1980	The glycosaminoglycan fraction obtained from the AB-CBF1-MCT-1 mastocytoma cultured in vitro consisted predominantly of dermatan sulfate-like material.	Glycosaminoglycans	4-21	modifier of curly tail 1	Mus musculus	57-62
6773589-5	1980	On the other hand, the major components of the glycosaminoglycan fractions of the AB-CXBG-MCT-1 and AB-CXBI-MCT-1 and Furth tumors were observed to behave like heparin or heparan sulfate.	Glycosaminoglycans	47-64	modifier of curly tail 1	Mus musculus	90-95
6773589-5	1980	On the other hand, the major components of the glycosaminoglycan fractions of the AB-CXBG-MCT-1 and AB-CXBI-MCT-1 and Furth tumors were observed to behave like heparin or heparan sulfate.	Glycosaminoglycans	47-64	modifier of curly tail 1	Mus musculus	108-113
7209966-7	1980	The present observations provided with evidence for the action of endo-beta-glucuronidase and endo-beta-N-acetylhexosaminidase on the tissue GAG, specifically on chondroitin sulfates.	Glycosaminoglycans	141-144	O-GlcNAcase	Homo sapiens	99-126
7368150-1	1980	The technique of crossed immunoelectrophoresis has been used to study the binding to purified antithrombin III (At III) of heparin and other mucopolysaccharides.	Glycosaminoglycans	141-160	serpin family C member 1	Homo sapiens	94-110
6774983-2	1980	Intracellular transport of sulfated glycosaminoglycans and glycoproteins of the bovine prolactin granule matrix.	Glycosaminoglycans	36-54	prolactin	Bos taurus	87-96
6154316-2	1980	Synthetic sulfonated glycosaminoglycans instilled intraluminally into bladders whose natural mucin layer has been removed are as effective as the natural mucin in preventing bacterial adherence.	Glycosaminoglycans	21-39	LOC100508689	Homo sapiens	93-98
6154316-3	1980	It also appears that adherence of calcium and protein is reduced in the presence of both the natural mucin layer and the synthetic sulfonated glycosaminoglycan sodium pentosanpolysulfate, suggesting that the antiadherence activity of both natural and synthetic surface glycosaminoglycans in the bladder extends to the molecular and ionic levels.	Glycosaminoglycans	269-287	LOC100508689	Homo sapiens	101-106
7362391-3	1980	Excess mucopolysaccharide deposition is stimulated by growth hormone and is characteristic of both cystic medial necrosis and myxomatous degeneration.	Glycosaminoglycans	7-25	growth hormone 1	Homo sapiens	54-68
6788049-1	1980	Glycosaminoglycans extracted by CPC precipitation from chick embryo skin at 9, 12, 15, 18, 21 days of incubation were separated by three different electrophoretic methods on acetate cellulose strips.	Glycosaminoglycans	0-18	Carcass protein content	Gallus gallus	32-35
6771264-0	1980	Characterization of fibronectin interactions with glycosaminoglycans and identification of active proteolytic fragments.	Glycosaminoglycans	50-68	fibronectin 1	Gallus gallus	20-31
6771264-1	1980	Fibronectin is a major cell-surface glycoprotein which has been reported to interact with glycosaminoglycans.	Glycosaminoglycans	90-108	fibronectin 1	Gallus gallus	0-11
6771264-5	1980	The binding of both molecules to fibronectin is not blocked by EDTA or by other glycosaminoglycans, and is only moderately inhibited by elevated ionic strength.	Glycosaminoglycans	80-98	fibronectin 1	Gallus gallus	33-44
6771264-6	1980	Scatchard analyses revealed nonlinear, high affinity binding to fibronectin with a KD of approximately 10(-7) to 10(-8) M for these glycosaminoglycans.	Glycosaminoglycans	132-150	fibronectin 1	Gallus gallus	64-75
6771264-9	1980	The possible involvement of such high affinity binding sites of fibronectin in the binding of glycosaminoglycans to the cell surface or in the organization of extracellular matrices is discussed.	Glycosaminoglycans	94-112	fibronectin 1	Gallus gallus	64-75
7410341-6	1980	These findings support the view that beta-glucuronidase can hydrolyze certain alpha-L-iduronide bonds and raise the possibility that beta-glucuronidase may play a role in the catabolism of iduronic acid-containing glycosaminoglycans.	Glycosaminoglycans	214-232	glucuronidase, beta	Rattus norvegicus	37-55
7410341-6	1980	These findings support the view that beta-glucuronidase can hydrolyze certain alpha-L-iduronide bonds and raise the possibility that beta-glucuronidase may play a role in the catabolism of iduronic acid-containing glycosaminoglycans.	Glycosaminoglycans	214-232	glucuronidase, beta	Rattus norvegicus	133-151
7419576-2	1980	Characterization of glycosaminoglycans and glycoproteins of the bovine prolactin matrix.	Glycosaminoglycans	20-38	prolactin	Bos taurus	71-80
7389116-2	1980	In comparison to controls we detected significant differences, in that diabetics with changed (alpha-1-) mobility on immunoelectrophoresis revealed increased urinary acid glycosaminoglycan excretion (p less than 0.01) and elevated HbAIc concentrations in plasma (p less than 0.01).	Glycosaminoglycans	171-188	adrenoceptor alpha 1D	Homo sapiens	95-104
6154129-13	1980	These results are consistent with the view that p65 is the precursor of gag gene-derived core proteins of BLV.	Glycosaminoglycans	72-75	synaptotagmin 1	Bos taurus	48-51
7353540-1	1980	A basic somatomedin preparation results in a 2-fold stimulation of incorporation of both [3H]leucine into protein and 35SO4 into glycosaminoglycans by cultured chick sternal chondrocytes.	Glycosaminoglycans	129-147	insulin like growth factor 1	Gallus gallus	8-19
7353540-3	1980	Somatomedin stimulates incorporation of leucine into glycosaminoglycans to the same extent to which it stimulates incorporation of sulfate into glycosaminoglycans, suggesting involvement of core protein synthesis.	Glycosaminoglycans	53-71	insulin like growth factor 1	Gallus gallus	0-11
7353540-3	1980	Somatomedin stimulates incorporation of leucine into glycosaminoglycans to the same extent to which it stimulates incorporation of sulfate into glycosaminoglycans, suggesting involvement of core protein synthesis.	Glycosaminoglycans	144-162	insulin like growth factor 1	Gallus gallus	0-11
7368150-1	1980	The technique of crossed immunoelectrophoresis has been used to study the binding to purified antithrombin III (At III) of heparin and other mucopolysaccharides.	Glycosaminoglycans	141-160	serpin family C member 1	Homo sapiens	112-118
7368628-5	1980	Glycosaminoglycans appear to be not only important participants in the effect of the antidiuretic hormone on the permeability of intersticial structures; they also play a certain role in the increase of osmolality of the renal papillar intersticium under the conditions of the antidiuresis, providing the release of loosely bound sodium.	Glycosaminoglycans	0-18	arginine vasopressin	Homo sapiens	85-105
7454730-10	1980	Glycosaminoglycans bind to collagen-fibronectin complexes resulting in a complex more stable to disruption with urea than complexes of any two of the components.	Glycosaminoglycans	0-18	fibronectin 1	Homo sapiens	36-47
6446899-0	1980	Isolation and characterization of sulphated mucopolysaccharides from rat leukaemic (RBL-1) basophils.	Glycosaminoglycans	44-63	RB transcriptional corepressor like 1	Rattus norvegicus	84-89
6768163-0	1980	Effect of glycosaminoglycans on thrombin-induced clotting of normal and antithrombin III-deficient plasmas.	Glycosaminoglycans	10-28	coagulation factor II, thrombin	Homo sapiens	32-40
420716-3	1979	Connective tissue activating peptide-III (CTAP-III) isolated from human platelets is a potent mitogen for human connective tissue cells in culture in addition to stimulating glycosaminoglycan synthesis, glucose consumption, and lactate formation.	Glycosaminoglycans	174-191	pro-platelet basic protein	Homo sapiens	0-40
86525-7	1979	On the other hand, a part (10-15%) of the MCSA was bound to the anti-p15 column, indicating that MCSA is linked to the gag p15.	Glycosaminoglycans	119-122	cyclin dependent kinase inhibitor 2B	Homo sapiens	69-72
86525-7	1979	On the other hand, a part (10-15%) of the MCSA was bound to the anti-p15 column, indicating that MCSA is linked to the gag p15.	Glycosaminoglycans	119-122	cyclin dependent kinase inhibitor 2B	Homo sapiens	123-126
86531-0	1979	Correlation between Alcian Blue stainig of glycosaminoglycans of cat nucleus pulposus and TEM x-ray probe microanalysis.	Glycosaminoglycans	43-61	MFT2	Homo sapiens	90-93
92574-3	1979	The glycosylated gag gene product gPr85gag, although containing sequences characteristic of all four core proteins plus additional sequences not found in Pr65gag, lacked a major tyrosine-containing p30 tryptic peptide, suggesting that gPr85gag is not processed to p30.	Glycosaminoglycans	17-20	centromere protein V	Homo sapiens	264-267
455246-0	1979	Electrophoresis of tissue glycosaminoglycans as an aid in the diagnosis of mesotheliomas.	Glycosaminoglycans	26-44	activation induced cytidine deaminase	Homo sapiens	51-54
446749-0	1979	Lectin from embryonic chick muscle that interacts with glycosaminoglycans.	Glycosaminoglycans	55-73	galectin 3	Gallus gallus	0-6
420716-3	1979	Connective tissue activating peptide-III (CTAP-III) isolated from human platelets is a potent mitogen for human connective tissue cells in culture in addition to stimulating glycosaminoglycan synthesis, glucose consumption, and lactate formation.	Glycosaminoglycans	174-191	pro-platelet basic protein	Homo sapiens	42-50
570737-0	1978	Inhibition of thrombin by antithrombin III in the presence of certain glycosaminoglycans found in the mammalian aorta.	Glycosaminoglycans	70-88	coagulation factor II, thrombin	Homo sapiens	14-22
153251-3	1979	Cultured skin fibroblasts from both insulin-dependent and noninsulin-dependent diabetics were found to have increased proportions of heparan sulfate in the media relative to the other sulfated glycosaminoglycans.	Glycosaminoglycans	193-211	insulin	Homo sapiens	36-43
215951-0	1978	Application of the cytochrome c adjective reaction to the histochemical demonstration of sulfated mucopolysaccharides--with special reference to leucopatent blue-hydrogen peroxide as substrates.	Glycosaminoglycans	98-117	cytochrome c, somatic	Homo sapiens	19-31
522483-3	1979	One of these, called lectin-2, interacts with specific glycosaminoglycans, especially heparin and dermatan sulfate.	Glycosaminoglycans	55-73	galectin 3	Gallus gallus	21-27
522483-8	1979	The results of these studies raise the possibility that lectin-2 functions by interacting with glycosaminoglycans, either associated with the cell surface or with the extracellular matrix.	Glycosaminoglycans	95-113	galectin 3	Gallus gallus	56-62
570737-0	1978	Inhibition of thrombin by antithrombin III in the presence of certain glycosaminoglycans found in the mammalian aorta.	Glycosaminoglycans	70-88	serpin family C member 1	Homo sapiens	26-42
212595-1	1978	Mink cells nonproductively transformed by the T-8 strain of mink cell focus-inducing virus express two type C viral amino terminal gag gene-coded structural proteins, p15 and p12, in the form of a 90,000 to 110,000 molecular weight polyprotein that lacks detectable immunological reactivity with other known type C virus-coded translational products.	Glycosaminoglycans	131-134	cyclin dependent kinase inhibitor 2B	Homo sapiens	167-170
212595-1	1978	Mink cells nonproductively transformed by the T-8 strain of mink cell focus-inducing virus express two type C viral amino terminal gag gene-coded structural proteins, p15 and p12, in the form of a 90,000 to 110,000 molecular weight polyprotein that lacks detectable immunological reactivity with other known type C virus-coded translational products.	Glycosaminoglycans	131-134	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	175-178
641404-6	1978	A major part of the capacity of normal serum to stimulate sulfate incorporation into GAG"s may reside in CTAP-III.	Glycosaminoglycans	85-88	pro-platelet basic protein	Homo sapiens	105-113
212760-1	1978	The serological properties of the gag gene products p15 and p12 of N- and B-tropic viruses of C57BL mice have been examined.	Glycosaminoglycans	34-37	cyclin dependent kinase inhibitor 2B	Mus musculus	52-55
646135-4	1978	Incorporation of both isotopic precursors into GAG of the brachymorphic proliferative zone was reduced to a greater extent than in the reserve zone.	Glycosaminoglycans	47-50	3'-phosphoadenosine 5'-phosphosulfate synthase 2	Mus musculus	58-71
209919-0	1978	In vitro studies of the interaction of isolated Lp(a) lipoprotein and other serum lipoproteins with glycosaminoglycans.	Glycosaminoglycans	100-118	lipoprotein(a)	Homo sapiens	48-53
209919-1	1978	The interaction of isolated Lp(a) lipoprotein or other lipoprotein classes with different glycosaminoglycans (GAG) bound to activated Sepharose was studied.	Glycosaminoglycans	90-108	lipoprotein(a)	Homo sapiens	28-33
209919-1	1978	The interaction of isolated Lp(a) lipoprotein or other lipoprotein classes with different glycosaminoglycans (GAG) bound to activated Sepharose was studied.	Glycosaminoglycans	110-113	lipoprotein(a)	Homo sapiens	28-33
209919-5	1978	Addition of GAG in solution revealed that this binding may be the only one existing under physiological conditions, and it appears possible that the Lp(a) lipoprotein is bound more firmly to GAG than is LDL under such conditions.	Glycosaminoglycans	191-194	lipoprotein(a)	Homo sapiens	149-154
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
678216-5	1978	The activity of glucosaminephosphate isomerase (glutamine-forming) and UDPglucose dehydrogenase, both key enzymes in the biosynthetic pathway of glycosaminoglycans, decreased in rats given low doses of pyridoxine and increased in rats given high doses.	Glycosaminoglycans	145-163	UDP-glucose 6-dehydrogenase	Rattus norvegicus	16-95
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	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	154-157
716766-1	1978	The effect of insulin on the concentration of different glycosaminoglycan (CG) fractions was different in different segments of aorta.	Glycosaminoglycans	56-73	insulin	Oryctolagus cuniculus	14-21
76313-1	1978	A strategy based on the identification of type-specific antigenic determinants in the transitional products of gag (p15, p12, and p30 proteins), pol (reverse transcriptase), and env (gp70 glycoproteins) genes of mammalian type C viruses has been used to study genetic recombination between these RNA viruses.	Glycosaminoglycans	111-114	cyclin dependent kinase inhibitor 2B	Homo sapiens	116-119
67898-4	1977	These findings, along with previous studies indicating immunologic cross-reactivity between their major internal antigens, p30, demonstrate that each of the gag gene-coded proteins of murine type C viruses has a analogue in viruses of the RD114/baboon group.	Glycosaminoglycans	157-160	high mobility group box 1	Mus musculus	123-126
154991-2	1978	These cartilages are composed of at least two series of proteoglycan variants whose glycosaminoglycan side chains display microheterogeneity with respect to the proportions of 4- and 6-linked ester sulfate.	Glycosaminoglycans	84-101	versican	Gallus gallus	56-68
720453-8	1978	The supernatant of the fibrinogen-thrombin-reaction, separated after 3 hours, likewise increased glucose consumption, GAG and hyaluronic acid concentration possibly due to effects of the fibrinopeptides A or B.	Glycosaminoglycans	118-121	coagulation factor II	Rattus norvegicus	34-42
409573-3	1977	In contrast, lysosomal neuraminidase activity in vitro was enhanced by the addition of glycosaminoglycans.	Glycosaminoglycans	87-105	neuraminidase 1	Homo sapiens	23-36
200928-4	1977	In addition, we have compared the tryptic peptides of the gag gene products p30 and p15 from several of these viruses.	Glycosaminoglycans	58-61	high mobility group box 1	Mus musculus	76-79
137073-0	1976	Purification of carcinoembryonic antigen by removal of contaminating mucopolysaccharides.	Glycosaminoglycans	69-88	CEACAM5	Bos taurus	16-40
70942-3	1977	Plasmin is localized in the connective tissue and its function is to regulate the turnover of glycosaminoglycans.	Glycosaminoglycans	94-112	plasminogen	Homo sapiens	0-7
831354-1	1977	Histochemical staining of bladder tissue has demonstrated a discrete layer of mucopolysaccharide (mucin) at the surface of rabbit and human bladders.	Glycosaminoglycans	78-96	LOC100508689	Homo sapiens	98-103
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
1006735-1	1976	Part 5: relationship between cholesterol deposition and glycosaminoglycans.	Glycosaminoglycans	56-74	tankyrase	Homo sapiens	0-6
1001249-0	1976	Lack of somatotropin effect on glycosaminoglycan content of canine coronary arteries.	Glycosaminoglycans	31-48	somatotropin	Canis lupus familiaris	8-20
825015-1	1976	The human heteroploid cell line D98/AH-2 shows a low level of glycosaminoglycans (GAG) synthesis as compared with normal human diploid fibroblasts.	Glycosaminoglycans	62-80	zinc finger RANBP2-type containing 3	Homo sapiens	36-40
825015-1	1976	The human heteroploid cell line D98/AH-2 shows a low level of glycosaminoglycans (GAG) synthesis as compared with normal human diploid fibroblasts.	Glycosaminoglycans	82-85	zinc finger RANBP2-type containing 3	Homo sapiens	36-40
60707-1	1976	The translation product of the gag gene of mammalian type-c- RNA viruses is a 65,000-68,000 molecular weight precursor polypeptide (Pr65) whose cleavage leads to the formation of four virion proteins, p30, p15, p12 and p10.	Glycosaminoglycans	31-34	centromere protein V	Homo sapiens	201-204
136211-5	1976	The network almost disappeared after treatment with hyaluronidase for 30 min, suggesting that it may consist of aid mucopolysaccharide.	Glycosaminoglycans	116-134	activation-induced cytidine deaminase	Rattus norvegicus	112-115
60707-1	1976	The translation product of the gag gene of mammalian type-c- RNA viruses is a 65,000-68,000 molecular weight precursor polypeptide (Pr65) whose cleavage leads to the formation of four virion proteins, p30, p15, p12 and p10.	Glycosaminoglycans	31-34	cyclin dependent kinase inhibitor 2B	Homo sapiens	206-209
60707-1	1976	The translation product of the gag gene of mammalian type-c- RNA viruses is a 65,000-68,000 molecular weight precursor polypeptide (Pr65) whose cleavage leads to the formation of four virion proteins, p30, p15, p12 and p10.	Glycosaminoglycans	31-34	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	211-214
60707-1	1976	The translation product of the gag gene of mammalian type-c- RNA viruses is a 65,000-68,000 molecular weight precursor polypeptide (Pr65) whose cleavage leads to the formation of four virion proteins, p30, p15, p12 and p10.	Glycosaminoglycans	31-34	S100 calcium binding protein A10	Homo sapiens	219-222
1023336-1	1976	In the byosinthesis of glycosaminoglycans, UDP-glucose is utilized by two enzymes: UDP-glucose dehydrogenase which produces UDP-glucuronic acid (chondroitin sulphate precursor), and UDP-glucose 4"-epimerase which produces UDP-galactose (keratan sulphate precursor).	Glycosaminoglycans	23-41	UDP-glucose 6-dehydrogenase	Homo sapiens	83-108
134044-6	1976	In the relatively normal intima, the mean concentrations of the GAGs were found to be 4.7, 20.9, 1.3, and 5.1 mg/g of dry, defatted, decalcified tissue for CSB, CSC, HA, and HS, respectively.	Glycosaminoglycans	64-68	ERCC excision repair 6, chromatin remodeling factor	Homo sapiens	156-159
821471-5	1976	Analysis for glycosyltransferase activity confirmed that glycosaminoglycans were formed chiefly in particles sedimenting at 20000g.	Glycosaminoglycans	57-75	protein O-linked mannose beta 1,4-N-acetylglucosaminyltransferase 2	Mus musculus	13-32
941794-11	1976	Catalase brought about an almost complete recovery of GAG content, together with an important increase in 35S incorporation.	Glycosaminoglycans	54-57	catalase	Homo sapiens	0-8
1023336-1	1976	In the byosinthesis of glycosaminoglycans, UDP-glucose is utilized by two enzymes: UDP-glucose dehydrogenase which produces UDP-glucuronic acid (chondroitin sulphate precursor), and UDP-glucose 4"-epimerase which produces UDP-galactose (keratan sulphate precursor).	Glycosaminoglycans	23-41	UDP-galactose-4-epimerase	Homo sapiens	182-206
123039-0	1975	Role of growth hormone in glycosaminoglycan synthesis by articular cartilage.	Glycosaminoglycans	26-43	growth hormone 1	Homo sapiens	8-22
123777-0	1975	Apparent sulfation of glycosaminoglycans by ascorbic acid 2-[3 5-S] sulfate: an explanation.	Glycosaminoglycans	22-40	PTOV1 extended AT-hook containing adaptor protein	Homo sapiens	53-59
123777-1	1975	The sulfation of glycosaminoglycans by ascorbic acid 2-[35S]sulfate was studied in costal cartilage and chondrocytes in vitro.	Glycosaminoglycans	17-35	PTOV1 extended AT-hook containing adaptor protein	Homo sapiens	48-54
123777-2	1975	Negligable (if any) sulfation of glycosaminoglycans was detected with immediately isolated ascorbic acid 2-[35S]sulfate.	Glycosaminoglycans	33-51	PTOV1 extended AT-hook containing adaptor protein	Homo sapiens	100-106
123777-4	1975	The [35S]glycosaminoglycans did not result from the direct transfer of 35S from ascorbic acid 2-sulfate but rather from a decomposition product of ascorbic acid 2-[35S]sulfate.	Glycosaminoglycans	9-27	PTOV1 extended AT-hook containing adaptor protein	Homo sapiens	89-95
123777-4	1975	The [35S]glycosaminoglycans did not result from the direct transfer of 35S from ascorbic acid 2-sulfate but rather from a decomposition product of ascorbic acid 2-[35S]sulfate.	Glycosaminoglycans	9-27	PTOV1 extended AT-hook containing adaptor protein	Homo sapiens	156-162
123643-1	1975	Somatomedin potencies of sera were assayed by following sulfation of mucopolysaccharides in chick embryo sterna in vitro.	Glycosaminoglycans	69-88	insulin like growth factor 1	Gallus gallus	0-11
1182196-4	1975	Glycosaminoglycans were eluted stepwise from the column with NaC1.	Glycosaminoglycans	0-18	nucleus accumbens associated 1	Homo sapiens	61-65
126129-8	1975	The physiological meaning of UDP-glucose 4"-epimerase in glycosaminoglycan biosynthesis in the two tissues under study is discussed on the basis of the Km values of UDP-glucose 4"-epimerase and UDP-glucose dehydrogenase and on the basis of the rate of UDP-glucose and UDP-galactose utilization.	Glycosaminoglycans	57-74	UDP-galactose-4-epimerase	Bos taurus	29-53
166544-17	1975	Enzymes of the mucopolysaccharide metabolism were not found at all (beta-glucuronidase) or showed only a weak reactivity, such as xylitol dehydrogenase.	Glycosaminoglycans	15-33	beta-glucuronidase	Callithrix jacchus	68-86
126129-8	1975	The physiological meaning of UDP-glucose 4"-epimerase in glycosaminoglycan biosynthesis in the two tissues under study is discussed on the basis of the Km values of UDP-glucose 4"-epimerase and UDP-glucose dehydrogenase and on the basis of the rate of UDP-glucose and UDP-galactose utilization.	Glycosaminoglycans	57-74	UDP-galactose-4-epimerase	Bos taurus	165-189
126129-8	1975	The physiological meaning of UDP-glucose 4"-epimerase in glycosaminoglycan biosynthesis in the two tissues under study is discussed on the basis of the Km values of UDP-glucose 4"-epimerase and UDP-glucose dehydrogenase and on the basis of the rate of UDP-glucose and UDP-galactose utilization.	Glycosaminoglycans	57-74	UDP-glucose 6-dehydrogenase	Bos taurus	194-219
170710-12	1975	In view of the unusually large size and lipid composition of lamellar bodies, a mechanism involving hydration of mucopolysaccharide contents as an aid to expulsion of lamellar contents is suggested.	Glycosaminoglycans	113-131	activation induced cytidine deaminase	Homo sapiens	147-150
167303-0	1975	Proceedings: Regulation of glycosaminoglycan formation in fibroblasts: opposite effects of cyclic 3",5"-AMP and cyclic 3",5"-GMP.	Glycosaminoglycans	27-44	5'-nucleotidase, cytosolic II	Homo sapiens	125-128
14390824-0	1955	[Relation of haptoglobin index to alpha 2-globulin and circulating mucopolysaccharides in various pathological conditions].	Glycosaminoglycans	67-86	haptoglobin	Homo sapiens	13-24
5541767-0	1971	The isolation and characterization of a mucopolysaccharide secreted by the snail, Otella lactea.	Glycosaminoglycans	40-58	snail family transcriptional repressor 1	Homo sapiens	75-80
4244783-0	1970	The rotatory relaxation of fibrinogen in mucopolysaccharide solution detected by fluorescence-depolarization.	Glycosaminoglycans	41-59	fibrinogen beta chain	Homo sapiens	27-37
14017678-2	1963	Relations between beta-glucuronidase and acid mucopolysaccharides in growth cartilage].	Glycosaminoglycans	46-65	glucuronidase beta	Homo sapiens	18-36
13572631-0	1958	[Possible relation between mucopolysaccharides (hexosamine) and protein part in elastin].	Glycosaminoglycans	27-46	elastin	Homo sapiens	80-87
16742805-6	1973	This glycosaminoglycan, found in both cells and growth medium, was almost entirely chondroitin 4-sulphate.	Glycosaminoglycans	5-22	carbohydrate sulfotransferase 11	Mus musculus	83-96
4261008-0	1972	The release of glycosaminoglycans during exposure of human platelets to thrombin and polystyrene latex particles.	Glycosaminoglycans	15-33	coagulation factor II, thrombin	Homo sapiens	72-80
4336087-2	1970	Studies of the dynamics of ACTH on mucopolysaccharides of arterial wall].	Glycosaminoglycans	35-54	proopiomelanocortin	Homo sapiens	27-31
4241141-0	1969	Effect of a single neonatal dose of ACTH, TSH, STH, thyroxine and aldosterone on serum heparin and tissue mucopolysaccharides.	Glycosaminoglycans	106-125	proopiomelanocortin	Homo sapiens	36-40
4225405-0	1967	The nature of C-reactive protein in acute phase serum: evidence for an equilibrium form containing a mucopolysaccharide of serum.	Glycosaminoglycans	101-119	C-reactive protein	Homo sapiens	14-32
4222592-0	1965	[Changes in the blood properdin level in normal and irradiated animals under the effect of a mucopolysaccharide preparation from cattle spleen].	Glycosaminoglycans	93-111	complement factor properdin	Bos taurus	22-31
14194638-0	1964	EFFECT OF PARATHYROID HORMONE ON MUCOPOLYSACCHARIDE SYNTHESIS IN RACHITIC RAT CARTILAGE IN VITRO.	Glycosaminoglycans	33-51	parathyroid hormone	Rattus norvegicus	10-29
13198940-0	1954	Mucopolysaccharides bound to thyroglobulin; a histochemical and paper-electrophoretic investigation.	Glycosaminoglycans	0-19	thyroglobulin	Homo sapiens	29-42
34053170-7	2021	COG3 knock out (KO) cells had particularly reduced ability to polymerize GAG chains.	Glycosaminoglycans	73-76	component of oligomeric golgi complex 3	Homo sapiens	0-4
33757902-2	2021	DYT1 dystonia is one of the most common genetic dystonias, and most patients carry heterozygous DYT1  GAG mutations causing a loss of a glutamic acid of the protein torsinA.	Glycosaminoglycans	102-105	torsin family 1 member A	Homo sapiens	0-4
33781652-0	2021	Glycosaminoglycans located on neutrophils and monocytes impact on CXCL8- and CCL2-induced cell migration.	Glycosaminoglycans	0-18	C-X-C motif chemokine ligand 8	Homo sapiens	66-71
33781652-0	2021	Glycosaminoglycans located on neutrophils and monocytes impact on CXCL8- and CCL2-induced cell migration.	Glycosaminoglycans	0-18	C-C motif chemokine ligand 2	Homo sapiens	77-81
33740688-4	2021	The overall objective of this study was to characterize the role PRG4 and HA play in the lubricating function of collagen-glycosaminoglycan (GAG) scaffolds for cartilage repair.	Glycosaminoglycans	141-144	proteoglycan 4	Bos taurus	65-69
33740688-9	2021	Immunohistochemistry demonstrated that PRG4 from recombinant human (rh) and bovine sources adsorbed to collagen-GAG scaffolds and the coefficient of friction for scaffolds immersed in rhPRG4 (0.067 +- 0.027) and normal bSF (0.056 +- 0.020) solution decreased compared to PBS (0.118 +- 0.21, both p < 0.05, at epsilon = 0.2).	Glycosaminoglycans	112-115	proteoglycan 4	Homo sapiens	39-43
14830656-0	1951	[Research on the mechanism of liberation of bacterial mucopolysaccharides by action of lysozyme].	Glycosaminoglycans	54-73	lysozyme	Homo sapiens	87-95
33757902-2	2021	DYT1 dystonia is one of the most common genetic dystonias, and most patients carry heterozygous DYT1  GAG mutations causing a loss of a glutamic acid of the protein torsinA.	Glycosaminoglycans	102-105	torsin family 1 member A	Homo sapiens	165-172
33985463-2	2021	MPS VI is a multisystemic disease resulting from a deficiency in arylsulfatase B causing an accumulation of glycosaminoglycans in the tissues and organs of the body.	Glycosaminoglycans	108-126	arylsulfatase B	Homo sapiens	65-80
34038745-8	2021	Besides, BRD7 overexpression reversed the reductions in sulfated glycosaminoglycan levels induced by TNF-alpha, but this effect was blocked by PI3K or YAP1 inhibitors.	Glycosaminoglycans	65-82	bromodomain containing 7	Homo sapiens	9-13
34038745-8	2021	Besides, BRD7 overexpression reversed the reductions in sulfated glycosaminoglycan levels induced by TNF-alpha, but this effect was blocked by PI3K or YAP1 inhibitors.	Glycosaminoglycans	65-82	tumor necrosis factor	Homo sapiens	101-110
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
33857420-0	2021	Golgi apparatus-synthesized sulfated glycosaminoglycans mediate polymerization and activation of the cGAMP sensor STING.	Glycosaminoglycans	37-55	stimulator of interferon response cGAMP interactor 1	Mus musculus	114-119
33857420-2	2021	Using a genome-wide CRISPR-Cas9 screen to define factors critical for STING activation in cells, we identified proteins critical for biosynthesis of sulfated glycosaminoglycans (sGAGs) in the Golgi apparatus.	Glycosaminoglycans	158-176	stimulator of interferon response cGAMP interactor 1	Mus musculus	70-75
33857420-7	2021	Reducing the expression of Slc35b2 to inhibit GAG sulfation in mice impaired responses to vaccinia virus infection.	Glycosaminoglycans	46-49	solute carrier family 35, member B2	Mus musculus	27-34
33145772-1	2021	Mucopolysaccharidosis type I (MPS I) is a lysosomal storage disorder caused by mutations in the IDUA gene, that codifies the alpha-L-iduronidase enzyme, which deficiency leads to storage of glycosaminoglycans, with multiple clinical manifestations.	Glycosaminoglycans	190-208	iduronidase, alpha-L	Mus musculus	96-100
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
33175445-2	2021	Arc has homology to retroviral Gag protein and is capable of self-assembly into virus-like capsids implicated in the intercellular transfer of RNA.	Glycosaminoglycans	31-34	activity regulated cytoskeleton associated protein	Homo sapiens	0-3
33960103-1	2021	Mucopolysaccharidosis type II (MPS II) is an X-linked inherited disease caused by pathogenic variants in the IDS gene, leading to deficiency of the lysosomal enzyme iduronate-2-sulfatase and consequent widespread storage of glycosaminoglycans, leading to several clinical consequences, with progressive manifestations which most times includes cognitive decline.	Glycosaminoglycans	224-242	iduronate 2-sulfatase	Homo sapiens	109-112
33960103-1	2021	Mucopolysaccharidosis type II (MPS II) is an X-linked inherited disease caused by pathogenic variants in the IDS gene, leading to deficiency of the lysosomal enzyme iduronate-2-sulfatase and consequent widespread storage of glycosaminoglycans, leading to several clinical consequences, with progressive manifestations which most times includes cognitive decline.	Glycosaminoglycans	224-242	iduronate 2-sulfatase	Homo sapiens	165-186
33859108-9	2021	P2 demonstrated a striking increase in the frequency of gag-specific central and effector memory CD8+ T cells producing IFN-gamma, TNF-alpha, and CD107a following anti-PD1 and anti-CTLA-4.	Glycosaminoglycans	56-59	CD8a molecule	Homo sapiens	97-100
33581610-0	2021	Murine leukemia virus resists producer cell APOBEC3A by its Glycosylated Gag but not target cell APOBEC3A.	Glycosaminoglycans	73-76	apolipoprotein B mRNA editing enzyme catalytic subunit 3A	Homo sapiens	44-52
33581610-4	2021	Furthermore, glycosylated Gag (glycoGag) of MLV inhibits the encapsidation of human A3A, but target cell A3A was not affected by glycoGag and exerted deamination of viral DNA.	Glycosaminoglycans	26-29	apolipoprotein B mRNA editing enzyme catalytic subunit 3A	Homo sapiens	84-87
33923651-5	2021	In human vascular smooth muscle cells, LPA induces Rho-associated protein kinase (ROCK) dependent transforming growth factor receptor (TGFBR1) transactivation, leading to glycosaminoglycan chain elongation.	Glycosaminoglycans	171-188	transforming growth factor beta receptor 1	Homo sapiens	135-141
32678931-13	2021	MMP-9, MMP-13, and total MMP activity had moderate negative correlations to tissue GAG.	Glycosaminoglycans	83-86	matrix metallopeptidase 9	Homo sapiens	0-5
32678931-13	2021	MMP-9, MMP-13, and total MMP activity had moderate negative correlations to tissue GAG.	Glycosaminoglycans	83-86	matrix metallopeptidase 1	Homo sapiens	0-3
33926568-12	2021	Activin A stimulated collagen type II gene expression and glycosaminoglycan synthesis in TGF-beta3 treated MenSCs but not in BMMSCs, both in vitro and in vivo, although the effects of TGF-beta3 alone were more pronounced in BMMSCs in vitro.	Glycosaminoglycans	58-75	transforming growth factor, beta 3	Mus musculus	89-98
33923025-4	2021	In this study, we generated the functional HIV-1 Gag epitope SL9-specific CTLs from the induced PSC (iPSCs), i.e., iPSC-CTLs, and investigated the suppression of SL9-specific iPSC-CTLs on viral replication and the protection of CD4+ T cells.	Glycosaminoglycans	49-52	CD4 molecule	Homo sapiens	228-231
33859108-9	2021	P2 demonstrated a striking increase in the frequency of gag-specific central and effector memory CD8+ T cells producing IFN-gamma, TNF-alpha, and CD107a following anti-PD1 and anti-CTLA-4.	Glycosaminoglycans	56-59	interferon gamma	Homo sapiens	120-129
33859108-9	2021	P2 demonstrated a striking increase in the frequency of gag-specific central and effector memory CD8+ T cells producing IFN-gamma, TNF-alpha, and CD107a following anti-PD1 and anti-CTLA-4.	Glycosaminoglycans	56-59	tumor necrosis factor	Homo sapiens	131-140
33859108-9	2021	P2 demonstrated a striking increase in the frequency of gag-specific central and effector memory CD8+ T cells producing IFN-gamma, TNF-alpha, and CD107a following anti-PD1 and anti-CTLA-4.	Glycosaminoglycans	56-59	lysosomal associated membrane protein 1	Homo sapiens	146-152
33859108-9	2021	P2 demonstrated a striking increase in the frequency of gag-specific central and effector memory CD8+ T cells producing IFN-gamma, TNF-alpha, and CD107a following anti-PD1 and anti-CTLA-4.	Glycosaminoglycans	56-59	programmed cell death 1	Homo sapiens	168-171
33859108-9	2021	P2 demonstrated a striking increase in the frequency of gag-specific central and effector memory CD8+ T cells producing IFN-gamma, TNF-alpha, and CD107a following anti-PD1 and anti-CTLA-4.	Glycosaminoglycans	56-59	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	181-187
33606521-5	2021	TGF-beta1 influenced construct contraction rate and glycosaminoglycan (GAG) production with two half-maximal effective concentration (EC50) ranges, which are 0.23 to 0.28 and 0.53 to 1.71 ng/mL, respectively.	Glycosaminoglycans	52-69	transforming growth factor beta 1	Homo sapiens	0-9
33606521-6	2021	At concentrations less than the EC50, for the GAG production and contraction rate, TGF-beta1 treatment resulted in less organized collagen fibers.	Glycosaminoglycans	46-49	transforming growth factor beta 1	Homo sapiens	83-92
33606521-5	2021	TGF-beta1 influenced construct contraction rate and glycosaminoglycan (GAG) production with two half-maximal effective concentration (EC50) ranges, which are 0.23 to 0.28 and 0.53 to 1.71 ng/mL, respectively.	Glycosaminoglycans	71-74	transforming growth factor beta 1	Homo sapiens	0-9
33476687-2	2021	Most DYT1 dystonia patients have a heterozygous trinucleotide GAG deletion in DYT1 or TOR1A gene, with a loss of a glutamic acid residue of the protein torsinA.	Glycosaminoglycans	62-65	torsin family 1 member A	Homo sapiens	5-9
33476687-2	2021	Most DYT1 dystonia patients have a heterozygous trinucleotide GAG deletion in DYT1 or TOR1A gene, with a loss of a glutamic acid residue of the protein torsinA.	Glycosaminoglycans	62-65	torsin family 1 member A	Homo sapiens	78-82
33476687-2	2021	Most DYT1 dystonia patients have a heterozygous trinucleotide GAG deletion in DYT1 or TOR1A gene, with a loss of a glutamic acid residue of the protein torsinA.	Glycosaminoglycans	62-65	torsin family 1 member A	Homo sapiens	86-91
33754692-0	2021	Injectable Glycosaminoglycan-Based Cryogels from Well-Defined Microscale Templates for Local Growth Factor Delivery.	Glycosaminoglycans	11-28	myotrophin	Rattus norvegicus	93-106
33827271-9	2021	The results showed that the scaffold delivered TGF-beta3 for up to 8 days of culture which resulted in 15-fold increase in GAG production, and 6-fold increase in collagen synthesis with respect to the No TGF-beta3 group.	Glycosaminoglycans	123-126	transforming growth factor beta 3	Homo sapiens	47-56
34056184-10	2021	Further, the binding surface of these flavonols to CCL2 orthologs was observed to be extensively overlapped with that of the receptor/GAG-binding surface, thus suggesting attenuation of CCL2-CCR2/GAG interactions in their presence.	Glycosaminoglycans	134-137	chemokine (C-C motif) ligand 2	Mus musculus	51-55
33751850-11	2021	TGF-beta1 and IGF-1 releasing COX rods induced higher Glycosaminoglycan (GAG)/DNA amounts than the other GF releasing COX rods.	Glycosaminoglycans	54-71	transforming growth factor beta 1	Homo sapiens	0-9
34056184-10	2021	Further, the binding surface of these flavonols to CCL2 orthologs was observed to be extensively overlapped with that of the receptor/GAG-binding surface, thus suggesting attenuation of CCL2-CCR2/GAG interactions in their presence.	Glycosaminoglycans	134-137	chemokine (C-C motif) ligand 2	Mus musculus	186-190
34056184-10	2021	Further, the binding surface of these flavonols to CCL2 orthologs was observed to be extensively overlapped with that of the receptor/GAG-binding surface, thus suggesting attenuation of CCL2-CCR2/GAG interactions in their presence.	Glycosaminoglycans	134-137	C-C motif chemokine receptor 2	Homo sapiens	191-195
34056184-10	2021	Further, the binding surface of these flavonols to CCL2 orthologs was observed to be extensively overlapped with that of the receptor/GAG-binding surface, thus suggesting attenuation of CCL2-CCR2/GAG interactions in their presence.	Glycosaminoglycans	196-199	chemokine (C-C motif) ligand 2	Mus musculus	51-55
34056184-10	2021	Further, the binding surface of these flavonols to CCL2 orthologs was observed to be extensively overlapped with that of the receptor/GAG-binding surface, thus suggesting attenuation of CCL2-CCR2/GAG interactions in their presence.	Glycosaminoglycans	196-199	chemokine (C-C motif) ligand 2	Mus musculus	186-190
33832800-1	2021	BACKGROUND: DYT-TOR1A is caused by a GAG deletion in the TOR1A gene.	Glycosaminoglycans	37-40	torsin family 1 member A	Homo sapiens	16-21
33832800-1	2021	BACKGROUND: DYT-TOR1A is caused by a GAG deletion in the TOR1A gene.	Glycosaminoglycans	37-40	torsin family 1 member A	Homo sapiens	57-62
33832800-8	2021	Whole exome sequencing eventually revealed a single GAG deletion in the TOR1A gene.	Glycosaminoglycans	52-55	torsin family 1 member A	Homo sapiens	72-77
33832800-9	2021	CONCLUSION: Monozygotic twins whose only mutation was a GAG deletion in TOR1A exhibited DYT/PARK-GCH1-asssociated features and jerking movements reminiscent of myoclonus.	Glycosaminoglycans	56-59	torsin family 1 member A	Homo sapiens	72-77
33832800-9	2021	CONCLUSION: Monozygotic twins whose only mutation was a GAG deletion in TOR1A exhibited DYT/PARK-GCH1-asssociated features and jerking movements reminiscent of myoclonus.	Glycosaminoglycans	56-59	GTP cyclohydrolase 1	Homo sapiens	97-101
33662819-0	2021	Histologic evaluation of therapeutic responses in ischemic myocardium elicited by dual growth factor delivery from composite glycosaminoglycan hydrogels.	Glycosaminoglycans	125-142	myotrophin	Rattus norvegicus	87-100
33751850-11	2021	TGF-beta1 and IGF-1 releasing COX rods induced higher Glycosaminoglycan (GAG)/DNA amounts than the other GF releasing COX rods.	Glycosaminoglycans	54-71	insulin like growth factor 1	Homo sapiens	14-19
33751850-11	2021	TGF-beta1 and IGF-1 releasing COX rods induced higher Glycosaminoglycan (GAG)/DNA amounts than the other GF releasing COX rods.	Glycosaminoglycans	73-76	transforming growth factor beta 1	Homo sapiens	0-9
33751850-11	2021	TGF-beta1 and IGF-1 releasing COX rods induced higher Glycosaminoglycan (GAG)/DNA amounts than the other GF releasing COX rods.	Glycosaminoglycans	73-76	insulin like growth factor 1	Homo sapiens	14-19
33247415-4	2021	The GAG deletion in TOR1A is associated with generalized dystonia with onset in childhood in the lower limbs.	Glycosaminoglycans	4-7	torsin family 1 member A	Homo sapiens	20-25
33463716-7	2021	Overexpression of glycosphingolipid precursor enzyme UGCG improved transfection efficiency by 17% and knocking-down the Gag-binding protein CNP improved 2.5-fold VLP specific productivity.	Glycosaminoglycans	120-123	2',3'-cyclic nucleotide 3' phosphodiesterase	Homo sapiens	140-143
33463716-7	2021	Overexpression of glycosphingolipid precursor enzyme UGCG improved transfection efficiency by 17% and knocking-down the Gag-binding protein CNP improved 2.5-fold VLP specific productivity.	Glycosaminoglycans	120-123	VHL like	Homo sapiens	162-165
32881070-3	2021	Cxcl1 and Cxcl2 exist as monomers and dimers, and exert their function by activating the Cxcr2 receptor and binding glycosaminoglycans (GAGs).	Glycosaminoglycans	116-134	chemokine (C-X-C motif) ligand 1	Mus musculus	0-5
32881070-3	2021	Cxcl1 and Cxcl2 exist as monomers and dimers, and exert their function by activating the Cxcr2 receptor and binding glycosaminoglycans (GAGs).	Glycosaminoglycans	116-134	chemokine (C-X-C motif) ligand 2	Mus musculus	10-15
32881070-10	2021	We propose that the ability of Cxcl1 and Cxcl2 to reversibly exist as monomers and dimers and differences in their Cxcr2 activity and GAG interactions coordinate neutrophil recruitment and activation, which play a critical role for successful resolution of inflammation.	Glycosaminoglycans	134-137	chemokine (C-X-C motif) ligand 2	Mus musculus	41-46
33860088-3	2021	Our recent study revealed that sulfated glycosaminoglycans, especially highly sulfated domains of heparan sulfate (heparan sulfate S-domains), participate in cancer pathology by mediating transcellular propagation of p53 aggregates.	Glycosaminoglycans	40-58	tumor protein p53	Homo sapiens	217-220
33479807-15	2021	Further increase in the expression of SIRT1, cartilage marker genes Aggrecan and collagen 2 (alpha1) by overexpression of lncRNA-CRNDE also indicated elevated GAG content.	Glycosaminoglycans	159-162	sirtuin 1	Rattus norvegicus	38-43
33485691-6	2021	Here we propose an Arc "life cycle", based on what is known about retroviral Gag, and discuss how elucidating these biological processes may lead to novel insights into brain plasticity and memory.	Glycosaminoglycans	77-80	activity regulated cytoskeleton associated protein	Homo sapiens	19-22
34027339-9	2021	In particular, these data suggest that, although both subpopulations collaborate in the production and organisation of extracellular matrix, GPC3 + HSCs specifically express genes involved in the metabolism of glycosaminoglycans, whereas DBH + HSCs display a gene signature that is reminiscent of antigen-presenting cells.	Glycosaminoglycans	210-228	glypican 3	Homo sapiens	141-145
33796087-0	2021	Improved Detection of HIV Gag p24 Protein Using a Combined Immunoprecipitation and Digital ELISA Method.	Glycosaminoglycans	26-29	transmembrane p24 trafficking protein 2	Homo sapiens	30-33
33796087-7	2021	Immunocapture of HIV gag p24 followed by elution in a Simoa-compatible format resulted in higher protein recovery and lower background from various biological matrices and sample volumes.	Glycosaminoglycans	21-24	transmembrane p24 trafficking protein 2	Homo sapiens	25-28
33719080-2	2021	In this condition, a functional beta-glucuronidase deficiency results in the accumulation of glycosaminoglycans (GAGs) in cells and tissues where beta-glucuronidase is important in GAG degradation.	Glycosaminoglycans	93-111	glucuronidase beta	Canis lupus familiaris	32-50
33841658-8	2021	Moreover, explants cultured with 10 ng/ml TGF-beta1 under hypoxic (1% O2) in combination with a bioreactor, significantly enhanced the expression of aggrecan and type II collagen, but were lacking in the production of Glycosaminoglycans (GAGs), as evidenced by alcian blue staining.	Glycosaminoglycans	238-242	transforming growth factor beta 1	Sus scrofa	42-51
33663609-8	2021	RESULTS: Glycosaminoglycan content and the expression levels of chondrogenic genes were decreased in the WJ-MSCs from IUGR, and the expression levels of chondrogenic genes were further reduced after IL-1beta treatment, while the expression levels of catabolic factors were increased.	Glycosaminoglycans	9-26	interleukin 1 alpha	Homo sapiens	199-207
33382197-9	2021	The results indicate that increasing MC-GAG stiffness induces osteogenic differentiation via the mechanotransduction mediators YAP/TAZ and the canonical Wnt signaling pathway, whereas the canonical BMPR signaling pathway is activated independent of stiffness.	Glycosaminoglycans	40-43	Yes1 associated transcriptional regulator	Homo sapiens	127-130
33538605-4	2021	PLL-MNP assessed GAG depletion by Chondroitinase ABC in vitro rat cartilage and intact ex vivo mouse knee joint.	Glycosaminoglycans	17-20	modifier of Niemann Pick type C1	Mus musculus	4-7
33674572-7	2021	Gag-specific CD8+ T cell responses are predominantly observed in secondary lymphoid organs in animals chronically infected prior to ART and these responses are dominated by CD69+ populations.	Glycosaminoglycans	0-3	CD69 molecule	Macaca mulatta	173-177
33506337-1	2021	Chondroitin sulfate (CS) is a widely studied class of glycosaminoglycans, responsible for diverse biological functions.	Glycosaminoglycans	54-72	citrate synthase	Homo sapiens	21-23
33504177-0	2021	Chondroitin Sulfate N-acetylgalactosaminyltransferase-2 Impacts Foam Cell Formation and Atherosclerosis by Altering Macrophage Glycosaminoglycan Chain.	Glycosaminoglycans	127-144	chondroitin sulfate N-acetylgalactosaminyltransferase 2	Mus musculus	0-55
33504177-3	2021	Approach and Results: ChGn-2-deficient mice showed decreased and shortened glycosaminoglycans.	Glycosaminoglycans	75-93	chondroitin sulfate N-acetylgalactosaminyltransferase 2	Mus musculus	22-28
33719080-2	2021	In this condition, a functional beta-glucuronidase deficiency results in the accumulation of glycosaminoglycans (GAGs) in cells and tissues where beta-glucuronidase is important in GAG degradation.	Glycosaminoglycans	113-116	glucuronidase beta	Canis lupus familiaris	32-50
32601684-1	2021	Loss-of-function variants in CHST14 cause a dermatan 4-O-sulfotransferase deficiency named musculocontractural Ehlers-Danlos syndrome-CHST14 (mcEDS-CHST14), resulting in complete depletion of the dermatan sulfate moiety of decorin glycosaminoglycan (GAG) chains, which is replaced by chondroitin sulfate.	Glycosaminoglycans	231-248	carbohydrate sulfotransferase 14	Mus musculus	29-35
33359244-9	2021	CONCLUSION: Modification of hADSCs by the antioxidants Sod2 and Cat improved the pathological condition of intervertebral disc tissues with increased GAG and COL2 expression, as well as reduced inflammation, thereby demonstrating a therapeutic effect in IVD.	Glycosaminoglycans	150-153	superoxide dismutase 2, mitochondrial	Mus musculus	55-59
33359244-9	2021	CONCLUSION: Modification of hADSCs by the antioxidants Sod2 and Cat improved the pathological condition of intervertebral disc tissues with increased GAG and COL2 expression, as well as reduced inflammation, thereby demonstrating a therapeutic effect in IVD.	Glycosaminoglycans	150-153	catalase	Mus musculus	64-67
33825882-4	2021	In this study, we have imparted collagenolytic property to cathepsin-L, by systematically engineering proline-specificity and glycosaminoglycans (GAG)-binding surface in the protease.	Glycosaminoglycans	126-144	cathepsin L	Homo sapiens	59-70
33825882-4	2021	In this study, we have imparted collagenolytic property to cathepsin-L, by systematically engineering proline-specificity and glycosaminoglycans (GAG)-binding surface in the protease.	Glycosaminoglycans	146-149	cathepsin L	Homo sapiens	59-70
32601684-1	2021	Loss-of-function variants in CHST14 cause a dermatan 4-O-sulfotransferase deficiency named musculocontractural Ehlers-Danlos syndrome-CHST14 (mcEDS-CHST14), resulting in complete depletion of the dermatan sulfate moiety of decorin glycosaminoglycan (GAG) chains, which is replaced by chondroitin sulfate.	Glycosaminoglycans	250-253	carbohydrate sulfotransferase 14	Mus musculus	29-35
32601684-10	2021	Through EM-based CB staining, rod-shaped linear GAG chains were found to be attached at one end to collagen fibrils and protruded outside of the fibrils, in contrast to them being round and wrapping the collagen fibrils in Chst14+/+ mice.	Glycosaminoglycans	48-51	carbohydrate sulfotransferase 14	Mus musculus	223-229
32601684-12	2021	Chst14-/- mice, exhibiting similar abnormalities in the GAG structure of decorin and collagen networks in the skin, could be a reasonable model for skin fragility of patients with mcEDS-CHST14, shedding light on the role of dermatan sulfate in maintaining skin strength.	Glycosaminoglycans	56-59	carbohydrate sulfotransferase 14	Mus musculus	0-6
32785657-0	2021	AMPK differentially alters sulfated glycosaminoglycans under normal and high glucose milieu in proximal tubular cells.	Glycosaminoglycans	36-54	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	0-4
32785657-3	2021	Here, we have looked into the effect of AMPK modulation on sulfated GAG (sGAG) levels of tubular cells of proximal and distal origin to understand the mechanism of hyperglycemia-mediated pathogenesis of the diabetic nephropathy.	Glycosaminoglycans	68-71	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	40-44
33450585-10	2021	Biochemical analysis and second harmonic generation microscopy showed that the release of IL4+IL13 increased total sulfated glycosaminoglycan content and decreased fibril alignment, which is typically associated with less fibrotic tissue.	Glycosaminoglycans	124-141	interleukin 4	Mus musculus	90-93
33434858-1	2021	Mucopolysaccharidosis type I (MPS I) is a lysosomal storage disorder characterized by alpha-L-iduronidase (IDUA) deficiency, an enzyme responsible for glycosaminoglycan degradation.	Glycosaminoglycans	151-168	iduronidase, alpha-L	Mus musculus	86-105
33434858-1	2021	Mucopolysaccharidosis type I (MPS I) is a lysosomal storage disorder characterized by alpha-L-iduronidase (IDUA) deficiency, an enzyme responsible for glycosaminoglycan degradation.	Glycosaminoglycans	151-168	iduronidase, alpha-L	Mus musculus	107-111
33450585-10	2021	Biochemical analysis and second harmonic generation microscopy showed that the release of IL4+IL13 increased total sulfated glycosaminoglycan content and decreased fibril alignment, which is typically associated with less fibrotic tissue.	Glycosaminoglycans	124-141	interleukin 13	Mus musculus	94-98
33572941-2	2021	IDUA catalyzes the degradation of the glycosaminoglycans dermatan and heparan sulfate (DS and HS, respectively).	Glycosaminoglycans	38-56	alpha-L-iduronidase	Homo sapiens	0-4
33176060-9	2021	In addition to the chain length, the type and extent of sulfation of glycosaminoglycans influenced the ability of skeletal muscle myosin to neutralize the polysaccharide"s ability to enhance antithrombin"s activity.	Glycosaminoglycans	69-87	serpin family C member 1	Homo sapiens	191-203
33372388-4	2021	Using Western blotting, immunoprecipitation, qPCR, immunofluorescence and Dimethylmethylene blue assays, and ELISA and transmission electron microscope techniques, we found that PLCgamma1 inhibitor U73122 enhanced Collagen II, Aggrecan and GAG levels, accompanied with increased LC3B-II/I ratio and decreased P62 expression level, whereas autophagy inhibitor Chloroquine partially diminished its effect.	Glycosaminoglycans	240-243	phospholipase C, gamma 1	Rattus norvegicus	178-187
33465243-6	2021	FOXF1 transfection significantly altered gene expression by upregulating healthy NP markers [FOXF1, keratin 19 (KRT19)], decreasing inflammatory cytokines [interleukin (IL)-1beta, -6], catabolic enzymes [metalloproteinase 13 (MMP13)] and nerve growth factor (NGF), with significant increases in glycosaminoglycan accumulation in human NP cells.	Glycosaminoglycans	295-312	forkhead box F1	Homo sapiens	0-5
33494617-7	2022	Inhibiting TRPC3 and TRPV4 decreased S-GAG content; however, only the inhibition of TRPV1 partially attenuated the hydrostatic loading-induced reduction in S-GAG content.	Glycosaminoglycans	39-42	transient receptor potential cation channel subfamily C member 3	Homo sapiens	11-16
33494617-7	2022	Inhibiting TRPC3 and TRPV4 decreased S-GAG content; however, only the inhibition of TRPV1 partially attenuated the hydrostatic loading-induced reduction in S-GAG content.	Glycosaminoglycans	39-42	transient receptor potential cation channel subfamily V member 4	Homo sapiens	21-26
33494617-7	2022	Inhibiting TRPC3 and TRPV4 decreased S-GAG content; however, only the inhibition of TRPV1 partially attenuated the hydrostatic loading-induced reduction in S-GAG content.	Glycosaminoglycans	158-161	transient receptor potential cation channel subfamily V member 1	Homo sapiens	84-89
33537031-5	2020	K-PLP with a pI of ~11, was found to form visible aggregates in the presence of glycosaminoglycans and persist at the injection site and draining lymph nodes in vivo, similar to GA.	Glycosaminoglycans	80-98	proteolipid protein (myelin) 1	Mus musculus	2-5
33373240-4	2021	For example, murid herpesvirus 4, the current model for human gammaherpesvirus infection, can bind to cell surface glycosaminoglycans using both glycoproteins gp70 and gH/gL.	Glycosaminoglycans	115-133	embigin	Homo sapiens	159-163
33452387-6	2021	Glycosaminoglycans of endothelial cells derived from MMD and control induced pluripotent stem cells demonstrated a decreased amount of CS, especially sulfated CS, in MMD.	Glycosaminoglycans	0-18	citrate synthase	Homo sapiens	135-137
33452387-6	2021	Glycosaminoglycans of endothelial cells derived from MMD and control induced pluripotent stem cells demonstrated a decreased amount of CS, especially sulfated CS, in MMD.	Glycosaminoglycans	0-18	citrate synthase	Homo sapiens	159-161
33373240-4	2021	For example, murid herpesvirus 4, the current model for human gammaherpesvirus infection, can bind to cell surface glycosaminoglycans using both glycoproteins gp70 and gH/gL.	Glycosaminoglycans	115-133	gamma-glutamyl hydrolase	Homo sapiens	168-170
33373240-6	2021	Single-virus force spectroscopy experiments demonstrate that gH/gL is the main actor in glycosaminoglycan binding, engaging more numerous and more stable interactions.	Glycosaminoglycans	88-105	gamma-glutamyl hydrolase	Homo sapiens	61-63
33382968-5	2021	These screens uncovered host factors and pathways with pan-coronavirus and virus-specific functional roles, including major dependency on glycosaminoglycan biosynthesis, sterol regulatory element-binding protein (SREBP) signaling, bone morphogenetic protein (BMP) signaling, and glycosylphosphatidylinositol biosynthesis, as well as a requirement for several poorly characterized proteins.	Glycosaminoglycans	138-155	adenosine deaminase 2	Homo sapiens	55-58
33418542-4	2021	Addition of TCL extended the chondrogenic phenotype to P11 and significantly enhanced GAG content and type II collagen staining at all passages.	Glycosaminoglycans	86-89	ras homolog family member J	Homo sapiens	12-15
33488893-1	2021	Mucopolysaccharidosis type 2 is a congenital lysosomal disease characterized by iduronate-2-sulfatase deficiency, which leads to excessive accumulation of glycosaminoglycans in tissue.	Glycosaminoglycans	155-173	iduronate 2-sulfatase	Homo sapiens	80-101
33315406-6	2021	Previously, 4-azido-xylose-alpha-UDP sugar inhibited both xylosyltransferase (XYLT-1) and beta-1,4-galactosyltransferase-7 (beta-GALT-7)-the first and second enzymes of GAG biosynthesis-when microinjected into a cell.	Glycosaminoglycans	169-172	xylosyltransferase 1	Homo sapiens	78-84
33315406-6	2021	Previously, 4-azido-xylose-alpha-UDP sugar inhibited both xylosyltransferase (XYLT-1) and beta-1,4-galactosyltransferase-7 (beta-GALT-7)-the first and second enzymes of GAG biosynthesis-when microinjected into a cell.	Glycosaminoglycans	169-172	beta-1,4-galactosyltransferase 7	Homo sapiens	90-122
33456569-6	2021	The glycosaminoglycan (GAG) chains of SRGN were characterized using fluorophore-assisted carbohydrate electrophoresis.	Glycosaminoglycans	4-21	serglycin	Homo sapiens	38-42
32653886-2	2021	OBJECTIVE: This study aims to investigate the effects of GAG from Urechis unicinctus on ADP-induced platelet calcium and membrane glycoprotein expressions in rats.	Glycosaminoglycans	57-60	CD86 molecule	Rattus norvegicus	121-142
32653886-5	2021	RESULTS: The results showed that the GAG from U. unicinctus significantly inhibited the release of platelet calcium (p < 0.01) and the expressions of platelet GPII b/IIIa and P-selectin (p < 0.01) induced by ADP in rats but had no significant effect on the influx of platelet calcium (p > 0.01).	Glycosaminoglycans	37-40	selectin P	Rattus norvegicus	175-185
32653886-6	2021	CONCLUSIONS: This study indicated that GAG may inhibit platelet activation and aggregation by reducing the release of Ca2+ and ADP-induced expression of platelet membrane glycoprotein in rats.	Glycosaminoglycans	39-42	CD86 molecule	Rattus norvegicus	162-183
33968333-0	2021	Evidence of a Putative Glycosaminoglycan Binding Site on the Glycosylated SARS-CoV-2 Spike Protein N-terminal domain.	Glycosaminoglycans	23-40	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	85-90
33968333-4	2021	Here, we performed bioinformatics and molecular dynamics simulations of the spike protein to investigate the existence of additional GAG binding sites on the receptor-binding domain (RBD), separate from previously reported heparin-binding sites.	Glycosaminoglycans	133-136	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	76-81
33403027-9	2021	Moreover, gene set enrichment analysis showed that cases of HNSCC with FOXD1 overexpression were enriched in bladder cancer, cell cycle, DNA replication, glycosaminoglycan biosynthesis chondroitin sulfate, homologous recombination, glycan biosynthesis, nucleotide excision repair, p53 signaling pathway, pyrimidine metabolism, and spliceosome pathways.	Glycosaminoglycans	154-171	forkhead box D1	Homo sapiens	71-76
32749901-3	2021	The enzyme uridine diphosphate (UDP)-glucose dehydrogenase (UGDH) produces UDP-glucuronate, an essential precursor for new glycosaminoglycan synthesis that is tightly controlled at multiple levels.	Glycosaminoglycans	123-140	UDP-glucose 6-dehydrogenase	Homo sapiens	11-58
32749901-3	2021	The enzyme uridine diphosphate (UDP)-glucose dehydrogenase (UGDH) produces UDP-glucuronate, an essential precursor for new glycosaminoglycan synthesis that is tightly controlled at multiple levels.	Glycosaminoglycans	123-140	UDP-glucose 6-dehydrogenase	Homo sapiens	60-64
33045764-5	2021	Co-culture of the FM defect with Cx43 antisense and plug increased collagen levels but reduced GAG.	Glycosaminoglycans	95-98	fibromodulin	Homo sapiens	18-20
33045764-5	2021	Co-culture of the FM defect with Cx43 antisense and plug increased collagen levels but reduced GAG.	Glycosaminoglycans	95-98	gap junction protein alpha 1	Homo sapiens	33-37
33129446-5	2021	Here, we report that hLF binds to chondroitin sulfate (CS)-E, a GAG subtype involved in various neurodegenerative diseases.	Glycosaminoglycans	64-67	HLF transcription factor, PAR bZIP family member	Homo sapiens	21-24
33129446-5	2021	Here, we report that hLF binds to chondroitin sulfate (CS)-E, a GAG subtype involved in various neurodegenerative diseases.	Glycosaminoglycans	64-67	choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity)	Homo sapiens	34-60
33271281-6	2021	Moreover, interaction of MPO, which is carrying a cationic charge, with anionic glycosaminoglycans (GAGs) resulted in reduction of their relative charge.	Glycosaminoglycans	80-98	myeloperoxidase	Homo sapiens	25-28
33271281-6	2021	Moreover, interaction of MPO, which is carrying a cationic charge, with anionic glycosaminoglycans (GAGs) resulted in reduction of their relative charge.	Glycosaminoglycans	100-104	myeloperoxidase	Homo sapiens	25-28
33271281-7	2021	By means of micro-viscometry and atomic force microscopy, we disclosed that MPO can crosslink GAG chains.	Glycosaminoglycans	94-97	myeloperoxidase	Homo sapiens	76-79
33271281-12	2021	Altogether, these findings provide evidence that MPO through interaction with GAGs modulates overall charge of the GLX, causing modification of its structure and thus affecting EC function.	Glycosaminoglycans	78-82	myeloperoxidase	Homo sapiens	49-52
33319323-1	2021	Mucopolysaccharidosis type I (MPS I) is a lysosomal storage disease caused by a mutation in the IDUA gene, which codes alpha-L-iduronidase (IDUA), a lysosomal hydrolase that degrades two glycosaminoglycans (GAGs): heparan sulfate (HS) and dermatan sulfate (DS).	Glycosaminoglycans	187-205	iduronidase, alpha-L	Mus musculus	96-100
33319323-1	2021	Mucopolysaccharidosis type I (MPS I) is a lysosomal storage disease caused by a mutation in the IDUA gene, which codes alpha-L-iduronidase (IDUA), a lysosomal hydrolase that degrades two glycosaminoglycans (GAGs): heparan sulfate (HS) and dermatan sulfate (DS).	Glycosaminoglycans	187-205	iduronidase, alpha-L	Mus musculus	140-144
33319323-1	2021	Mucopolysaccharidosis type I (MPS I) is a lysosomal storage disease caused by a mutation in the IDUA gene, which codes alpha-L-iduronidase (IDUA), a lysosomal hydrolase that degrades two glycosaminoglycans (GAGs): heparan sulfate (HS) and dermatan sulfate (DS).	Glycosaminoglycans	207-211	iduronidase, alpha-L	Mus musculus	96-100
33319323-1	2021	Mucopolysaccharidosis type I (MPS I) is a lysosomal storage disease caused by a mutation in the IDUA gene, which codes alpha-L-iduronidase (IDUA), a lysosomal hydrolase that degrades two glycosaminoglycans (GAGs): heparan sulfate (HS) and dermatan sulfate (DS).	Glycosaminoglycans	207-211	iduronidase, alpha-L	Mus musculus	140-144
33164842-6	2021	RESULTS: Flavopiridol and JQ1 inhibitors act synergistically, and a combination of both almost completely prevented the activation of most IL-1beta-induced PRGs in vitro by microarray analysis, and prevented IL-1beta-induced glycosaminoglycan release from cartilage explants.	Glycosaminoglycans	225-242	interleukin 1 alpha	Mus musculus	139-147
33456569-6	2021	The glycosaminoglycan (GAG) chains of SRGN were characterized using fluorophore-assisted carbohydrate electrophoresis.	Glycosaminoglycans	23-26	serglycin	Homo sapiens	38-42
33456569-11	2021	In addition, SRGN interacted with MDK and matrix metalloproteinase 2 in ESCC via its GAG chains, which were mainly decorated with chondroitin sulfate comprising of  di-4S and  di-6S CS.	Glycosaminoglycans	85-88	serglycin	Homo sapiens	13-17
33456569-11	2021	In addition, SRGN interacted with MDK and matrix metalloproteinase 2 in ESCC via its GAG chains, which were mainly decorated with chondroitin sulfate comprising of  di-4S and  di-6S CS.	Glycosaminoglycans	85-88	matrix metallopeptidase 2	Homo sapiens	42-68
33490919-5	2021	Binding of tagged CXCL12 to either chemokine receptors or membrane glycosaminoglycans could be monitored due to the steric constraints of nanoluciferase complementation.	Glycosaminoglycans	67-85	C-X-C motif chemokine ligand 12	Homo sapiens	18-24
33490919-6	2021	Furthermore, binding of native CXCL12-HiBiT to AlexaFluor488-tagged CXCR4 chemokine receptors could also be distinguished from glycosaminoglycan binding and pharmacologically analyzed using BRET.	Glycosaminoglycans	127-144	C-X-C motif chemokine ligand 12	Homo sapiens	31-37
33328567-7	2020	Specifically, superior sustained systemic and mucosal HIV Gag-specific poly-functional/cytotoxic CD4+ and CD8+ T cells were detected with the IL-4R antagonist adjuvanted strategy compared to the unadjuvanted control.	Glycosaminoglycans	58-61	CD4 molecule	Homo sapiens	97-100
33318190-4	2020	Here, we identified sulfated GAGs as molecules that mediate prion-like behavior of p53 aggregates.	Glycosaminoglycans	29-33	tumor protein p53	Homo sapiens	83-86
33318190-5	2020	Sulfated GAGs at the cell surface were required for cellular uptake of recombinant and cancer cell-derived p53 aggregates and extracellular release of p53 from cancer cells.	Glycosaminoglycans	9-13	tumor protein p53	Homo sapiens	107-110
33318190-5	2020	Sulfated GAGs at the cell surface were required for cellular uptake of recombinant and cancer cell-derived p53 aggregates and extracellular release of p53 from cancer cells.	Glycosaminoglycans	9-13	tumor protein p53	Homo sapiens	151-154
33318190-7	2020	Finally, sulfated GAG-dependent cellular uptake of p53 aggregates was critical for subsequent extracellular release of the aggregates and gain of oncogenic function in recipient cells.	Glycosaminoglycans	18-21	tumor protein p53	Homo sapiens	51-54
33318190-8	2020	Our work provides a mechanism of prion-like behavior of p53 aggregates and will shed light on sulfated GAGs as a common mediator of prions.	Glycosaminoglycans	103-107	tumor protein p53	Homo sapiens	56-59
33414095-4	2021	The authors sought to assess the use of collagen-GAG bilayer wound matrices on STSG take for NF wounds.	Glycosaminoglycans	49-52	neurofascin	Homo sapiens	93-95
33328567-7	2020	Specifically, superior sustained systemic and mucosal HIV Gag-specific poly-functional/cytotoxic CD4+ and CD8+ T cells were detected with the IL-4R antagonist adjuvanted strategy compared to the unadjuvanted control.	Glycosaminoglycans	58-61	CD8a molecule	Homo sapiens	106-109
33328567-7	2020	Specifically, superior sustained systemic and mucosal HIV Gag-specific poly-functional/cytotoxic CD4+ and CD8+ T cells were detected with the IL-4R antagonist adjuvanted strategy compared to the unadjuvanted control.	Glycosaminoglycans	58-61	interleukin 4 receptor	Homo sapiens	142-147
33317052-0	2020	Glycosaminoglycan Modification of Decorin Depends on MMP14 Activity and Regulates Collagen Assembly.	Glycosaminoglycans	0-17	matrix metallopeptidase 14 (membrane-inserted)	Mus musculus	53-58
33287330-3	2020	The subsequent complete deficiency of alpha l-iduronidase enzyme is directly responsible of a progressive accumulation of glycosaminoglycans (GAG) in lysosomes which affects the functions of many tissues.	Glycosaminoglycans	122-140	alpha-L-iduronidase	Homo sapiens	38-57
32745937-1	2020	The impact of glycosaminoglycan (chondroitin sulphate, CS) on bone morphogenetic protein - 2 (BMP - 2) structure, stability (thermal and chemical), association kinetics and conformation was monitored by multiple spectroscopic techniques (UV-Visible, fluorescence and circular dichroism).	Glycosaminoglycans	14-31	bone morphogenetic protein 2	Homo sapiens	62-92
33159882-7	2020	As heparan sulfate modulates FGF-mediated signaling, we found a significantly decreased activation of the MAP kinases ERK1/2 in FGF-2-stimulated cell lines of affected individuals that could be restored by addition of heparin, a GAG similar to heparan sulfate.	Glycosaminoglycans	229-232	fibroblast growth factor 2	Homo sapiens	29-32
33287330-3	2020	The subsequent complete deficiency of alpha l-iduronidase enzyme is directly responsible of a progressive accumulation of glycosaminoglycans (GAG) in lysosomes which affects the functions of many tissues.	Glycosaminoglycans	142-145	alpha-L-iduronidase	Homo sapiens	38-57
32976982-1	2020	DYT1 dystonia is an inherited movement disorder caused by a heterozygous trinucleotide (GAG) deletion in DYT1/TOR1A, coding for torsinA.	Glycosaminoglycans	88-91	torsin family 1, member A (torsin A)	Mus musculus	0-4
33159882-7	2020	As heparan sulfate modulates FGF-mediated signaling, we found a significantly decreased activation of the MAP kinases ERK1/2 in FGF-2-stimulated cell lines of affected individuals that could be restored by addition of heparin, a GAG similar to heparan sulfate.	Glycosaminoglycans	229-232	mitogen-activated protein kinase 3	Homo sapiens	118-124
33159882-7	2020	As heparan sulfate modulates FGF-mediated signaling, we found a significantly decreased activation of the MAP kinases ERK1/2 in FGF-2-stimulated cell lines of affected individuals that could be restored by addition of heparin, a GAG similar to heparan sulfate.	Glycosaminoglycans	229-232	fibroblast growth factor 2	Homo sapiens	128-133
33390947-8	2020	All GAG formulations significantly reduced the production of the pro-inflammatory cytokine IL-8 under basal conditions, while no GAG treatment suppressed cytokine production under any other condition.	Glycosaminoglycans	4-7	C-X-C motif chemokine ligand 8	Homo sapiens	91-95
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
32920014-6	2020	We observed that LPA via ROCK dependent pathways transactivates the TGFBR1 to stimulate genes associated with GAG chain elongation.	Glycosaminoglycans	110-113	transforming growth factor beta receptor 1	Homo sapiens	68-74
32976982-1	2020	DYT1 dystonia is an inherited movement disorder caused by a heterozygous trinucleotide (GAG) deletion in DYT1/TOR1A, coding for torsinA.	Glycosaminoglycans	88-91	torsin family 1, member A (torsin A)	Mus musculus	105-109
32976982-1	2020	DYT1 dystonia is an inherited movement disorder caused by a heterozygous trinucleotide (GAG) deletion in DYT1/TOR1A, coding for torsinA.	Glycosaminoglycans	88-91	torsin family 1, member A (torsin A)	Mus musculus	110-115
32976982-1	2020	DYT1 dystonia is an inherited movement disorder caused by a heterozygous trinucleotide (GAG) deletion in DYT1/TOR1A, coding for torsinA.	Glycosaminoglycans	88-91	torsin family 1, member A (torsin A)	Mus musculus	128-135
32715779-13	2020	(p < .05) GAG content, chondrogenic protein and gene expression level of SOX-9, COL-II, ACAN, and HIF pathway related gene (HIF-1alpha) were significantly higher in IGF-1 PLGA/PDA/PCL scaffolds group compared to other groups.	Glycosaminoglycans	10-13	insulin like growth factor 1	Homo sapiens	165-170
33218277-5	2020	The ability of rAAV9-UPII-TK-EGFP to penetrate the glycosaminoglycan (GAG) layer on the surface of bladder cells and to transduce the bladder cells in vivo was very high.	Glycosaminoglycans	51-68	uroplakin 2	Homo sapiens	21-25
33218277-5	2020	The ability of rAAV9-UPII-TK-EGFP to penetrate the glycosaminoglycan (GAG) layer on the surface of bladder cells and to transduce the bladder cells in vivo was very high.	Glycosaminoglycans	70-73	uroplakin 2	Homo sapiens	21-25
33357723-5	2020	The results showed that quercetin significantly up-regulated the expression of chondrogenesis genes and stimulated the secretion of GAG (glycosaminoglycan) through activating the ERK, P38 and AKT signalling pathways in a dose-dependent manner.	Glycosaminoglycans	137-154	Eph receptor B1	Rattus norvegicus	179-182
33357723-5	2020	The results showed that quercetin significantly up-regulated the expression of chondrogenesis genes and stimulated the secretion of GAG (glycosaminoglycan) through activating the ERK, P38 and AKT signalling pathways in a dose-dependent manner.	Glycosaminoglycans	137-154	mitogen activated protein kinase 14	Rattus norvegicus	184-187
32919534-1	2020	Chondroitin sulfate (CS) is one of the major and widespread glycosaminoglycans, a family of structurally complex, linear, anionic hetero-co-polysaccharides.	Glycosaminoglycans	60-78	citrate synthase	Homo sapiens	21-23
33324681-4	2020	While GAG-PrP interactions had been previously reported, the specific glycan structures that facilitate interactions with different regions of PrP and their binding kinetics have not been systematically investigated.	Glycosaminoglycans	6-9	prion protein	Mus musculus	10-13
33324681-6	2020	Additionally, we found the specific structural determinants required for GAG binding to the four PrP constructs with chemically defined derivatives of heparin and other GAGs by an SPR competition assay.	Glycosaminoglycans	73-76	prion protein	Mus musculus	97-100
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
33002580-2	2020	In this study, we showed the effect of biglycan (Bgn), a small leucine-rich proteoglycan enriched in extracellular matrix of bone and the associated GAG subtype, chondroitin sulfate (CS), on the toughness of bone in vivo, using wild-type (WT) and Bgn deficient mice.	Glycosaminoglycans	149-152	biglycan	Mus musculus	39-47
33002580-2	2020	In this study, we showed the effect of biglycan (Bgn), a small leucine-rich proteoglycan enriched in extracellular matrix of bone and the associated GAG subtype, chondroitin sulfate (CS), on the toughness of bone in vivo, using wild-type (WT) and Bgn deficient mice.	Glycosaminoglycans	149-152	biglycan	Mus musculus	49-52
33002580-3	2020	The amount of total GAGs and CS in the mineralized compartment of Bgn KO mouse bone matrix decreased significantly, associated with the reduction of the toughness of bone, in comparison with those of WT mice.	Glycosaminoglycans	20-24	biglycan	Mus musculus	66-69
33198351-1	2020	The lysosomal storage disorder, mucopolysaccharidosis I (MPSI), results from mutations in IDUA, the gene that encodes the glycosaminoglycan-degrading enzyme alpha-L-iduronidase.	Glycosaminoglycans	122-139	alpha-L-iduronidase	Homo sapiens	90-94
33198351-1	2020	The lysosomal storage disorder, mucopolysaccharidosis I (MPSI), results from mutations in IDUA, the gene that encodes the glycosaminoglycan-degrading enzyme alpha-L-iduronidase.	Glycosaminoglycans	122-139	alpha-L-iduronidase	Homo sapiens	157-176
32763434-5	2020	Subsequently, released IGF-1 from Coa could effectively induce chondrogenic differentiation of embedded ADSCs in the hydrogel, by showing enhanced glycosaminoglycan deposition and expression of chondrogenesis-associated genes.	Glycosaminoglycans	147-164	insulin like growth factor 1	Homo sapiens	23-28
33187224-0	2020	Molecular Changes in Dengue Envelope Protein Domain III upon Interaction with Glycosaminoglycans.	Glycosaminoglycans	78-96	envelope protein domain iii	None	28-55
32771428-4	2020	BmNPV/SAG-SRS-Gag was expressed in silkworms and characterized.	Glycosaminoglycans	14-17	S-antigen visual arrestin	Homo sapiens	6-9
32580029-12	2020	Knocking-down plectin impacted on pathways reported to have a role in OA, including Wnt signalling, glycosaminoglycan biosynthesis and immune regulation.	Glycosaminoglycans	100-117	plectin	Homo sapiens	14-21
32868072-1	2020	Pleotropic growth factor, transforming growth factor (TGF)-beta drives the modification and elongation of glycosaminoglycan (GAG) chains on proteoglycans.	Glycosaminoglycans	106-123	transforming growth factor alpha	Homo sapiens	26-63
32868072-1	2020	Pleotropic growth factor, transforming growth factor (TGF)-beta drives the modification and elongation of glycosaminoglycan (GAG) chains on proteoglycans.	Glycosaminoglycans	125-128	transforming growth factor alpha	Homo sapiens	26-63
32868072-3	2020	We have identified that phosphorylation of Smad2 linker region drives GAG chain modification.	Glycosaminoglycans	70-73	SMAD family member 2	Homo sapiens	43-48
32868072-4	2020	The identification of an inhibitor of Smad2 linker region phosphorylation and GAG chain modification signifies a potential therapeutic for cardiovascular diseases.	Glycosaminoglycans	78-81	SMAD family member 2	Homo sapiens	38-43
33131383-6	2020	There are two glycosaminoglycan attachment domains CSalpha and CSbeta.	Glycosaminoglycans	14-31	chorionic somatomammotropin hormone 1	Homo sapiens	51-58
33131383-6	2020	There are two glycosaminoglycan attachment domains CSalpha and CSbeta.	Glycosaminoglycans	14-31	chorionic somatomammotropin hormone 1	Homo sapiens	63-69
33424000-14	2020	Degenerated mucopolysaccharide may be a precursor of nitrogen or "the gas itself" in DH-CoG.	Glycosaminoglycans	12-30	gastrin	Homo sapiens	70-73
32621519-2	2020	FGE is necessary for the activation of sulfatases, a family of enzymes that are involved in the degradation of sulfated substrates such as glycosaminoglycans and sulfolipids.	Glycosaminoglycans	139-157	sulfatase modifying factor 1	Homo sapiens	0-3
33115953-6	2020	When Ad-MKX-transduced MSCs were seeded on TGF-beta3-conjugated decellularized meniscus scaffold (DMS) and inserted into experimental tears in meniscus explants, they increased glycosaminoglycan content, extracellular matrix interconnectivity, cell infiltration into the DMS, and improved biomechanical properties.	Glycosaminoglycans	177-194	mohawk homeobox	Mus musculus	8-11
33126404-0	2020	Systemic Glycosaminoglycan Clearance by HARE/Stabilin-2 Activates Intracellular Signaling.	Glycosaminoglycans	9-26	stabilin 2	Homo sapiens	45-55
33126404-9	2020	This review focuses on the HARE-mediated GAG activation of intracellular signaling, particularly the Extracellular Signal-Regulated Kinase 1/2 pathway.	Glycosaminoglycans	41-44	mitogen-activated protein kinase 1	Homo sapiens	101-142
33138172-0	2020	A Versatile Macromer-Based Glycosaminoglycan (sHA3) Decorated Biomaterial for Pro-Osteogenic Scavenging of Wnt Antagonists.	Glycosaminoglycans	27-44	Wnt family member 3A	Homo sapiens	107-110
33115953-6	2020	When Ad-MKX-transduced MSCs were seeded on TGF-beta3-conjugated decellularized meniscus scaffold (DMS) and inserted into experimental tears in meniscus explants, they increased glycosaminoglycan content, extracellular matrix interconnectivity, cell infiltration into the DMS, and improved biomechanical properties.	Glycosaminoglycans	177-194	transforming growth factor beta 3	Homo sapiens	43-52
33192558-0	2020	Cyclooxygenase-2 Modulates Glycosaminoglycan Production in the Skin During Salt Overload.	Glycosaminoglycans	27-44	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	0-16
33192558-4	2020	A link between the COX-2/PGE2 system and GAG synthesis was also suggested.	Glycosaminoglycans	41-44	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	19-24
33192558-12	2020	In conclusion, high-salt environment could induce GAG production of DFs in a COX-2/PGE2-dependent manner.	Glycosaminoglycans	50-53	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	77-82
33192558-6	2020	Our further aim was to demonstrate that the elevation of the GAG content is ceased by COX-2 inhibition in a salt overloaded animal model.	Glycosaminoglycans	61-64	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	86-91
33192558-13	2020	Moreover, the COX-2 inhibition resulted in a decreased skin GAG content of the salt overloaded rats.	Glycosaminoglycans	60-63	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	14-19
33050659-10	2020	We conclude that PTGs of cmiRNA-1246 and key pathways, namely, ubiquitin-mediated proteolysis, glycosaminoglycan binding, the DNA metabolic process, and the PI3K-Akt-mTOR signaling pathway, the neurotrophin and cardiomyopathy signaling pathway, and the MAPK signaling pathway provide new insights on a noninvasive prognostic biomarker for LUAD.	Glycosaminoglycans	95-112	brain derived neurotrophic factor	Homo sapiens	194-206
33090996-9	2020	This SV interrupted UDP-glucose 6-dehydrogenase (UGDH), a gene involved in the biosynthesis of glycosaminoglycans.	Glycosaminoglycans	95-113	UDP-glucose 6-dehydrogenase	Felis catus	20-47
33090996-9	2020	This SV interrupted UDP-glucose 6-dehydrogenase (UGDH), a gene involved in the biosynthesis of glycosaminoglycans.	Glycosaminoglycans	95-113	UDP-glucose 6-dehydrogenase	Felis catus	49-53
33050843-4	2022	Recent experimental findings insinuate that heparan sulphate (HS), a glycosaminoglycans, exhibits binding with SAA1 to promote its aggregation.	Glycosaminoglycans	69-87	serum amyloid A1	Homo sapiens	111-115
32979832-5	2020	However, this protective effect diminished quickly after seven days, followed by a rapid reduction of GAG-specific CD8+T cell number and activity, and viral persistence.	Glycosaminoglycans	102-105	CD8a molecule	Homo sapiens	115-118
32589819-4	2020	Reported herein is a nanoscale covalent organic framework (NCOF)-based nanoagent, namely CaCO 3 @COF-BODIPY-2I@GAG ( 4 ), which is embedded with CaCO 3 nanoparticle (NP) and surface decorated with BODIPY-2I as photosensitizer (PS) and glycosaminoglycan (GAG) targeting agent for CD44 receptors on the digestive tract tumor cells.	Glycosaminoglycans	111-114	CD44 molecule (Indian blood group)	Homo sapiens	279-283
32822214-5	2020	Furthermore, we showed by real-time PCR that this dimension modification of endothelial glycocalyx may be attributed to a significant downregulation of heparan sulfate proteoglycan (HSPG)-related genes, including syndecan-3, glypican-1, and EXT1, not resulting from an enhanced shedding of sulfated glycosaminoglycans (sGAGs) from the vessel wall to the plasma.	Glycosaminoglycans	299-317	syndecan 3	Rattus norvegicus	213-223
32822214-5	2020	Furthermore, we showed by real-time PCR that this dimension modification of endothelial glycocalyx may be attributed to a significant downregulation of heparan sulfate proteoglycan (HSPG)-related genes, including syndecan-3, glypican-1, and EXT1, not resulting from an enhanced shedding of sulfated glycosaminoglycans (sGAGs) from the vessel wall to the plasma.	Glycosaminoglycans	299-317	glypican 1	Rattus norvegicus	225-235
32822214-5	2020	Furthermore, we showed by real-time PCR that this dimension modification of endothelial glycocalyx may be attributed to a significant downregulation of heparan sulfate proteoglycan (HSPG)-related genes, including syndecan-3, glypican-1, and EXT1, not resulting from an enhanced shedding of sulfated glycosaminoglycans (sGAGs) from the vessel wall to the plasma.	Glycosaminoglycans	299-317	exostosin glycosyltransferase 1	Rattus norvegicus	241-245
33072082-3	2020	CD160+ CD8+ T cells derived from HIV+ patients correlated with slow progressions both in a cross-sectional study and in a 60-month longitudinal cohort, displaying enhanced cytotoxicity and proliferative capacity in response to HIV Gag stimulation; triggering CD160 promoted their functionalities through MEK-ERK and PI3K-AKT pathways.	Glycosaminoglycans	231-234	CD160 molecule	Homo sapiens	0-5
32483835-0	2020	Glycosaminoglycans bind human IL-27 and regulate its activity.	Glycosaminoglycans	0-18	interleukin 27	Homo sapiens	30-35
32483835-4	2020	Here, we show that different glycosaminoglycans (GAGs) modulate human IL-27 activity in vitro.	Glycosaminoglycans	29-47	interleukin 27	Homo sapiens	70-75
32827291-1	2020	beta1,4-galactosyltransferase 4 (B4GalT4) is one of seven B4GalTs that belong to CAZy glycosyltransferase family 7 and transfer galactose to growing sugar moieties of proteins, glycolipids, glycosaminoglycans as well as single sugar for lactose synthesis.	Glycosaminoglycans	190-208	beta-1,4-galactosyltransferase 4	Homo sapiens	0-31
32827291-1	2020	beta1,4-galactosyltransferase 4 (B4GalT4) is one of seven B4GalTs that belong to CAZy glycosyltransferase family 7 and transfer galactose to growing sugar moieties of proteins, glycolipids, glycosaminoglycans as well as single sugar for lactose synthesis.	Glycosaminoglycans	190-208	beta-1,4-galactosyltransferase 4	Homo sapiens	33-40
32162324-5	2020	Moreover, loss of OC and OPN compromises the extracellular matrix integrity and maturation, observed by an unexpected enhancement of glycosaminoglycans content that are associated with a more primitive skeletal connective tissue, and by a delay on the maturation of mineral species produced.	Glycosaminoglycans	133-151	bone gamma-carboxyglutamate protein 2	Mus musculus	18-20
32162324-5	2020	Moreover, loss of OC and OPN compromises the extracellular matrix integrity and maturation, observed by an unexpected enhancement of glycosaminoglycans content that are associated with a more primitive skeletal connective tissue, and by a delay on the maturation of mineral species produced.	Glycosaminoglycans	133-151	secreted phosphoprotein 1	Mus musculus	25-28
32992671-5	2020	We observed an anabolic response in NP cells treated with recombinant GDF6 (increased expression of matrix and NP-phenotypic markers; increased glycosaminoglycan production; no change in catabolic enzyme expression), and identified the signalling pathways involved in these responses (SMAD1/5/8 and ERK1/2 phosphorylation, validated by blocking studies).	Glycosaminoglycans	144-161	growth differentiation factor 6	Homo sapiens	70-74
32948012-3	2020	We report that the ESCRT proteins transiently co-localize with virions after completion of virion assembly for durations of 45 +- 30 s. We show that mutagenizing the YP domain of Gag which is the primary ALIX binding site or depleting ALIX from cells results in multiple recruitments of the full ESCRT machinery on the same virion (referred to as stuttering where the number of recruitments to the same virion >3).	Glycosaminoglycans	179-182	programmed cell death 6 interacting protein	Homo sapiens	204-208
32948012-3	2020	We report that the ESCRT proteins transiently co-localize with virions after completion of virion assembly for durations of 45 +- 30 s. We show that mutagenizing the YP domain of Gag which is the primary ALIX binding site or depleting ALIX from cells results in multiple recruitments of the full ESCRT machinery on the same virion (referred to as stuttering where the number of recruitments to the same virion >3).	Glycosaminoglycans	179-182	programmed cell death 6 interacting protein	Homo sapiens	235-239
32828295-5	2020	One clonal line, named ASC52telo-SOX9, displayed increased GAG and type II collagen synthesis and was found to be responsive to both mechanical and inflammatory stimuli in a manner similar to native chondrocytes.	Glycosaminoglycans	59-62	SRY-box transcription factor 9	Homo sapiens	33-37
33072082-3	2020	CD160+ CD8+ T cells derived from HIV+ patients correlated with slow progressions both in a cross-sectional study and in a 60-month longitudinal cohort, displaying enhanced cytotoxicity and proliferative capacity in response to HIV Gag stimulation; triggering CD160 promoted their functionalities through MEK-ERK and PI3K-AKT pathways.	Glycosaminoglycans	231-234	CD8a molecule	Homo sapiens	7-10
33072082-3	2020	CD160+ CD8+ T cells derived from HIV+ patients correlated with slow progressions both in a cross-sectional study and in a 60-month longitudinal cohort, displaying enhanced cytotoxicity and proliferative capacity in response to HIV Gag stimulation; triggering CD160 promoted their functionalities through MEK-ERK and PI3K-AKT pathways.	Glycosaminoglycans	231-234	CD160 molecule	Homo sapiens	259-264
33072082-3	2020	CD160+ CD8+ T cells derived from HIV+ patients correlated with slow progressions both in a cross-sectional study and in a 60-month longitudinal cohort, displaying enhanced cytotoxicity and proliferative capacity in response to HIV Gag stimulation; triggering CD160 promoted their functionalities through MEK-ERK and PI3K-AKT pathways.	Glycosaminoglycans	231-234	mitogen-activated protein kinase kinase 7	Homo sapiens	304-307
33072082-3	2020	CD160+ CD8+ T cells derived from HIV+ patients correlated with slow progressions both in a cross-sectional study and in a 60-month longitudinal cohort, displaying enhanced cytotoxicity and proliferative capacity in response to HIV Gag stimulation; triggering CD160 promoted their functionalities through MEK-ERK and PI3K-AKT pathways.	Glycosaminoglycans	231-234	mitogen-activated protein kinase 1	Homo sapiens	308-311
33072082-3	2020	CD160+ CD8+ T cells derived from HIV+ patients correlated with slow progressions both in a cross-sectional study and in a 60-month longitudinal cohort, displaying enhanced cytotoxicity and proliferative capacity in response to HIV Gag stimulation; triggering CD160 promoted their functionalities through MEK-ERK and PI3K-AKT pathways.	Glycosaminoglycans	231-234	AKT serine/threonine kinase 1	Homo sapiens	321-324
32982525-8	2020	Glycosaminoglycan-related pathways were significantly upregulated in the EGFR mutant group.	Glycosaminoglycans	0-17	epidermal growth factor receptor	Homo sapiens	73-77
32993972-11	2020	Taken together, this study demonstrates that the RALA-siMMP-9 activated Col/GAG scaffolds possess high potential as a promising regenerative platform for improved DFU healing.	Glycosaminoglycans	76-79	RAS like proto-oncogene A	Homo sapiens	49-53
32993972-3	2020	To fulfil this aim, collagen/GAG (Col/GAG) scaffolds activated by MMP-9-targeting siRNA (siMMP-9) were developed in this study.	Glycosaminoglycans	29-32	matrix metallopeptidase 9	Homo sapiens	66-71
32993972-3	2020	To fulfil this aim, collagen/GAG (Col/GAG) scaffolds activated by MMP-9-targeting siRNA (siMMP-9) were developed in this study.	Glycosaminoglycans	38-41	matrix metallopeptidase 9	Homo sapiens	66-71
32843678-7	2020	The Akt inhibitor suppressed the enhancement of GAG production induced by TD-198946.	Glycosaminoglycans	48-51	thymoma viral proto-oncogene 1	Mus musculus	4-7
32993972-8	2020	In the 3D culture of fibroblasts, the siMMP-9 activated Col/GAG scaffolds displayed excellent cytocompatibility and ~60% and 40% MMP-9 gene downregulation in low and high glucose culture, respectively.	Glycosaminoglycans	60-63	matrix metallopeptidase 9	Homo sapiens	40-45
32983121-7	2020	In contrast, immunizations with the Gag/Env vaccine persistently increased the levels of multiple cytokines/chemokines.	Glycosaminoglycans	36-39	endogenous retrovirus group W member 1, envelope	Homo sapiens	40-43
32983121-10	2020	18 weeks after final boost with a higher dosage, IP-10 levels (P = 0.0313) in the Gag/Env group remained higher than baseline.	Glycosaminoglycans	82-85	C-X-C motif chemokine ligand 10	Homo sapiens	49-54
32983121-10	2020	18 weeks after final boost with a higher dosage, IP-10 levels (P = 0.0313) in the Gag/Env group remained higher than baseline.	Glycosaminoglycans	82-85	endogenous retrovirus group W member 1, envelope	Homo sapiens	86-89
32641479-9	2020	Here, we show that P50, generated from an alternatively spliced RNA encoded in gag, counteracts APOBEC3 by blocking its packaging.	Glycosaminoglycans	79-82	apolipoprotein B mRNA editing enzyme, catalytic polypeptide 3	Mus musculus	96-103
32843678-11	2020	TD-198946 exhibited therapeutic effects on IDD by enhancing GAG production via PI3K/Akt signaling.	Glycosaminoglycans	60-63	thymoma viral proto-oncogene 1	Mus musculus	84-87
32846949-2	2020	In bacterial sepsis, PF4 binds to glycosaminoglycans (GAGs) on the surface of aerobic bacteria, giving rise to an antigenic complex that induces the early formation of anti-PF4 IgG-IgA-IgM.	Glycosaminoglycans	34-52	platelet factor 4	Homo sapiens	21-24
32923824-10	2020	As the residues R18, R24, and K49 of hCCL2 are crucial determinants of monocyte trafficking through receptor/glycosaminoglycans (GAG) binding in CCL2 human/murine orthologs, we propose that baicalin engaging these residues in complex formation will result in attenuation of CCL2 binding to the receptor/GAGs, thus inhibiting the chemokine-regulated leukocyte trafficking.	Glycosaminoglycans	109-127	C-C motif chemokine ligand 2	Homo sapiens	37-42
32923824-10	2020	As the residues R18, R24, and K49 of hCCL2 are crucial determinants of monocyte trafficking through receptor/glycosaminoglycans (GAG) binding in CCL2 human/murine orthologs, we propose that baicalin engaging these residues in complex formation will result in attenuation of CCL2 binding to the receptor/GAGs, thus inhibiting the chemokine-regulated leukocyte trafficking.	Glycosaminoglycans	109-127	C-C motif chemokine ligand 2	Homo sapiens	38-42
32923824-10	2020	As the residues R18, R24, and K49 of hCCL2 are crucial determinants of monocyte trafficking through receptor/glycosaminoglycans (GAG) binding in CCL2 human/murine orthologs, we propose that baicalin engaging these residues in complex formation will result in attenuation of CCL2 binding to the receptor/GAGs, thus inhibiting the chemokine-regulated leukocyte trafficking.	Glycosaminoglycans	109-127	chemokine (C-C motif) ligand 2	Mus musculus	145-149
32923824-10	2020	As the residues R18, R24, and K49 of hCCL2 are crucial determinants of monocyte trafficking through receptor/glycosaminoglycans (GAG) binding in CCL2 human/murine orthologs, we propose that baicalin engaging these residues in complex formation will result in attenuation of CCL2 binding to the receptor/GAGs, thus inhibiting the chemokine-regulated leukocyte trafficking.	Glycosaminoglycans	129-132	C-C motif chemokine ligand 2	Homo sapiens	37-42
32923824-10	2020	As the residues R18, R24, and K49 of hCCL2 are crucial determinants of monocyte trafficking through receptor/glycosaminoglycans (GAG) binding in CCL2 human/murine orthologs, we propose that baicalin engaging these residues in complex formation will result in attenuation of CCL2 binding to the receptor/GAGs, thus inhibiting the chemokine-regulated leukocyte trafficking.	Glycosaminoglycans	129-132	C-C motif chemokine ligand 2	Homo sapiens	38-42
32923824-10	2020	As the residues R18, R24, and K49 of hCCL2 are crucial determinants of monocyte trafficking through receptor/glycosaminoglycans (GAG) binding in CCL2 human/murine orthologs, we propose that baicalin engaging these residues in complex formation will result in attenuation of CCL2 binding to the receptor/GAGs, thus inhibiting the chemokine-regulated leukocyte trafficking.	Glycosaminoglycans	129-132	chemokine (C-C motif) ligand 2	Mus musculus	145-149
32790806-5	2020	RESULTS: Chondrogenesis in MSCs was consistently and strongly induced in collagen I hydrogels by the transgenes SOX9, TGFB1 and BMP2 as evidenced by positive staining for proteoglycans, chondroitin-4-sulfate (CS4) and collagen (COL) type II, increased levels of glycosaminoglycan (GAG) synthesis, and expression of mRNAs associated with chondrogenesis.	Glycosaminoglycans	281-284	bone morphogenetic protein 2	Homo sapiens	128-132
32820216-7	2020	Notably, RhCMV-Gag and RhCMV-Env vaccines elicited anti-Gag and anti-Env antibodies in RhCMV-seronegative RM, an unexpected contrast to vaccination of RhCMV-seropositive RM.	Glycosaminoglycans	15-18	endogenous retrovirus group K member 20	Homo sapiens	69-72
32824699-3	2020	Previous reports have suggested that the glycosaminoglycan heparin is a ligand for the natural cytotoxicity receptors NKp30, NKp44 (human), and NKp46 (both human and mouse).	Glycosaminoglycans	41-58	natural cytotoxicity triggering receptor 3	Homo sapiens	118-123
32824699-3	2020	Previous reports have suggested that the glycosaminoglycan heparin is a ligand for the natural cytotoxicity receptors NKp30, NKp44 (human), and NKp46 (both human and mouse).	Glycosaminoglycans	41-58	natural cytotoxicity triggering receptor 2	Homo sapiens	125-130
32824699-3	2020	Previous reports have suggested that the glycosaminoglycan heparin is a ligand for the natural cytotoxicity receptors NKp30, NKp44 (human), and NKp46 (both human and mouse).	Glycosaminoglycans	41-58	natural cytotoxicity triggering receptor 1	Homo sapiens	144-149
32855969-13	2020	TIMP-1 (an ADAMTS inhibitor) and TIMP-1 combined with the sIL-13Ralpha2-Fc intervention increased the levels of GAG and HA, inhibited the expression of type I collagen, and promoted the expression of type II collagen.	Glycosaminoglycans	112-115	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	0-6
32855969-13	2020	TIMP-1 (an ADAMTS inhibitor) and TIMP-1 combined with the sIL-13Ralpha2-Fc intervention increased the levels of GAG and HA, inhibited the expression of type I collagen, and promoted the expression of type II collagen.	Glycosaminoglycans	112-115	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	33-39
32855969-14	2020	Conclusion: Adamts8 may participate in the degradation of ECM components such as GAG and HA and lead to an imbalance in the ECM of the intervertebral disc, resulting in intervertebral disc degeneration.	Glycosaminoglycans	81-84	ADAM metallopeptidase with thrombospondin type 1 motif, 8	Rattus norvegicus	12-19
32790806-5	2020	RESULTS: Chondrogenesis in MSCs was consistently and strongly induced in collagen I hydrogels by the transgenes SOX9, TGFB1 and BMP2 as evidenced by positive staining for proteoglycans, chondroitin-4-sulfate (CS4) and collagen (COL) type II, increased levels of glycosaminoglycan (GAG) synthesis, and expression of mRNAs associated with chondrogenesis.	Glycosaminoglycans	262-279	bone morphogenetic protein 2	Homo sapiens	128-132
32751752-1	2020	We recently developed a blood-brain barrier (BBB)-penetrating enzyme transport vehicle (ETV) fused to the lysosomal enzyme iduronate 2-sulfatase (ETV:IDS) and demonstrated its ability to reduce glycosaminoglycan (GAG) accumulation in the brains of a mouse model of mucopolysaccharidosis (MPS) II.	Glycosaminoglycans	194-211	iduronate 2-sulfatase	Mus musculus	123-144
32986582-5	2020	RESULTS: In the in vitro analysis, cells treated with experimental media containing TGF-beta3, BMP-4, and TIMP-2 exhibited staining indicative of GAG production and began to exhibit a chondrocytic morphology.	Glycosaminoglycans	146-149	bone morphogenetic protein 4	Oryctolagus cuniculus	95-100
32986582-5	2020	RESULTS: In the in vitro analysis, cells treated with experimental media containing TGF-beta3, BMP-4, and TIMP-2 exhibited staining indicative of GAG production and began to exhibit a chondrocytic morphology.	Glycosaminoglycans	146-149	metalloproteinase inhibitor 2	Oryctolagus cuniculus	106-112
32631737-1	2020	Mucopolysaccharidosis type II (MPS II) is a lysosomal storage disease (LSD) caused by a deficiency of the iduronate-2-sulfatase (IDS) that catabolizes glycosaminoglycans (GAGs).	Glycosaminoglycans	151-169	iduronate 2-sulfatase	Mus musculus	129-132
32784891-3	2020	We reasoned that the synthetic non-sugar mimetics of glycosaminoglycans may inhibit MMP-8 because natural glycosaminoglycans are known to modulate the functions of various MMPs.	Glycosaminoglycans	53-71	matrix metallopeptidase 8	Homo sapiens	84-89
32784891-3	2020	We reasoned that the synthetic non-sugar mimetics of glycosaminoglycans may inhibit MMP-8 because natural glycosaminoglycans are known to modulate the functions of various MMPs.	Glycosaminoglycans	53-71	matrix metallopeptidase 8	Homo sapiens	172-176
32784891-3	2020	We reasoned that the synthetic non-sugar mimetics of glycosaminoglycans may inhibit MMP-8 because natural glycosaminoglycans are known to modulate the functions of various MMPs.	Glycosaminoglycans	106-124	matrix metallopeptidase 8	Homo sapiens	84-89
32784891-3	2020	We reasoned that the synthetic non-sugar mimetics of glycosaminoglycans may inhibit MMP-8 because natural glycosaminoglycans are known to modulate the functions of various MMPs.	Glycosaminoglycans	106-124	matrix metallopeptidase 8	Homo sapiens	172-176
32784891-8	2020	Overall, this work provides the first proof that the sulfated mimetics of glycosaminoglycans could lead to potent, selective, and catalytic activity-tunable, small molecular inhibitors of MMP-8.	Glycosaminoglycans	74-92	matrix metallopeptidase 8	Homo sapiens	188-193
32591402-4	2020	We isolated Gag- and Nef-specific CTL clones with different TCR sequences from the PBMC of donors in acute and chronic infection.	Glycosaminoglycans	12-15	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	60-63
32751752-1	2020	We recently developed a blood-brain barrier (BBB)-penetrating enzyme transport vehicle (ETV) fused to the lysosomal enzyme iduronate 2-sulfatase (ETV:IDS) and demonstrated its ability to reduce glycosaminoglycan (GAG) accumulation in the brains of a mouse model of mucopolysaccharidosis (MPS) II.	Glycosaminoglycans	213-216	iduronate 2-sulfatase	Mus musculus	123-144
32664967-0	2020	FAM20B-catalyzed glycosaminoglycans control murine tooth number by restricting FGFR2b signaling.	Glycosaminoglycans	17-35	FAM20B, glycosaminoglycan xylosylkinase	Mus musculus	0-6
32709038-6	2020	The NEC-1 microbiome had increased glycosaminoglycan degradation and lysosome activity by the first 10-days of life, and was more sensitive to childbirth, low birth weight and gestational age, than healthy microbiome.	Glycosaminoglycans	35-52	proprotein convertase subtilisin/kexin type 1	Homo sapiens	4-9
32664967-3	2020	RESULTS: In this study, we present evidence that disrupting glycosaminoglycans (GAGs) in the dental epithelium of mice by inactivating FAM20B, a xylose kinase essential for GAG assembly, leads to supernumerary tooth formation in a pattern reminiscent of replacement teeth.	Glycosaminoglycans	60-78	FAM20B, glycosaminoglycan xylosylkinase	Mus musculus	135-141
32664967-3	2020	RESULTS: In this study, we present evidence that disrupting glycosaminoglycans (GAGs) in the dental epithelium of mice by inactivating FAM20B, a xylose kinase essential for GAG assembly, leads to supernumerary tooth formation in a pattern reminiscent of replacement teeth.	Glycosaminoglycans	80-84	FAM20B, glycosaminoglycan xylosylkinase	Mus musculus	135-141
32664967-3	2020	RESULTS: In this study, we present evidence that disrupting glycosaminoglycans (GAGs) in the dental epithelium of mice by inactivating FAM20B, a xylose kinase essential for GAG assembly, leads to supernumerary tooth formation in a pattern reminiscent of replacement teeth.	Glycosaminoglycans	80-83	FAM20B, glycosaminoglycan xylosylkinase	Mus musculus	135-141
32664967-4	2020	The dental epithelial GAGs confine murine tooth number by restricting the homeostasis of Sox2(+) dental epithelial stem/progenitor cells in a non-autonomous manner.	Glycosaminoglycans	22-26	SRY (sex determining region Y)-box 2	Mus musculus	89-93
32664967-5	2020	FAM20B-catalyzed GAGs regulate the cell fate of dental lamina by restricting FGFR2b signaling at the initial stage of tooth development to maintain a subtle balance between the renewal and differentiation of Sox2(+) cells.	Glycosaminoglycans	17-21	FAM20B, glycosaminoglycan xylosylkinase	Mus musculus	0-6
32664967-5	2020	FAM20B-catalyzed GAGs regulate the cell fate of dental lamina by restricting FGFR2b signaling at the initial stage of tooth development to maintain a subtle balance between the renewal and differentiation of Sox2(+) cells.	Glycosaminoglycans	17-21	SRY (sex determining region Y)-box 2	Mus musculus	208-212
32181981-7	2020	Culture with IL-1beta (10 ng/ml) decreased pellet size and DNA amount, and severely compromised glycosaminoglycan (GAG) and collagen content.	Glycosaminoglycans	96-113	interleukin 1 alpha	Homo sapiens	13-21
33005889-5	2020	Here we confirm that dextran sulphate, a sulphated glycosaminoglycan, induces the assembly of recombinant tau protein into filaments in vitro.	Glycosaminoglycans	51-68	microtubule associated protein tau	Homo sapiens	106-109
32647227-0	2020	Therapeutic vaccine-mediated Gag-specific CD8+ T-cell induction under anti-retroviral therapy augments anti-virus efficacy of CD8+ cells in simian immunodeficiency virus-infected macaques.	Glycosaminoglycans	29-32	CD8a molecule	Homo sapiens	42-45
32647227-0	2020	Therapeutic vaccine-mediated Gag-specific CD8+ T-cell induction under anti-retroviral therapy augments anti-virus efficacy of CD8+ cells in simian immunodeficiency virus-infected macaques.	Glycosaminoglycans	29-32	CD8a molecule	Homo sapiens	126-129
32647227-8	2020	In the vaccinated animals, the anti-SIV efficacy of CD8+ cells at week 34 was correlated positively with Gag-specific CD8+ T-cell frequencies and inversely with rebound viral loads at week 34.	Glycosaminoglycans	105-108	CD8a molecule	Homo sapiens	52-55
32647227-8	2020	In the vaccinated animals, the anti-SIV efficacy of CD8+ cells at week 34 was correlated positively with Gag-specific CD8+ T-cell frequencies and inversely with rebound viral loads at week 34.	Glycosaminoglycans	105-108	CD8a molecule	Homo sapiens	118-121
32556741-2	2020	The binding occurs through a multimeric positively-charged motif of NT4 that interacts with negatively charged motives in both glycosaminoglycans and LRP receptors.	Glycosaminoglycans	127-145	neurotrophin 4	Homo sapiens	68-71
32181981-7	2020	Culture with IL-1beta (10 ng/ml) decreased pellet size and DNA amount, and severely compromised glycosaminoglycan (GAG) and collagen content.	Glycosaminoglycans	115-118	interleukin 1 alpha	Homo sapiens	13-21
32616241-6	2020	The results of entropy analysis of the sequences of gag, pol, and env revealed that the env gene had the largest variation, and the gag gene nonconserved sites are mainly concentrated in p19, p10, and p12.	Glycosaminoglycans	52-55	endogenous retrovirus group K member 20	Homo sapiens	88-91
32439268-1	2020	Mucopolysaccharidosis type I (MPS-I), a lysosomal storage disorder caused by a deficiency of alpha-L-iduronidase enzyme, results in the progressive accumulation of glycosaminoglycans and consequent multiorgan dysfunction.	Glycosaminoglycans	164-182	iduronidase, alpha-L	Mus musculus	93-112
32616241-6	2020	The results of entropy analysis of the sequences of gag, pol, and env revealed that the env gene had the largest variation, and the gag gene nonconserved sites are mainly concentrated in p19, p10, and p12.	Glycosaminoglycans	52-55	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	201-204
32616241-6	2020	The results of entropy analysis of the sequences of gag, pol, and env revealed that the env gene had the largest variation, and the gag gene nonconserved sites are mainly concentrated in p19, p10, and p12.	Glycosaminoglycans	132-135	endogenous retrovirus group K member 20	Homo sapiens	66-69
32616241-6	2020	The results of entropy analysis of the sequences of gag, pol, and env revealed that the env gene had the largest variation, and the gag gene nonconserved sites are mainly concentrated in p19, p10, and p12.	Glycosaminoglycans	132-135	interleukin 23 subunit alpha	Homo sapiens	187-190
32616241-6	2020	The results of entropy analysis of the sequences of gag, pol, and env revealed that the env gene had the largest variation, and the gag gene nonconserved sites are mainly concentrated in p19, p10, and p12.	Glycosaminoglycans	132-135	S100 calcium binding protein A10	Homo sapiens	192-195
32616241-6	2020	The results of entropy analysis of the sequences of gag, pol, and env revealed that the env gene had the largest variation, and the gag gene nonconserved sites are mainly concentrated in p19, p10, and p12.	Glycosaminoglycans	132-135	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	201-204
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
32637402-7	2020	VLP interaction with the ATF hollow fibers was studied via confocal microscopy, field emission scanning electron microscopy, and nanoparticle tracking analysis to design a bioprocess capable of separating unassembled Gag monomers and concentrate VLPs in one step.	Glycosaminoglycans	217-220	glial cell derived neurotrophic factor	Homo sapiens	25-28
32330426-1	2020	MPS I is caused by mutations in alpha-l-iduronidase (IDUA), a ubiquitous enzyme that catalyzes the hydrolysis of glycosaminoglycans.	Glycosaminoglycans	113-131	alpha-L-iduronidase	Canis lupus familiaris	32-51
32321820-5	2020	We here examined the impact of HLA-B*52:01-associated viral polymorphisms within the immunodominant C-clade Gag epitope RMTSPVSI ("RI8"; Gag residues 275-282) on viral replicative capacity (VRC), since HLA-mediated reduction in VRC is a central mechanism implicated in HLA-associated control of HIV.	Glycosaminoglycans	108-111	major histocompatibility complex, class I, B	Homo sapiens	31-36
32595622-0	2020	Antiviral Activity of Feline BCA2 Is Mainly Dependent on Its Interference With Proviral Transcription Rather Than Degradation of FIV Gag.	Glycosaminoglycans	133-136	ring finger protein 115	Homo sapiens	29-33
32595622-6	2020	Furthermore, for both fBCA2 and hBCA2, restricting viral transcription is the main anti-FIV mechanism compared to degradation of FIV Gag or promoting viral degradation.	Glycosaminoglycans	133-136	ring finger protein 115	Homo sapiens	32-37
32330426-1	2020	MPS I is caused by mutations in alpha-l-iduronidase (IDUA), a ubiquitous enzyme that catalyzes the hydrolysis of glycosaminoglycans.	Glycosaminoglycans	113-131	alpha-L-iduronidase	Canis lupus familiaris	53-57
32461912-1	2020	Mucopolysaccharidosis type I (MPS I) is an inherited metabolic disorder caused by deficiency of alpha-L-iduronidase (IDUA), resulting in accumulation of heparan and dermatan sulfate glycosaminoglycans (GAGs).	Glycosaminoglycans	202-206	alpha-L-iduronidase	Homo sapiens	117-121
32277574-9	2020	These findings indicate that CANT1 is involved in the synthesis of GAG and regulation of chondrocyte differentiation in the cartilage and contribute to a better understanding of the pathogenesis of DD type 1.	Glycosaminoglycans	67-70	calcium activated nucleotidase 1	Mus musculus	29-34
32539154-18	2020	In this context, elevated GAG values are suspected to participate in hampering formation of the fibrillin-1 network (r = -0.2475; P = 0.04687), which explains its decline over time.	Glycosaminoglycans	26-29	fibrillin 1	Homo sapiens	96-107
32481593-7	2020	Taken together, these data indicate that heparin controls the specificity of kallistatin, such that kinin generation by KLK1 within the microcirculation will be locally protected by the binding of kallistatin to the heparin-like glycosaminoglycans of the endothelium.	Glycosaminoglycans	229-247	serpin family A member 4	Homo sapiens	77-88
32481593-7	2020	Taken together, these data indicate that heparin controls the specificity of kallistatin, such that kinin generation by KLK1 within the microcirculation will be locally protected by the binding of kallistatin to the heparin-like glycosaminoglycans of the endothelium.	Glycosaminoglycans	229-247	serpin family A member 4	Homo sapiens	197-208
32466274-6	2020	Furthermore, investigations regarding the mechanism of anti-inflammatory activity of GAG were focused on nuclear transcription factor-kB (NF-kappaB)-related signal transduction.	Glycosaminoglycans	85-88	nuclear factor kappa B subunit 1	Homo sapiens	138-147
32466274-7	2020	Immunofluorescence staining of the p65 subunit of NF-kappaB and immunoblotting were performed that showed a significant decrease in NF-kappaB level in macrophages on GAG-based multilayers.	Glycosaminoglycans	166-169	RELA proto-oncogene, NF-kB subunit	Homo sapiens	35-59
32466274-7	2020	Immunofluorescence staining of the p65 subunit of NF-kappaB and immunoblotting were performed that showed a significant decrease in NF-kappaB level in macrophages on GAG-based multilayers.	Glycosaminoglycans	166-169	nuclear factor kappa B subunit 1	Homo sapiens	50-59
32466274-10	2020	The results provide an insight on the anti-inflammatory effects of GAG not only based on their physicochemical properties, but also related to their mechanism of action toward NF-kappaB signal transduction.	Glycosaminoglycans	67-70	nuclear factor kappa B subunit 1	Homo sapiens	176-185
32382564-0	2020	Plasma Glycosaminoglycan Profiles in Systemic Sclerosis: Associations with MMP-3, MMP-10, TIMP-1, TIMP-2, and TGF-Beta.	Glycosaminoglycans	7-24	matrix metallopeptidase 3	Homo sapiens	75-80
32477302-6	2020	Additional modifications to HIV-1 gag in some of the macaque-tropic HIV-1 have also been done to overcome TRIM5alpha restriction in rhesus and cynomolgus macaques.	Glycosaminoglycans	34-37	tripartite motif containing 5	Homo sapiens	106-116
32239467-1	2020	DYT-TOR1A is the most common inherited dystonia caused by a three nucleotide (GAG) deletion (dE) in the TOR1A gene.	Glycosaminoglycans	78-81	torsin family 1 member A	Homo sapiens	4-9
32239467-1	2020	DYT-TOR1A is the most common inherited dystonia caused by a three nucleotide (GAG) deletion (dE) in the TOR1A gene.	Glycosaminoglycans	78-81	torsin family 1 member A	Homo sapiens	104-109
32433527-5	2020	Following 14 days of induction, micropellets exposed to TGF-beta1 alone or TGF-beta1 + KGN in combination were larger and produced more glycosominoglycan (GAG) than KGN-only cultures.	Glycosaminoglycans	155-158	transforming growth factor beta 1	Homo sapiens	56-65
32433527-5	2020	Following 14 days of induction, micropellets exposed to TGF-beta1 alone or TGF-beta1 + KGN in combination were larger and produced more glycosominoglycan (GAG) than KGN-only cultures.	Glycosaminoglycans	155-158	transforming growth factor beta 1	Homo sapiens	75-84
32433527-6	2020	When TGF-beta1 + KGN was used, GAG quantities were similar or slightly greater than the TGF-beta1-only cultures, depending on the BMSC donor.	Glycosaminoglycans	31-34	transforming growth factor beta 1	Homo sapiens	5-14
32429351-5	2020	There is strong evidence that formation of the Gag lattice on the PM is a prerequisite for the incorporation of Env into budding particles.	Glycosaminoglycans	47-50	endogenous retrovirus group K member 20	Homo sapiens	112-115
32429351-6	2020	It is also suggested that Env incorporation is mediated by an interaction between its cytoplasmic tail (gp41CT) and the MA domain of Gag.	Glycosaminoglycans	133-136	endogenous retrovirus group K member 20	Homo sapiens	26-29
32429351-8	2020	Elucidation of the molecular determinants of Gag-Env-membrane interactions may help in the development of new antiviral therapeutic agents that inhibit particle assembly, Env incorporation and ultimately virus production.	Glycosaminoglycans	45-48	endogenous retrovirus group K member 20	Homo sapiens	49-52
32429351-8	2020	Elucidation of the molecular determinants of Gag-Env-membrane interactions may help in the development of new antiviral therapeutic agents that inhibit particle assembly, Env incorporation and ultimately virus production.	Glycosaminoglycans	45-48	endogenous retrovirus group K member 20	Homo sapiens	171-174
32414121-5	2020	As the majority of sulfatases are localized to the lysosome, loss of sulfatase activity induces lysosomal storage of glycosaminoglycans and sulfatides and subsequent cellular pathology.	Glycosaminoglycans	117-135	arylsulfatase family member H	Homo sapiens	19-28
32187531-5	2020	Our binding analyses further revealed that glycosaminoglycans, heparin and heparan sulfate, are ligands for OTK and thus may play a role in the Sema1a-PlexA axon guidance system.	Glycosaminoglycans	43-61	off-track	Drosophila melanogaster	108-111
32187531-5	2020	Our binding analyses further revealed that glycosaminoglycans, heparin and heparan sulfate, are ligands for OTK and thus may play a role in the Sema1a-PlexA axon guidance system.	Glycosaminoglycans	43-61	Semaphorin 1a	Drosophila melanogaster	144-150
32187531-5	2020	Our binding analyses further revealed that glycosaminoglycans, heparin and heparan sulfate, are ligands for OTK and thus may play a role in the Sema1a-PlexA axon guidance system.	Glycosaminoglycans	43-61	Plexin A	Drosophila melanogaster	151-156
32462053-0	2020	Preclinical Development and Clinical-Scale Manufacturing of HIV Gag-Specific, LentivirusModified CD4 T Cells for HIV Functional Cure.	Glycosaminoglycans	64-67	CD4 molecule	Homo sapiens	97-100
32462053-5	2020	We developed a method for manufacturing autologous CD4+ T cell products highly enriched with Gag-specific T cells.	Glycosaminoglycans	93-96	CD4 molecule	Homo sapiens	51-54
32462053-6	2020	Rare Gag-specific CD4 T cells in peripheral blood mononuclear cells (PBMCs) were increased nearly 1,000-fold by stimulating PBMC with Gag peptides, followed by depleting nontarget cells and transducing with lentivirus vector AGT103 to protect against HIV-mediated depletion and inhibit HIV release from latently infected cells.	Glycosaminoglycans	5-8	CD4 molecule	Homo sapiens	18-21
31858998-0	2020	Off-line coupling of capillary isotachophoresis separation to IRMPD spectroscopy for glycosaminoglycans analysis: Application to the chondroitin sulfate disaccharides model solutes.	Glycosaminoglycans	85-103	citrate synthase	Homo sapiens	133-152
32391006-8	2020	In this review, we summarize the current status of research on how GAG interactions regulate ELR-chemokine activation of CXCR1 and CXCR2 receptors, and discuss knowledge gaps that must be overcome to establish causal relationships governing the impact of GAG interactions on chemokine function in human health and disease.	Glycosaminoglycans	67-70	C-X-C motif chemokine receptor 1	Homo sapiens	121-126
32391006-8	2020	In this review, we summarize the current status of research on how GAG interactions regulate ELR-chemokine activation of CXCR1 and CXCR2 receptors, and discuss knowledge gaps that must be overcome to establish causal relationships governing the impact of GAG interactions on chemokine function in human health and disease.	Glycosaminoglycans	67-70	C-X-C motif chemokine receptor 2	Homo sapiens	131-136
32382564-0	2020	Plasma Glycosaminoglycan Profiles in Systemic Sclerosis: Associations with MMP-3, MMP-10, TIMP-1, TIMP-2, and TGF-Beta.	Glycosaminoglycans	7-24	matrix metallopeptidase 10	Homo sapiens	82-88
32382564-0	2020	Plasma Glycosaminoglycan Profiles in Systemic Sclerosis: Associations with MMP-3, MMP-10, TIMP-1, TIMP-2, and TGF-Beta.	Glycosaminoglycans	7-24	TIMP metallopeptidase inhibitor 1	Homo sapiens	90-96
32382564-0	2020	Plasma Glycosaminoglycan Profiles in Systemic Sclerosis: Associations with MMP-3, MMP-10, TIMP-1, TIMP-2, and TGF-Beta.	Glycosaminoglycans	7-24	TIMP metallopeptidase inhibitor 2	Homo sapiens	98-104
32382564-0	2020	Plasma Glycosaminoglycan Profiles in Systemic Sclerosis: Associations with MMP-3, MMP-10, TIMP-1, TIMP-2, and TGF-Beta.	Glycosaminoglycans	7-24	transforming growth factor beta 1	Homo sapiens	110-118
32268600-0	2020	Domesticated gag Gene of Drosophila LTR Retrotransposons Is Involved in Response to Oxidative Stress.	Glycosaminoglycans	13-16	ltr	Drosophila melanogaster	36-39
32268600-3	2020	The present work is devoted to studying the role of the domesticated gag gene, Gagr, in the Drosophila genome.	Glycosaminoglycans	69-72	Gag-related	Drosophila melanogaster	79-83
32256629-1	2020	Objectives: Mucopolysaccharidosis type VII (MPS VII) or Sly syndrome is a rare autosomal recessive disorder caused by deficiency of beta-glucuronidase enzyme, which is involved in degradation of glycosaminoglycans.	Glycosaminoglycans	195-213	glucuronidase beta	Homo sapiens	132-150
31976578-7	2020	Our finding suggested that the variant haplotype GAG in TLR10 is associated with decreased risk of PM in Chinese children.	Glycosaminoglycans	49-52	toll like receptor 10	Homo sapiens	56-61
32077689-5	2020	We showed that Evasin-3-bound CXCL1 is unable to activate the CXCR2 receptor, but retains affinity to glycosaminoglycans.	Glycosaminoglycans	102-120	C-X-C motif chemokine ligand 1	Homo sapiens	30-35
32162173-2	2020	IDUA degrades two types of glycosaminoglycans (GAGs): heparan and dermatan sulfates, important components of extracellular matrix, with signaling and structural functions.	Glycosaminoglycans	27-45	iduronidase, alpha-L	Mus musculus	0-4
32566917-5	2020	In this study we sought to investigate the role of LPS in proteoglycan modification and GAG chain elongation, and we hypothesize that LPS will signal via Smad2 dependent pathways to regulate GAG chain elongation.	Glycosaminoglycans	88-91	SMAD family member 2	Homo sapiens	154-159
31941773-1	2020	The cellular protein SERINC5 inhibits the infectivity of diverse retroviruses, and its activity is counteracted by the glycosylated Gag (glycoGag) protein of murine leukemia virus (MLV), the S2 protein of equine infectious anemia virus (EIAV), and the Nef protein of human immunodeficiency virus type 1 (HIV-1).	Glycosaminoglycans	132-135	serine incorporator 5	Homo sapiens	21-28
31941773-1	2020	The cellular protein SERINC5 inhibits the infectivity of diverse retroviruses, and its activity is counteracted by the glycosylated Gag (glycoGag) protein of murine leukemia virus (MLV), the S2 protein of equine infectious anemia virus (EIAV), and the Nef protein of human immunodeficiency virus type 1 (HIV-1).	Glycosaminoglycans	132-135	S100 calcium binding protein B	Homo sapiens	252-255
31969431-7	2020	Moreover, the late domain (L-domain) of Gag played a central role in Alix recruitment, which promoted endosomal sorting complex required for transport I (ESCRT-I) formation and amphisome accumulation by facilitating late endosome formation.	Glycosaminoglycans	40-43	programmed cell death 6 interacting protein	Homo sapiens	69-73
32566917-5	2020	In this study we sought to investigate the role of LPS in proteoglycan modification and GAG chain elongation, and we hypothesize that LPS will signal via Smad2 dependent pathways to regulate GAG chain elongation.	Glycosaminoglycans	191-194	SMAD family member 2	Homo sapiens	154-159
32566917-9	2020	LPS via TLR4 stimulates the expression of GAG synthesizing enzymes to an equal extent to traditional cardiovascular agonists.	Glycosaminoglycans	42-45	toll like receptor 4	Homo sapiens	8-12
32566917-10	2020	LPS phosphorylates the Smad2 linker region via TAK-1/MAPK dependent pathways which correlated with genes associated with GAG chain initiation and elongation.	Glycosaminoglycans	121-124	SMAD family member 2	Homo sapiens	23-28
32566917-10	2020	LPS phosphorylates the Smad2 linker region via TAK-1/MAPK dependent pathways which correlated with genes associated with GAG chain initiation and elongation.	Glycosaminoglycans	121-124	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	47-52
32100548-8	2021	The GAG-ECM area of the CTPs and their progeny was increased in presence of HGL (P = 0.027).	Glycosaminoglycans	4-7	lipase F, gastric type	Homo sapiens	76-79
31743109-5	2020	Our results show that using an immunodominant peptide (I10) or the complete GALNS enzyme to orally induce tolerance to GALNS prior to ERT resulted in several improvements to ERT in mice: (a) decreased splenocyte proliferation after in vitro GALNS stimulation, (b) modulation of the cytokine secretion profile, (c) decrease in GALNS-specific IgG or IgE in plasma, (d) decreased GAG storage in liver, and (e) fewer circulating immune complexes in plasma.	Glycosaminoglycans	377-380	galactosamine (N-acetyl)-6-sulfate sulfatase	Mus musculus	119-124
31705726-5	2020	CSGALNACT1 encodes CSGalNAcT-1, a key enzyme in the biosynthesis of sulfated glycosaminoglycans chondroitin and dermatan sulfate.	Glycosaminoglycans	77-95	chondroitin sulfate N-acetylgalactosaminyltransferase 1	Homo sapiens	0-10
31705726-5	2020	CSGALNACT1 encodes CSGalNAcT-1, a key enzyme in the biosynthesis of sulfated glycosaminoglycans chondroitin and dermatan sulfate.	Glycosaminoglycans	77-95	chondroitin sulfate N-acetylgalactosaminyltransferase 1	Homo sapiens	19-30
32252157-7	2020	RESULTS: AFCs and cartilaginous CEPCs stimulated with each 100-ng/mL L51P and BMP2, showed a significant upregulation in GAG (AFCs: p = 0.00347 and CEPCs: p = 0.0115) and DNA production (AFCs: p = 0.0182 and CEPCs: p = 0.0179) compared to control.	Glycosaminoglycans	121-124	bone morphogenetic protein 2	Homo sapiens	78-82
32121123-2	2020	IDUA deficiency leads to glycosaminoglycan (GAG) accumulation resulting in cellular degeneration and multi-organ dysfunction.	Glycosaminoglycans	25-42	alpha-L-iduronidase	Canis lupus familiaris	0-4
32121123-2	2020	IDUA deficiency leads to glycosaminoglycan (GAG) accumulation resulting in cellular degeneration and multi-organ dysfunction.	Glycosaminoglycans	44-47	alpha-L-iduronidase	Canis lupus familiaris	0-4
32151961-6	2020	In addition, FzD7 CRD increased the expression of glycosaminoglycans (GAGs), Collagen II, aggrecan and reduced the expression of matrix metalloproteinase (MMP)-1, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS-5) in Wnt3a-stimulated human chondrocytes.	Glycosaminoglycans	50-68	frizzled class receptor 7	Mus musculus	13-17
31743109-5	2020	Our results show that using an immunodominant peptide (I10) or the complete GALNS enzyme to orally induce tolerance to GALNS prior to ERT resulted in several improvements to ERT in mice: (a) decreased splenocyte proliferation after in vitro GALNS stimulation, (b) modulation of the cytokine secretion profile, (c) decrease in GALNS-specific IgG or IgE in plasma, (d) decreased GAG storage in liver, and (e) fewer circulating immune complexes in plasma.	Glycosaminoglycans	377-380	galactosamine (N-acetyl)-6-sulfate sulfatase	Mus musculus	76-81
31743109-5	2020	Our results show that using an immunodominant peptide (I10) or the complete GALNS enzyme to orally induce tolerance to GALNS prior to ERT resulted in several improvements to ERT in mice: (a) decreased splenocyte proliferation after in vitro GALNS stimulation, (b) modulation of the cytokine secretion profile, (c) decrease in GALNS-specific IgG or IgE in plasma, (d) decreased GAG storage in liver, and (e) fewer circulating immune complexes in plasma.	Glycosaminoglycans	377-380	galactosamine (N-acetyl)-6-sulfate sulfatase	Mus musculus	119-124
31743109-5	2020	Our results show that using an immunodominant peptide (I10) or the complete GALNS enzyme to orally induce tolerance to GALNS prior to ERT resulted in several improvements to ERT in mice: (a) decreased splenocyte proliferation after in vitro GALNS stimulation, (b) modulation of the cytokine secretion profile, (c) decrease in GALNS-specific IgG or IgE in plasma, (d) decreased GAG storage in liver, and (e) fewer circulating immune complexes in plasma.	Glycosaminoglycans	377-380	galactosamine (N-acetyl)-6-sulfate sulfatase	Mus musculus	119-124
31705726-8	2020	Our data indicate that biallelic loss-of-function mutations in CSGALNACT1 disturb glycosaminoglycan synthesis and cause a mild skeletal dysplasia with advanced bone age, CSGALNACT1-CDG.	Glycosaminoglycans	82-99	chondroitin sulfate N-acetylgalactosaminyltransferase 1	Homo sapiens	63-73
32175296-1	2020	UDP-glucose dehydrogenase (UGDH) encodes an oxidoreductase that converts two successive oxidations of UDP-glucose to produce UDP-glucuronic acid, a key component in the synthesis of several polysaccharides such as glycosaminoglycan and the disaccharide hyaluronic acid.	Glycosaminoglycans	214-231	UDP-glucose 6-dehydrogenase	Homo sapiens	0-25
32175296-1	2020	UDP-glucose dehydrogenase (UGDH) encodes an oxidoreductase that converts two successive oxidations of UDP-glucose to produce UDP-glucuronic acid, a key component in the synthesis of several polysaccharides such as glycosaminoglycan and the disaccharide hyaluronic acid.	Glycosaminoglycans	214-231	UDP-glucose 6-dehydrogenase	Homo sapiens	27-31
32175296-1	2020	UDP-glucose dehydrogenase (UGDH) encodes an oxidoreductase that converts two successive oxidations of UDP-glucose to produce UDP-glucuronic acid, a key component in the synthesis of several polysaccharides such as glycosaminoglycan and the disaccharide hyaluronic acid.	Glycosaminoglycans	214-231	hydroxysteroid 17-beta dehydrogenase 6	Homo sapiens	44-58
32564788-1	2020	Pleiotrophin (PTN) is a potent mitogenic cytokine with a high affinity for the polysaccharide glycosaminoglycan (GAG).	Glycosaminoglycans	113-116	pleiotrophin	Homo sapiens	0-12
32149109-9	2020	Furthermore, Apelin increased GAG content of NP cells and mRNA/protein expressions of NP matrix macromolecules (Collagen II and Aggrecan) and promoted autophagic flux (LC3II/I increased and p62 decreased) under oxidative stress.	Glycosaminoglycans	30-33	apelin	Homo sapiens	13-19
31889024-4	2020	ET showed a higher proportion of cytokine-producing ENV- and GAG-specific CD4 and CD8 T cells compared with LT.	Glycosaminoglycans	61-64	CD4 molecule	Homo sapiens	74-77
31679559-2	2020	IDUA degrades heparan and dermatan sulfates, two types of glycosaminoglycan (GAG), important signalling and structural molecules of the extracellular matrix.	Glycosaminoglycans	58-75	iduronidase, alpha-L	Mus musculus	0-4
31679559-2	2020	IDUA degrades heparan and dermatan sulfates, two types of glycosaminoglycan (GAG), important signalling and structural molecules of the extracellular matrix.	Glycosaminoglycans	77-80	iduronidase, alpha-L	Mus musculus	0-4
31679559-7	2020	Epithelial GAG storage, especially in the cauda epididymidis, was seen in Idua-/- mice.	Glycosaminoglycans	11-14	iduronidase, alpha-L	Mus musculus	74-78
31922599-6	2020	RESULTS: The proband and his second son both carried a heterozygous 5521G>A (GAG to AAG) missense variant in exon 38 of the MYH9 gene, leading to p.Glu1841Lys substitution at position 1841 of amino acid sequence.	Glycosaminoglycans	77-80	myosin heavy chain 9	Homo sapiens	124-128
31250000-2	2020	The flavivirus nonstructural protein 1 (NS1) alters glycosaminoglycans on the endothelium, causing hyperpermeability in vitro and vascular leakage in vivo in a tissue-dependent manner.	Glycosaminoglycans	52-70	influenza virus NS1A binding protein	Homo sapiens	40-43
31250000-9	2020	CONCLUSIONS: These findings suggest that ZIKV NS1 contributes to placental dysfunction via modulation of glycosaminoglycans on trophoblasts and chorionic villi, resulting in increased permeability of human placentas.	Glycosaminoglycans	105-123	influenza virus NS1A binding protein	Homo sapiens	46-49
33073008-1	2020	The glycosaminoglycans (GAGs), dermatan sulfate (DS) and heparan sulfate (HS) are both substrates for alpha-l-iduronidase (IDUA).	Glycosaminoglycans	4-22	alpha-L-iduronidase	Homo sapiens	123-127
31661461-5	2020	Rhesus macaques with low viral loads (VLs) harbored higher frequencies of polyfunctional CXCR5+ SIV-specific CD8+ T cells in various lymphoid tissues and higher proportions of unique Gag-specific CD8+ T cell clonotypes in the mesenteric lymph nodes relative to rhesus macaques with high VLs.	Glycosaminoglycans	183-186	CD8a molecule	Homo sapiens	196-199
31661461-6	2020	In addition, public Gag-specific CD8+ T cell clonotypes were more commonly shared across distinct anatomical sites than the corresponding private clonotypes, which tended to form tissue-specific repertoires, especially in the peripheral blood and the gastrointestinal tract.	Glycosaminoglycans	20-23	CD8a molecule	Homo sapiens	33-36
32036969-8	2020	Kyoto encyclopedia of genes and genomes pathway-enrichment analyses of DEG revealed 10 significant pathways (P < 0.05) represented by calcium signaling pathway (7 genes including CACNA1G, PDE1C, PDGFRB, and SLC8A1) and glycosaminoglycan biosynthesis (B3GNT7, CSGALNACT1, GLCE, and ST3GAL1).	Glycosaminoglycans	219-236	calcium voltage-gated channel subunit alpha1 G	Gallus gallus	179-186
32564788-1	2020	Pleiotrophin (PTN) is a potent mitogenic cytokine with a high affinity for the polysaccharide glycosaminoglycan (GAG).	Glycosaminoglycans	113-116	pleiotrophin	Homo sapiens	14-17
32274707-1	2020	Heparanase is an endo-beta-glucuronidase that cleaves at a limited number of internal sites the glycosaminoglycan heparan sulfate (HS).	Glycosaminoglycans	96-113	heparanase	Homo sapiens	0-10
32564788-4	2020	In particular, PTN has now been shown to bind a diverse collection of receptors including many GAG-containing proteoglycans.	Glycosaminoglycans	95-98	pleiotrophin	Homo sapiens	15-18
32274709-1	2020	The retaining endo-beta-D-glucuronidase Heparanase (HPSE) is the primary mammalian enzyme responsible for breakdown of the glycosaminoglycan heparan sulfate (HS).	Glycosaminoglycans	123-140	heparanase	Homo sapiens	52-56
32564788-6	2020	Structural studies of PTN in complex with both GAG and domains from its non-proteoglycan receptors reveal a binding mechanism that relies on electrostatic interactions and points to PTN-induced receptor oligomerization as one of the possible ways PTN uses to control cellular functions.	Glycosaminoglycans	47-50	pleiotrophin	Homo sapiens	22-25
31658834-7	2019	After adjusting for disease severity, DMMB-GAG was significantly associated with parasitemia [partial correlation coefficient (Pcorr) = 0.34; P = 0.01] and plasma TNF (Pcorr = 0.26; P = 0.04) and inversely with plasma and urine NO oxidation products [Pcorr = -0.31 (P = 0.01) and Pcorr = -0.26 (P = 0.03), respectively].	Glycosaminoglycans	43-46	tumor necrosis factor	Homo sapiens	163-166
31330080-5	2020	Based on the results from loss-of-function studies, SGK1 silencing promoted the deposition of glycosaminoglycans in interleukin 1 beta (IL-1beta)-treated chondrocytes, and significantly alleviated IL-1beta-induced downregulation of Collagen II and Aggrecan, as well as the upregulation of a disintegrin and metalloproteinase with thrombospondin motifs 5 and matrix metalloproteinase-13.	Glycosaminoglycans	94-112	serum/glucocorticoid regulated kinase 1	Homo sapiens	52-56
31330080-5	2020	Based on the results from loss-of-function studies, SGK1 silencing promoted the deposition of glycosaminoglycans in interleukin 1 beta (IL-1beta)-treated chondrocytes, and significantly alleviated IL-1beta-induced downregulation of Collagen II and Aggrecan, as well as the upregulation of a disintegrin and metalloproteinase with thrombospondin motifs 5 and matrix metalloproteinase-13.	Glycosaminoglycans	94-112	interleukin 1 beta	Homo sapiens	116-134
31330080-5	2020	Based on the results from loss-of-function studies, SGK1 silencing promoted the deposition of glycosaminoglycans in interleukin 1 beta (IL-1beta)-treated chondrocytes, and significantly alleviated IL-1beta-induced downregulation of Collagen II and Aggrecan, as well as the upregulation of a disintegrin and metalloproteinase with thrombospondin motifs 5 and matrix metalloproteinase-13.	Glycosaminoglycans	94-112	interleukin 1 beta	Homo sapiens	136-144
33280329-3	2020	The correlation analysis, performed in different age groups, revealed significant associations of VEGF-A level with lipid parameters (CS, LDL-C, Apo B, atherogenicity coefficient, Apo B /Apo A1 ratio) and extracellular matrix metabolism (blood TIMP-4, MMP-2, MMP-3, MMP-9, hyaluronan, total and peptide-bound hydroxyproline, glycosaminoglycans).	Glycosaminoglycans	325-343	vascular endothelial growth factor A	Homo sapiens	98-104
33138761-5	2020	Intrathecal or intracerebroventricular ERT and intravenous ERT with fusion proteins, presently under development, seem to be able to reduce the levels of GAGs in the CNS and have the potential of reducing the impact of the neurological burden of the disease.	Glycosaminoglycans	154-158	E74 like ETS transcription factor 3	Homo sapiens	39-42
33138761-5	2020	Intrathecal or intracerebroventricular ERT and intravenous ERT with fusion proteins, presently under development, seem to be able to reduce the levels of GAGs in the CNS and have the potential of reducing the impact of the neurological burden of the disease.	Glycosaminoglycans	154-158	E74 like ETS transcription factor 3	Homo sapiens	59-62
32306341-2	2020	ZG16p binds to mannose via the well-conserved GXXXD loop among mJRLs and sulfated glycosaminoglycans (e.g., heparin and heparan sulfate) via the basic patch of molecular surface.	Glycosaminoglycans	82-100	zymogen granule protein 16	Rattus norvegicus	0-5
31834922-2	2019	IDUA codes for alpha-L-iduronidase (IDUA), a lysosomal hydrolase that degrades glycosaminoglycans (GAGs): heparan sulphate and dermatan sulphate.	Glycosaminoglycans	79-97	iduronidase, alpha-L	Mus musculus	0-4
31834922-2	2019	IDUA codes for alpha-L-iduronidase (IDUA), a lysosomal hydrolase that degrades glycosaminoglycans (GAGs): heparan sulphate and dermatan sulphate.	Glycosaminoglycans	79-97	iduronidase, alpha-L	Mus musculus	36-40
31805123-1	2019	In early-onset generalized torsion dystonia, caused by a GAG deletion in TOR1A (DYT1), enhanced striatal cholinergic activity has been suggested to be critically involved.	Glycosaminoglycans	57-60	torsin family 1, member A (torsin A)	Mus musculus	73-78
31805123-1	2019	In early-onset generalized torsion dystonia, caused by a GAG deletion in TOR1A (DYT1), enhanced striatal cholinergic activity has been suggested to be critically involved.	Glycosaminoglycans	57-60	torsin family 1, member A (torsin A)	Mus musculus	80-84
31290007-1	2019	Protease activated receptors (PARs) transactivate both epidermal growth factor receptors (EGFR) and transforming growth factor (TGF)-beta receptors (TGFBR1) in vascular smooth muscle leading to the increased expression of genes (CHST11 and CHSY1) which are rate limiting for the enzymes that mediate hyperelongation of glycosaminoglycan (GAG) chains on the lipid-binding proteoglycan, biglycan.	Glycosaminoglycans	319-336	epidermal growth factor receptor	Homo sapiens	55-88
31550528-8	2019	Moreover, quercetin induced M2 polarization of macrophages and upregulated the expression of transforming growth factor beta (TGF-beta) and insulin-like growth factor (IGF), which in turn created a pro-chondrogenic microenvironment for chondrocytes and promoted the synthesis of glycosaminoglycan (GAG) in chondrocytes.	Glycosaminoglycans	279-296	transforming growth factor alpha	Rattus norvegicus	126-134
31550528-8	2019	Moreover, quercetin induced M2 polarization of macrophages and upregulated the expression of transforming growth factor beta (TGF-beta) and insulin-like growth factor (IGF), which in turn created a pro-chondrogenic microenvironment for chondrocytes and promoted the synthesis of glycosaminoglycan (GAG) in chondrocytes.	Glycosaminoglycans	298-301	transforming growth factor alpha	Rattus norvegicus	126-134
31290007-1	2019	Protease activated receptors (PARs) transactivate both epidermal growth factor receptors (EGFR) and transforming growth factor (TGF)-beta receptors (TGFBR1) in vascular smooth muscle leading to the increased expression of genes (CHST11 and CHSY1) which are rate limiting for the enzymes that mediate hyperelongation of glycosaminoglycan (GAG) chains on the lipid-binding proteoglycan, biglycan.	Glycosaminoglycans	338-341	epidermal growth factor receptor	Homo sapiens	55-88
31290007-1	2019	Protease activated receptors (PARs) transactivate both epidermal growth factor receptors (EGFR) and transforming growth factor (TGF)-beta receptors (TGFBR1) in vascular smooth muscle leading to the increased expression of genes (CHST11 and CHSY1) which are rate limiting for the enzymes that mediate hyperelongation of glycosaminoglycan (GAG) chains on the lipid-binding proteoglycan, biglycan.	Glycosaminoglycans	338-341	epidermal growth factor receptor	Homo sapiens	90-94
31290007-1	2019	Protease activated receptors (PARs) transactivate both epidermal growth factor receptors (EGFR) and transforming growth factor (TGF)-beta receptors (TGFBR1) in vascular smooth muscle leading to the increased expression of genes (CHST11 and CHSY1) which are rate limiting for the enzymes that mediate hyperelongation of glycosaminoglycan (GAG) chains on the lipid-binding proteoglycan, biglycan.	Glycosaminoglycans	338-341	transforming growth factor beta receptor 1	Homo sapiens	149-155
31290007-1	2019	Protease activated receptors (PARs) transactivate both epidermal growth factor receptors (EGFR) and transforming growth factor (TGF)-beta receptors (TGFBR1) in vascular smooth muscle leading to the increased expression of genes (CHST11 and CHSY1) which are rate limiting for the enzymes that mediate hyperelongation of glycosaminoglycan (GAG) chains on the lipid-binding proteoglycan, biglycan.	Glycosaminoglycans	319-336	epidermal growth factor receptor	Homo sapiens	90-94
31290007-1	2019	Protease activated receptors (PARs) transactivate both epidermal growth factor receptors (EGFR) and transforming growth factor (TGF)-beta receptors (TGFBR1) in vascular smooth muscle leading to the increased expression of genes (CHST11 and CHSY1) which are rate limiting for the enzymes that mediate hyperelongation of glycosaminoglycan (GAG) chains on the lipid-binding proteoglycan, biglycan.	Glycosaminoglycans	319-336	transforming growth factor beta receptor 1	Homo sapiens	149-155
31290007-1	2019	Protease activated receptors (PARs) transactivate both epidermal growth factor receptors (EGFR) and transforming growth factor (TGF)-beta receptors (TGFBR1) in vascular smooth muscle leading to the increased expression of genes (CHST11 and CHSY1) which are rate limiting for the enzymes that mediate hyperelongation of glycosaminoglycan (GAG) chains on the lipid-binding proteoglycan, biglycan.	Glycosaminoglycans	319-336	carbohydrate sulfotransferase 11	Homo sapiens	229-235
31290007-1	2019	Protease activated receptors (PARs) transactivate both epidermal growth factor receptors (EGFR) and transforming growth factor (TGF)-beta receptors (TGFBR1) in vascular smooth muscle leading to the increased expression of genes (CHST11 and CHSY1) which are rate limiting for the enzymes that mediate hyperelongation of glycosaminoglycan (GAG) chains on the lipid-binding proteoglycan, biglycan.	Glycosaminoglycans	338-341	carbohydrate sulfotransferase 11	Homo sapiens	229-235
31473686-2	2019	Lack or improper amount of the IDUA enzyme results in the improper metabolism of mucopolysaccharides or glycosaminoglycans (GAGs).	Glycosaminoglycans	81-100	alpha-L-iduronidase	Homo sapiens	31-35
31473686-2	2019	Lack or improper amount of the IDUA enzyme results in the improper metabolism of mucopolysaccharides or glycosaminoglycans (GAGs).	Glycosaminoglycans	104-122	alpha-L-iduronidase	Homo sapiens	31-35
31033097-7	2019	Moreover, the per cell expression of CSF1R determined by its mean pixel intensity (MPI) correlated positively with the MPI of SIV Gag p28 in SIV-infected PVMs.	Glycosaminoglycans	130-133	colony stimulating factor 1 receptor	Homo sapiens	37-42
31536840-5	2019	This study aims to determine the optimal loading and release kinetics of TGF-beta1 bound to an engineered GAG hydrogel to promote optimal cartilaginous matrix production in absence of TGF-beta1 media-supplementation.	Glycosaminoglycans	106-109	transforming growth factor beta 1	Homo sapiens	73-82
31536840-6	2019	We show that heparin, a GAG known to bind a wide range of GFs, covalently conjugated to a hyaluronan hydrogel, leads to a sustained release of TGF-beta1.	Glycosaminoglycans	24-27	transforming growth factor beta 1	Homo sapiens	143-152
31033097-7	2019	Moreover, the per cell expression of CSF1R determined by its mean pixel intensity (MPI) correlated positively with the MPI of SIV Gag p28 in SIV-infected PVMs.	Glycosaminoglycans	130-133	golgi SNAP receptor complex member 1	Homo sapiens	134-137
30963568-11	2019	Our results demonstrate a novel mechanism underlying the function of HOTAIR in tumor progression through programming the context of cell surface glycosaminoglycans.	Glycosaminoglycans	145-163	HOX transcript antisense RNA	Homo sapiens	69-75
31216050-5	2019	Further, HIV-specific responses were dominated by gag-specific CD4+ T cells in virologically suppressed HIV-D individuals, suggesting retention of T cell memory for both viruses.	Glycosaminoglycans	50-53	CD4 molecule	Homo sapiens	63-66
31301135-4	2019	Along those lines, vaccine recipients with higher HLA-I adaptation to the Gag vaccine insert mounted less polyfunctional CD8 T-cell responses at the protein-level.	Glycosaminoglycans	74-77	CD8a molecule	Homo sapiens	121-124
33455219-0	2019	Modulation of Human CXCL12 Binding Properties to Glycosaminoglycans To Enhance Chemotactic Gradients.	Glycosaminoglycans	49-67	C-X-C motif chemokine ligand 12	Homo sapiens	20-26
33455219-3	2019	hCXCL12 variants were designed to bind to glycosaminoglycans (GAGs) with different affinities in order to modulate its release.	Glycosaminoglycans	42-60	C-X-C motif chemokine ligand 12	Homo sapiens	0-7
33455219-6	2019	The reduced GAG affinity led to a fast release of hCXCL12 K24/K27/R41/R47A, whereas hCXCL12 Q48K was slowly released over 2 weeks due to its increased binding strength compared to wild type hCXCL12.	Glycosaminoglycans	12-15	C-X-C motif chemokine ligand 12	Homo sapiens	50-57
31286562-9	2019	We observed long-term Brachyury expression, significant increased expression of NP phenotypic markers FOXF1, KRT19, and chondrogenic marker SOX9 with decreases in inflammatory cytokines IL1-beta/IL6, NGF, and MMPs and significant increases in glycosaminoglycan accumulation.	Glycosaminoglycans	243-260	T-box transcription factor 1	Homo sapiens	22-31
31267683-9	2019	Glycosaminoglycan levels decreased in the decellularized lung and increased in the recellularized lung, especially in the ASC-treated group.	Glycosaminoglycans	0-17	PYD and CARD domain containing	Rattus norvegicus	122-125
31196538-0	2019	Structure and heparanase inhibitory activity of a new glycosaminoglycan from the slug Limacus flavus.	Glycosaminoglycans	54-71	heparanase	Homo sapiens	14-24
31341044-10	2019	Testican-2/SPOCK2 is a complex type of secreted proteoglycan with heparan sulfate GAG chains attached to the core protein.	Glycosaminoglycans	82-85	sparc/osteonectin, cwcv and kazal-like domains proteoglycan 2	Mus musculus	11-17
31533830-2	2019	CXCL12 activity has been shown to be heavily influenced by its binding to extracellular glycosaminoglycans (GAG) by modulating its presentation to its receptors and by generating haptotactic gradients.	Glycosaminoglycans	88-106	chemokine (C-X-C motif) ligand 12	Mus musculus	0-6
31533830-2	2019	CXCL12 activity has been shown to be heavily influenced by its binding to extracellular glycosaminoglycans (GAG) by modulating its presentation to its receptors and by generating haptotactic gradients.	Glycosaminoglycans	108-111	chemokine (C-X-C motif) ligand 12	Mus musculus	0-6
31325655-3	2019	Exome sequencing revealed a biallelic loss of function mutation in CSGALNACT1, which encodes chondroitin sulfate N-acetylgalactosaminyltransferase 1 and plays a major role in the chondroitin sulfate chain biosynthesis and therefore in the synthesis of glycosaminoglycans.	Glycosaminoglycans	252-270	chondroitin sulfate N-acetylgalactosaminyltransferase 1	Homo sapiens	67-77
31325655-3	2019	Exome sequencing revealed a biallelic loss of function mutation in CSGALNACT1, which encodes chondroitin sulfate N-acetylgalactosaminyltransferase 1 and plays a major role in the chondroitin sulfate chain biosynthesis and therefore in the synthesis of glycosaminoglycans.	Glycosaminoglycans	252-270	chondroitin sulfate N-acetylgalactosaminyltransferase 1	Homo sapiens	93-148
31196538-6	2019	Bioactivity assays showed that LF-GAG could potently inhibit human heparanase (IC50, 0.10 muM).	Glycosaminoglycans	34-37	heparanase	Homo sapiens	67-77
31196538-8	2019	Structure-activity relationship analysis indicated that the chain length and sulfate substitution of LF-GAG are essential for its heparanase inhibitory activity.	Glycosaminoglycans	104-107	heparanase	Homo sapiens	130-140
30778123-3	2019	Therefore, PGs and their GAGs could be significant to adipose tissue homeostasis.	Glycosaminoglycans	25-29	WD and tetratricopeptide repeats 1	Mus musculus	54-61
31207331-4	2019	Expression of SOX9, Collagen10 and Collagen2 proved the chondro-inductive effect of GAG-grafted scaffolds.	Glycosaminoglycans	84-87	SRY-box transcription factor 9	Homo sapiens	14-18
31002379-1	2019	AIM: To investigate whether glycosaminoglycans (GAGs) binding to high-dose LL37 eliminates its cytotoxicity to dental pulp cells (hDPCs) whilst retaining undiminished antimicrobial and LPS-neutralizing abilities.	Glycosaminoglycans	28-46	cathelicidin antimicrobial peptide	Homo sapiens	75-79
30778123-4	2019	The purpose of this study was to determine the role of ECM sulfated GAGs in adipose tissue homeostasis.	Glycosaminoglycans	68-72	WD and tetratricopeptide repeats 1	Mus musculus	76-83
30778123-12	2019	CONCLUSIONS: Decreased GAGs due to the loss of the key GAG assembly enzyme XylT2 causes reduced steady state adipose tissue stores leading to a unique lipodystrophic model.	Glycosaminoglycans	23-27	WD and tetratricopeptide repeats 1	Mus musculus	109-116
30778123-12	2019	CONCLUSIONS: Decreased GAGs due to the loss of the key GAG assembly enzyme XylT2 causes reduced steady state adipose tissue stores leading to a unique lipodystrophic model.	Glycosaminoglycans	23-26	WD and tetratricopeptide repeats 1	Mus musculus	109-116
30778123-14	2019	Therefore, adipose tissue GAGs are important in the homeostasis of adipose tissue by mediating control of adipose precursor development, tissue inflammation, and vascular development.	Glycosaminoglycans	26-30	WD and tetratricopeptide repeats 1	Mus musculus	11-18
30778123-14	2019	Therefore, adipose tissue GAGs are important in the homeostasis of adipose tissue by mediating control of adipose precursor development, tissue inflammation, and vascular development.	Glycosaminoglycans	26-30	WD and tetratricopeptide repeats 1	Mus musculus	67-74
30778123-14	2019	Therefore, adipose tissue GAGs are important in the homeostasis of adipose tissue by mediating control of adipose precursor development, tissue inflammation, and vascular development.	Glycosaminoglycans	26-30	WD and tetratricopeptide repeats 1	Mus musculus	67-74
31544795-1	2019	IDUA contributes to the degradation of the glycosaminoglycans, including heparan sulphate and dermatan sulphate.	Glycosaminoglycans	43-61	alpha-L-iduronidase	Homo sapiens	0-4
31544795-2	2019	Deficient activity of IDUA generates accumulation of glycosaminoglycans in lysosomes leading to MPS I.	Glycosaminoglycans	53-71	alpha-L-iduronidase	Homo sapiens	22-26
31106390-0	2019	Correction to: Genetically engineered probiotic Saccharomyces cerevisiae strains mature human dendritic cells and stimulate gag-specific memory CD8+ T cells ex vivo.	Glycosaminoglycans	124-127	CD8a molecule	Homo sapiens	144-147
31125187-0	2019	A non-circulating pool of factor XI associated with glycosaminoglycans in mice.	Glycosaminoglycans	52-70	coagulation factor XI	Mus musculus	26-35
31125187-11	2019	Most FXI in mice is noncovalently associated with GAGs on blood vessel endothelium and does not circulate in plasma.	Glycosaminoglycans	50-54	coagulation factor XI	Mus musculus	5-8
31085206-11	2019	Taken together, these findings demonstrate that the dual targeting of DENV virions and NS1 using GAG analogues offers a new avenue for DENV drug development.	Glycosaminoglycans	97-100	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	87-90
30932321-1	2019	Chondroitin sulfate E (CS-E) is a glycosaminoglycan containing type-E disaccharide units (sulfated at C-4 and C-6 of N-acetylgalactosamine).	Glycosaminoglycans	34-51	complement C4A (Rodgers blood group)	Homo sapiens	102-105
30932321-1	2019	Chondroitin sulfate E (CS-E) is a glycosaminoglycan containing type-E disaccharide units (sulfated at C-4 and C-6 of N-acetylgalactosamine).	Glycosaminoglycans	34-51	complement C6	Homo sapiens	110-113
31365577-4	2019	Sodium storage capacity was decreased in Ext1+/-Ext2+/- mice as reflected by a 77% reduction in endothelial surface layer thickness and a lower skin sodium-to-glycosaminoglycan ratio.	Glycosaminoglycans	159-176	exostosin glycosyltransferase 1	Mus musculus	41-45
31365577-4	2019	Sodium storage capacity was decreased in Ext1+/-Ext2+/- mice as reflected by a 77% reduction in endothelial surface layer thickness and a lower skin sodium-to-glycosaminoglycan ratio.	Glycosaminoglycans	159-176	exostosin glycosyltransferase 2	Mus musculus	48-52
31336923-7	2019	Furthermore, tbx5a knockdown interfered with ECM formation in pectoral fins, affecting glycosaminoglycans, fibronectin, hyaluronic acid (HA), and N-cadherin.	Glycosaminoglycans	87-105	T-box transcription factor 5a	Danio rerio	13-18
31080121-2	2019	Arc exhibits homology to the capsid-forming Gag proteins from retroviruses and can encapsulate its own mRNA and transport it to neighboring neurons.	Glycosaminoglycans	44-47	activity regulated cytoskeleton associated protein	Homo sapiens	0-3
31167981-8	2019	Although BMP-2 significantly increased glycosaminoglycan production, Safranin O-negative outer layer was formed and the mRNA expression of COL10 relating to cartilage hypertrophy was also significantly upregulated (P<0.05).	Glycosaminoglycans	39-56	bone morphogenetic protein 2	Canis lupus familiaris	9-14
31434236-9	2019	In the presence of IL-1beta, these donors showed a significant increase in cartilage matrix gene expression and GAG content relative to hyperoxic conditions.	Glycosaminoglycans	112-115	interleukin 1 alpha	Homo sapiens	19-27
31440231-4	2019	While the two domains, namely, N-terminal and C-terminal domains (NTD and CTD), have been the central target for Gag research, the linker region connecting the two has been poorly studied.	Glycosaminoglycans	113-116	fuzzy planar cell polarity protein	Homo sapiens	66-69
31440231-4	2019	While the two domains, namely, N-terminal and C-terminal domains (NTD and CTD), have been the central target for Gag research, the linker region connecting the two has been poorly studied.	Glycosaminoglycans	113-116	CTD	Homo sapiens	74-77
31034775-6	2019	In addition, CCR5 is highly expressed on SIV gag-specific (CM9+) CD8+ T cells in SIV-infected macaques, yet CCR5+CD8+ T cells are significantly reduced in mucosal lymphoid tissues with disease progression.	Glycosaminoglycans	45-48	C-C motif chemokine receptor 5	Homo sapiens	13-17
31034775-6	2019	In addition, CCR5 is highly expressed on SIV gag-specific (CM9+) CD8+ T cells in SIV-infected macaques, yet CCR5+CD8+ T cells are significantly reduced in mucosal lymphoid tissues with disease progression.	Glycosaminoglycans	45-48	CD8a molecule	Homo sapiens	65-68
30439444-0	2019	Calcium activated nucleotidase 1 (CANT1) is critical for glycosaminoglycan biosynthesis in cartilage and endochondral ossification.	Glycosaminoglycans	57-74	calcium activated nucleotidase 1	Mus musculus	0-32
30439444-0	2019	Calcium activated nucleotidase 1 (CANT1) is critical for glycosaminoglycan biosynthesis in cartilage and endochondral ossification.	Glycosaminoglycans	57-74	calcium activated nucleotidase 1	Mus musculus	34-39
30439444-3	2019	Specifically, the glycosaminoglycan synthesis was decreased in chondrocytes from Cant1 knock-out mice and their hydrodynamic size was reduced, whilst the sulfation was increased and the overall proteoglycan secretion was delayed.	Glycosaminoglycans	18-35	calcium activated nucleotidase 1	Mus musculus	81-86
31167921-15	2019	There have been no effective therapeutics available for HAM/TSP, but recently, a semisynthetic glycosaminoglycan, named pentosan polysulfate (PPS), has been found to alleviate the symptoms of HAM/TSP.	Glycosaminoglycans	95-112	thrombospondin 1	Homo sapiens	196-199
31175155-8	2019	These results provide first evidence that mast cells produce HYAL4 and that this enzyme may play a specific role in maintaining alpha-granule homeostasis in these cells by cleaving CS glycosaminoglycan chains attached to serglycin.	Glycosaminoglycans	184-201	hyaluronidase 4	Homo sapiens	61-66
31151856-0	2019	Arc Oligomerization Is Regulated by CaMKII Phosphorylation of the GAG Domain: An Essential Mechanism for Plasticity and Memory Formation.	Glycosaminoglycans	66-69	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	36-42
31151856-5	2019	CaMKII phosphorylates the N-lobe of the Arc GAG domain and disrupts an interaction surface essential for high-order oligomerization.	Glycosaminoglycans	44-47	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	0-6
31002939-7	2019	A higher production of sulfated glycosaminoglycans (sGAG)/DNA was observed for CD146+ pellets, while in organ cultures, sGAG synthesis rate was higher for IVDs treated with CD146- MSCs by either homing or injection.	Glycosaminoglycans	32-50	melanoma cell adhesion molecule	Homo sapiens	79-84
30914273-1	2019	B4GALT7 encodes beta-1,4-galactosyltransferase which links glycosaminoglycans to proteoglycans in connective tissues.	Glycosaminoglycans	59-77	beta-1,4-galactosyltransferase 7	Homo sapiens	0-7
30720852-7	2019	RESULTS: The results of this study showed that MIF antagonist (p425) significantly decreased urine protein and GAG excretion, urine protein/creatinine ratio, and serum BUN and Cr in the streptozotocin-induced DN in the rats.	Glycosaminoglycans	111-114	macrophage migration inhibitory factor	Rattus norvegicus	47-50
31061498-7	2019	Therefore, sulfation patterns determine the length of the glycosaminoglycan segment that bind to PTPRsigma and define the fate of axonal regeneration through a mechanism involving PTPRsigma, cortactin and autophagy.	Glycosaminoglycans	58-75	cortactin	Homo sapiens	191-200
31832432-8	2019	Results: The frequencies of CAG>GAG, ATG>GTG, GTC>GTA, and GTG>ATG polymorphisms in exon 25 of the PKD1 gene were 34 (94.44%), 33 (91.67%), 26 (72.22%), and 5 (13.89%), respectively.	Glycosaminoglycans	32-35	polycystin 1, transient receptor potential channel interacting	Homo sapiens	99-103
30809816-3	2019	This study addressed the question whether ET-1 by activating the Rho kinase and cytoskeletal rearrangement can transactivate the TGF-beta receptor leading to phosphorylation of the transcription factor Smad2 and increased expression of the GAG chain synthesizing enzyme such as chondroitin synthase-1 (CHSY-1) in bovine aortic endothelial cells (BAECs).	Glycosaminoglycans	240-243	endothelin 1	Bos taurus	42-46
31242641-4	2019	The greatest COL2A1/COL10A1 ratio was detected in cells exposed to a combination medium containing 10 ng/mL BMP-2 and 1 ng/mL TGF-beta1 in the absence of dexamethasone, and this was reflected in the total amount of glycosaminoglycans produced.	Glycosaminoglycans	215-233	collagen type II alpha 1 chain	Homo sapiens	13-19
31242641-4	2019	The greatest COL2A1/COL10A1 ratio was detected in cells exposed to a combination medium containing 10 ng/mL BMP-2 and 1 ng/mL TGF-beta1 in the absence of dexamethasone, and this was reflected in the total amount of glycosaminoglycans produced.	Glycosaminoglycans	215-233	collagen, type X, alpha 1	Mus musculus	20-27
31242641-4	2019	The greatest COL2A1/COL10A1 ratio was detected in cells exposed to a combination medium containing 10 ng/mL BMP-2 and 1 ng/mL TGF-beta1 in the absence of dexamethasone, and this was reflected in the total amount of glycosaminoglycans produced.	Glycosaminoglycans	215-233	bone morphogenetic protein 2	Mus musculus	108-119
31242641-4	2019	The greatest COL2A1/COL10A1 ratio was detected in cells exposed to a combination medium containing 10 ng/mL BMP-2 and 1 ng/mL TGF-beta1 in the absence of dexamethasone, and this was reflected in the total amount of glycosaminoglycans produced.	Glycosaminoglycans	215-233	transforming growth factor, beta 1	Mus musculus	126-135
30417274-3	2019	In this study, our aim was to identify the TGF-beta1 mediated signalling pathway involving reactive oxygen species (ROS) and Smad2 linker region phosphorylation that regulate the mRNA expression of GAG synthesizing enzymes, chondroitin 4-O-sulfotransferase 1 (CHST11) and chondroitin sulfate synthase 1 (CHSY1) which are the rate limiting enzymes involved in GAG chain elongation.	Glycosaminoglycans	198-201	transforming growth factor beta 1	Homo sapiens	43-52
30417274-3	2019	In this study, our aim was to identify the TGF-beta1 mediated signalling pathway involving reactive oxygen species (ROS) and Smad2 linker region phosphorylation that regulate the mRNA expression of GAG synthesizing enzymes, chondroitin 4-O-sulfotransferase 1 (CHST11) and chondroitin sulfate synthase 1 (CHSY1) which are the rate limiting enzymes involved in GAG chain elongation.	Glycosaminoglycans	198-201	SMAD family member 2	Homo sapiens	125-130
30417274-3	2019	In this study, our aim was to identify the TGF-beta1 mediated signalling pathway involving reactive oxygen species (ROS) and Smad2 linker region phosphorylation that regulate the mRNA expression of GAG synthesizing enzymes, chondroitin 4-O-sulfotransferase 1 (CHST11) and chondroitin sulfate synthase 1 (CHSY1) which are the rate limiting enzymes involved in GAG chain elongation.	Glycosaminoglycans	198-201	carbohydrate sulfotransferase 11	Homo sapiens	260-266
30417274-3	2019	In this study, our aim was to identify the TGF-beta1 mediated signalling pathway involving reactive oxygen species (ROS) and Smad2 linker region phosphorylation that regulate the mRNA expression of GAG synthesizing enzymes, chondroitin 4-O-sulfotransferase 1 (CHST11) and chondroitin sulfate synthase 1 (CHSY1) which are the rate limiting enzymes involved in GAG chain elongation.	Glycosaminoglycans	198-201	chondroitin sulfate synthase 1	Homo sapiens	272-302
30417274-3	2019	In this study, our aim was to identify the TGF-beta1 mediated signalling pathway involving reactive oxygen species (ROS) and Smad2 linker region phosphorylation that regulate the mRNA expression of GAG synthesizing enzymes, chondroitin 4-O-sulfotransferase 1 (CHST11) and chondroitin sulfate synthase 1 (CHSY1) which are the rate limiting enzymes involved in GAG chain elongation.	Glycosaminoglycans	198-201	chondroitin sulfate synthase 1	Homo sapiens	304-309
31013423-5	2019	Engineering the surface charge of CCL21 reduced its nonspecific binding to glycosaminoglycans, a property of chemokines that complicates their targeted delivery.	Glycosaminoglycans	75-93	C-C motif chemokine ligand 21	Homo sapiens	34-39
31168439-1	2019	The rat aryl sulfotransferases IV (AST IV) has been used to catalyze 3"-phosphoadenosine-5"-phosphate (PAP) into the sulfuryl group donor 3"-phosphoadenosine-5"-phosphosulfate (PAPS) in biotechnological production of glycosaminoglycans.	Glycosaminoglycans	217-235	sulfotransferase family 1A member 1	Rattus norvegicus	8-33
31168439-1	2019	The rat aryl sulfotransferases IV (AST IV) has been used to catalyze 3"-phosphoadenosine-5"-phosphate (PAP) into the sulfuryl group donor 3"-phosphoadenosine-5"-phosphosulfate (PAPS) in biotechnological production of glycosaminoglycans.	Glycosaminoglycans	217-235	sulfotransferase family 1A member 1	Rattus norvegicus	35-41
30869126-1	2019	The glycosaminoglycan dermatan sulfate (DS) is a well-known activator of heparin cofactor II-dependent inactivation of thrombin.	Glycosaminoglycans	4-21	coagulation factor II, thrombin	Homo sapiens	119-127
31010851-7	2019	Enzymatic removal of neutrophil glycosaminoglycans was observed to ablate neutrophil navigation of a CXCL8 gradient, whereas navigation of an fMLF gradient remained largely intact.	Glycosaminoglycans	32-50	C-X-C motif chemokine ligand 8	Homo sapiens	101-106
29739272-12	2019	IL-1beta reduced GAG and DNA content, but the addition of NCM relative to BM improved GAG and DNA content.	Glycosaminoglycans	17-20	interleukin 1 alpha	Bos taurus	0-8
30894475-9	2019	Finally, we demonstrate how our methodology can be adapted to interrogate interactions between membrane-associated Env and the matrix domain of Gag.	Glycosaminoglycans	144-147	endogenous retrovirus group K member 20	Homo sapiens	115-118
30825594-7	2019	We identified an MMP3-inducing fraction in the range of 40 kDa after gel filtration, and we confirmed our findings in three-dimensional PPAC cultures, where SF-CM also reduced the glycosaminoglycan content.	Glycosaminoglycans	180-197	matrix metallopeptidase 3	Homo sapiens	17-21
31100859-5	2019	A marine-derived, heparan sulphate-containing glycosaminoglycan extract, isolated from the crab Portunus pelagicus, was identified to inhibit human BACE1 with comparable bioactivity to that of mammalian heparin (IC50 = 1.85 mug mL-1 (R2 = 0.94) and 2.43 mug mL-1 (R2 = 0.93), respectively), while possessing highly attenuated anticoagulant activities.	Glycosaminoglycans	46-63	beta-secretase 1	Homo sapiens	148-153
31100859-5	2019	A marine-derived, heparan sulphate-containing glycosaminoglycan extract, isolated from the crab Portunus pelagicus, was identified to inhibit human BACE1 with comparable bioactivity to that of mammalian heparin (IC50 = 1.85 mug mL-1 (R2 = 0.94) and 2.43 mug mL-1 (R2 = 0.93), respectively), while possessing highly attenuated anticoagulant activities.	Glycosaminoglycans	46-63	L1 cell adhesion molecule	Mus musculus	228-232
31100859-5	2019	A marine-derived, heparan sulphate-containing glycosaminoglycan extract, isolated from the crab Portunus pelagicus, was identified to inhibit human BACE1 with comparable bioactivity to that of mammalian heparin (IC50 = 1.85 mug mL-1 (R2 = 0.94) and 2.43 mug mL-1 (R2 = 0.93), respectively), while possessing highly attenuated anticoagulant activities.	Glycosaminoglycans	46-63	L1 cell adhesion molecule	Mus musculus	258-262
30666821-4	2019	We demonstrated extended release of rhBMP-2 from CS-GAG scaffolds compared to their collagen sponge counterparts, and further extended release from CS-GAG gels seeded with BMP-2 MSC.	Glycosaminoglycans	52-55	bone morphogenetic protein 2	Homo sapiens	38-43
31100859-0	2019	A Glycosaminoglycan Extract from Portunus pelagicus Inhibits BACE1, the beta Secretase Implicated in Alzheimer"s Disease.	Glycosaminoglycans	2-19	beta-secretase 1	Homo sapiens	61-66
31100859-2	2019	The glycosaminoglycan heparin, widely used as a clinical anticoagulant, has previously been shown to inhibit the Alzheimer"s disease-relevant beta-secretase 1 (BACE1).	Glycosaminoglycans	4-21	beta-secretase 1	Homo sapiens	160-165
30905864-12	2019	The resulting localized delivery of transforming growth factor beta1 increases glycosaminoglycan and collagen production within the micromasses without exogenous stimulation in the medium.	Glycosaminoglycans	79-96	transforming growth factor beta 1	Homo sapiens	36-68
31193135-1	2019	Iduronate-2-sulfatase (IDS) is a lysosomal enzyme involved in the metabolism of the glycosaminoglycans heparan (HS) and dermatan (DS) sulfate.	Glycosaminoglycans	84-102	iduronate 2-sulfatase	Mus musculus	0-21
31193135-1	2019	Iduronate-2-sulfatase (IDS) is a lysosomal enzyme involved in the metabolism of the glycosaminoglycans heparan (HS) and dermatan (DS) sulfate.	Glycosaminoglycans	84-102	iduronate 2-sulfatase	Mus musculus	23-26
31022913-1	2019	Mucopolysaccharidosis type II (MPSII) is a lysosomal storage disorder due to the deficit of the enzyme iduronate 2-sulfatase (IDS), which leads to the accumulation of glycosaminoglycans in most organ-systems, including the brain, and resulting in neurological involvement in about two-thirds of the patients.	Glycosaminoglycans	167-185	iduronate 2-sulfatase	Homo sapiens	103-124
30685487-1	2019	OBJECTIVE: We investigated the effects of 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f) on xylosyltransferase-1 (XT-1), an essential anabolic enzyme that catalyzes the initial and rate-determining step in glycosaminoglycan chain synthesis, in human primary chondrocytes.	Glycosaminoglycans	216-233	xylosyltransferase 1	Homo sapiens	102-122
30685487-1	2019	OBJECTIVE: We investigated the effects of 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f) on xylosyltransferase-1 (XT-1), an essential anabolic enzyme that catalyzes the initial and rate-determining step in glycosaminoglycan chain synthesis, in human primary chondrocytes.	Glycosaminoglycans	216-233	xylosyltransferase 1	Homo sapiens	124-128
30685487-11	2019	CONCLUSION: These results demonstrate that 29-kDa FN-f negatively affects cartilage anabolism by regulating glycosaminoglycan formation through XT-1.	Glycosaminoglycans	108-125	xylosyltransferase 1	Homo sapiens	144-148
30803152-6	2019	Unlike Col-GAG, hMSCs on MC-GAG expressed increased amounts of osteoprotegerin (OPG) protein, the major endogenous osteoclast inhibitor.	Glycosaminoglycans	28-31	TNF receptor superfamily member 11b	Homo sapiens	63-78
30803152-6	2019	Unlike Col-GAG, hMSCs on MC-GAG expressed increased amounts of osteoprotegerin (OPG) protein, the major endogenous osteoclast inhibitor.	Glycosaminoglycans	28-31	TNF receptor superfamily member 11b	Homo sapiens	80-83
30803152-8	2019	Collectively, these results suggested that the MC-GAG material both directly inhibited the osteoclast viability, proliferation, and resorptive activity as well as induced hMSCs to secrete osteoprotegerin, an antiosteoclastogenic factor, via a signalling pathway distinct from osteogenic differentiation.	Glycosaminoglycans	50-53	TNF receptor superfamily member 11b	Homo sapiens	188-203
31022913-1	2019	Mucopolysaccharidosis type II (MPSII) is a lysosomal storage disorder due to the deficit of the enzyme iduronate 2-sulfatase (IDS), which leads to the accumulation of glycosaminoglycans in most organ-systems, including the brain, and resulting in neurological involvement in about two-thirds of the patients.	Glycosaminoglycans	167-185	iduronate 2-sulfatase	Homo sapiens	126-129
31022913-4	2019	Fibroblasts from MPSII patients were treated for 7 days with NPs loaded with the IDS enzyme; an induced IDS activity like the one detected in healthy cells was measured, together with a reduction of GAG content to non-pathological levels.	Glycosaminoglycans	199-202	iduronate 2-sulfatase	Homo sapiens	81-84
30952887-4	2019	Three of 12 vaccinees were completely protected and these animals elicited sustained Gag-specific poly-functional, cytotoxic mucosal CD4+ T cells, complemented by systemic poly-functional CD4+ and CD8+ T cell immunity.	Glycosaminoglycans	85-88	T-cell surface glycoprotein CD4	Macaca nemestrina	133-136
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
29663644-6	2019	Safranin-O staining demonstrated a typical depletion of glycosaminoglycans in TNF-alpha-treated micromasses but not in the presence of the hydrogel.	Glycosaminoglycans	56-74	tumor necrosis factor	Homo sapiens	78-87
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
31065277-1	2019	Mucopolysaccharidosis type 1 (MPS-1), also known as Hurler"s disease, is a congenital metabolic disorder caused by a mutation in the alpha-L-iduronidase (IDUA) gene, which results in the loss of lysosomal enzyme function for the degradation of glycosaminoglycans.	Glycosaminoglycans	244-262	iduronidase, alpha-L	Mus musculus	133-152
31065277-1	2019	Mucopolysaccharidosis type 1 (MPS-1), also known as Hurler"s disease, is a congenital metabolic disorder caused by a mutation in the alpha-L-iduronidase (IDUA) gene, which results in the loss of lysosomal enzyme function for the degradation of glycosaminoglycans.	Glycosaminoglycans	244-262	iduronidase, alpha-L	Mus musculus	154-158
30894640-8	2019	Our combined experimental and theoretical approach provides valuable new insights on how GAG interfere with MMP2 activity and MMP2/TIMP3 complex formation.	Glycosaminoglycans	89-92	matrix metallopeptidase 2	Homo sapiens	108-112
31016187-6	2019	In vivo, the exogenous genes enhanced COL2A1, ACAN, and TIMP-1 expression in cartilage and reduced cartilage Mankin score and the contents of NO, IL-1beta, TNF-alpha, and GAG contents in synovial fluid of rabbits, MMP-13, ADAMTS-5, COL1A2, and COL10A1 levels in cartilage.	Glycosaminoglycans	171-174	collagen alpha-1(II) chain	Oryctolagus cuniculus	38-44
31016187-6	2019	In vivo, the exogenous genes enhanced COL2A1, ACAN, and TIMP-1 expression in cartilage and reduced cartilage Mankin score and the contents of NO, IL-1beta, TNF-alpha, and GAG contents in synovial fluid of rabbits, MMP-13, ADAMTS-5, COL1A2, and COL10A1 levels in cartilage.	Glycosaminoglycans	171-174	aggrecan core protein	Oryctolagus cuniculus	46-50
31016187-6	2019	In vivo, the exogenous genes enhanced COL2A1, ACAN, and TIMP-1 expression in cartilage and reduced cartilage Mankin score and the contents of NO, IL-1beta, TNF-alpha, and GAG contents in synovial fluid of rabbits, MMP-13, ADAMTS-5, COL1A2, and COL10A1 levels in cartilage.	Glycosaminoglycans	171-174	metalloproteinase inhibitor 1	Oryctolagus cuniculus	56-62
30921340-8	2019	It was observed that DNA priming and MVA boosting induced Env and Gag specific bi-functional and multi-functional CD4+ and CD8+ T cells expressing IFN-gamma, TNF-alpha and IL-2.	Glycosaminoglycans	66-69	CD4 molecule	Homo sapiens	114-117
30921340-8	2019	It was observed that DNA priming and MVA boosting induced Env and Gag specific bi-functional and multi-functional CD4+ and CD8+ T cells expressing IFN-gamma, TNF-alpha and IL-2.	Glycosaminoglycans	66-69	CD8a molecule	Homo sapiens	123-126
30921340-8	2019	It was observed that DNA priming and MVA boosting induced Env and Gag specific bi-functional and multi-functional CD4+ and CD8+ T cells expressing IFN-gamma, TNF-alpha and IL-2.	Glycosaminoglycans	66-69	interferon gamma	Homo sapiens	147-156
30921340-8	2019	It was observed that DNA priming and MVA boosting induced Env and Gag specific bi-functional and multi-functional CD4+ and CD8+ T cells expressing IFN-gamma, TNF-alpha and IL-2.	Glycosaminoglycans	66-69	tumor necrosis factor	Homo sapiens	158-167
30921340-8	2019	It was observed that DNA priming and MVA boosting induced Env and Gag specific bi-functional and multi-functional CD4+ and CD8+ T cells expressing IFN-gamma, TNF-alpha and IL-2.	Glycosaminoglycans	66-69	interleukin 2	Homo sapiens	172-176
30894640-0	2019	Glycosaminoglycans influence enzyme activity of MMP2 and MMP2/TIMP3 complex formation - Insights at cellular and molecular level.	Glycosaminoglycans	0-18	matrix metallopeptidase 2	Homo sapiens	48-52
30894640-0	2019	Glycosaminoglycans influence enzyme activity of MMP2 and MMP2/TIMP3 complex formation - Insights at cellular and molecular level.	Glycosaminoglycans	0-18	matrix metallopeptidase 2	Homo sapiens	57-61
30894640-8	2019	Our combined experimental and theoretical approach provides valuable new insights on how GAG interfere with MMP2 activity and MMP2/TIMP3 complex formation.	Glycosaminoglycans	89-92	matrix metallopeptidase 2	Homo sapiens	126-130
30894640-8	2019	Our combined experimental and theoretical approach provides valuable new insights on how GAG interfere with MMP2 activity and MMP2/TIMP3 complex formation.	Glycosaminoglycans	89-92	TIMP metallopeptidase inhibitor 3	Homo sapiens	131-136
30894640-0	2019	Glycosaminoglycans influence enzyme activity of MMP2 and MMP2/TIMP3 complex formation - Insights at cellular and molecular level.	Glycosaminoglycans	0-18	TIMP metallopeptidase inhibitor 3	Homo sapiens	62-67
30735356-2	2019	Herpes simplex virus type 1 (HSV-1), for example, exhibits a mucin-like region on its glycoprotein gC, a viral protein involved in initial recruitment of the virus to the cell surface via interaction with sulfated glycosaminoglycans.	Glycosaminoglycans	214-232	LOC100508689	Homo sapiens	61-66
30894640-4	2019	Here, we investigated the molecular interplay of MMP2 with different GAG (chondroitin sulfate, hyaluronan (HA), sulfated hyaluronan (SH) and heparin (HE)) and the impact of GAG on MMP2/TIMP3 complex formation using in vitro-experiments with human bone marrow stromal cells, in silico docking and molecular dynamics simulations.	Glycosaminoglycans	69-72	matrix metallopeptidase 2	Homo sapiens	49-53
30735356-3	2019	So far, this mucin-like region has been proposed to play a key role in modulating the interactions with cellular glycosaminoglycans, and in particular to promote release of HSV-1 virions from infected cells.	Glycosaminoglycans	113-131	LOC100508689	Homo sapiens	13-18
30735356-7	2019	Our data suggest that the mucin-like region modulates virus-glycosaminoglycan interactions by regulating the affinity, type, and number of glycoproteins involved in the virus-glycosaminoglycan interaction.	Glycosaminoglycans	60-77	LOC100508689	Homo sapiens	26-31
30735356-7	2019	Our data suggest that the mucin-like region modulates virus-glycosaminoglycan interactions by regulating the affinity, type, and number of glycoproteins involved in the virus-glycosaminoglycan interaction.	Glycosaminoglycans	175-192	LOC100508689	Homo sapiens	26-31
30735356-8	2019	This study therefore presents new evidence for a role of the mucin-like region in balancing the interaction of HSV-1 with glycosaminoglycans and provides further insights into the molecular mechanisms used by the virus to ensure both successful cell entry and release from the infected cell.	Glycosaminoglycans	122-140	LOC100508689	Homo sapiens	61-66
30660005-6	2019	Docking and molecular dynamics analysis of a molecular model of HB-EGF led to the identification of residues in the heparin-binding domain of the protein being essential for the recognition of GAG derivatives.	Glycosaminoglycans	193-196	heparin binding EGF like growth factor	Homo sapiens	64-70
30845788-4	2019	Possible inter-species differences in the GAG-binding sites on antithrombin III, heparanase, and chemokines of the CCL and CXCL families were examined by sequence alignments, molecular modelling and assessment of surface electrostatic potentials to determine if one species of laboratory animal is likely to result in more clinically relevant data than another.	Glycosaminoglycans	42-45	serpin family C member 1	Homo sapiens	63-79
32254916-3	2019	Chondroitin sulfate (CS), a sulfated glycosaminoglycan (GAG), is distributed throughout animal bodies, including cartilage and the extracellular matrix (ECM), and it has been widely utilized in the dietary supplement and pharmaceutical industries.	Glycosaminoglycans	56-59	citrate synthase	Homo sapiens	21-23
30861996-7	2019	Moderate glycosaminoglycan (GAG) staining was observed in untreated and NE-treated cells, while IL-1beta strongly decreased GAG deposition.	Glycosaminoglycans	124-127	interleukin 1 beta	Homo sapiens	96-104
30857263-1	2019	beta-glucuronidase is a lysosomal glycosidase enzyme which catalyzes the extracellular matrix of cancer and normal cells and the glycosaminoglycans of the cell membrane, which is important for cancer cell proliferation, invasion, and metastasis.	Glycosaminoglycans	129-147	glucuronidase beta	Homo sapiens	0-18
30447344-8	2019	Furthermore, DKK1 stimulated expression of collagen type II (COL2A1) and glycosaminoglycans (GAGs), which represent healthy articular cartilage markers.	Glycosaminoglycans	73-91	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	13-17
30852161-8	2019	Upon engaging with glycosaminoglycans on the membrane of fimbrial epithelial cells, PAPP-A cleaves IGFBPs and releases IGF2 to bind with IGF-1R.	Glycosaminoglycans	19-37	pappalysin 1	Homo sapiens	84-90
30852161-8	2019	Upon engaging with glycosaminoglycans on the membrane of fimbrial epithelial cells, PAPP-A cleaves IGFBPs and releases IGF2 to bind with IGF-1R.	Glycosaminoglycans	19-37	insulin like growth factor binding protein 2	Homo sapiens	99-105
30852161-8	2019	Upon engaging with glycosaminoglycans on the membrane of fimbrial epithelial cells, PAPP-A cleaves IGFBPs and releases IGF2 to bind with IGF-1R.	Glycosaminoglycans	19-37	insulin like growth factor 2	Homo sapiens	119-123
30852161-8	2019	Upon engaging with glycosaminoglycans on the membrane of fimbrial epithelial cells, PAPP-A cleaves IGFBPs and releases IGF2 to bind with IGF-1R.	Glycosaminoglycans	19-37	insulin like growth factor 1 receptor	Homo sapiens	137-143
30811489-8	2019	We identified 15 conserved epitopes in Pol (11), Gag (3), and Nef (1) according to their potential presentation by the dominant HLA-A and B alleles and now propose to use the corresponding conserved peptides in a multi-epitopic vaccine (HLA-fitted VAC, HFVAC).	Glycosaminoglycans	49-52	major histocompatibility complex, class I, A	Homo sapiens	128-139
30863107-6	2019	Kyoto Encyclopedia of Genes and Genomes analysis showed that target genes of miR-4792 were enriched in aminoacyltRNA biosynthesis, AGE-RAGE signaling pathway in diabetic complications, sphingolipid signaling pathway, neuroactive ligand-receptor interaction, glycosaminoglycan degradation, and regulation of lipolysis in adipocytes.	Glycosaminoglycans	258-275	microRNA 4792	Homo sapiens	77-85
30528777-6	2019	Interestingly, the hydrophobic pocket is in the vicinity of GAG binding region of CXCL3, a molecular determinant in leukocyte trafficking.	Glycosaminoglycans	60-63	C-X-C motif chemokine ligand 3	Homo sapiens	82-87
30698412-7	2019	In different regions of the bovine eyes, CS was the major GAG, and the amounts of hyaluronic acid or keratan sulfate varied depending on the region of the eye.	Glycosaminoglycans	58-61	citrate synthase	Bos taurus	41-43
30830870-4	2019	Immunization with HVVs induced very high-magnitude Gag-specific CD8+ T cell responses in blood and tissue-resident CD8+ memory T cells in vaginal mucosa.	Glycosaminoglycans	51-54	CD8a molecule	Homo sapiens	64-67
30669426-0	2019	Microcarriers Based on Glycosaminoglycan-Like Marine Exopolysaccharide for TGF-beta1 Long-Term Protection.	Glycosaminoglycans	23-40	transforming growth factor beta 1	Homo sapiens	75-84
30710015-2	2019	It is a linear glycosaminoglycan composed of disaccharide units of GlcNAc and d-glucuronic acid with alternating beta-1,4 and beta-1,3 glycosidic bonds that can be repeated 20,000 or more times, a molecular mass &gt;8 million Da, and a length &gt;20 mum.	Glycosaminoglycans	15-32	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	113-121
30710015-2	2019	It is a linear glycosaminoglycan composed of disaccharide units of GlcNAc and d-glucuronic acid with alternating beta-1,4 and beta-1,3 glycosidic bonds that can be repeated 20,000 or more times, a molecular mass &gt;8 million Da, and a length &gt;20 mum.	Glycosaminoglycans	15-32	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	126-134
30595526-1	2019	Hunter syndrome (mucopolysaccharidosis II [MPS II]), a deficiency of iduronate-2-sulfatase (IDS), causes an accumulation of glycosaminoglycans, giving rise to multiple systemic and CNS symptoms.	Glycosaminoglycans	124-142	iduronate 2-sulfatase	Homo sapiens	69-90
30595526-1	2019	Hunter syndrome (mucopolysaccharidosis II [MPS II]), a deficiency of iduronate-2-sulfatase (IDS), causes an accumulation of glycosaminoglycans, giving rise to multiple systemic and CNS symptoms.	Glycosaminoglycans	124-142	iduronate 2-sulfatase	Homo sapiens	92-95
30500378-2	2019	The capacity of the side glycosaminoglycan chain heparan sulfate (HS) being able to interact with diverse protein ligands relies on its complex structure that is generated by a controlled biosynthesis process, involving the actions of glycosyl-transferases, sulfotransferases and the glucuronyl C5-epimerase.	Glycosaminoglycans	25-42	glucuronic acid epimerase	Homo sapiens	284-307
30557915-3	2019	Among the treatment regimens, the combination of the three stimuli (TCL treatment) led to the most robust glycosaminoglycan content, total collagen content, and type II collagen production.	Glycosaminoglycans	106-123	ras homolog family member J	Homo sapiens	68-71
30563944-7	2019	Hspg2 exon 3 null intervertebral discs accumulated significantly greater glycosaminoglycan in the nucleus pulposus, annulus fibrosus, and vertebral growth plates than C57BL/6 wild-type (WT) I intervertebral discs.	Glycosaminoglycans	73-90	perlecan (heparan sulfate proteoglycan 2)	Mus musculus	0-5
30611221-13	2019	CONCLUSIONS: Glycosaminoglycan, CaG can strengthen ECM by increasing activity of TIMP-2 and adhesion activity on collagen known to inhibit changes of ECM, leading to tumor cell invasion and progression.	Glycosaminoglycans	13-30	tissue inhibitor of metalloproteinase 2	Mus musculus	81-87
30528089-1	2019	Mucopolysaccharidosis type I (MPS I) is a severe disease due to deficiency of the lysosomal hydrolase alpha-L-iduronidase (IDUA) and the subsequent accumulation of the glycosaminoglycans (GAG), leading to progressive, systemic disease and a shortened lifespan.	Glycosaminoglycans	168-186	iduronidase, alpha-L	Mus musculus	102-121
30528089-1	2019	Mucopolysaccharidosis type I (MPS I) is a severe disease due to deficiency of the lysosomal hydrolase alpha-L-iduronidase (IDUA) and the subsequent accumulation of the glycosaminoglycans (GAG), leading to progressive, systemic disease and a shortened lifespan.	Glycosaminoglycans	168-186	iduronidase, alpha-L	Mus musculus	123-127
30528089-1	2019	Mucopolysaccharidosis type I (MPS I) is a severe disease due to deficiency of the lysosomal hydrolase alpha-L-iduronidase (IDUA) and the subsequent accumulation of the glycosaminoglycans (GAG), leading to progressive, systemic disease and a shortened lifespan.	Glycosaminoglycans	188-191	iduronidase, alpha-L	Mus musculus	123-127
30028513-3	2018	A protein interaction site is present in the ARC C-terminal domain (CTD), a bilobar structure homologous to the retroviral Gag capsid domain.	Glycosaminoglycans	123-126	activity-regulated cytoskeleton-associated protein	Rattus norvegicus	45-48
29984655-1	2019	BACKGROUND: The small leucine-rich proteoglycans (SLRPs) biglycan (BGN) and decorin (DCN) linked with sulfated glycosaminoglycan (GAG) chains exhibit oncogenic or tumor suppressive potentials depending on the cellular context and association with GAGs.	Glycosaminoglycans	111-128	biglycan	Homo sapiens	67-70
29984655-1	2019	BACKGROUND: The small leucine-rich proteoglycans (SLRPs) biglycan (BGN) and decorin (DCN) linked with sulfated glycosaminoglycan (GAG) chains exhibit oncogenic or tumor suppressive potentials depending on the cellular context and association with GAGs.	Glycosaminoglycans	130-133	biglycan	Homo sapiens	67-70
30774881-4	2019	Through an experimental and computational approach using fluorescence polarization, ITC, docking and molecular dynamics simulations we investigate the binding of these functionalized GAG derivatives to ten representative regulatory proteins including IL-8, IL-10, BMP-2, sclerostin, TIMP-3, CXCL-12, TGF-beta, FGF-1, FGF-2, and AT-III, and we establish structure-activity relationships for GAG recognition.	Glycosaminoglycans	183-186	C-X-C motif chemokine ligand 8	Homo sapiens	251-255
30774881-4	2019	Through an experimental and computational approach using fluorescence polarization, ITC, docking and molecular dynamics simulations we investigate the binding of these functionalized GAG derivatives to ten representative regulatory proteins including IL-8, IL-10, BMP-2, sclerostin, TIMP-3, CXCL-12, TGF-beta, FGF-1, FGF-2, and AT-III, and we establish structure-activity relationships for GAG recognition.	Glycosaminoglycans	183-186	interleukin 10	Homo sapiens	257-262
30774881-4	2019	Through an experimental and computational approach using fluorescence polarization, ITC, docking and molecular dynamics simulations we investigate the binding of these functionalized GAG derivatives to ten representative regulatory proteins including IL-8, IL-10, BMP-2, sclerostin, TIMP-3, CXCL-12, TGF-beta, FGF-1, FGF-2, and AT-III, and we establish structure-activity relationships for GAG recognition.	Glycosaminoglycans	183-186	bone morphogenetic protein 2	Homo sapiens	264-269
30774881-4	2019	Through an experimental and computational approach using fluorescence polarization, ITC, docking and molecular dynamics simulations we investigate the binding of these functionalized GAG derivatives to ten representative regulatory proteins including IL-8, IL-10, BMP-2, sclerostin, TIMP-3, CXCL-12, TGF-beta, FGF-1, FGF-2, and AT-III, and we establish structure-activity relationships for GAG recognition.	Glycosaminoglycans	183-186	TIMP metallopeptidase inhibitor 3	Homo sapiens	283-289
30774881-4	2019	Through an experimental and computational approach using fluorescence polarization, ITC, docking and molecular dynamics simulations we investigate the binding of these functionalized GAG derivatives to ten representative regulatory proteins including IL-8, IL-10, BMP-2, sclerostin, TIMP-3, CXCL-12, TGF-beta, FGF-1, FGF-2, and AT-III, and we establish structure-activity relationships for GAG recognition.	Glycosaminoglycans	183-186	C-X-C motif chemokine ligand 12	Homo sapiens	291-298
30774881-4	2019	Through an experimental and computational approach using fluorescence polarization, ITC, docking and molecular dynamics simulations we investigate the binding of these functionalized GAG derivatives to ten representative regulatory proteins including IL-8, IL-10, BMP-2, sclerostin, TIMP-3, CXCL-12, TGF-beta, FGF-1, FGF-2, and AT-III, and we establish structure-activity relationships for GAG recognition.	Glycosaminoglycans	183-186	fibroblast growth factor 1	Homo sapiens	310-315
30774881-4	2019	Through an experimental and computational approach using fluorescence polarization, ITC, docking and molecular dynamics simulations we investigate the binding of these functionalized GAG derivatives to ten representative regulatory proteins including IL-8, IL-10, BMP-2, sclerostin, TIMP-3, CXCL-12, TGF-beta, FGF-1, FGF-2, and AT-III, and we establish structure-activity relationships for GAG recognition.	Glycosaminoglycans	183-186	fibroblast growth factor 2	Homo sapiens	317-322
30774881-4	2019	Through an experimental and computational approach using fluorescence polarization, ITC, docking and molecular dynamics simulations we investigate the binding of these functionalized GAG derivatives to ten representative regulatory proteins including IL-8, IL-10, BMP-2, sclerostin, TIMP-3, CXCL-12, TGF-beta, FGF-1, FGF-2, and AT-III, and we establish structure-activity relationships for GAG recognition.	Glycosaminoglycans	183-186	serpin family C member 1	Homo sapiens	328-334
30423352-10	2019	The target pathways (excluding Jnk) were involved in the expression of the GAG elongation genes (C4ST-1 and CHSY-1).	Glycosaminoglycans	75-78	mitogen-activated protein kinase 8	Homo sapiens	31-34
30423352-10	2019	The target pathways (excluding Jnk) were involved in the expression of the GAG elongation genes (C4ST-1 and CHSY-1).	Glycosaminoglycans	75-78	carbohydrate sulfotransferase 11	Homo sapiens	97-103
30423352-10	2019	The target pathways (excluding Jnk) were involved in the expression of the GAG elongation genes (C4ST-1 and CHSY-1).	Glycosaminoglycans	75-78	chondroitin sulfate synthase 1	Homo sapiens	108-114
30507579-2	2019	Brain ECM is abundant in hyaluronan (HA), a non-sulfated glycosaminoglycan synthesized by HA synthases (HAS) 1-3 in a high molecular weight (MW) form that is degraded into lower MW fragments.	Glycosaminoglycans	57-74	hyaluronan synthase 1	Homo sapiens	90-112
30564243-6	2018	In vitro study shows that IL-33 promotes the expression of IFN-gamma by Gag stimulated CD4+ and CD8+T cells from HIV-infected patients to a certain extent.	Glycosaminoglycans	72-75	interleukin 33	Homo sapiens	26-31
30564243-6	2018	In vitro study shows that IL-33 promotes the expression of IFN-gamma by Gag stimulated CD4+ and CD8+T cells from HIV-infected patients to a certain extent.	Glycosaminoglycans	72-75	interferon gamma	Homo sapiens	59-68
30564243-6	2018	In vitro study shows that IL-33 promotes the expression of IFN-gamma by Gag stimulated CD4+ and CD8+T cells from HIV-infected patients to a certain extent.	Glycosaminoglycans	72-75	CD4 molecule	Homo sapiens	87-90
30564243-6	2018	In vitro study shows that IL-33 promotes the expression of IFN-gamma by Gag stimulated CD4+ and CD8+T cells from HIV-infected patients to a certain extent.	Glycosaminoglycans	72-75	CD8a molecule	Homo sapiens	96-99
30555231-6	2018	Results: A linear correlation exists between the GAG assay and the qPCR for the quantification of the TOP1 and TDP2 mRNA transcripts (101-104 copies).	Glycosaminoglycans	49-52	tyrosyl-DNA phosphodiesterase 2	Homo sapiens	111-115
30205243-2	2018	Glycosaminoglycan (GAG) sugars are known to enhance BMP activity in vitro and in vivo; here the interactions of BMP-2 with various glycosaminoglycan classes were compared and shown to be selective for heparin over other comparable saccharides.	Glycosaminoglycans	131-148	bone morphogenetic protein 2	Homo sapiens	112-117
29173042-1	2018	Antithrombin (AT) is a serpin that inhibits mainly thrombin and fXa after being activated by binding to glycosaminoglycans as heparin and heparan sulfate.	Glycosaminoglycans	104-122	serpin family C member 1	Homo sapiens	0-12
29173042-1	2018	Antithrombin (AT) is a serpin that inhibits mainly thrombin and fXa after being activated by binding to glycosaminoglycans as heparin and heparan sulfate.	Glycosaminoglycans	104-122	coagulation factor II, thrombin	Homo sapiens	4-12
29173042-1	2018	Antithrombin (AT) is a serpin that inhibits mainly thrombin and fXa after being activated by binding to glycosaminoglycans as heparin and heparan sulfate.	Glycosaminoglycans	104-122	coagulation factor X	Homo sapiens	64-67
29978271-1	2018	Mucopolysaccharidosis II (MPS II) is caused by a deficiency of iduronate-2-sulfatase that results in accumulation of glycosaminoglycans (GAG), including heparan sulfate (HS), which is considered to contribute to neuropathology.	Glycosaminoglycans	117-135	iduronate 2-sulfatase	Mus musculus	63-84
29978271-1	2018	Mucopolysaccharidosis II (MPS II) is caused by a deficiency of iduronate-2-sulfatase that results in accumulation of glycosaminoglycans (GAG), including heparan sulfate (HS), which is considered to contribute to neuropathology.	Glycosaminoglycans	137-140	iduronate 2-sulfatase	Mus musculus	63-84
30170069-1	2018	Mucopolysaccharidosis type I (MPS I) is a multisystemic disorder caused by the deficiency of alpha-L-iduronidase (IDUA) that leads to intracellular accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	164-182	alpha-L-iduronidase	Homo sapiens	93-112
30259667-0	2018	Novel Surface Coatings Using Oxidized Glycosaminoglycans as Delivery Systems of Bone Morphogenetic Protein 2 (BMP-2) for Bone Regeneration.	Glycosaminoglycans	38-56	bone morphogenetic protein 2	Homo sapiens	80-108
30259667-0	2018	Novel Surface Coatings Using Oxidized Glycosaminoglycans as Delivery Systems of Bone Morphogenetic Protein 2 (BMP-2) for Bone Regeneration.	Glycosaminoglycans	38-56	bone morphogenetic protein 2	Homo sapiens	110-115
30170069-1	2018	Mucopolysaccharidosis type I (MPS I) is a multisystemic disorder caused by the deficiency of alpha-L-iduronidase (IDUA) that leads to intracellular accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	164-182	alpha-L-iduronidase	Homo sapiens	114-118
30170069-1	2018	Mucopolysaccharidosis type I (MPS I) is a multisystemic disorder caused by the deficiency of alpha-L-iduronidase (IDUA) that leads to intracellular accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	184-187	alpha-L-iduronidase	Homo sapiens	93-112
30170069-1	2018	Mucopolysaccharidosis type I (MPS I) is a multisystemic disorder caused by the deficiency of alpha-L-iduronidase (IDUA) that leads to intracellular accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	184-187	alpha-L-iduronidase	Homo sapiens	114-118
30356641-9	2018	Glycosaminoglycan chain interactions of Neurocan were required for inhibition of Sema3F-induced spine elimination, but the C-terminal sushi domain was dispensable.	Glycosaminoglycans	0-17	sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3F	Mus musculus	81-87
30257828-6	2018	ELISA assays showed obvious deficiency of NAGLU and higher (P&lt;0.05) glycosaminoglycan levels in multiple tissues from NAGLU +/- pigs.	Glycosaminoglycans	71-88	NAGLU	Sus scrofa	121-126
30230320-5	2018	In CXCL8, both histidines exist in the Nepsilon2 tautomeric state in the free, GAG-bound, and receptor-bound forms.	Glycosaminoglycans	79-82	C-X-C motif chemokine ligand 8	Homo sapiens	3-8
30184438-3	2018	This region of IGFBP-3 was shown earlier to bind certain glycosaminoglycans including hyaluronan (HA).	Glycosaminoglycans	57-75	insulin like growth factor binding protein 3	Homo sapiens	15-22
32165899-1	2019	Mucopolysaccharidosis type I (MPS I or Hurler syndrome) is a multisystem genetic disorder caused by alpha-L-iduronidase (IDUA) deficiency, which leads to widespread accumulation of glycosaminoglycans triggering tissue damage and organ dysfunction.	Glycosaminoglycans	181-199	alpha-L-iduronidase	Homo sapiens	100-119
32165899-1	2019	Mucopolysaccharidosis type I (MPS I or Hurler syndrome) is a multisystem genetic disorder caused by alpha-L-iduronidase (IDUA) deficiency, which leads to widespread accumulation of glycosaminoglycans triggering tissue damage and organ dysfunction.	Glycosaminoglycans	181-199	alpha-L-iduronidase	Homo sapiens	121-125
29754316-4	2018	Likely due to the long half-life of vascular elastin, most mechanical changes in the arterial wall resulted largely from a distributed increase in collagen, including thicker fibers in the media, and localized increases in glycosaminoglycans.	Glycosaminoglycans	223-241	elastin	Mus musculus	45-52
30371322-6	2018	Total glycosaminoglycans increased similarly in both DCM groups but exhibited a significantly lower affinity for transforming growth factor-beta in adult DCMs versus pediatric DCMs, resulting in increased bioavailability of transforming growth factor-beta1 and a significantly higher activity of the Smad2/3 pathway in adult DCMs.	Glycosaminoglycans	6-24	transforming growth factor beta 1	Homo sapiens	224-256
30371322-6	2018	Total glycosaminoglycans increased similarly in both DCM groups but exhibited a significantly lower affinity for transforming growth factor-beta in adult DCMs versus pediatric DCMs, resulting in increased bioavailability of transforming growth factor-beta1 and a significantly higher activity of the Smad2/3 pathway in adult DCMs.	Glycosaminoglycans	6-24	SMAD family member 2	Homo sapiens	300-307
30105814-2	2018	A newly identified kinase - family with sequence similarity 20 member B (FAM20B) - is essential for the formation of GAG chains.	Glycosaminoglycans	117-120	FAM20B, glycosaminoglycan xylosylkinase	Mus musculus	73-79
30031224-4	2018	Our in vitro data show that SCII induces M2 polarization of macrophages, and activates macrophages to express pro-chondrogenic genes (TGF-beta and IGF), which greatly improves the microenvironment around chondrocytes to produce type II collagen and glycosaminoglycan.	Glycosaminoglycans	249-266	transforming growth factor, beta 1	Rattus norvegicus	134-142
29294496-11	2018	Glycosaminoglycans (GAG) content decreased significantly (p = 0.009) in the IL-1 group compared with the NC group.	Glycosaminoglycans	0-18	interleukin 1 beta	Canis lupus familiaris	76-80
29294496-11	2018	Glycosaminoglycans (GAG) content decreased significantly (p = 0.009) in the IL-1 group compared with the NC group.	Glycosaminoglycans	20-23	interleukin 1 beta	Canis lupus familiaris	76-80
30068652-7	2018	Using a molecular dynamic simulation, we observed that both gag-PTAP and ORF3-PSAP motifs bind to the same site in UEV-TSG101 by hydrogen bonding.	Glycosaminoglycans	60-63	prosaposin	Homo sapiens	78-82
29644940-9	2018	When exposed to cyclic strain, Scx-overexpressing cells maintained the elongated phenotype exhibited in static constructs, increased GAG production compared to static culture, and increased expression of the ligament-related genes collagen type I, decorin, and tenascin-C compared to strained LacZ controls.	Glycosaminoglycans	133-136	scleraxis	Mus musculus	31-34
30068652-7	2018	Using a molecular dynamic simulation, we observed that both gag-PTAP and ORF3-PSAP motifs bind to the same site in UEV-TSG101 by hydrogen bonding.	Glycosaminoglycans	60-63	tumor susceptibility 101	Homo sapiens	119-125
30068652-8	2018	HIV-released inhibitory CPs also displayed binding to the same site in UEV-TSG101, indicating that they may compete with ORF3-PSAP or gag-PTAP for binding to UEV-TSG101.	Glycosaminoglycans	134-137	tumor susceptibility 101	Homo sapiens	75-81
30068652-8	2018	HIV-released inhibitory CPs also displayed binding to the same site in UEV-TSG101, indicating that they may compete with ORF3-PSAP or gag-PTAP for binding to UEV-TSG101.	Glycosaminoglycans	134-137	tumor susceptibility 101	Homo sapiens	162-168
30227885-0	2018	Effects of a 15-month anti-TNF-alpha treatment on plasma levels of glycosaminoglycans in women with rheumatoid arthritis.	Glycosaminoglycans	67-85	tumor necrosis factor	Homo sapiens	27-36
30227885-1	2018	BACKGROUND: In this study, the effect of 15-month anti-tumor necrosis factor alpha (TNF-alpha) treatment on circulating levels of plasma sulfated glycosaminoglycans (GAGs) and the nonsulfated GAG hyaluronic acid (HA) in female rheumatoid arthritis (RA) patients was assessed.	Glycosaminoglycans	146-164	tumor necrosis factor	Homo sapiens	84-93
30227885-8	2018	Anti-TNF-alpha treatment resulted in normalization of plasma total GAG and HA levels in RA patients, without any effect on KS levels.	Glycosaminoglycans	67-70	tumor necrosis factor	Homo sapiens	5-14
29518374-6	2018	We summarize information on expression of the IAPP gene, the regulation of the hormone by post-translational modifications, the structural properties of the peptide in various states, the kinetics of misfolding to amyloid fibrils, and the interactions of the peptide with insulin, membranes, glycosaminoglycans, and nanoparticles.	Glycosaminoglycans	292-310	islet amyloid polypeptide	Homo sapiens	46-50
29940298-1	2018	Mucopolysaccharidosis type I (MPS I) is caused by the lysosomal accumulation of glycosaminoglycans (GAGs) due to the deficiency of the enzyme alpha-L-iduronidase (IDUA).	Glycosaminoglycans	80-98	iduronidase, alpha-L	Mus musculus	163-167
29940298-1	2018	Mucopolysaccharidosis type I (MPS I) is caused by the lysosomal accumulation of glycosaminoglycans (GAGs) due to the deficiency of the enzyme alpha-L-iduronidase (IDUA).	Glycosaminoglycans	100-104	iduronidase, alpha-L	Mus musculus	163-167
30227887-7	2018	In contrast, very little staining for TGFbeta and dermatan sulfate epimerase, an enzyme involved in glycosylation of glycosaminoglycan chains, was observed in these foci and other cells in both control and DSLD-affected tendons and SLs.	Glycosaminoglycans	117-134	dermatan sulfate epimerase	Equus caballus	50-76
29944975-4	2018	Collagen-GAG scaffolds that incorporate beta-cyclodextrin show improved sequestration as well as extended retention and release of TGF-beta1.	Glycosaminoglycans	9-12	transforming growth factor beta 1	Homo sapiens	131-140
29402725-4	2018	CCL18 can also modulate tissue inflammation by inhibiting cell recruitment through binding to glycosaminoglycans with high affinity, thereby displacing other chemokines bound to the endothelial surface.	Glycosaminoglycans	94-112	C-C motif chemokine ligand 18	Homo sapiens	0-5
29704279-5	2018	Brazilin was found to reduce the GAG loss from cartilage explants stimulated with IL-1beta and TNF-alpha.	Glycosaminoglycans	33-36	interleukin 1 beta	Homo sapiens	82-90
29704279-5	2018	Brazilin was found to reduce the GAG loss from cartilage explants stimulated with IL-1beta and TNF-alpha.	Glycosaminoglycans	33-36	tumor necrosis factor	Homo sapiens	95-104
30064964-1	2018	Mucopolysaccharidosis type II (MPS II or Hunter syndrome) is a lysosomal storage disorder caused by a deficiency of iduronate-2-sulfatase (IDS), an enzyme that catabolizes glycosaminoglycans (GAGs) including heparan sulfate (HS) and dermatan sulfate (DS).	Glycosaminoglycans	172-190	iduronate 2-sulfatase	Mus musculus	139-142
30064964-4	2018	We recently developed a BBB-penetrating IDS fusion protein, JR-141, and demonstrated its ability to reduce GAG accumulation in the brain of human transferrin receptor knock-in and Ids knock-out mice (TFRC-KI/Ids-KO), an animal model of MPS II, following intravenous administration.	Glycosaminoglycans	107-110	iduronate 2-sulfatase	Homo sapiens	40-43
29914979-2	2018	PF4 released from platelets binds to surface glycosaminoglycans on hematopoietic and vascular cells that are heterogenous in composition and differ in affinity for PF4.	Glycosaminoglycans	45-63	platelet factor 4	Mus musculus	0-3
29737194-5	2018	In addition, Gag-specific cytolytic activity (CD107a/b+) was decreased in HAND compared with NL individuals and correlated with their neurological testing, suggesting a potential role of cytotoxic CD8+ T cells in the mechanism of HAND development.	Glycosaminoglycans	13-16	lysosomal associated membrane protein 1	Homo sapiens	46-52
30082715-0	2018	SLC10A7 mutations cause a skeletal dysplasia with amelogenesis imperfecta mediated by GAG biosynthesis defects.	Glycosaminoglycans	86-89	solute carrier family 10 member 7	Homo sapiens	0-7
29733455-6	2018	CXCL9(74-103) competes with CXCL6 and CCL3 for binding to the glycosaminoglycans heparan sulfate and chondroitin sulfate in vitro.	Glycosaminoglycans	62-80	chemokine (C-X-C motif) ligand 9	Mus musculus	0-5
29903730-5	2018	MPO binding to the glycocalyx was further characterized using Chinese hamster ovary cells and its glycosaminoglycan mutants-pgsA-745 (mutant Chinese hamster ovary cells lacking heparan sulfate and chondroitin sulfate glycosaminoglycan) and pgsD-677 (mutant Chinese hamster ovary cells lacking heparan sulfate glycosaminoglycan), which revealed heparan sulfate as the main mediator of MPO binding.	Glycosaminoglycans	98-115	myeloperoxidase	Cricetulus griseus	0-3
29733455-6	2018	CXCL9(74-103) competes with CXCL6 and CCL3 for binding to the glycosaminoglycans heparan sulfate and chondroitin sulfate in vitro.	Glycosaminoglycans	62-80	chemokine (C-X-C motif) ligand 5	Mus musculus	28-33
29768676-2	2018	This difference is attributed to 1) a stronger interaction of the basic C-terminal tail of CCL21 with acidic glycosaminoglycans (GAGs) in the environment and 2) an autoinhibitory function of this C-terminal tail.	Glycosaminoglycans	109-127	C-C motif chemokine ligand 21	Homo sapiens	91-96
29733455-6	2018	CXCL9(74-103) competes with CXCL6 and CCL3 for binding to the glycosaminoglycans heparan sulfate and chondroitin sulfate in vitro.	Glycosaminoglycans	62-80	chemokine (C-C motif) ligand 3	Mus musculus	38-42
29768676-9	2018	Together these results indicate that ligands containing CCL21 core and C-terminal tail (CCL21 and CCL21CCL19-N-term ) are most restricted in their cAMP signaling; a phenotype attributed to a stronger GAG binding of CCL21 and defined structural differences between CCL19 and CCL21.	Glycosaminoglycans	200-203	C-C motif chemokine ligand 21	Homo sapiens	56-61
29768676-9	2018	Together these results indicate that ligands containing CCL21 core and C-terminal tail (CCL21 and CCL21CCL19-N-term ) are most restricted in their cAMP signaling; a phenotype attributed to a stronger GAG binding of CCL21 and defined structural differences between CCL19 and CCL21.	Glycosaminoglycans	200-203	C-C motif chemokine ligand 21	Homo sapiens	88-93
29768676-9	2018	Together these results indicate that ligands containing CCL21 core and C-terminal tail (CCL21 and CCL21CCL19-N-term ) are most restricted in their cAMP signaling; a phenotype attributed to a stronger GAG binding of CCL21 and defined structural differences between CCL19 and CCL21.	Glycosaminoglycans	200-203	C-C motif chemokine ligand 21	Homo sapiens	98-115
29481844-9	2018	The second glycoform, referred to as "NG" (non-glycanated) biglycan, lacks the GAG side chains.	Glycosaminoglycans	79-82	biglycan	Mus musculus	59-67
29768676-9	2018	Together these results indicate that ligands containing CCL21 core and C-terminal tail (CCL21 and CCL21CCL19-N-term ) are most restricted in their cAMP signaling; a phenotype attributed to a stronger GAG binding of CCL21 and defined structural differences between CCL19 and CCL21.	Glycosaminoglycans	200-203	C-C motif chemokine ligand 21	Homo sapiens	88-93
29768676-9	2018	Together these results indicate that ligands containing CCL21 core and C-terminal tail (CCL21 and CCL21CCL19-N-term ) are most restricted in their cAMP signaling; a phenotype attributed to a stronger GAG binding of CCL21 and defined structural differences between CCL19 and CCL21.	Glycosaminoglycans	200-203	C-C motif chemokine ligand 19	Homo sapiens	103-108
29768676-9	2018	Together these results indicate that ligands containing CCL21 core and C-terminal tail (CCL21 and CCL21CCL19-N-term ) are most restricted in their cAMP signaling; a phenotype attributed to a stronger GAG binding of CCL21 and defined structural differences between CCL19 and CCL21.	Glycosaminoglycans	200-203	C-C motif chemokine ligand 21	Homo sapiens	88-93
29773673-10	2018	Combinatorial treatments with other here identified missorted enzymes of this degradation pathway might further correct glycosaminoglycan accumulation and will provide a useful basis to reveal mechanisms of selective, Gnptg-dependent formation of M6P residues on lysosomal proteins.	Glycosaminoglycans	120-137	N-acetylglucosamine-1-phosphotransferase, gamma subunit	Mus musculus	218-223
30006605-4	2018	Here we show that the nonstimulatory, HIV-derived peptide GAG enhances a specific human cytotoxic T lymphocyte response to HBV-derived epitopes presented by HLA-A*02:01.	Glycosaminoglycans	58-61	major histocompatibility complex, class I, A	Homo sapiens	157-162
30042467-2	2018	IDS is one of the sulfatase enzymes required for lysosomal degradation of glycosaminoglycans.	Glycosaminoglycans	74-92	iduronate 2-sulfatase	Homo sapiens	0-3
30042467-2	2018	IDS is one of the sulfatase enzymes required for lysosomal degradation of glycosaminoglycans.	Glycosaminoglycans	74-92	arylsulfatase family member H	Homo sapiens	18-27
29926706-6	2018	Compared with those in control rats, the ID-CBT5101 treatments significantly reduced the serum concentration of inflammation and bone metabolism markers (i.e., COX-2, IL-6, LTB4, and COMP), and significantly increased the concentration of IFN-gamma and glycosaminoglycans.	Glycosaminoglycans	253-271	interferon gamma	Rattus norvegicus	239-248
29420785-2	2018	Both chondroitin sulphate (CS) and heparan sulphate (HS) are important constituents of GAG ligands for RPTPsigma, although they have opposite effects on neuronal cells.	Glycosaminoglycans	87-90	protein tyrosine phosphatase receptor type S	Homo sapiens	103-112
29648490-7	2018	The full-length p57gag DNA vaccine, which contains the CE, increased overall Gag-specific responses but did not increase CE responses in any animals (0/4).	Glycosaminoglycans	77-80	cyclin dependent kinase inhibitor 1C	Homo sapiens	16-19
30042949-2	2018	Genetic mutation/deletion of GAG from TorsonA"s gene resulting in DeltaE303 (which weakens the binding between TorsinA and its activator, such as LULL1) primarily cause this neurodegenerative disorder.	Glycosaminoglycans	29-32	torsin family 1 member A	Homo sapiens	111-118
30042949-2	2018	Genetic mutation/deletion of GAG from TorsonA"s gene resulting in DeltaE303 (which weakens the binding between TorsinA and its activator, such as LULL1) primarily cause this neurodegenerative disorder.	Glycosaminoglycans	29-32	torsin 1A interacting protein 2	Homo sapiens	146-151
29752409-0	2018	Specific glycosaminoglycan chain length and sulfation patterns are required for cell uptake of tau versus alpha-synuclein and beta-amyloid aggregates.	Glycosaminoglycans	9-26	microtubule associated protein tau	Homo sapiens	95-98
29752409-0	2018	Specific glycosaminoglycan chain length and sulfation patterns are required for cell uptake of tau versus alpha-synuclein and beta-amyloid aggregates.	Glycosaminoglycans	9-26	synuclein alpha	Homo sapiens	106-121
29752409-4	2018	Here, we measured direct interaction with modified heparins to determine the size and sulfation requirements for tau, alpha-synuclein, and beta-amyloid (Abeta) aggregate binding to glycosaminoglycans (GAGs).	Glycosaminoglycans	181-199	microtubule associated protein tau	Homo sapiens	113-116
29752409-4	2018	Here, we measured direct interaction with modified heparins to determine the size and sulfation requirements for tau, alpha-synuclein, and beta-amyloid (Abeta) aggregate binding to glycosaminoglycans (GAGs).	Glycosaminoglycans	181-199	amyloid beta precursor protein	Homo sapiens	153-158
29752409-6	2018	Tau aggregates required a precise GAG architecture with defined sulfate moieties in the N- and 6-O-positions, whereas the binding of alpha-synuclein and Abeta aggregates was less stringent.	Glycosaminoglycans	34-37	microtubule associated protein tau	Homo sapiens	0-3
29752409-9	2018	In summary, tau aggregates display specific interactions with HSPGs that depend on GAG length and sulfate moiety position, whereas alpha-synuclein and Abeta aggregates exhibit more flexible interactions with HSPGs.	Glycosaminoglycans	83-86	microtubule associated protein tau	Homo sapiens	12-15
29420785-4	2018	We prepared recombinant RPTPsigma N-terminal fragment containing the GAG binding site and various types of biotin-conjugated GAG (CS and HS) with chemical modification and chemo-enzymatic synthesis.	Glycosaminoglycans	69-72	protein tyrosine phosphatase receptor type S	Homo sapiens	24-33
29930254-5	2018	Cell treatment with chondroitinase ABC ablated migration, suggesting that cis presentation of CXCL4 by cell surface glycosaminoglycans to a GPCR is required.	Glycosaminoglycans	116-134	platelet factor 4	Homo sapiens	94-99
29943542-5	2018	Addition of 100 ng/mL IFN-beta1a to regular TGF-beta3 chondrogenic differentiation medium could improve the concentration of GAG, increase the size of pellets, promote the formation of aggrecan and up-regulate the expression of CollangenII and Sox9.	Glycosaminoglycans	125-128	transforming growth factor beta 3	Homo sapiens	44-53
29706017-12	2018	Deposition of C3 fragments is also needed, which implies that in aHUS, the problem is in simultaneous recognition of C3 fragments and glycosaminoglycans or sialic acids by FH, not just the inability of FH to recognize glomerular endothelium as such.	Glycosaminoglycans	134-152	ferritin heavy polypeptide 1	Mus musculus	172-174
30042881-15	2018	The amplified catabolic phenotype of Hspg2Delta3 - /Delta3 - mice may account for the age-dependent decline in GAG observed in tail tendon over 3 to 12 weeks.	Glycosaminoglycans	111-114	delta like canonical Notch ligand 3	Mus musculus	37-58
29890089-5	2018	FoxA2 overexpression significantly enhanced NP-specific gene expression and the synthesis of glycosaminoglycan and collagen, whereas FoxA2 knockdown decreased NP-like differentiation and the expression of aggrecan and collagen II.	Glycosaminoglycans	93-110	forkhead box A2	Homo sapiens	0-5
29620716-7	2018	Although p24 IgG1 levels were enriched in patients with elevated Gag-specific T-cell responses, these levels remained an independent predictor of low-viral loads (P = 0.04) and high CD4+ cell counts (P = 0.004) after adjusting for Gag-specific T-cell responses and for protective HLA class I alleles.	Glycosaminoglycans	65-68	transmembrane p24 trafficking protein 2	Homo sapiens	9-12
29620716-7	2018	Although p24 IgG1 levels were enriched in patients with elevated Gag-specific T-cell responses, these levels remained an independent predictor of low-viral loads (P = 0.04) and high CD4+ cell counts (P = 0.004) after adjusting for Gag-specific T-cell responses and for protective HLA class I alleles.	Glycosaminoglycans	231-234	transmembrane p24 trafficking protein 2	Homo sapiens	9-12
29904116-0	2018	Neutrophil TLR4 and PKR are targets of breast cancer cell glycosaminoglycans and effectors of glycosaminoglycan-induced APRIL secretion.	Glycosaminoglycans	58-76	toll like receptor 4	Homo sapiens	11-15
29904116-0	2018	Neutrophil TLR4 and PKR are targets of breast cancer cell glycosaminoglycans and effectors of glycosaminoglycan-induced APRIL secretion.	Glycosaminoglycans	58-76	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	20-23
29904116-0	2018	Neutrophil TLR4 and PKR are targets of breast cancer cell glycosaminoglycans and effectors of glycosaminoglycan-induced APRIL secretion.	Glycosaminoglycans	58-75	toll like receptor 4	Homo sapiens	11-15
29904116-0	2018	Neutrophil TLR4 and PKR are targets of breast cancer cell glycosaminoglycans and effectors of glycosaminoglycan-induced APRIL secretion.	Glycosaminoglycans	58-75	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	20-23
29904116-3	2018	We found that breast cancer cells do stimulate neutrophils to secrete APRIL through their glycosaminoglycans.	Glycosaminoglycans	90-108	TNF superfamily member 13	Homo sapiens	70-75
29883024-2	2018	CPN is constitutively active, whereas CPB2 circulates as a precursor, procarboxypeptidase B2 (proCPB2), that needs to be activated by the thrombin-thrombomodulin complex or plasmin bound to glycosaminoglycans.	Glycosaminoglycans	190-208	carboxypeptidase B2 (plasma)	Mus musculus	38-42
29874596-2	2018	In this issue of Structure, Briggs and Hohenester (2018) determined the crystal structure of xylosyltransferase 1 and its structure in ternary complex with UDP-xylose donor and peptide acceptors, providing a mechanistic insight into the role of xylosyltransferase for glycosaminoglycan site selection.	Glycosaminoglycans	268-285	xylosyltransferase 1	Homo sapiens	93-113
29371215-2	2018	In the monogenic disease mucopolysaccharidosis VI, loss-of-function mutations in arylsulfatase B lead to myocardial accumulation of chondroitin sulfate (CS) glycosaminoglycans, manifesting as myriad cardiac symptoms.	Glycosaminoglycans	157-175	arylsulfatase B	Homo sapiens	81-96
29568866-4	2018	In the present study, a HIV gag-based VLP strategy and Bac-to-Bac system were utilized to construct Trop-2, CD40L and gag recombinant baculoviruses, which were then used to infect TN5 cells in order to form Trop-2 VLPs or Trop-2-CD40L VLPs.	Glycosaminoglycans	28-31	tumor-associated calcium signal transducer 2	Mus musculus	100-106
29571744-0	2018	The NC domain of HIV-1 Gag contributes to the interaction of Gag with TSG101.	Glycosaminoglycans	23-26	tumor susceptibility 101	Homo sapiens	70-76
29571744-0	2018	The NC domain of HIV-1 Gag contributes to the interaction of Gag with TSG101.	Glycosaminoglycans	61-64	tumor susceptibility 101	Homo sapiens	70-76
29571744-4	2018	To investigate the role of GagNC in this recruitment, we analysed its impact on TSG101 and ALIX localisations and interactions in cells expressing Gag.	Glycosaminoglycans	27-30	tumor susceptibility 101	Homo sapiens	80-86
29571744-4	2018	To investigate the role of GagNC in this recruitment, we analysed its impact on TSG101 and ALIX localisations and interactions in cells expressing Gag.	Glycosaminoglycans	27-30	programmed cell death 6 interacting protein	Homo sapiens	91-95
29571744-7	2018	RESULTS: We show that deletion of NC or of its two zinc fingers decreases the amount of Gag-TSG101 interacting complexes in cells.	Glycosaminoglycans	88-91	tumor susceptibility 101	Homo sapiens	92-98
29571744-10	2018	CONCLUSION: The NC zinc fingers and p6 domain of Gag participate in the formation of the Gag-TSG101 complex and in its cellular localisation.	Glycosaminoglycans	49-52	tumor susceptibility 101	Homo sapiens	93-99
29571744-10	2018	CONCLUSION: The NC zinc fingers and p6 domain of Gag participate in the formation of the Gag-TSG101 complex and in its cellular localisation.	Glycosaminoglycans	89-92	tumor susceptibility 101	Homo sapiens	93-99
29571744-12	2018	In addition, details on the Gag-TSG101 complex were obtained by combining two high resolution biophysical techniques.	Glycosaminoglycans	28-31	tumor susceptibility 101	Homo sapiens	32-38
29443383-3	2018	This gene encodes Beta-1,3-galactosyltransferase 6 (beta3GalT6), an essential component of the glycosaminoglycan synthesis pathway.	Glycosaminoglycans	95-112	beta-1,3-galactosyltransferase 6	Homo sapiens	18-50
29443383-3	2018	This gene encodes Beta-1,3-galactosyltransferase 6 (beta3GalT6), an essential component of the glycosaminoglycan synthesis pathway.	Glycosaminoglycans	95-112	beta-1,3-galactosyltransferase 6	Homo sapiens	52-62
29568866-4	2018	In the present study, a HIV gag-based VLP strategy and Bac-to-Bac system were utilized to construct Trop-2, CD40L and gag recombinant baculoviruses, which were then used to infect TN5 cells in order to form Trop-2 VLPs or Trop-2-CD40L VLPs.	Glycosaminoglycans	28-31	CD40 ligand	Mus musculus	108-113
29668274-3	2018	The versatility of melittin in interacting with various biological substrates, such as membranes, glycosaminoglycans, and a variety of proteins, has inspired a slew of studies that aim to improve our understanding of the structural basis of such interactions.	Glycosaminoglycans	98-116	melittin	Apis mellifera	19-27
29783732-8	2018	Safranin-O staining demonstrated a typical depletion of GAG in TNF-alpha-treated micromasses (-73%), although the extent was limited in the presence of HA (-39%).	Glycosaminoglycans	56-59	tumor necrosis factor	Homo sapiens	63-72
30023916-2	2018	In this study, we synthesized GLP-1 derivatives that were conjugated with glycosaminoglycans (GAGs), i.e., chondroitin (CH) or heparosan (HPN), to address the major limitation in their clinical use of GLP-1, which is its short half-life in the body.	Glycosaminoglycans	74-92	glucagon	Mus musculus	30-35
29748537-5	2018	We postulate that this neck-biased distribution is regulated by vesicular retention and steric complementarity of Env during independent Gag lattice formation.	Glycosaminoglycans	137-140	endogenous retrovirus group K member 20	Homo sapiens	114-117
29762123-3	2018	Arylsulfatase B (ARSB) selectively cleaves 4S groups from the non-reducing ends of GAG chains without disrupting other, growth-permissive motifs.	Glycosaminoglycans	83-86	arylsulfatase B	Homo sapiens	0-15
29762123-3	2018	Arylsulfatase B (ARSB) selectively cleaves 4S groups from the non-reducing ends of GAG chains without disrupting other, growth-permissive motifs.	Glycosaminoglycans	83-86	arylsulfatase B	Homo sapiens	17-21
29606503-2	2018	Since IDS catalyzes the degradation of glycosaminoglycans (GAGs), deficiency in this enzyme leads to accumulation of GAGs in most cells in all tissues and organs, resulting in severe somatic and neurological disorders.	Glycosaminoglycans	39-57	iduronate 2-sulfatase	Mus musculus	6-9
29739909-3	2018	HIV-specific cTfh (Tet+), detected by Gag-major histocompatibility complex class II (MHC-II) tetramer labeling in the CD45RA- CXCR5+ CD4+ T cell population, proved more frequent in the controller group (P = 0.002).	Glycosaminoglycans	38-41	C-X-C motif chemokine receptor 5	Homo sapiens	126-131
29540475-6	2018	The cell adhesion was partially blocked by anti-Mac-1 mAb and inhibition was enhanced when anti-Mac-1 antibodies were combined with glycosaminoglycans, suggesting that cell-surface proteoglycans act cooperatively with Mac-1.	Glycosaminoglycans	132-150	integrin subunit alpha M	Homo sapiens	48-53
29168879-5	2018	This decrease in glycosaminoglycans was also related to abnormal nuclear B3GALT6 expression in neuroblastic cells.	Glycosaminoglycans	17-35	beta-1,3-galactosyltransferase 6	Homo sapiens	73-80
29462330-4	2018	In contrast, the CSPG4 expressed by a colon carcinoma cell line, WiDr, was predominantly as a protein core on the cell surface lacking glycosaminoglycan (GAG) chains.	Glycosaminoglycans	135-152	chondroitin sulfate proteoglycan 4	Homo sapiens	17-22
29436595-0	2018	Anti-apoptotic effects of glycosaminoglycans via inhibition of ERK/AP-1 signaling in TNF-alpha-stimulated human dermal fibroblasts.	Glycosaminoglycans	26-44	tumor necrosis factor	Homo sapiens	85-94
29462330-4	2018	In contrast, the CSPG4 expressed by a colon carcinoma cell line, WiDr, was predominantly as a protein core on the cell surface lacking glycosaminoglycan (GAG) chains.	Glycosaminoglycans	154-157	chondroitin sulfate proteoglycan 4	Homo sapiens	17-22
29073831-8	2018	RESULTS: PTHrP overexpression increased glycosaminoglycan (GAG) production by MSCs irrespective of TGF-beta1 treatment, and exerted differential effects on chondrogenic and hypertrophic gene expression when MSCs were cultured in the presence of a PTHrP signaling gradient.	Glycosaminoglycans	40-57	parathyroid hormone like hormone	Homo sapiens	9-14
28645130-6	2018	Concentrations of TGF-beta1 in the media were up to three times greater with the CS-GAG gels and were significantly (p &lt; 0.05) greater than with PRF on days 3, 5, 7, 9, and 13.	Glycosaminoglycans	84-87	transforming growth factor beta 1	Homo sapiens	18-27
28645130-7	2018	Furthermore, TGF-beta1 elution was still substantial at day 13 with the use of the CS-GAG gels.	Glycosaminoglycans	86-89	transforming growth factor beta 1	Homo sapiens	13-22
28645130-8	2018	Additional in vitro work is warranted to characterize TGF-beta1 elution from this CS-GAG gel with human PRP and to determine whether the use of these CS-GAG gels can augment cartilage repair in vivo.	Glycosaminoglycans	85-88	transforming growth factor beta 1	Homo sapiens	54-63
29479058-1	2018	UDP-glucose 6-dehydrogenase (UGDH) produces UDP-alpha-D-glucuronic acid, the precursors for glycosaminoglycans (GAGs) and proteoglycans of the extracellular matrix.	Glycosaminoglycans	92-110	UDP-glucose 6-dehydrogenase	Homo sapiens	29-33
29479058-6	2018	UGDH knockdown decreases GAG abundance in GBM cells, as well as cell proliferation and migration in vitro.	Glycosaminoglycans	25-28	UDP-glucose 6-dehydrogenase	Homo sapiens	0-4
29073831-8	2018	RESULTS: PTHrP overexpression increased glycosaminoglycan (GAG) production by MSCs irrespective of TGF-beta1 treatment, and exerted differential effects on chondrogenic and hypertrophic gene expression when MSCs were cultured in the presence of a PTHrP signaling gradient.	Glycosaminoglycans	59-62	parathyroid hormone like hormone	Homo sapiens	9-14
29570275-2	2018	Glycosaminoglycan chains, including heparan sulfate (HS) and chondroitin sulfate (CS), act as ligands that regulate LAR signaling.	Glycosaminoglycans	0-17	protein tyrosine phosphatase receptor type F	Homo sapiens	116-119
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
29482445-7	2018	CD271+ MNCs showed the highest proliferation rate, cell viability, sulfated glycosaminoglycan deposition, and cartilage marker expression compared to the CD271- or unseparated MNC fractions in 3D culture.	Glycosaminoglycans	76-93	nerve growth factor receptor	Homo sapiens	0-5
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
28477140-3	2018	The CSPG glycosaminoglycan side chains composed of chondroitin sulfate (CS) are responsible for its inhibitory activity on neurite outgrowth and are dependent on RhoA activation.	Glycosaminoglycans	9-26	ras homolog family member A	Homo sapiens	162-166
29580682-1	2018	Mucopolysaccharidosis type II (MPS II) is an X-linked recessive lysosomal disorder caused by deficiency of iduronate 2-sulfatase (IDS), leading to accumulation of glycosaminoglycans (GAGs) in tissues of affected individuals, progressive disease, and shortened lifespan.	Glycosaminoglycans	163-181	iduronate 2-sulfatase	Homo sapiens	130-133
29082918-5	2018	CXCL12 fulfills its functions in homeostatic and pathological conditions by interacting with its receptors CXC chemokine receptor 4 (CXCR4) and atypical chemokine receptor 3 (ACKR3) and by binding to glycosaminoglycans (GAGs) in tissues and on the endothelium to allow a proper presentation to passing leukocytes.	Glycosaminoglycans	200-218	C-X-C motif chemokine ligand 12	Homo sapiens	0-6
28906016-9	2018	CXCL10 also trended toward a reduction in IL-1alpha-stimulated total MMP activity (p = 0.09) and S-GAG (p = 0.09), but not NO release.	Glycosaminoglycans	99-102	chemokine (C-X-C motif) ligand 10	Mus musculus	0-6
28906016-9	2018	CXCL10 also trended toward a reduction in IL-1alpha-stimulated total MMP activity (p = 0.09) and S-GAG (p = 0.09), but not NO release.	Glycosaminoglycans	99-102	interleukin 1 alpha	Mus musculus	42-51
29438988-2	2018	Phosphorylation of the transcription factor Smad has emerged as a critical step in the signaling pathways that control the synthesis of biglycan, both the core protein and the GAG chains.	Glycosaminoglycans	176-179	biglycan	Homo sapiens	136-144
29568314-11	2018	The intense alician blue staining indicated an increased production of mucopolysaccharides in the differentiated pellets, which also showed elevated expression of SOX9.	Glycosaminoglycans	71-90	SRY-box transcription factor 9	Homo sapiens	163-167
29148104-8	2018	Nrg-1 therapy remarkably attenuated the upregulated expression chondroitin sulfate proteoglycans (CSPGs) specific glycosaminoglycans in the extracellular matrix of demyelinating foci and promoted interleukin-10 (IL-10) production by immune cells.	Glycosaminoglycans	114-132	neuregulin 1	Homo sapiens	0-5
28694053-7	2018	Together with its two endogenous ligands CCL19 and CCL21, of which the carboxy terminal tail of CCL21 displays an extraordinarily strong glycosaminoglycan (GAG) binding, CCR7 plays a central role in coordinating the meeting between mature antigen presenting DCs and naive T-cells which normally takes place in the lymph nodes (LNs).	Glycosaminoglycans	156-159	C-C motif chemokine ligand 19	Homo sapiens	41-46
28694053-7	2018	Together with its two endogenous ligands CCL19 and CCL21, of which the carboxy terminal tail of CCL21 displays an extraordinarily strong glycosaminoglycan (GAG) binding, CCR7 plays a central role in coordinating the meeting between mature antigen presenting DCs and naive T-cells which normally takes place in the lymph nodes (LNs).	Glycosaminoglycans	156-159	C-C motif chemokine ligand 21	Homo sapiens	51-56
28694053-7	2018	Together with its two endogenous ligands CCL19 and CCL21, of which the carboxy terminal tail of CCL21 displays an extraordinarily strong glycosaminoglycan (GAG) binding, CCR7 plays a central role in coordinating the meeting between mature antigen presenting DCs and naive T-cells which normally takes place in the lymph nodes (LNs).	Glycosaminoglycans	156-159	C-C motif chemokine ligand 21	Homo sapiens	96-101
28694053-7	2018	Together with its two endogenous ligands CCL19 and CCL21, of which the carboxy terminal tail of CCL21 displays an extraordinarily strong glycosaminoglycan (GAG) binding, CCR7 plays a central role in coordinating the meeting between mature antigen presenting DCs and naive T-cells which normally takes place in the lymph nodes (LNs).	Glycosaminoglycans	156-159	C-C motif chemokine receptor 7	Homo sapiens	170-174
30271866-0	2018	Osteogenic differentiation enhances the MC3T3-E1 secretion of glycosaminoglycans with an affinity for basic fibroblast growth factor and bone morphogenetic protein-2.	Glycosaminoglycans	62-80	fibroblast growth factor 2	Mus musculus	102-132
30271866-0	2018	Osteogenic differentiation enhances the MC3T3-E1 secretion of glycosaminoglycans with an affinity for basic fibroblast growth factor and bone morphogenetic protein-2.	Glycosaminoglycans	62-80	bone morphogenetic protein 2	Mus musculus	137-165
30271866-7	2018	Significantly higher amount of GAG secreted was detected for cells cultured in the DM containing BMP-2, in contrast to other culture conditions.	Glycosaminoglycans	31-34	bone morphogenetic protein 2	Mus musculus	97-102
30271866-8	2018	The GAG secreted had an affinity for BMP-2 and basic fibroblast growth factor (bFGF).	Glycosaminoglycans	4-7	bone morphogenetic protein 2	Mus musculus	37-42
30271866-8	2018	The GAG secreted had an affinity for BMP-2 and basic fibroblast growth factor (bFGF).	Glycosaminoglycans	4-7	fibroblast growth factor 2	Mus musculus	47-77
30271866-8	2018	The GAG secreted had an affinity for BMP-2 and basic fibroblast growth factor (bFGF).	Glycosaminoglycans	4-7	fibroblast growth factor 2	Mus musculus	79-83
30271866-10	2018	Conclusion: It was found that the osteogenic differentiation allowed cells to enhance the secretion of GAG with an affinity for BMP-2 and bFGF.	Glycosaminoglycans	103-106	bone morphogenetic protein 2	Mus musculus	128-133
30271866-10	2018	Conclusion: It was found that the osteogenic differentiation allowed cells to enhance the secretion of GAG with an affinity for BMP-2 and bFGF.	Glycosaminoglycans	103-106	fibroblast growth factor 2	Mus musculus	138-142
29547721-3	2018	Here we report that chondroitin-4-sulfate (CHSA), a natural glycosaminoglycan approved as a dietary supplement used for osteoarthritis, selectively promotes the tumor growth potential of BRAF V600E-expressing human melanoma cells in patient- and cell line-derived xenograft mice and confers resistance to BRAF inhibitors.	Glycosaminoglycans	60-77	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	187-191
28926869-0	2018	- No Title - The receptor for advanced glycation end-products (RAGE) is a multi-ligand receptor which belongs to the pattern recognition receptor family and can bind to various ligands such as advanced glycation end-products (AGEs), members of the S100 protein family, glycosaminoglycans, amyloid beta peptides, high-mobility group box-1 (HMGB1) and nucleic acids through its extracellular domain.	Glycosaminoglycans	269-287	advanced glycosylation end product-specific receptor	Mus musculus	17-61
28926869-0	2018	- No Title - The receptor for advanced glycation end-products (RAGE) is a multi-ligand receptor which belongs to the pattern recognition receptor family and can bind to various ligands such as advanced glycation end-products (AGEs), members of the S100 protein family, glycosaminoglycans, amyloid beta peptides, high-mobility group box-1 (HMGB1) and nucleic acids through its extracellular domain.	Glycosaminoglycans	269-287	advanced glycosylation end product-specific receptor	Mus musculus	63-67
28926869-0	2018	- No Title - The receptor for advanced glycation end-products (RAGE) is a multi-ligand receptor which belongs to the pattern recognition receptor family and can bind to various ligands such as advanced glycation end-products (AGEs), members of the S100 protein family, glycosaminoglycans, amyloid beta peptides, high-mobility group box-1 (HMGB1) and nucleic acids through its extracellular domain.	Glycosaminoglycans	269-287	high mobility group box 1	Mus musculus	312-337
28926869-0	2018	- No Title - The receptor for advanced glycation end-products (RAGE) is a multi-ligand receptor which belongs to the pattern recognition receptor family and can bind to various ligands such as advanced glycation end-products (AGEs), members of the S100 protein family, glycosaminoglycans, amyloid beta peptides, high-mobility group box-1 (HMGB1) and nucleic acids through its extracellular domain.	Glycosaminoglycans	269-287	high mobility group box 1	Mus musculus	339-344
29198892-13	2018	Together, these results showed that infusion of IDUAL allowed for significant IDUA levels and GAG reduction in the brain and subsequent neurological benefits.	Glycosaminoglycans	94-97	iduronidase, alpha-L	Mus musculus	48-52
28968258-1	2018	A rare autosomal recessive disorder caused by mutations in the B3GALT6 gene on chromosome 1p36 results in deficiency of beta-1,3-galactosyltransferase 6, an enzyme critical for glycosaminoglycan biosynthesis.	Glycosaminoglycans	177-194	beta-1,3-galactosyltransferase 6	Homo sapiens	63-70
28968258-1	2018	A rare autosomal recessive disorder caused by mutations in the B3GALT6 gene on chromosome 1p36 results in deficiency of beta-1,3-galactosyltransferase 6, an enzyme critical for glycosaminoglycan biosynthesis.	Glycosaminoglycans	177-194	beta-1,3-galactosyltransferase 6	Homo sapiens	120-152
28969431-5	2018	After three HIV-DNA immunizations, IFN-gamma ELISpot responses to Gag were detected in 9/17 (53%) vaccinees, while none responded to Envelope (Env).	Glycosaminoglycans	66-69	interferon gamma	Homo sapiens	35-44
28556569-6	2018	Safranin O staining revealed that matrilin-3 (140 and 280 ng) treatment significantly improved cartilage regeneration and glycosaminoglycan accumulation.	Glycosaminoglycans	122-139	matrilin 3	Rattus norvegicus	34-44
28548569-6	2018	In contrast, another growth factor, TGFbeta1, increased the GAG content in excess of threefold more than the increase in collagen.	Glycosaminoglycans	60-63	transforming growth factor beta 1	Homo sapiens	36-44
29495527-1	2018	In this editorial to MDPI Pharmaceuticals special issue "Glycosaminoglycans and Proteoglycans" we describe in outline the common structural features of glycosaminoglycans and the characteristics of proteoglycans, including the intracellular proteoglycan, serglycin, cell-surface proteoglycans, like syndecans and glypicans, and the extracellular matrix proteoglycans, like aggrecan, perlecan, and small leucine-rich proteoglycans.	Glycosaminoglycans	57-75	serglycin	Homo sapiens	255-264
29495527-1	2018	In this editorial to MDPI Pharmaceuticals special issue "Glycosaminoglycans and Proteoglycans" we describe in outline the common structural features of glycosaminoglycans and the characteristics of proteoglycans, including the intracellular proteoglycan, serglycin, cell-surface proteoglycans, like syndecans and glypicans, and the extracellular matrix proteoglycans, like aggrecan, perlecan, and small leucine-rich proteoglycans.	Glycosaminoglycans	152-170	serglycin	Homo sapiens	255-264
29282986-1	2018	Monosubstituted naphthoxylosides have been shown to function as substrates for, and inhibitors of, the enzyme beta4GalT7, a key enzyme in the biosynthetic pathway leading to glycosaminoglycans and proteoglycans.	Glycosaminoglycans	174-192	beta-1,4-galactosyltransferase 7	Homo sapiens	110-120
29167337-13	2018	These findings indicate that the immunodominant HLA-B*27:02-restricted Nef response adds to protection mediated by the Gag and Pol specificities that dominate anti-HIV CD8+ T-cell activity in HLA-B*27:05-positive subjects.	Glycosaminoglycans	119-122	major histocompatibility complex, class I, B	Homo sapiens	48-53
29289480-2	2018	However, a chaperone compound for mucopolysaccharidosis type II (MPS II), which is an X-linked lysosomal storage disorder characterized by a deficiency of iduronate-2-sulfatase (IDS) and the accumulation of glycosaminoglycans (GAGs), has still not been developed.	Glycosaminoglycans	227-231	iduronate 2-sulfatase	Homo sapiens	155-176
29167337-13	2018	These findings indicate that the immunodominant HLA-B*27:02-restricted Nef response adds to protection mediated by the Gag and Pol specificities that dominate anti-HIV CD8+ T-cell activity in HLA-B*27:05-positive subjects.	Glycosaminoglycans	119-122	CD8a molecule	Homo sapiens	168-171
29167337-13	2018	These findings indicate that the immunodominant HLA-B*27:02-restricted Nef response adds to protection mediated by the Gag and Pol specificities that dominate anti-HIV CD8+ T-cell activity in HLA-B*27:05-positive subjects.	Glycosaminoglycans	119-122	major histocompatibility complex, class I, B	Homo sapiens	192-197
30107380-17	2018	Such knowledge should be useful in developing glycosaminoglycan-based compounds that target HGF/Met signaling.	Glycosaminoglycans	46-63	hepatocyte growth factor	Cricetulus griseus	92-95
29370775-11	2018	EC1 mounted high frequency HIV-specific CD8+ T cell responses, including a B*81:01-restricted Gag TL9 response.	Glycosaminoglycans	94-97	Susceptibility to lysis by alloreactive natural killer cells	Homo sapiens	0-3
29329231-6	2018	Collagen retention was demonstrated in all groups except ST 1%, and a significant decrease in glycosaminoglycans was observed in the TST 1% and TET 1% groups.	Glycosaminoglycans	94-112	despair 2	Mus musculus	133-138
29329231-6	2018	Collagen retention was demonstrated in all groups except ST 1%, and a significant decrease in glycosaminoglycans was observed in the TST 1% and TET 1% groups.	Glycosaminoglycans	94-112	tet methylcytosine dioxygenase 1	Mus musculus	144-149
29338738-8	2018	Analysis of an HLA-B*27:05/B*57:01 non-progressor, in contrast, demonstrated minimal virus sequence diversification (1.1% Gag amino acid sequence change over 10 years), and dominant HIV-specific CTL responses previously shown to be effective in control of viraemia were maintained.	Glycosaminoglycans	122-125	major histocompatibility complex, class I, B	Homo sapiens	15-20
29063236-9	2018	WIKIPATHWAYS, REACTOME, PID_NCI and KEGG pathway analysis showed the down-regulated DEGs were enriched endochondral ossification, TGF beta signalling pathway, integrin cell surface interactions, beta1 integrin cell surface interactions, malaria and glycosaminoglycan biosynthesis-chondroitin sulfate/dermatan sulphate.	Glycosaminoglycans	249-266	transforming growth factor beta 1	Homo sapiens	130-138
29063236-9	2018	WIKIPATHWAYS, REACTOME, PID_NCI and KEGG pathway analysis showed the down-regulated DEGs were enriched endochondral ossification, TGF beta signalling pathway, integrin cell surface interactions, beta1 integrin cell surface interactions, malaria and glycosaminoglycan biosynthesis-chondroitin sulfate/dermatan sulphate.	Glycosaminoglycans	249-266	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	195-200
28882767-1	2018	Mucopolysaccharidosis type I (MPS I) is an autosomal recessive disease caused by deficiency of alpha-l-iduronidase (IDUA), which results in the lysosomal accumulation of glycosaminoglycans (GAG) leading to widespread clinical manifestations.	Glycosaminoglycans	170-188	iduronidase, alpha-L	Mus musculus	95-114
29749312-11	2018	IL-1beta mediated suppression of GAG synthesis was not rescued by IL-10.	Glycosaminoglycans	33-36	interleukin-1 beta	Equus caballus	0-8
28882767-1	2018	Mucopolysaccharidosis type I (MPS I) is an autosomal recessive disease caused by deficiency of alpha-l-iduronidase (IDUA), which results in the lysosomal accumulation of glycosaminoglycans (GAG) leading to widespread clinical manifestations.	Glycosaminoglycans	170-188	iduronidase, alpha-L	Mus musculus	116-120
28882767-1	2018	Mucopolysaccharidosis type I (MPS I) is an autosomal recessive disease caused by deficiency of alpha-l-iduronidase (IDUA), which results in the lysosomal accumulation of glycosaminoglycans (GAG) leading to widespread clinical manifestations.	Glycosaminoglycans	190-193	iduronidase, alpha-L	Mus musculus	95-114
28882767-1	2018	Mucopolysaccharidosis type I (MPS I) is an autosomal recessive disease caused by deficiency of alpha-l-iduronidase (IDUA), which results in the lysosomal accumulation of glycosaminoglycans (GAG) leading to widespread clinical manifestations.	Glycosaminoglycans	190-193	iduronidase, alpha-L	Mus musculus	116-120
28762182-9	2017	Furthermore, there was a comparatively decreased binding of GAGs from hypercholesterolemic rats to lipoprotein lipase.	Glycosaminoglycans	60-64	lipoprotein lipase	Rattus norvegicus	99-117
30194597-1	2018	Binding of serine protease inhibitors (serpins) to nonprotein ligands such as glycosaminoglycans or phospholipids has been shown to modify their inhibitory activity and-at least in the case of SERPINA5-to mediate serpin internalization into cells.	Glycosaminoglycans	78-96	serpin family A member 5	Homo sapiens	193-201
29024190-1	2017	Xyloside analogues with substitution of the endocyclic oxygen atom by sulfur or carbon were investigated as substrates for beta-1,4-galactosyltransferase 7 (beta4GalT7), a key enzyme in the biosynthesis of glycosaminoglycan chains.	Glycosaminoglycans	206-223	beta-1,4-galactosyltransferase 7	Homo sapiens	123-155
29024190-1	2017	Xyloside analogues with substitution of the endocyclic oxygen atom by sulfur or carbon were investigated as substrates for beta-1,4-galactosyltransferase 7 (beta4GalT7), a key enzyme in the biosynthesis of glycosaminoglycan chains.	Glycosaminoglycans	206-223	beta-1,4-galactosyltransferase 7	Homo sapiens	157-167
28958576-1	2017	Iduronidase (IDUA)-deficient mice accumulate glycosaminoglycans in cells and tissues and exhibit many of the same neuropathological symptoms of patients suffering from Mucopolysaccharidosis I.	Glycosaminoglycans	45-63	iduronidase, alpha-L	Mus musculus	0-11
28958576-1	2017	Iduronidase (IDUA)-deficient mice accumulate glycosaminoglycans in cells and tissues and exhibit many of the same neuropathological symptoms of patients suffering from Mucopolysaccharidosis I.	Glycosaminoglycans	45-63	iduronidase, alpha-L	Mus musculus	13-17
28945007-2	2017	Previously, a correlation was described between the osteogenic capabilities of nanoparticulate mineralized collagen glycosaminoglycan scaffolds (MC-GAG) and an autogenous activation of small mothers against decapentaplegic ( Smad1/5) in the canonical bone morphogenetic protein receptor (BMPR) pathway with a diminished extracellular signal regulated kinase 1/2 (ERK1/2) activation when compared to nonmineralized collagen glycosaminoglycan scaffolds (Col-GAG).	Glycosaminoglycans	116-133	SMAD family member 1	Homo sapiens	225-232
28945007-2	2017	Previously, a correlation was described between the osteogenic capabilities of nanoparticulate mineralized collagen glycosaminoglycan scaffolds (MC-GAG) and an autogenous activation of small mothers against decapentaplegic ( Smad1/5) in the canonical bone morphogenetic protein receptor (BMPR) pathway with a diminished extracellular signal regulated kinase 1/2 (ERK1/2) activation when compared to nonmineralized collagen glycosaminoglycan scaffolds (Col-GAG).	Glycosaminoglycans	116-133	mitogen-activated protein kinase 1	Homo sapiens	320-361
28945007-2	2017	Previously, a correlation was described between the osteogenic capabilities of nanoparticulate mineralized collagen glycosaminoglycan scaffolds (MC-GAG) and an autogenous activation of small mothers against decapentaplegic ( Smad1/5) in the canonical bone morphogenetic protein receptor (BMPR) pathway with a diminished extracellular signal regulated kinase 1/2 (ERK1/2) activation when compared to nonmineralized collagen glycosaminoglycan scaffolds (Col-GAG).	Glycosaminoglycans	116-133	mitogen-activated protein kinase 3	Homo sapiens	363-369
28945007-2	2017	Previously, a correlation was described between the osteogenic capabilities of nanoparticulate mineralized collagen glycosaminoglycan scaffolds (MC-GAG) and an autogenous activation of small mothers against decapentaplegic ( Smad1/5) in the canonical bone morphogenetic protein receptor (BMPR) pathway with a diminished extracellular signal regulated kinase 1/2 (ERK1/2) activation when compared to nonmineralized collagen glycosaminoglycan scaffolds (Col-GAG).	Glycosaminoglycans	423-440	SMAD family member 1	Homo sapiens	225-232
28945007-8	2017	The MEK/ERK cascade, intimately tied to JNK activation, is necessary for Runx2-independent osteogenesis on Col-GAG, while completely dispensable in osteogenesis on MC-GAG.	Glycosaminoglycans	111-114	mitogen-activated protein kinase kinase 7	Homo sapiens	4-7
28945007-8	2017	The MEK/ERK cascade, intimately tied to JNK activation, is necessary for Runx2-independent osteogenesis on Col-GAG, while completely dispensable in osteogenesis on MC-GAG.	Glycosaminoglycans	111-114	mitogen-activated protein kinase 1	Homo sapiens	8-11
28945007-8	2017	The MEK/ERK cascade, intimately tied to JNK activation, is necessary for Runx2-independent osteogenesis on Col-GAG, while completely dispensable in osteogenesis on MC-GAG.	Glycosaminoglycans	111-114	mitogen-activated protein kinase 8	Homo sapiens	40-43
28945007-8	2017	The MEK/ERK cascade, intimately tied to JNK activation, is necessary for Runx2-independent osteogenesis on Col-GAG, while completely dispensable in osteogenesis on MC-GAG.	Glycosaminoglycans	111-114	RUNX family transcription factor 2	Homo sapiens	73-78
28734840-1	2017	Human beta-glucuronidase (GUS; EC 3.2.1.31) is a lysosomal enzyme that catalyzes the hydrolysis of beta-d-glucuronic acid residues from the non-reducing termini of glycosaminoglycans.	Glycosaminoglycans	164-182	beta-glucuronidase	Cricetulus griseus	6-24
28734840-1	2017	Human beta-glucuronidase (GUS; EC 3.2.1.31) is a lysosomal enzyme that catalyzes the hydrolysis of beta-d-glucuronic acid residues from the non-reducing termini of glycosaminoglycans.	Glycosaminoglycans	164-182	beta-glucuronidase	Cricetulus griseus	26-29
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
29671225-2	2018	Deficiency of the lysosomal enzyme, iduronate-2-sulfatase (EC 3.1.6.13) results in deposition of the glycosaminoglycans, dermatan, and heparan sulfate in various tissues.	Glycosaminoglycans	101-119	iduronate 2-sulfatase	Homo sapiens	36-57
29287114-9	2017	Histological analysis of epiphyseal cartilage from Col2-DKO mice revealed disrupted endochondral ossification, characterized by drastic GAG reduction in the ECM.	Glycosaminoglycans	136-139	collagen, type II, alpha 1	Mus musculus	51-55
29287114-11	2017	Conversely, primary chondrocyte cultures from Col2-DKO knee cartilage had the same proliferation rate as WT chondrocytes and low GAG expression levels, indicating that the chondrocytes themselves had an intact proliferative ability.	Glycosaminoglycans	129-132	collagen, type II, alpha 1	Mus musculus	46-50
29207576-7	2017	Enzymatic GAG depolymerization via heparinase III and chondroitinase ABC was used to emulate the effect of glycocalyx remodeling on CXCL8-induced endothelial downstream signaling.	Glycosaminoglycans	10-13	C-X-C motif chemokine ligand 8	Homo sapiens	132-137
29067744-5	2017	The extract suppressed glycosaminoglycan release from the cartilage explant in the presence of Interleukin-1beta.	Glycosaminoglycans	23-40	interleukin 1 beta	Rattus norvegicus	95-112
29033235-9	2017	Higher GAG priming activity is attributed to the formation of more stable interactions between the 1,5-linked xylosides and beta-1,4-galactosyltransferase 7 (beta4GalT7).	Glycosaminoglycans	7-10	beta-1,4-galactosyltransferase 7	Homo sapiens	124-156
29033235-9	2017	Higher GAG priming activity is attributed to the formation of more stable interactions between the 1,5-linked xylosides and beta-1,4-galactosyltransferase 7 (beta4GalT7).	Glycosaminoglycans	7-10	beta-1,4-galactosyltransferase 7	Homo sapiens	158-168
29163168-0	2017	Atheroregressive Potential of the Treatment with a Chimeric Monoclonal Antibody against Sulfated Glycosaminoglycans on Pre-existing Lesions in Apolipoprotein E-Deficient Mice.	Glycosaminoglycans	97-115	apolipoprotein E	Mus musculus	143-159
28940845-1	2017	Syndecan 2 (SDC2) belongs to a four-member family of evolutionary conserved small type I transmembrane proteoglycans consisting of a protein core to which glycosaminoglycan chains are covalently attached.	Glycosaminoglycans	155-172	syndecan 2	Homo sapiens	0-10
28940845-1	2017	Syndecan 2 (SDC2) belongs to a four-member family of evolutionary conserved small type I transmembrane proteoglycans consisting of a protein core to which glycosaminoglycan chains are covalently attached.	Glycosaminoglycans	155-172	syndecan 2	Homo sapiens	12-16
28570296-11	2017	RESULTS: Genetic depletion of ADAMTS5 prevented vertebral bone loss, substantially reduced loss of disc GAG content, and completely obviated ADAMTS-mediated proteolysis of disc aggrecan within its interglobular domain (IGD) in mice following exposure to tobacco smoke.	Glycosaminoglycans	104-107	a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 5 (aggrecanase-2)	Mus musculus	30-37
28878089-9	2017	We focus on HLA-B*14, unique among HLAs associated with control of HIV in that the dominant CTL response is Env specific, not Gag specific.	Glycosaminoglycans	126-129	major histocompatibility complex, class I, B	Homo sapiens	12-17
28878089-10	2017	We demonstrate that Env-specific HLA-B*14-restricted activity is substantially more efficacious than the subdominant HLA-B*14-restricted Gag response.	Glycosaminoglycans	137-140	major histocompatibility complex, class I, B	Homo sapiens	117-122
28878089-12	2017	This reflects the increased functional avidity of the Env response over Gag, substantially more marked for HLA-B*14:02.	Glycosaminoglycans	72-75	major histocompatibility complex, class I, B	Homo sapiens	107-112
28963928-7	2017	Additionally, cessation of IL-1beta rescued T-2-elicited tilt of matrix homeostasis toward catabolism by elevating the transcription of collagen II and aggrecan, promoting release of sulphated glycosaminoglycans (sGAG) and TIMP1, and suppressing matrix metalloproteinases production including MMP-1, MMP-3 and MMP-13.	Glycosaminoglycans	193-211	interleukin 1 beta	Homo sapiens	27-35
28963928-7	2017	Additionally, cessation of IL-1beta rescued T-2-elicited tilt of matrix homeostasis toward catabolism by elevating the transcription of collagen II and aggrecan, promoting release of sulphated glycosaminoglycans (sGAG) and TIMP1, and suppressing matrix metalloproteinases production including MMP-1, MMP-3 and MMP-13.	Glycosaminoglycans	193-211	solute carrier family 25 member 5	Homo sapiens	44-47
29123919-13	2017	The short T1(Gd) centrally may reflect lower glycosaminoglycan content, whereas the increase in T2 medially indicates increased cartilage hydration.	Glycosaminoglycans	45-62	interleukin 1 receptor like 1	Homo sapiens	10-16
28570296-11	2017	RESULTS: Genetic depletion of ADAMTS5 prevented vertebral bone loss, substantially reduced loss of disc GAG content, and completely obviated ADAMTS-mediated proteolysis of disc aggrecan within its interglobular domain (IGD) in mice following exposure to tobacco smoke.	Glycosaminoglycans	104-107	a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 1	Mus musculus	30-36
29078966-8	2017	Gag reflex was also significantly decreased after stimulating PC6 acupuncture point with LLLT.	Glycosaminoglycans	0-3	proprotein convertase subtilisin/kexin type 5	Homo sapiens	62-65
28851629-4	2017	Additionally, Gag-specific TNF-alpha secreting CD8+ and CD4+ T cells and Env-specific IL-2 secreting T cells were also elicited by mice immunized with Gag and Env constructs, respectively, as estimated by intracellular cytokine staining assay.	Glycosaminoglycans	14-17	tumor necrosis factor	Mus musculus	27-36
28851629-4	2017	Additionally, Gag-specific TNF-alpha secreting CD8+ and CD4+ T cells and Env-specific IL-2 secreting T cells were also elicited by mice immunized with Gag and Env constructs, respectively, as estimated by intracellular cytokine staining assay.	Glycosaminoglycans	14-17	CD4 antigen	Mus musculus	56-59
28851629-4	2017	Additionally, Gag-specific TNF-alpha secreting CD8+ and CD4+ T cells and Env-specific IL-2 secreting T cells were also elicited by mice immunized with Gag and Env constructs, respectively, as estimated by intracellular cytokine staining assay.	Glycosaminoglycans	14-17	melanoma antigen	Mus musculus	159-162
29091184-0	2017	Prevalence of gag mutations associated with in vitro resistance to capsid inhibitor GS-CA1 in HIV-1 antiretroviral-naive patients.	Glycosaminoglycans	14-17	carbonic anhydrase 1	Homo sapiens	87-90
28232224-8	2017	Using a murine model of radiation-induced proctitis, the prophylactic delivery of a single dose of GAG from a SELP matrix administered prior to irradiation significantly reduced radiation-induced pain after 3, 7, and 21days by 53+-4%, 47+-10%, and 12+-6%, respectively.	Glycosaminoglycans	99-102	selectin, platelet	Mus musculus	110-114
28232224-9	2017	Matrix-mediated delivery of GAG by SELP represents an innovative method for more effective treatment of RIP and promises to improve quality of life of cancer patients by allowing higher radiotherapy doses with improved safety.	Glycosaminoglycans	28-31	selectin P	Homo sapiens	35-39
28991552-3	2017	Recent studies suggest that HIT antibodies activate platelets by recognizing PF4 in a complex with platelet glycosaminoglycans (and/or polyphosphates) and that an assay based on this principle, the PF4-dependent P-selectin expression assay (PEA), may be even more accurate than the SRA for HIT diagnosis.	Glycosaminoglycans	108-126	platelet factor 4	Homo sapiens	77-80
28991552-3	2017	Recent studies suggest that HIT antibodies activate platelets by recognizing PF4 in a complex with platelet glycosaminoglycans (and/or polyphosphates) and that an assay based on this principle, the PF4-dependent P-selectin expression assay (PEA), may be even more accurate than the SRA for HIT diagnosis.	Glycosaminoglycans	108-126	platelet factor 4	Homo sapiens	198-201
28991552-3	2017	Recent studies suggest that HIT antibodies activate platelets by recognizing PF4 in a complex with platelet glycosaminoglycans (and/or polyphosphates) and that an assay based on this principle, the PF4-dependent P-selectin expression assay (PEA), may be even more accurate than the SRA for HIT diagnosis.	Glycosaminoglycans	108-126	selectin P	Homo sapiens	212-222
28019703-10	2017	Human MSC within the hydrogel cultured with or without TGF-beta1 showed significantly higher GAG production compared to control medium.	Glycosaminoglycans	93-96	transforming growth factor beta 1	Homo sapiens	55-64
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
28916807-5	2017	This mobility increase is dependent on Gag-interacting Env tail but not on changes in viral envelope lipid order.	Glycosaminoglycans	39-42	endogenous retrovirus group K member 20	Homo sapiens	55-58
28629082-2	2017	The composition of hECM was evaluated by quantifying the content of sulphated glycosaminoglycans (sGAG), fibronectin and laminin.	Glycosaminoglycans	78-96	multimerin 1	Homo sapiens	19-23
29070611-0	2017	Solution structure of CXCL13 and heparan sulfate binding show that GAG binding site and cellular signalling rely on distinct domains.	Glycosaminoglycans	67-70	C-X-C motif chemokine ligand 13	Homo sapiens	22-28
28478702-4	2017	Real-time polymerase chain reaction, enzyme-linked immunosorbent assays, and Western blot results suggested that the levels of type II collagen and GAG were increased after incubating BMSCs with SDF-1 compared with the without SDF-1 group.	Glycosaminoglycans	148-151	C-X-C motif chemokine ligand 12	Homo sapiens	195-200
28389983-2	2017	Complete structural elucidation of glycosaminoglycans necessitates the unambiguous assignments of sulfo modifications and the C-5 uronic acid stereochemistry.	Glycosaminoglycans	35-53	complement C5	Homo sapiens	126-129
28696225-5	2017	Consistent with this, GPC6 interacts with Hh through its core protein and with Ptc1 through its glycosaminoglycan chains.	Glycosaminoglycans	96-113	glypican 6	Homo sapiens	22-26
28696225-5	2017	Consistent with this, GPC6 interacts with Hh through its core protein and with Ptc1 through its glycosaminoglycan chains.	Glycosaminoglycans	96-113	patched 1	Homo sapiens	79-83
27061379-8	2017	RHEB-overexpressing chondrocytes successfully formed cartilage tissue in vitro as well as in vivo, with increased expression of GAG matrix and chondrogenic markers.	Glycosaminoglycans	128-131	Ras homolog, mTORC1 binding	Homo sapiens	0-4
28426371-7	2017	A chemically defined media condition that incorporated TGF-beta3 promoted the deposition of GAG and collagen in DAPS in vitro, the maintenance of accumulated matrix in vivo, and minimal changes in the metabolic activity of cells within the construct.	Glycosaminoglycans	92-95	transforming growth factor, beta 3	Rattus norvegicus	55-64
28859141-8	2017	The glycosaminoglycan content and structure in Aspn-/- skin was profoundly altered: chondroitin/dermatan sulfate was more than doubled and had an altered composition, while heparan sulfate was halved and had a decreased sulfation.	Glycosaminoglycans	4-21	asporin	Mus musculus	47-51
28159936-5	2017	Mass spectrometry of CFH isolated from AMD eyes revealed nitrated residues in domains critical for binding to heparan sulphate glycosaminoglycans (GAGs), lipid peroxidation by-products and complement (C) 3b.Functional studies revealed that nitrated CFH did not bind to lipid peroxidation products, nor to the GAG of perlecan nor to C3b.	Glycosaminoglycans	147-151	complement factor H	Homo sapiens	21-24
29088739-5	2017	Previous studies have shown that serglycin, the only known intracellular proteoglycan, functions mainly in the storage of basically charged components within the intracellular granules/vesicles via serglycin"s densely clustered, negatively charged glycosaminoglycan chains.	Glycosaminoglycans	248-265	serglycin	Homo sapiens	33-42
29088739-5	2017	Previous studies have shown that serglycin, the only known intracellular proteoglycan, functions mainly in the storage of basically charged components within the intracellular granules/vesicles via serglycin"s densely clustered, negatively charged glycosaminoglycan chains.	Glycosaminoglycans	248-265	serglycin	Homo sapiens	198-207
28573980-7	2017	In vitro studies analyzing cell-material interactions revealed scaffold cytocompatibility with higher cell viability and cell proliferation as well as higher glycosaminoglycan secretion for POST scaffolds with respect to PRE.	Glycosaminoglycans	158-175	solute carrier family 35 member G1	Homo sapiens	190-194
28594230-3	2017	In this study, we explore the occurrence of patterns of Gag p24 recognition among untreated HIV-1-infected patients by identifying the epitopes that compose such patterns and how they distinctly associate with disease progression.	Glycosaminoglycans	56-59	transmembrane p24 trafficking protein 2	Homo sapiens	60-63
28750862-4	2017	AT III activity was decreased as a result of a negative acute phase response, degradation by elastase, reduced availability of glycosaminoglycans, and, most importantly, consumption as a consequence of thrombin formation.	Glycosaminoglycans	127-145	serpin family C member 1	Canis lupus familiaris	0-6
28478695-6	2017	Sustained IDS expression had a profound effect on normalization of GAG in all tested tissues and on prevention of hepatomegaly.	Glycosaminoglycans	67-70	iduronate 2-sulfatase	Mus musculus	10-13
28837619-0	2017	LL-37 causes cell death of human nasal epithelial cells, which is inhibited with a synthetic glycosaminoglycan.	Glycosaminoglycans	93-110	cathelicidin antimicrobial peptide	Homo sapiens	0-5
28837619-4	2017	Recent findings suggest that a synthetic glycosaminoglycan (GM-0111) can protect against LL-37-induced sinonasal mucosal inflammation and cell death in a murine model of acute RS.	Glycosaminoglycans	41-58	cathelicidin antimicrobial peptide	Homo sapiens	89-94
28600129-5	2017	When the GAG mimetic nanofiber gels were injected in the infarct site of rodent myocardial infarct model, increased VEGF-A expression and recruitment of vascular cells was observed.	Glycosaminoglycans	9-12	vascular endothelial growth factor A	Rattus norvegicus	116-122
28763512-6	2017	These effects were achieved via the secreted xyloside-primed glycosaminoglycans (GAG) chains that in part, act through an ERK1/2 mediated signaling pathway.	Glycosaminoglycans	61-79	mitogen-activated protein kinase 3	Homo sapiens	122-128
28763512-6	2017	These effects were achieved via the secreted xyloside-primed glycosaminoglycans (GAG) chains that in part, act through an ERK1/2 mediated signaling pathway.	Glycosaminoglycans	81-84	mitogen-activated protein kinase 3	Homo sapiens	122-128
28159936-5	2017	Mass spectrometry of CFH isolated from AMD eyes revealed nitrated residues in domains critical for binding to heparan sulphate glycosaminoglycans (GAGs), lipid peroxidation by-products and complement (C) 3b.Functional studies revealed that nitrated CFH did not bind to lipid peroxidation products, nor to the GAG of perlecan nor to C3b.	Glycosaminoglycans	147-150	complement factor H	Homo sapiens	21-24
26612824-9	2017	A bolus injection of OP-1 partially restored GAG content to the native level in half of the donors, while the sustained release of OP-1 did not affect the NP explants.	Glycosaminoglycans	45-48	bone morphogenetic protein 7	Homo sapiens	21-25
28804565-10	2017	Compared to that in the control group, tissue engineered cartilage constructed by thrombospondin-1 transfected adipose derived stem cells in vivo showed a higher GAG content and lower compressive modulus, which indicating lower level of ossification.	Glycosaminoglycans	162-165	thrombospondin 1	Homo sapiens	82-98
28703769-3	2017	In the present study, we found that different glycosaminoglycans (GAGs) protect the CXCR3 ligands against proteolytic processing by CD26 without directly affecting the enzymatic activity of CD26.	Glycosaminoglycans	46-64	dipeptidylpeptidase 4	Mus musculus	132-136
27808352-7	2017	Sulf-1 injection into the mouse osteoarthritic knee significantly suppressed glycosaminoglycan loss and MMP-13 expression.	Glycosaminoglycans	77-94	sulfatase 1	Mus musculus	0-6
28616978-4	2017	The CA4+ CECT attenuation obtained from imaging ex vivo human hip cartilage correlates with the glycosaminoglycan content, equilibrium modulus, and coefficient of friction, which are key indicators of cartilage functional performance and osteoarthritis stage.	Glycosaminoglycans	96-113	carbonic anhydrase 4	Homo sapiens	4-7
28323137-7	2017	Snorc was demonstrated to have a glycosaminoglycan independent affinity to FGF2 and it inhibited FGF2 dependent cell growth of C3H101/2 cells.	Glycosaminoglycans	33-50	secondary ossification center associated regulator of chondrocyte maturation	Mus musculus	0-5
28323137-7	2017	Snorc was demonstrated to have a glycosaminoglycan independent affinity to FGF2 and it inhibited FGF2 dependent cell growth of C3H101/2 cells.	Glycosaminoglycans	33-50	fibroblast growth factor 2	Mus musculus	75-79
28716818-12	2017	The increased lipoprotein retention in intimal hyperplasia can be targeted by blocking the interaction between apoB lipoproteins and glycosaminoglycans in the extracellular matrix.	Glycosaminoglycans	133-151	apolipoprotein B	Mus musculus	111-115
28209294-3	2017	OBJECTIVE: The aim of this study is to clarify the effects of sulfated GAGs on dermal cell behaviors triggered by the TGF-beta signaling, along with its possible regulators basic fibroblast growth factor (bFGF) and cell surface epimorphin.	Glycosaminoglycans	71-75	transforming growth factor beta 1	Homo sapiens	118-126
28585336-1	2017	Mucopolysaccharidosis type 1 (MPS1) is an inherited lysosomal storage disorder caused by a deficiency in the glycosaminoglycan (GAG)-degrading enzyme alpha-l-iduronidase (IDUA).	Glycosaminoglycans	128-131	iduronidase, alpha-L	Mus musculus	150-169
28585336-1	2017	Mucopolysaccharidosis type 1 (MPS1) is an inherited lysosomal storage disorder caused by a deficiency in the glycosaminoglycan (GAG)-degrading enzyme alpha-l-iduronidase (IDUA).	Glycosaminoglycans	128-131	iduronidase, alpha-L	Mus musculus	171-175
28661485-4	2017	We used a transgenic mouse model with high syndecan-2 expression in osteoblasts to enrich the bone surface with cellular GAGs.	Glycosaminoglycans	121-125	syndecan 2	Mus musculus	43-53
28947964-8	2017	Moreover, GAG increased both CD4+FoxP3+ and CD8+CD122+PD-1+ Treg numbers in both spleens and lymph nodes of NOD mice.	Glycosaminoglycans	10-13	CD4 antigen	Mus musculus	29-32
28947964-8	2017	Moreover, GAG increased both CD4+FoxP3+ and CD8+CD122+PD-1+ Treg numbers in both spleens and lymph nodes of NOD mice.	Glycosaminoglycans	10-13	forkhead box P3	Mus musculus	33-38
28947964-9	2017	In particular, GAG could reverse a decline in CD4+FoxP3+ Tregs resulted from CsA treatments.	Glycosaminoglycans	15-18	CD4 antigen	Mus musculus	46-49
28947964-9	2017	In particular, GAG could reverse a decline in CD4+FoxP3+ Tregs resulted from CsA treatments.	Glycosaminoglycans	15-18	forkhead box P3	Mus musculus	50-55
28947964-12	2017	Thus, we demonstrated that GAG ameliorated autoimmune T1DM by upregulating both CD4+FoxP3+ and CD8+CD122+PD-1+ Tregs while GAG synergized with CsA to further suppress autoimmunity and T1DM by reversing the decline in CD4+FoxP3+ Tregs resulted from CsA treatments.	Glycosaminoglycans	27-30	CD4 antigen	Mus musculus	80-83
28947964-12	2017	Thus, we demonstrated that GAG ameliorated autoimmune T1DM by upregulating both CD4+FoxP3+ and CD8+CD122+PD-1+ Tregs while GAG synergized with CsA to further suppress autoimmunity and T1DM by reversing the decline in CD4+FoxP3+ Tregs resulted from CsA treatments.	Glycosaminoglycans	27-30	forkhead box P3	Mus musculus	84-89
28947964-12	2017	Thus, we demonstrated that GAG ameliorated autoimmune T1DM by upregulating both CD4+FoxP3+ and CD8+CD122+PD-1+ Tregs while GAG synergized with CsA to further suppress autoimmunity and T1DM by reversing the decline in CD4+FoxP3+ Tregs resulted from CsA treatments.	Glycosaminoglycans	27-30	CD4 antigen	Mus musculus	217-220
28947964-12	2017	Thus, we demonstrated that GAG ameliorated autoimmune T1DM by upregulating both CD4+FoxP3+ and CD8+CD122+PD-1+ Tregs while GAG synergized with CsA to further suppress autoimmunity and T1DM by reversing the decline in CD4+FoxP3+ Tregs resulted from CsA treatments.	Glycosaminoglycans	27-30	forkhead box P3	Mus musculus	221-226
28649514-1	2017	Mucopolysaccharidosis type II (MPS II - Hunter syndrome) is an X-linked lysosomal storage disorder caused by a deficiency in the enzyme iduronate-2 sulfatase (I2S), leading to the accumulation of the glycosaminoglycans, affecting multiple organs and systems.	Glycosaminoglycans	200-218	iduronate 2-sulfatase	Homo sapiens	136-157
28649514-1	2017	Mucopolysaccharidosis type II (MPS II - Hunter syndrome) is an X-linked lysosomal storage disorder caused by a deficiency in the enzyme iduronate-2 sulfatase (I2S), leading to the accumulation of the glycosaminoglycans, affecting multiple organs and systems.	Glycosaminoglycans	200-218	iduronate 2-sulfatase	Homo sapiens	159-162
27744520-7	2017	Interestingly, EXT1-depleted cells showed a downregulation of the UDP-sugar transporter SLC35D1, whereas SLC35D2 was downregulated in beta4GalT7-depleted cells, indicating an intricate regulatory network that connects all glycosaminoglycans synthesis.	Glycosaminoglycans	222-240	exostosin glycosyltransferase 1	Homo sapiens	15-19
27744520-7	2017	Interestingly, EXT1-depleted cells showed a downregulation of the UDP-sugar transporter SLC35D1, whereas SLC35D2 was downregulated in beta4GalT7-depleted cells, indicating an intricate regulatory network that connects all glycosaminoglycans synthesis.	Glycosaminoglycans	222-240	solute carrier family 35 member D2	Homo sapiens	105-112
27744520-7	2017	Interestingly, EXT1-depleted cells showed a downregulation of the UDP-sugar transporter SLC35D1, whereas SLC35D2 was downregulated in beta4GalT7-depleted cells, indicating an intricate regulatory network that connects all glycosaminoglycans synthesis.	Glycosaminoglycans	222-240	beta-1,4-galactosyltransferase 7	Homo sapiens	134-144
28588666-1	2017	Hunter syndrome (or mucopolysaccharidosis type II, MPS II) is an X-linked recessive disorder induced by a deficiency of the iduronate 2-sulfatase (IDS) enzyme, resulting in the accumulation of glycosaminoglycan substrates, heparan sulfate and dermatan sulfate, in the lysosomes.	Glycosaminoglycans	193-210	iduronate 2-sulfatase	Homo sapiens	124-145
28588666-1	2017	Hunter syndrome (or mucopolysaccharidosis type II, MPS II) is an X-linked recessive disorder induced by a deficiency of the iduronate 2-sulfatase (IDS) enzyme, resulting in the accumulation of glycosaminoglycan substrates, heparan sulfate and dermatan sulfate, in the lysosomes.	Glycosaminoglycans	193-210	iduronate 2-sulfatase	Homo sapiens	147-150
28569157-8	2017	The level of release and matrix accumulation of GAGs in IL-1beta pre-treated HAC pellets in the presence of sesamin was recovered.	Glycosaminoglycans	48-52	interleukin 1 beta	Homo sapiens	56-64
28539925-4	2017	It was demonstrated that CXCL9(74-103) binds with high affinity to GAGs, competed with active chemokines for GAG binding and thereby inhibited CXCL8- and monosodium urate (MSU) crystal-induced neutrophil migration to joints.	Glycosaminoglycans	67-70	chemokine (C-X-C motif) ligand 9	Mus musculus	25-30
28539925-11	2017	This could be explained by (1) the lower affinity of CXCL9(74-93) for CS, the most abundant GAG in joints, and (2) by reduced competition with GAG binding of CXCL1, the most abundant ELR+ CXC chemokine in this gout model.	Glycosaminoglycans	92-95	chemokine (C-X-C motif) ligand 9	Mus musculus	53-58
28539925-14	2017	In summary, both CXCL9 peptides inhibited neutrophil migration in vivo through interference with GAG interactions in several animal models.	Glycosaminoglycans	97-100	chemokine (C-X-C motif) ligand 9	Mus musculus	17-22
28539925-15	2017	Shortening CXCL9(74-103) from the COOH-terminus limited its GAG-binding spectrum.	Glycosaminoglycans	60-63	chemokine (C-X-C motif) ligand 9	Mus musculus	11-16
28264929-5	2017	Addressing this long-standing incongruity, we used calorimetry and magnetic resonance to probe interactions of AgRP peptides with glycosaminoglycans, including heparan sulfate.	Glycosaminoglycans	130-148	agouti related neuropeptide	Homo sapiens	111-115
27783214-6	2017	TNFalpha led to a significant raise of GAG release and NO production.	Glycosaminoglycans	39-42	tumor necrosis factor	Bos taurus	0-8
28204496-8	2017	However, GalNAc-4-ST1 has minimal activity toward glycosaminoglycans, instead modifying terminal beta1,4-linked GalNAc on N- and O-linked oligosaccharides on specific glycoproteins.	Glycosaminoglycans	50-68	carbohydrate sulfotransferase 8	Homo sapiens	9-21
28209294-3	2017	OBJECTIVE: The aim of this study is to clarify the effects of sulfated GAGs on dermal cell behaviors triggered by the TGF-beta signaling, along with its possible regulators basic fibroblast growth factor (bFGF) and cell surface epimorphin.	Glycosaminoglycans	71-75	syntaxin 2	Homo sapiens	228-238
28339078-9	2017	P-PRP promoted the mRNA and protein expression levels of cartilaginous markers and the production of GAG more effectively, compared with L-PRP.	Glycosaminoglycans	101-104	prion protein	Homo sapiens	2-5
27302693-2	2017	Therefore, this study evaluated whether contrast-enhanced computed tomography (CECT) attenuation and contrast agent flux using the iodinated contrast agents CA4+ and ioxaglate correlate with the glycosaminoglycan (GAG) content/distribution and water content in human menisci.	Glycosaminoglycans	195-212	carbonic anhydrase 4	Homo sapiens	157-160
27302693-3	2017	The optimal ioxaglate and CA4+ contrast agent concentrations for mapping meniscal GAG distribution were qualitatively determined by comparison of CECT color maps with Safranin-O stained histological sections.	Glycosaminoglycans	82-85	carbonic anhydrase 4	Homo sapiens	26-29
27302693-6	2017	The optimal concentrations for GAG depiction for ioxaglate and CA4+ were &gt;=80 and 12 mgI/ml, respectively.	Glycosaminoglycans	31-34	carbonic anhydrase 4	Homo sapiens	63-66
28194008-2	2017	Here, we show that a genetic point mutation in the glycosaminoglycan recognition motif of Otx2 broadly delays the maturation of pivotal parvalbumin-positive (PV+) interneurons not only in V1 but also in the primary auditory (A1) and medial prefrontal cortex (mPFC).	Glycosaminoglycans	51-68	orthodenticle homeobox 2	Mus musculus	90-94
28468283-8	2017	Any future exploitation of the TGF-beta cytokines in the therapy of chronic diseases will need to fully consider their interactions with glycosaminoglycans and the implications of this in terms of their bioavailability and biological activity.	Glycosaminoglycans	137-155	transforming growth factor beta 1	Homo sapiens	31-39
28179527-8	2017	For granzyme B, Tat/Rev was the most dominant whereas for IFN-gamma, Gag predominated.	Glycosaminoglycans	69-72	interferon gamma	Homo sapiens	58-67
28441755-5	2017	RHEB enhances the chondrogenic differentiation of ASCs in 3D culture via upregulation of SOX9 with concomitant increase in glycosaminoglycans (GAGs), and type II collagen (COL2).	Glycosaminoglycans	123-141	Ras homolog, mTORC1 binding	Homo sapiens	0-4
28161573-6	2017	Histological assessment of in vitro and subcutaneously implanted in vivo constructs demonstrated that CM-expanded cells followed by TGF-beta3 exposure resulted in highest cell proliferation, GAG accumulation, and collagen deposition.	Glycosaminoglycans	191-194	transforming growth factor beta 3	Homo sapiens	132-141
28224886-3	2017	Hyaluronate, a main component of glycosaminoglycans, provides CD44-specific interactions with chondrocytes but typically requires chemical cross-linking agents to fabricate hydrogels, which may cause unexpected side effects in the body.	Glycosaminoglycans	33-51	CD44 antigen	Mus musculus	62-66
28284342-2	2017	CCL21 contains an extended C-terminus, which increases binding to lymphatic glycosaminoglycans and provides a mechanism for cell trafficking by forming a stationary chemokine concentration gradient that allows cell migration via haptotaxis.	Glycosaminoglycans	76-94	C-C motif chemokine ligand 21	Homo sapiens	0-5
28445977-1	2017	Serglycin is an intracellular proteoglycan with a unique ability to adopt highly divergent structures by glycosylation with variable types of glycosaminoglycans (GAGs) when expressed by different cell types.	Glycosaminoglycans	142-160	serglycin	Homo sapiens	0-9
28432302-0	2017	A bacterial ABC transporter enables import of mammalian host glycosaminoglycans.	Glycosaminoglycans	61-79	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	12-27
28978009-4	2017	Here, we find that cancer cell internalization of CAIX is negatively regulated by post-translational modification with chondroitin or heparan sulfate glycosaminoglycan chains.	Glycosaminoglycans	150-167	carbonic anhydrase 9	Homo sapiens	50-54
28978009-5	2017	We show that perturbed glycosaminoglycan modification results in increased CAIX endocytosis.	Glycosaminoglycans	23-40	carbonic anhydrase 9	Homo sapiens	75-79
28978009-7	2017	In support of this concept, pharmacological inhibition of glycosaminoglycan biosynthesis with xylosides significantly potentiated the internalization and cytotoxic activity of an antibody-drug conjugate (ADC) targeted at CAIX.	Glycosaminoglycans	58-75	carbonic anhydrase 9	Homo sapiens	221-225
28978009-8	2017	Moreover, cells expressing glycosaminoglycan-deficient CAIX were significantly more sensitive to ADC treatment as compared with cells expressing wild-type CAIX.	Glycosaminoglycans	27-44	carbonic anhydrase 9	Homo sapiens	55-59
28978009-8	2017	Moreover, cells expressing glycosaminoglycan-deficient CAIX were significantly more sensitive to ADC treatment as compared with cells expressing wild-type CAIX.	Glycosaminoglycans	27-44	carbonic anhydrase 9	Homo sapiens	155-159
28115521-2	2017	PF4 is stored in platelet alpha-granules bound to the glycosaminoglycan (GAG) chains of serglycin.	Glycosaminoglycans	54-71	platelet factor 4	Homo sapiens	0-3
28333940-0	2017	Distinct transcriptome profiles of Gag-specific CD8+ T cells temporally correlated with the protection elicited by SIVDeltanef live attenuated vaccine.	Glycosaminoglycans	35-38	CD8a molecule	Homo sapiens	48-51
28333940-5	2017	We found that gene expression profiles of Gag-specific CD8+ T cells at 20 WPV are qualitatively different from those at 3 WPV.	Glycosaminoglycans	42-45	CD8a molecule	Homo sapiens	55-58
28333940-6	2017	At 20 WPV, the most significant transcriptional changes of Gag-specific CD8+ T cells were genes involved in TCR signaling, differentiation and maturation toward central memory cells, with increased expression of CCR7, TCRalpha, TCRbeta, CD28 and decreased expression of CTLA-4, IFN-gamma, RANTES, granzyme A and B.	Glycosaminoglycans	59-62	CD8a molecule	Homo sapiens	72-75
28333940-6	2017	At 20 WPV, the most significant transcriptional changes of Gag-specific CD8+ T cells were genes involved in TCR signaling, differentiation and maturation toward central memory cells, with increased expression of CCR7, TCRalpha, TCRbeta, CD28 and decreased expression of CTLA-4, IFN-gamma, RANTES, granzyme A and B.	Glycosaminoglycans	59-62	C-C motif chemokine receptor 7	Homo sapiens	212-216
28333940-6	2017	At 20 WPV, the most significant transcriptional changes of Gag-specific CD8+ T cells were genes involved in TCR signaling, differentiation and maturation toward central memory cells, with increased expression of CCR7, TCRalpha, TCRbeta, CD28 and decreased expression of CTLA-4, IFN-gamma, RANTES, granzyme A and B.	Glycosaminoglycans	59-62	T cell receptor alpha constant	Homo sapiens	218-226
28333940-6	2017	At 20 WPV, the most significant transcriptional changes of Gag-specific CD8+ T cells were genes involved in TCR signaling, differentiation and maturation toward central memory cells, with increased expression of CCR7, TCRalpha, TCRbeta, CD28 and decreased expression of CTLA-4, IFN-gamma, RANTES, granzyme A and B.	Glycosaminoglycans	59-62	T cell receptor beta constant 1	Homo sapiens	228-235
28333940-6	2017	At 20 WPV, the most significant transcriptional changes of Gag-specific CD8+ T cells were genes involved in TCR signaling, differentiation and maturation toward central memory cells, with increased expression of CCR7, TCRalpha, TCRbeta, CD28 and decreased expression of CTLA-4, IFN-gamma, RANTES, granzyme A and B.	Glycosaminoglycans	59-62	CD28 molecule	Homo sapiens	237-241
28333940-6	2017	At 20 WPV, the most significant transcriptional changes of Gag-specific CD8+ T cells were genes involved in TCR signaling, differentiation and maturation toward central memory cells, with increased expression of CCR7, TCRalpha, TCRbeta, CD28 and decreased expression of CTLA-4, IFN-gamma, RANTES, granzyme A and B.	Glycosaminoglycans	59-62	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	270-276
28333940-6	2017	At 20 WPV, the most significant transcriptional changes of Gag-specific CD8+ T cells were genes involved in TCR signaling, differentiation and maturation toward central memory cells, with increased expression of CCR7, TCRalpha, TCRbeta, CD28 and decreased expression of CTLA-4, IFN-gamma, RANTES, granzyme A and B.	Glycosaminoglycans	59-62	interferon gamma	Homo sapiens	278-287
28333940-6	2017	At 20 WPV, the most significant transcriptional changes of Gag-specific CD8+ T cells were genes involved in TCR signaling, differentiation and maturation toward central memory cells, with increased expression of CCR7, TCRalpha, TCRbeta, CD28 and decreased expression of CTLA-4, IFN-gamma, RANTES, granzyme A and B.	Glycosaminoglycans	59-62	C-C motif chemokine ligand 5	Homo sapiens	289-295
28333940-6	2017	At 20 WPV, the most significant transcriptional changes of Gag-specific CD8+ T cells were genes involved in TCR signaling, differentiation and maturation toward central memory cells, with increased expression of CCR7, TCRalpha, TCRbeta, CD28 and decreased expression of CTLA-4, IFN-gamma, RANTES, granzyme A and B.	Glycosaminoglycans	59-62	granzyme A	Homo sapiens	297-313
29744379-3	2017	We therefore hypothesized that fibroblast growth factor (FGF2) enriching chondroitin sulfate glycosaminoglycan (CS-GAG) matrices can maintain the undifferentiated state of neural stem cells (NSCs) and facilitate brain tissue repair subacutely post-TBI.	Glycosaminoglycans	115-118	fibroblast growth factor 2	Rattus norvegicus	57-61
29744379-6	2017	CS-GAG-NSC treated animals demonstrated significantly enhanced (p &lt; 0.05) FGF2 retention, and maintenance of PKH26GL labeled NSCs as indicated by enhanced Sox1+ and Ki67+ cell presence over other differentiated cell types.	Glycosaminoglycans	3-6	fibroblast growth factor 2	Rattus norvegicus	77-81
29744379-6	2017	CS-GAG-NSC treated animals demonstrated significantly enhanced (p &lt; 0.05) FGF2 retention, and maintenance of PKH26GL labeled NSCs as indicated by enhanced Sox1+ and Ki67+ cell presence over other differentiated cell types.	Glycosaminoglycans	3-6	SRY-box transcription factor 1	Rattus norvegicus	158-162
28154179-4	2017	Moreover, 1B6 recognized glycosaminoglycan (GAG)-bound CXCL10, resulting in target-mediated clearance, which was corroborated using CXCL10-deficient mice.	Glycosaminoglycans	25-42	chemokine (C-X-C motif) ligand 10	Mus musculus	55-61
28154179-4	2017	Moreover, 1B6 recognized glycosaminoglycan (GAG)-bound CXCL10, resulting in target-mediated clearance, which was corroborated using CXCL10-deficient mice.	Glycosaminoglycans	44-47	chemokine (C-X-C motif) ligand 10	Mus musculus	55-61
28154179-4	2017	Moreover, 1B6 recognized glycosaminoglycan (GAG)-bound CXCL10, resulting in target-mediated clearance, which was corroborated using CXCL10-deficient mice.	Glycosaminoglycans	44-47	chemokine (C-X-C motif) ligand 10	Mus musculus	132-138
28154179-5	2017	In contrast to 1B6, 1F11 inhibited the interaction of CXCL10 with GAGs, did not recognize GAG-bound CXCL10, and did not display target-mediated drug disposition.	Glycosaminoglycans	66-69	chemokine (C-X-C motif) ligand 10	Mus musculus	54-60
28327528-8	2017	The level of laminin in HMVEC-C cells or fibronectin in HFD rat hepatocytes was significantly affected by these GAG treatments, which regulated adipogenesis and adipocyte function.	Glycosaminoglycans	112-115	fibronectin 1	Rattus norvegicus	41-52
28115521-2	2017	PF4 is stored in platelet alpha-granules bound to the glycosaminoglycan (GAG) chains of serglycin.	Glycosaminoglycans	73-76	platelet factor 4	Homo sapiens	0-3
28115521-3	2017	This study revealed that platelet serglycin is decorated with chondroitin/dermatan sulfate and that PF4 binds to these GAG chains.	Glycosaminoglycans	119-122	platelet factor 4	Homo sapiens	100-103
28267150-4	2017	Neuropsin cleaves mature NRG1 (bound to extracellular glycosaminoglycans) in response to long-term potentiation or depression, liberating a soluble ligand that activates its receptor, ErbB4.	Glycosaminoglycans	54-72	opsin 5	Mus musculus	0-9
28099921-0	2017	Stiehopus japonieus acidic mucopolysaccharide inhibits the proliferation of pancreatic cancer SW1990 cells through Hippo-YAP pathway.	Glycosaminoglycans	27-45	Yes1 associated transcriptional regulator	Homo sapiens	121-124
28267150-4	2017	Neuropsin cleaves mature NRG1 (bound to extracellular glycosaminoglycans) in response to long-term potentiation or depression, liberating a soluble ligand that activates its receptor, ErbB4.	Glycosaminoglycans	54-72	neuregulin 1	Mus musculus	25-29
28267150-4	2017	Neuropsin cleaves mature NRG1 (bound to extracellular glycosaminoglycans) in response to long-term potentiation or depression, liberating a soluble ligand that activates its receptor, ErbB4.	Glycosaminoglycans	54-72	erb-b2 receptor tyrosine kinase 4	Mus musculus	184-189
27989561-4	2017	SERPINA5 binds glycosaminoglycans, phospholipids, and retinoic acid.	Glycosaminoglycans	15-33	serine (or cysteine) peptidase inhibitor, clade A, member 5	Mus musculus	0-8
28222208-2	2017	Therefore, this study aims to give insight into the interaction of cancer cells exhibiting different metastatic potential (MDA-MB-231, MDA-MB-468) with surface immobilized GAG interacting with serum proteins like fibronectin.	Glycosaminoglycans	172-175	fibronectin 1	Homo sapiens	213-224
28240227-0	2017	Nonsteroidal anti-inflammatory drugs modulate cellular glycosaminoglycan synthesis by affecting EGFR and PI3K signaling pathways.	Glycosaminoglycans	55-72	epidermal growth factor receptor	Homo sapiens	96-100
28240227-6	2017	This study documents that NSAIDs, and their mixtures with genistein modulate cellular glycosaminoglycan synthesis by affecting EGFR and PI3K signaling pathways.	Glycosaminoglycans	86-103	epidermal growth factor receptor	Homo sapiens	127-131
28245630-1	2017	CXCL7, a chemokine highly expressed in platelets, orchestrates neutrophil recruitment during thrombosis and related pathophysiological processes by interacting with CXCR2 receptor and sulfated glycosaminoglycans (GAG).	Glycosaminoglycans	193-211	pro-platelet basic protein	Homo sapiens	0-5
28245630-1	2017	CXCL7, a chemokine highly expressed in platelets, orchestrates neutrophil recruitment during thrombosis and related pathophysiological processes by interacting with CXCR2 receptor and sulfated glycosaminoglycans (GAG).	Glycosaminoglycans	213-216	pro-platelet basic protein	Homo sapiens	0-5
28245630-3	2017	Currently, nothing is known regarding the structural basis by which receptor and GAG interactions mediate CXCL7 function.	Glycosaminoglycans	81-84	pro-platelet basic protein	Homo sapiens	106-111
28000839-11	2017	Sulfated glycosaminoglycan production was also reduced upon chondrogenic differentiation in the presence of IL-6, but not IL-8.	Glycosaminoglycans	9-26	interleukin 6	Homo sapiens	108-112
28150116-1	2017	Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of alpha-L-iduronidase (IDUA), resulting in accumulation of glycosaminoglycans (GAG) in lysosomes.	Glycosaminoglycans	123-141	iduronidase, alpha-L	Mus musculus	66-85
28150116-1	2017	Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of alpha-L-iduronidase (IDUA), resulting in accumulation of glycosaminoglycans (GAG) in lysosomes.	Glycosaminoglycans	123-141	iduronidase, alpha-L	Mus musculus	87-91
28150116-1	2017	Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of alpha-L-iduronidase (IDUA), resulting in accumulation of glycosaminoglycans (GAG) in lysosomes.	Glycosaminoglycans	143-146	iduronidase, alpha-L	Mus musculus	66-85
28150116-1	2017	Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of alpha-L-iduronidase (IDUA), resulting in accumulation of glycosaminoglycans (GAG) in lysosomes.	Glycosaminoglycans	143-146	iduronidase, alpha-L	Mus musculus	87-91
28199387-7	2017	The competitive effect of heparin on DS binding to TG2 suggests that both glycosaminoglycans occupy the same binding site(s) on the protein molecule.	Glycosaminoglycans	74-92	transglutaminase 2	Homo sapiens	51-54
27863148-1	2017	HLA-DPB1*581:01 differs from DPB1*41:01:01 at codon 57, substituting codon GAG for GAC in exon 2.	Glycosaminoglycans	75-78	major histocompatibility complex, class II, DP beta 1	Homo sapiens	0-8
27887732-11	2017	CONCLUSIONS: Although reduction in inflammatory/angiogenic potential of the chondrogenically differentiated constructs highlights the superior effectiveness of PRP in comparison to TGFbeta for chondrogenic differentiation, yet further improvement of the PRP-based chondrogenic differentiation media is required to inhibit the production of angiogenic/inflammatory markers, calcification and the release of synthesized GAG out of the construct.	Glycosaminoglycans	418-421	prion protein	Homo sapiens	160-163
27887732-11	2017	CONCLUSIONS: Although reduction in inflammatory/angiogenic potential of the chondrogenically differentiated constructs highlights the superior effectiveness of PRP in comparison to TGFbeta for chondrogenic differentiation, yet further improvement of the PRP-based chondrogenic differentiation media is required to inhibit the production of angiogenic/inflammatory markers, calcification and the release of synthesized GAG out of the construct.	Glycosaminoglycans	418-421	prion protein	Homo sapiens	254-257
27976897-0	2017	Potent, Selective, Allosteric Inhibition of Human Plasmin by Sulfated Non-Saccharide Glycosaminoglycan Mimetics.	Glycosaminoglycans	85-102	plasminogen	Homo sapiens	50-57
27976897-3	2017	We report on the synthesis, biological activity, and mechanism of action of a group of small molecules, called non-saccharide glycosaminoglycan mimetics (NSGMs), as direct allosteric plasmin inhibitors.	Glycosaminoglycans	126-143	plasminogen	Homo sapiens	183-190
27863148-1	2017	HLA-DPB1*581:01 differs from DPB1*41:01:01 at codon 57, substituting codon GAG for GAC in exon 2.	Glycosaminoglycans	75-78	major histocompatibility complex, class II, DP beta 1	Homo sapiens	4-8
29359168-2	2017	Retroviruses have developed strategies to counteract the action of SERINC5, such as the expression of proteins like negative regulatory factor (Nef), S2, and glycosylated Gag (glycoGag).	Glycosaminoglycans	171-174	serine incorporator 5	Homo sapiens	67-74
28013294-0	2017	Mutation in VPS33A affects metabolism of glycosaminoglycans: a new type of mucopolysaccharidosis with severe systemic symptoms.	Glycosaminoglycans	41-59	VPS33A core subunit of CORVET and HOPS complexes	Homo sapiens	12-18
27599773-3	2017	CSGALNACT1 encodes chondroitin sulfate N-acetylgalactosaminyltransferase-1 (CSGalNAcT-1, ChGn-1), which initiates chondroitin sulfate (CS) chain biosynthesis on the so-called GAG-protein linker region tetrasaccharide.	Glycosaminoglycans	175-178	chondroitin sulfate N-acetylgalactosaminyltransferase 1	Homo sapiens	0-10
27599773-3	2017	CSGALNACT1 encodes chondroitin sulfate N-acetylgalactosaminyltransferase-1 (CSGalNAcT-1, ChGn-1), which initiates chondroitin sulfate (CS) chain biosynthesis on the so-called GAG-protein linker region tetrasaccharide.	Glycosaminoglycans	175-178	chondroitin sulfate N-acetylgalactosaminyltransferase 1	Homo sapiens	76-87
27658702-8	2017	The stimulation of GAG synthesis by dynamic compression was greater at 21 % than 5 % oxygen tension and this response was reduced with TNFalpha or reversed with L-NIO.	Glycosaminoglycans	19-22	tumor necrosis factor	Homo sapiens	135-143
24945362-2	2017	We report that the content of insoluble elastin in the dermis of cultured human skin can be increased though the use of two approaches that enhance elastogenesis by dermal fibroblasts, forced expression of versican variant V3, which lacks glycosaminoglycan (GAG) chains, and forced expression of versican antisense to decrease levels of versican variant V1 with GAG chains.	Glycosaminoglycans	239-256	elastin	Homo sapiens	40-47
24945362-2	2017	We report that the content of insoluble elastin in the dermis of cultured human skin can be increased though the use of two approaches that enhance elastogenesis by dermal fibroblasts, forced expression of versican variant V3, which lacks glycosaminoglycan (GAG) chains, and forced expression of versican antisense to decrease levels of versican variant V1 with GAG chains.	Glycosaminoglycans	258-261	elastin	Homo sapiens	40-47
24945362-2	2017	We report that the content of insoluble elastin in the dermis of cultured human skin can be increased though the use of two approaches that enhance elastogenesis by dermal fibroblasts, forced expression of versican variant V3, which lacks glycosaminoglycan (GAG) chains, and forced expression of versican antisense to decrease levels of versican variant V1 with GAG chains.	Glycosaminoglycans	362-365	elastin	Homo sapiens	40-47
28740513-6	2017	The abundance of glycosaminoglycan (GAG) was also significantly higher in the IGF-1-MSC group.	Glycosaminoglycans	17-34	insulin like growth factor 1	Homo sapiens	78-83
28740513-6	2017	The abundance of glycosaminoglycan (GAG) was also significantly higher in the IGF-1-MSC group.	Glycosaminoglycans	36-39	insulin like growth factor 1	Homo sapiens	78-83
27795436-4	2017	We recently reported that nuclear Naf1 promoted nuclear export of unspliced HIV-1 gag mRNA, leading to increased Gag production.	Glycosaminoglycans	113-116	Pr55(Gag)	Human immunodeficiency virus 1	82-85
28230922-3	2017	ALDH-positive cells were isolated by a fluorescence-activated cell sorting technique from Lewis rat"s stromal-vascular-fraction (SVF) and transplanted with c-GAG scaffolds in a rat full-thickness skin wound model.	Glycosaminoglycans	158-161	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	0-4
27720939-1	2016	Mucopolysaccharidosis type I (MPS I) is caused by deficiency of alpha-l-iduronidase, involved in degradation of glycosaminoglycans.	Glycosaminoglycans	112-130	iduronidase, alpha-L	Mus musculus	64-83
27936727-3	2016	Modification of ECM with CBP-heparin leads to increased deposition of functional heparin (by ~7.2-fold measured by glycosaminoglycan composition) and a corresponding reduction in platelet binding (&gt;70%) and whole blood clotting (&gt;80%) onto the ECM.	Glycosaminoglycans	115-132	CREB binding protein	Homo sapiens	25-28
27784788-2	2016	Transforming growth factor beta type III receptor (TbetaRIII/betaglycan) is a transmembrane proteoglycan co-receptor that exists with or without heparan and/or chondroitin sulfate glycosaminoglycan (GAG) modifications in cells and has established roles in development and cancer.	Glycosaminoglycans	199-202	transforming growth factor beta receptor 3	Homo sapiens	61-71
27784788-3	2016	Our studies here demonstrate that TbetaRIII, independent of its TGFbeta co-receptor function, regulates canonical Wnt3a signaling by controlling Wnt3a availability through its sulfated GAG chains.	Glycosaminoglycans	185-188	Wnt family member 3A	Homo sapiens	114-119
27502245-9	2016	NO production and GAG release by the cartilage was increased when cultured with M(IFNgamma+TNFalpha) MCM.	Glycosaminoglycans	18-21	interferon gamma	Homo sapiens	82-90
27860466-2	2016	Glycosaminoglycans (GAGs), known to complex and stabilize cytokines in vivo, are therefore used to form 3D-biohybrid polymer networks capable of aiding the effective administration of Interleukin-4, a key regulator of the inflammatory response.	Glycosaminoglycans	0-18	interleukin 4	Mus musculus	184-197
27784933-6	2016	The presence of a type II repeat is a characteristic feature of GBPs, which is similar in structure to the fibronectin type II domain (fn2), which has ability to bind multiple ligands including gelatin, glycosaminoglycans, choline phospholipids, and lipoproteins.	Glycosaminoglycans	203-221	fibronectin 1	Bos taurus	107-118
27898729-3	2016	Because relative expression of GAGs is dependent on cell-type and niche, isolating GAGs from cell cultures and tissues may provide insight into cell- and tissue-specific GAG structure and functions.	Glycosaminoglycans	83-87	melanoma antigen	Mus musculus	31-34
27905556-5	2016	Here we show that in Gag-expressing cells, secretion of biologically active p17 takes place at the plasma membrane and occurs following its interaction with phosphatidylinositol-(4,5)-bisphosphate and its subsequent cleavage from the precursor Gag (Pr55Gag) operated by cellular aspartyl proteases.	Glycosaminoglycans	21-24	family with sequence similarity 72 member B	Homo sapiens	76-79
27905556-5	2016	Here we show that in Gag-expressing cells, secretion of biologically active p17 takes place at the plasma membrane and occurs following its interaction with phosphatidylinositol-(4,5)-bisphosphate and its subsequent cleavage from the precursor Gag (Pr55Gag) operated by cellular aspartyl proteases.	Glycosaminoglycans	244-247	family with sequence similarity 72 member B	Homo sapiens	76-79
27898729-9	2016	GAG extracts from all examined cell lines and tissues contained varying amounts of contaminating RNA, which interfered with GAG quantification using DMMB assays and characterization of GAGs by barium acetate gel electrophoresis.	Glycosaminoglycans	185-189	melanoma antigen	Mus musculus	0-3
28018459-7	2016	The CLCNKB mutation analysis revealed a heterozygous c.139G&gt;A transition in exon 13 [p.Gly(GGG)465Glu(GAG)].	Glycosaminoglycans	105-108	chloride voltage-gated channel Kb	Homo sapiens	4-10
27829019-6	2016	The expression of PD-1 and PD-L1 was higher on Gag-specific CD8+ T cells as compared to CEF-specific CD8+ T cells, and the expression of these markers did not change significantly after Treg depletion or co-culture with Treg/HIV-, unlike on CEF-specific CD8+ T cells.	Glycosaminoglycans	47-50	programmed cell death 1	Homo sapiens	18-22
27829019-6	2016	The expression of PD-1 and PD-L1 was higher on Gag-specific CD8+ T cells as compared to CEF-specific CD8+ T cells, and the expression of these markers did not change significantly after Treg depletion or co-culture with Treg/HIV-, unlike on CEF-specific CD8+ T cells.	Glycosaminoglycans	47-50	CD274 molecule	Homo sapiens	27-32
27829019-6	2016	The expression of PD-1 and PD-L1 was higher on Gag-specific CD8+ T cells as compared to CEF-specific CD8+ T cells, and the expression of these markers did not change significantly after Treg depletion or co-culture with Treg/HIV-, unlike on CEF-specific CD8+ T cells.	Glycosaminoglycans	47-50	CD8a molecule	Homo sapiens	60-63
27301418-3	2016	Here we show that plasmin cleaves surface-bound CCL21 to release the C-terminal peptide responsible for CCL21 binding to glycosaminoglycans on the extracellular matrix and cell surfaces, thereby generating the soluble form.	Glycosaminoglycans	121-139	plasminogen	Homo sapiens	18-25
27301418-3	2016	Here we show that plasmin cleaves surface-bound CCL21 to release the C-terminal peptide responsible for CCL21 binding to glycosaminoglycans on the extracellular matrix and cell surfaces, thereby generating the soluble form.	Glycosaminoglycans	121-139	C-C motif chemokine ligand 21	Homo sapiens	48-53
27301418-3	2016	Here we show that plasmin cleaves surface-bound CCL21 to release the C-terminal peptide responsible for CCL21 binding to glycosaminoglycans on the extracellular matrix and cell surfaces, thereby generating the soluble form.	Glycosaminoglycans	121-139	C-C motif chemokine ligand 21	Homo sapiens	104-109
27871226-4	2016	Previously, homozygous missense variants within the B3GAT3 gene encoding beta 1,3 glucuronyltransferase 3(GlcAT-I) responsible for the biosynthesis of glycosaminoglycans have been described in 7 individuals.	Glycosaminoglycans	151-169	beta-1,3-glucuronyltransferase 3	Homo sapiens	52-58
27871226-4	2016	Previously, homozygous missense variants within the B3GAT3 gene encoding beta 1,3 glucuronyltransferase 3(GlcAT-I) responsible for the biosynthesis of glycosaminoglycans have been described in 7 individuals.	Glycosaminoglycans	151-169	beta-1,3-glucuronyltransferase 3	Homo sapiens	73-105
27871226-4	2016	Previously, homozygous missense variants within the B3GAT3 gene encoding beta 1,3 glucuronyltransferase 3(GlcAT-I) responsible for the biosynthesis of glycosaminoglycans have been described in 7 individuals.	Glycosaminoglycans	151-169	beta-1,3-glucuronyltransferase 3	Homo sapiens	106-113
27808176-3	2016	FN homes several binding sites for sulfated glycosaminoglycans (sGAG), such as heparin (Hep), which was previously shown to influence FN conformation and protein binding.	Glycosaminoglycans	44-62	fibronectin 1	Homo sapiens	0-2
27808176-3	2016	FN homes several binding sites for sulfated glycosaminoglycans (sGAG), such as heparin (Hep), which was previously shown to influence FN conformation and protein binding.	Glycosaminoglycans	44-62	fibronectin 1	Homo sapiens	134-136
27387409-4	2016	The results indicate a lower leaching of fibronectin, but a higher leaching of laminin and sulfated glycosaminoglycans from tissues decellularized with STX and TX, respectively.	Glycosaminoglycans	100-118	ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 2	Rattus norvegicus	152-155
27895229-5	2016	We found that the ability of PECAM-1 to stimulate cell migration, promote filopodia formation and trigger Cdc42 activation were lost if PECAM-1-dependent homophilic or heparin/GAG-dependent heterophilic ligand binding was disabled.	Glycosaminoglycans	176-179	platelet/endothelial cell adhesion molecule 1	Mus musculus	29-36
27445159-3	2016	The expressed serglycin was also decorated with chondroitin/dermatan sulfate chains and the relative abundance of these glycosaminoglycan chains changed under different concentrations of glucose in the culture medium.	Glycosaminoglycans	120-137	serglycin	Homo sapiens	14-23
27349464-8	2016	Administration of IL-10 significantly reduced the injury related cell death and release of GAG and NO, respectively.	Glycosaminoglycans	91-94	interleukin-10	Bos taurus	18-23
27895229-5	2016	We found that the ability of PECAM-1 to stimulate cell migration, promote filopodia formation and trigger Cdc42 activation were lost if PECAM-1-dependent homophilic or heparin/GAG-dependent heterophilic ligand binding was disabled.	Glycosaminoglycans	176-179	cell division cycle 42	Mus musculus	106-111
27798666-0	2016	A Novel Physiological Glycosaminoglycan-Deficient Splice Variant of Neuropilin-1 Is Anti-Tumorigenic In Vitro and In Vivo.	Glycosaminoglycans	22-39	neuropilin 1	Homo sapiens	68-80
27798666-4	2016	NRP1 is further post-translationally modified by the addition of glycosaminoglycans (GAG) side chains through an O-glycosylation site at serine612.	Glycosaminoglycans	65-83	neuropilin 1	Homo sapiens	0-4
27798666-4	2016	NRP1 is further post-translationally modified by the addition of glycosaminoglycans (GAG) side chains through an O-glycosylation site at serine612.	Glycosaminoglycans	85-88	neuropilin 1	Homo sapiens	0-4
27798666-7	2016	As expected, the high molecular weight products appearing as a smear in SDS-PAGE and reflecting the presence of GAG in NRP1-FS were undetectable in the NRP1-Delta7 protein.	Glycosaminoglycans	112-115	neuropilin 1	Homo sapiens	119-123
27582494-6	2016	TIMP-3 K26A/K45A retained higher affinity for sulfated glycosaminoglycans than K42A/K110A and exhibited increased affinity for ADAMTS-5 in the presence of heparin.	Glycosaminoglycans	55-73	TIMP metallopeptidase inhibitor 3	Homo sapiens	0-6
27487857-3	2016	The dual binding of HIT antibodies to platelet surface PF4/GAG complexes and to FcgammaRIIA likely leads to both platelet clearance and to their direct activation.	Glycosaminoglycans	59-62	platelet factor 4	Homo sapiens	55-58
27775651-1	2016	Chondroitin sulfate (CS), a type of glycosaminoglycan (GAG), is a factor involved in the suppression of myogenic differentiation.	Glycosaminoglycans	36-53	heat shock protein 9	Mus musculus	21-23
27775651-1	2016	Chondroitin sulfate (CS), a type of glycosaminoglycan (GAG), is a factor involved in the suppression of myogenic differentiation.	Glycosaminoglycans	55-58	heat shock protein 9	Mus musculus	21-23
27755597-3	2016	Here we report that the acid hydrolase HYAL1, a hyaluronidase able to degrade the glycosaminoglycans hyaluronic acid (HA) and chondroitin sulfate, is also upregulated upon osteoclastogenesis.	Glycosaminoglycans	82-100	hyaluronoglucosaminidase 1	Mus musculus	39-44
27711228-14	2016	In these 2, transient decreases in viremia were associated with Gag selection in known CD8+ T cell epitopes.	Glycosaminoglycans	64-67	CD8a molecule	Homo sapiens	87-90
27610455-6	2016	GAG derivatives as part of biomaterials might post-translationally modulate TIMP-3 levels stronger than native GAGs, thus exhibiting catabolic effects on the ECM, which could prevent extensive pathological matrix degradation and promote wound healing.	Glycosaminoglycans	0-3	TIMP metallopeptidase inhibitor 3	Homo sapiens	76-82
27716431-2	2016	The most frequent genetic cause is a GAG deletion in the Tor1a (DYT1) gene encoding torsinA with a reduced penetrance of 30-40 % suggesting additional genetic or environmental modifiers.	Glycosaminoglycans	37-40	torsin family 1, member A (torsin A)	Mus musculus	57-62
27716431-2	2016	The most frequent genetic cause is a GAG deletion in the Tor1a (DYT1) gene encoding torsinA with a reduced penetrance of 30-40 % suggesting additional genetic or environmental modifiers.	Glycosaminoglycans	37-40	torsin family 1, member A (torsin A)	Mus musculus	64-68
27716431-2	2016	The most frequent genetic cause is a GAG deletion in the Tor1a (DYT1) gene encoding torsinA with a reduced penetrance of 30-40 % suggesting additional genetic or environmental modifiers.	Glycosaminoglycans	37-40	torsin family 1, member A (torsin A)	Mus musculus	84-91
27799147-10	2016	Overexpression of miR-138-5p significantly increased the IL-1beta-induced downregulation of COL2A1, ACAN, and GAGs, and increased the IL-1beta-induced over expression of MMP-13.We found that FOXC1 is directly regulated by miR-138-5p.	Glycosaminoglycans	110-114	interleukin 1 beta	Homo sapiens	57-65
27799147-11	2016	Additionally, co-transfection with miR-138-5p mimics and pcDNA3.1 (+)-FOXC1 resulted in higher levels of COL2A1, ACAN, and GAGs, but lower levels of MMP-13.	Glycosaminoglycans	123-127	forkhead box C1	Homo sapiens	70-75
27471273-3	2016	Currently, nothing is known regarding the structural basis or molecular mechanisms underlying CXCL5-GAG interactions.	Glycosaminoglycans	100-103	C-X-C motif chemokine ligand 5	Homo sapiens	94-99
27515282-1	2016	AIMS: Exogenously administered biglycan (core protein with high-molecular weight glycosaminoglycan chains) has been shown to protect neonatal cardiomyocytes against simulated ischemia/reperfusion injury (SI/R), however, the mechanism of action is not clear.	Glycosaminoglycans	81-98	biglycan	Homo sapiens	31-39
27188707-13	2016	Genetic screening was negative in all patients for the GAG deletion in TOR1A (DYT1) and in the 5 exons currently associated with disease-causing mutations in TUBB4 (DYT4).	Glycosaminoglycans	55-58	torsin family 1 member A	Homo sapiens	71-76
27188707-13	2016	Genetic screening was negative in all patients for the GAG deletion in TOR1A (DYT1) and in the 5 exons currently associated with disease-causing mutations in TUBB4 (DYT4).	Glycosaminoglycans	55-58	torsin family 1 member A	Homo sapiens	78-82
27564657-3	2016	Thrombomodulin enhances thrombin-mediated TAFI activation and glycosaminoglycans enhance plasmin-mediated TAFI activation.	Glycosaminoglycans	62-80	plasminogen	Homo sapiens	89-96
27564657-3	2016	Thrombomodulin enhances thrombin-mediated TAFI activation and glycosaminoglycans enhance plasmin-mediated TAFI activation.	Glycosaminoglycans	62-80	carboxypeptidase B2	Homo sapiens	106-110
27427877-8	2016	Increases in CD4 and CD8 T-cell activation markers (P = 0.08 and P &lt; 0.001, respectively) and HIV-specific CD8 responses (P = 0.04 for p24 gag, P = 0.01 for p17 gag and P = 0.04 for total gag) were seen in vaccinees but not controls.	Glycosaminoglycans	142-145	CD8a molecule	Homo sapiens	21-24
26989120-5	2016	Compared with patients who were SAb-/GAg+, patients who were SAb+/GAg+ exhibited higher levels of proteinuria (P&lt;0.001) and a lower chance of proteinuria remission (P&lt;0.001).	Glycosaminoglycans	37-40	SH3 domain binding protein 5	Homo sapiens	61-64
26989120-5	2016	Compared with patients who were SAb-/GAg+, patients who were SAb+/GAg+ exhibited higher levels of proteinuria (P&lt;0.001) and a lower chance of proteinuria remission (P&lt;0.001).	Glycosaminoglycans	66-69	SH3 domain binding protein 5	Homo sapiens	61-64
27243901-2	2016	We detected anti-Gag (p24) and envelope (gp140) antibodies in both nasal fluid and salivary collections from all HIV-infected individuals, and cross-reactive anti-p24 antibodies were detected in 10% of HIV-uninfected individuals enrolled at one site.	Glycosaminoglycans	17-20	transmembrane p24 trafficking protein 2	Homo sapiens	22-25
27471273-9	2016	Further, binding interactions and GAG geometry in CXCL5 are novel and distinctly different compared with the related chemokines CXCL1 and CXCL8.	Glycosaminoglycans	34-37	C-X-C motif chemokine ligand 5	Homo sapiens	50-55
27471273-10	2016	We conclude that a finely tuned balance between the GAG-bound dimer and free soluble monomer regulates CXCL5-mediated receptor signaling and function.	Glycosaminoglycans	52-55	C-X-C motif chemokine ligand 5	Homo sapiens	103-108
27566567-8	2016	Also the affinity of CXCL12 and [3-NT7]CXCL12 for glycosaminoglycans, the G protein-coupled chemokine receptor CXCR4 and the atypical chemokine receptor ACKR3 were comparable.	Glycosaminoglycans	50-68	C-X-C motif chemokine ligand 12	Homo sapiens	21-27
27566567-8	2016	Also the affinity of CXCL12 and [3-NT7]CXCL12 for glycosaminoglycans, the G protein-coupled chemokine receptor CXCR4 and the atypical chemokine receptor ACKR3 were comparable.	Glycosaminoglycans	50-68	C-X-C motif chemokine ligand 12	Homo sapiens	39-45
27114232-7	2016	Furthermore, experimental evidence indicates that cathepsin D activity is linked to the metabolism of cholesterol and of glycosaminoglycans, which accounts for its involvement in neuronal plasticity.	Glycosaminoglycans	121-139	cathepsin D	Homo sapiens	50-61
27648839-7	2016	Vpr and Gag interaction is required to counteract TSG101 overexpression effect since Vpr A30F mutant which is unable to interact with Gag and incorporate into virions, reduced ability to prevent Gag accumulation and to rescue VLP production.	Glycosaminoglycans	8-11	Vpr	Human immunodeficiency virus 1	85-88
27648839-7	2016	Vpr and Gag interaction is required to counteract TSG101 overexpression effect since Vpr A30F mutant which is unable to interact with Gag and incorporate into virions, reduced ability to prevent Gag accumulation and to rescue VLP production.	Glycosaminoglycans	134-137	Vpr	Human immunodeficiency virus 1	0-3
27648839-7	2016	Vpr and Gag interaction is required to counteract TSG101 overexpression effect since Vpr A30F mutant which is unable to interact with Gag and incorporate into virions, reduced ability to prevent Gag accumulation and to rescue VLP production.	Glycosaminoglycans	134-137	tumor susceptibility 101	Homo sapiens	50-56
27648839-7	2016	Vpr and Gag interaction is required to counteract TSG101 overexpression effect since Vpr A30F mutant which is unable to interact with Gag and incorporate into virions, reduced ability to prevent Gag accumulation and to rescue VLP production.	Glycosaminoglycans	134-137	Vpr	Human immunodeficiency virus 1	0-3
27648839-7	2016	Vpr and Gag interaction is required to counteract TSG101 overexpression effect since Vpr A30F mutant which is unable to interact with Gag and incorporate into virions, reduced ability to prevent Gag accumulation and to rescue VLP production.	Glycosaminoglycans	134-137	tumor susceptibility 101	Homo sapiens	50-56
27648839-8	2016	In addition, GST pull-down assays and Biacore analysis revealed that Vpr competed with TSG101 for Gag binding.	Glycosaminoglycans	98-101	Vpr	Human immunodeficiency virus 1	69-72
27648839-8	2016	In addition, GST pull-down assays and Biacore analysis revealed that Vpr competed with TSG101 for Gag binding.	Glycosaminoglycans	98-101	tumor susceptibility 101	Homo sapiens	87-93
27648839-9	2016	These results indicate that Vpr overcomes the effects of TSG101 overexpression to support viral production by competing with TSG101 to bind Gag.	Glycosaminoglycans	140-143	Vpr	Human immunodeficiency virus 1	28-31
27648839-9	2016	These results indicate that Vpr overcomes the effects of TSG101 overexpression to support viral production by competing with TSG101 to bind Gag.	Glycosaminoglycans	140-143	tumor susceptibility 101	Homo sapiens	57-63
27648839-9	2016	These results indicate that Vpr overcomes the effects of TSG101 overexpression to support viral production by competing with TSG101 to bind Gag.	Glycosaminoglycans	140-143	tumor susceptibility 101	Homo sapiens	125-131
27625115-0	2016	Chemokine CXCL1 mediated neutrophil recruitment: Role of glycosaminoglycan interactions.	Glycosaminoglycans	57-74	C-X-C motif chemokine ligand 1	Homo sapiens	10-15
27625115-2	2016	CXCL1 exists reversibly as monomers and dimers, and mediates its function by binding glycosaminoglycans (GAG) and CXCR2 receptor.	Glycosaminoglycans	85-103	C-X-C motif chemokine ligand 1	Homo sapiens	0-5
27625115-2	2016	CXCL1 exists reversibly as monomers and dimers, and mediates its function by binding glycosaminoglycans (GAG) and CXCR2 receptor.	Glycosaminoglycans	105-108	C-X-C motif chemokine ligand 1	Homo sapiens	0-5
27625115-3	2016	We recently showed that both monomers and dimers are potent CXCR2 agonists, the dimer is the high-affinity GAG ligand, lysine and arginine residues located in two non-overlapping domains mediate GAG interactions, and there is extensive overlap between GAG and receptor-binding domains.	Glycosaminoglycans	107-110	C-X-C motif chemokine receptor 2	Homo sapiens	60-65
27625115-3	2016	We recently showed that both monomers and dimers are potent CXCR2 agonists, the dimer is the high-affinity GAG ligand, lysine and arginine residues located in two non-overlapping domains mediate GAG interactions, and there is extensive overlap between GAG and receptor-binding domains.	Glycosaminoglycans	195-198	C-X-C motif chemokine receptor 2	Homo sapiens	60-65
27625115-3	2016	We recently showed that both monomers and dimers are potent CXCR2 agonists, the dimer is the high-affinity GAG ligand, lysine and arginine residues located in two non-overlapping domains mediate GAG interactions, and there is extensive overlap between GAG and receptor-binding domains.	Glycosaminoglycans	195-198	C-X-C motif chemokine receptor 2	Homo sapiens	60-65
27440904-6	2016	Surprisingly, in all three cell types, a majority of Gag peptides derived from p15 rather than from the most immunogenic p24.	Glycosaminoglycans	53-56	cyclin dependent kinase inhibitor 2B	Homo sapiens	79-82
27515218-1	2016	We hypothesize that a plasma glycosaminoglycan, chondroitin sulfate, may be responsible for the biological and clinical effects attributed to the Gc protein-derived Macrophage Activating Factor (GcMAF), a protein that is extracted from human blood.	Glycosaminoglycans	29-46	GC vitamin D binding protein	Homo sapiens	146-193
27515218-1	2016	We hypothesize that a plasma glycosaminoglycan, chondroitin sulfate, may be responsible for the biological and clinical effects attributed to the Gc protein-derived Macrophage Activating Factor (GcMAF), a protein that is extracted from human blood.	Glycosaminoglycans	29-46	GC vitamin D binding protein	Homo sapiens	195-200
27648839-2	2016	However, some reports show that overexpression of TSG101 inhibits virus release by disruption of Gag targeting process.	Glycosaminoglycans	97-100	tumor susceptibility 101	Homo sapiens	50-56
27648839-3	2016	Since a HIV-1 accessory protein, Vpr binds to Gag p6 domain at the position close to the binding site for TSG101, whether Vpr implicates TSG101 overexpression effect has not been investigated.	Glycosaminoglycans	46-49	Vpr	Human immunodeficiency virus 1	33-36
27648839-5	2016	Co-transfection of TSG101 and Gag with Vpr prevented TSG101-induced Gag accumulation in endosomes and lysosomes.	Glycosaminoglycans	30-33	Vpr	Human immunodeficiency virus 1	39-42
27648839-5	2016	Co-transfection of TSG101 and Gag with Vpr prevented TSG101-induced Gag accumulation in endosomes and lysosomes.	Glycosaminoglycans	30-33	tumor susceptibility 101	Homo sapiens	53-59
27648839-7	2016	Vpr and Gag interaction is required to counteract TSG101 overexpression effect since Vpr A30F mutant which is unable to interact with Gag and incorporate into virions, reduced ability to prevent Gag accumulation and to rescue VLP production.	Glycosaminoglycans	8-11	tumor susceptibility 101	Homo sapiens	50-56
27251652-1	2016	Mucopolysaccharidosis type II (MPS II) is a lysosomal storage disease caused by a deficient activity of iduronate-2-sulfatase, leading to abnormal accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	163-181	iduronate 2-sulfatase	Homo sapiens	104-125
27251652-1	2016	Mucopolysaccharidosis type II (MPS II) is a lysosomal storage disease caused by a deficient activity of iduronate-2-sulfatase, leading to abnormal accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	183-186	iduronate 2-sulfatase	Homo sapiens	104-125
27342998-7	2016	Out of 8 pregnancies with a positive family history of MPS, 2 showed elevated glycosaminoglycans in the amniotic fluid (220 and 410mug/ml).	Glycosaminoglycans	78-96	iduronate 2-sulfatase	Homo sapiens	55-61
27693454-2	2016	This functional versatility arises from a wide array of decorin/protein interactions also including interactions with its single glycosaminoglycan side chain.	Glycosaminoglycans	129-146	decorin	Homo sapiens	56-63
27549192-2	2016	The FV Gag N-terminal region is responsible for capsid formation and particle budding via interaction with Env.	Glycosaminoglycans	7-10	endogenous retrovirus group K member 20	Homo sapiens	107-110
27069063-2	2016	GAG-trinucleotide repeat (TNR) polymorphisms in the glutamate-cysteine ligase catalytic gene (GCLC), the rate-limiting enzyme for GSH synthesis, are associated with schizophrenia.	Glycosaminoglycans	0-3	glutamate-cysteine ligase catalytic subunit	Homo sapiens	94-98
27579920-6	2016	Fluorescently-tagged PFV Gag, through its chromatin tethering function, selectively relocalized ectopically expressed eGFP-tagged PLK proteins to mitotic chromosomes in a Gag STP motif-dependent manner, confirming a specific and dominant nature of the Gag-PLK interaction in mammalian cells.	Glycosaminoglycans	25-28	polo like kinase 1	Homo sapiens	130-133
27579920-6	2016	Fluorescently-tagged PFV Gag, through its chromatin tethering function, selectively relocalized ectopically expressed eGFP-tagged PLK proteins to mitotic chromosomes in a Gag STP motif-dependent manner, confirming a specific and dominant nature of the Gag-PLK interaction in mammalian cells.	Glycosaminoglycans	25-28	sulfotransferase family 1A member 1	Homo sapiens	175-178
27579920-6	2016	Fluorescently-tagged PFV Gag, through its chromatin tethering function, selectively relocalized ectopically expressed eGFP-tagged PLK proteins to mitotic chromosomes in a Gag STP motif-dependent manner, confirming a specific and dominant nature of the Gag-PLK interaction in mammalian cells.	Glycosaminoglycans	25-28	polo like kinase 1	Homo sapiens	256-259
27579920-6	2016	Fluorescently-tagged PFV Gag, through its chromatin tethering function, selectively relocalized ectopically expressed eGFP-tagged PLK proteins to mitotic chromosomes in a Gag STP motif-dependent manner, confirming a specific and dominant nature of the Gag-PLK interaction in mammalian cells.	Glycosaminoglycans	171-174	polo like kinase 1	Homo sapiens	130-133
27579920-6	2016	Fluorescently-tagged PFV Gag, through its chromatin tethering function, selectively relocalized ectopically expressed eGFP-tagged PLK proteins to mitotic chromosomes in a Gag STP motif-dependent manner, confirming a specific and dominant nature of the Gag-PLK interaction in mammalian cells.	Glycosaminoglycans	171-174	sulfotransferase family 1A member 1	Homo sapiens	175-178
27579920-7	2016	The functional relevance of the Gag-PLK interaction was examined in the context of replication-competent FVs and single-round PFV vectors.	Glycosaminoglycans	32-35	polo like kinase 1	Homo sapiens	36-39
27549192-4	2016	RESULTS: Mutagenesis of N-terminal Gag residues of feline FV (FFV) reveals key residues essential for either capsid assembly and/or viral budding via interaction with the FFV Env leader protein (Elp).	Glycosaminoglycans	35-38	endogenous retrovirus group K member 20	Homo sapiens	175-178
27549192-4	2016	RESULTS: Mutagenesis of N-terminal Gag residues of feline FV (FFV) reveals key residues essential for either capsid assembly and/or viral budding via interaction with the FFV Env leader protein (Elp).	Glycosaminoglycans	35-38	nuclear receptor subfamily 5 group A member 1	Homo sapiens	195-198
27549192-5	2016	In an in vitro Gag-Elp interaction screen, Gag mutations abolishing particle assembly also interfered with Elp binding, indicating that Gag assembly is a prerequisite for this highly specific interaction.	Glycosaminoglycans	15-18	nuclear receptor subfamily 5 group A member 1	Homo sapiens	19-22
27549192-5	2016	In an in vitro Gag-Elp interaction screen, Gag mutations abolishing particle assembly also interfered with Elp binding, indicating that Gag assembly is a prerequisite for this highly specific interaction.	Glycosaminoglycans	15-18	nuclear receptor subfamily 5 group A member 1	Homo sapiens	107-110
27549192-5	2016	In an in vitro Gag-Elp interaction screen, Gag mutations abolishing particle assembly also interfered with Elp binding, indicating that Gag assembly is a prerequisite for this highly specific interaction.	Glycosaminoglycans	43-46	nuclear receptor subfamily 5 group A member 1	Homo sapiens	19-22
27549192-5	2016	In an in vitro Gag-Elp interaction screen, Gag mutations abolishing particle assembly also interfered with Elp binding, indicating that Gag assembly is a prerequisite for this highly specific interaction.	Glycosaminoglycans	43-46	nuclear receptor subfamily 5 group A member 1	Homo sapiens	107-110
27549192-5	2016	In an in vitro Gag-Elp interaction screen, Gag mutations abolishing particle assembly also interfered with Elp binding, indicating that Gag assembly is a prerequisite for this highly specific interaction.	Glycosaminoglycans	43-46	nuclear receptor subfamily 5 group A member 1	Homo sapiens	19-22
27549192-5	2016	In an in vitro Gag-Elp interaction screen, Gag mutations abolishing particle assembly also interfered with Elp binding, indicating that Gag assembly is a prerequisite for this highly specific interaction.	Glycosaminoglycans	43-46	nuclear receptor subfamily 5 group A member 1	Homo sapiens	107-110
27549192-11	2016	Discussion of these findings will be based on a recent model developed for Gag-Elp interactions in prototype FV.	Glycosaminoglycans	75-78	nuclear receptor subfamily 5 group A member 1	Homo sapiens	79-82
27307252-8	2016	Analysis of the UDP-sugar pools and flux through pathways downstream of UDP-glucuronate production revealed that these glucuronidation precursor metabolites were channeled through proteoglycan and glycosaminoglycan biosynthetic pathways, leading to increased surface expression of Notch1.	Glycosaminoglycans	197-214	notch receptor 1	Homo sapiens	281-287
27515235-6	2016	RESULTS: Here we report that RPL7, a major ribosomal protein involved in translation regulation, is a partner of Gag via its interaction with the NC domain.	Glycosaminoglycans	113-116	ribosomal protein L7	Homo sapiens	29-33
27515235-8	2016	Interestingly, RPL7 is shown for the first time to exhibit a potent DNA/RNA chaperone activity higher than that of Gag.	Glycosaminoglycans	115-118	ribosomal protein L7	Homo sapiens	15-19
27515235-10	2016	CONCLUSIONS: Our results show that GagNC interacts with the ribosomal protein RPL7 endowed with nucleic acid chaperone activity, favoring the notion that RPL7 could be a Gag helper chaperoning factor possibly contributing to the start of Gag assembly.	Glycosaminoglycans	35-38	ribosomal protein L7	Homo sapiens	78-82
27515235-10	2016	CONCLUSIONS: Our results show that GagNC interacts with the ribosomal protein RPL7 endowed with nucleic acid chaperone activity, favoring the notion that RPL7 could be a Gag helper chaperoning factor possibly contributing to the start of Gag assembly.	Glycosaminoglycans	35-38	ribosomal protein L7	Homo sapiens	154-158
27153775-3	2016	In human vascular smooth muscle, transforming growth factor-beta (TGF-beta) regulates glycosaminoglycan chain hyperelongation via ERK and p38 as well as Smad2 linker region (Smad2L) phosphorylation.	Glycosaminoglycans	86-103	mitogen-activated protein kinase 14	Homo sapiens	138-141
27153775-5	2016	Of six glycosaminoglycan synthesizing enzymes, xylosyltransferase-1, chondroitin sulfate synthase-1, and chondroitin sulfotransferase-1 were regulated by TGF-beta.	Glycosaminoglycans	7-24	xylosyltransferase 1	Homo sapiens	47-67
27153775-5	2016	Of six glycosaminoglycan synthesizing enzymes, xylosyltransferase-1, chondroitin sulfate synthase-1, and chondroitin sulfotransferase-1 were regulated by TGF-beta.	Glycosaminoglycans	7-24	chondroitin sulfate synthase 1	Homo sapiens	69-99
27427828-0	2016	Multitasking Human Lectin Galectin-3 Interacts with Sulfated Glycosaminoglycans and Chondroitin Sulfate Proteoglycans.	Glycosaminoglycans	61-79	galectin 3	Homo sapiens	26-36
27393384-3	2016	The actual discrimination is performed by factor H, which has binding sites for polyanions (sialic acids, glycosaminoglycans, phospholipids).	Glycosaminoglycans	106-124	complement factor H	Homo sapiens	42-50
27072078-6	2016	In parallel, PKCepsilon knock-down also leads to SOX9 and Collagen II (COL2) down-modulation and to a lower deposition of glycosaminoglycans (GAGs) in the extracellular matrix (ECM).	Glycosaminoglycans	122-140	protein kinase C epsilon	Homo sapiens	13-23
27139244-3	2016	The presence of hACs in the co-cultures significantly increases the osteogenic differentiation potential of hBMSCs based on ALP activity, RT-PCR for osteogenic markers, calcium analyses, and histological stainings, whereas hACs produces a significant amount of glycosaminoglycans (GAGs) for the cartilage region, even in the absence of growth factor TGF-beta family in the co-culture medium.	Glycosaminoglycans	261-279	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	16-20
27139244-3	2016	The presence of hACs in the co-cultures significantly increases the osteogenic differentiation potential of hBMSCs based on ALP activity, RT-PCR for osteogenic markers, calcium analyses, and histological stainings, whereas hACs produces a significant amount of glycosaminoglycans (GAGs) for the cartilage region, even in the absence of growth factor TGF-beta family in the co-culture medium.	Glycosaminoglycans	261-279	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	223-227
27279617-3	2016	CTL escape mutations restricted by protective HLA class I molecules are frequently located in the conserved p24 Gag sequence of HIV-1 that encodes the conical capsid core and have been suggested to reduce viral replication capacity.	Glycosaminoglycans	112-115	transmembrane p24 trafficking protein 2	Homo sapiens	108-111
27411850-7	2016	We found that FGF-2 supplementation during proliferation, but not differentiation, was able to increase glycosaminoglycan deposition, pellet size, and chondrogenic gene expression following chondrogenic induction, as well as increased calcium deposition, alkaline phosphatase activity, and expression of vital osteogenic differentiation genes following osteogenic induction.	Glycosaminoglycans	104-121	fibroblast growth factor 2	Homo sapiens	14-19
27305175-0	2016	A Complex Dance: The Importance of Glycosaminoglycans and Zinc in the Aggregation of Human Prolactin.	Glycosaminoglycans	35-53	prolactin	Homo sapiens	91-100
27427967-6	2016	Priming with BCG-GagM and boosting with MVA-GagM elicited higher Gag-specific IFN-gamma ELISPOT responses than the BCG-GagM only and MVA-GagM only homologous vaccination regimens.	Glycosaminoglycans	17-20	interferon gamma	Homo sapiens	78-87
27399760-11	2016	We demonstrated that the truncated Nef peptide binds to GagPol outside the protease region and by doing so probably blocks processing of both GagPol and Gag precursors at a very early stage.	Glycosaminoglycans	56-59	nef protein	Simian immunodeficiency virus	35-38
27405802-3	2016	When we conditionally inactivated FAM20B (Family with sequence similarity 20 member-B), which is a newly identified xylose kinase essential for glycosaminoglycan (GAG) formation on the protein core of proteoglycans, from the dental mesenchyme using Osr2-Cre, which is also strongly expressed in joint cartilage, we found chondrosarcoma in the knee joint and remarkable defects of postnatal ossification in the long bones.	Glycosaminoglycans	144-161	FAM20B, glycosaminoglycan xylosylkinase	Mus musculus	34-40
27405802-3	2016	When we conditionally inactivated FAM20B (Family with sequence similarity 20 member-B), which is a newly identified xylose kinase essential for glycosaminoglycan (GAG) formation on the protein core of proteoglycans, from the dental mesenchyme using Osr2-Cre, which is also strongly expressed in joint cartilage, we found chondrosarcoma in the knee joint and remarkable defects of postnatal ossification in the long bones.	Glycosaminoglycans	163-166	FAM20B, glycosaminoglycan xylosylkinase	Mus musculus	34-40
27305175-3	2016	Here we, for the first time, study the impact of GAGs in combination with Zn(2+) on the reversible hPRL aggregation across the pH range of 7.4-5.5.	Glycosaminoglycans	49-53	prolactin	Homo sapiens	99-103
27305175-5	2016	GAGs alone cause hPRL aggregation below pH 5.5.	Glycosaminoglycans	0-4	prolactin	Homo sapiens	17-21
27305175-6	2016	Comprehensive thermal stability investigations show that hPRL is particularly destabilized toward thermal denaturation at pH 5.5 and that GAGs increasingly destabilize hPRL at decreasing pH values.	Glycosaminoglycans	138-142	prolactin	Homo sapiens	168-172
27305175-7	2016	We propose that Zn(2+) causes hPRL aggregation through low-affinity Zn(2+) binding sites on hPRL with GAGs facilitating Zn(2+) binding by neutralizing repulsive positive charges of hPRL in the acidic environments of the TGN and mature secretory granules.	Glycosaminoglycans	102-106	prolactin	Homo sapiens	30-34
27305175-7	2016	We propose that Zn(2+) causes hPRL aggregation through low-affinity Zn(2+) binding sites on hPRL with GAGs facilitating Zn(2+) binding by neutralizing repulsive positive charges of hPRL in the acidic environments of the TGN and mature secretory granules.	Glycosaminoglycans	102-106	prolactin	Homo sapiens	92-96
27305175-7	2016	We propose that Zn(2+) causes hPRL aggregation through low-affinity Zn(2+) binding sites on hPRL with GAGs facilitating Zn(2+) binding by neutralizing repulsive positive charges of hPRL in the acidic environments of the TGN and mature secretory granules.	Glycosaminoglycans	102-106	prolactin	Homo sapiens	92-96
27170746-8	2016	Combined, these results suggest a stepwise model for viral cell-to-cell transmission wherein (i) Env-receptor interactions anchor target cells to infected cells, (ii) Env signals Gag"s recruitment to the cell-cell contact dependent on an intact Env CT and Gag MA, and (iii) Env CT and Gag MA, in conjunction with extracellular forces, combine to regulate VS stability and infectious outcomes.	Glycosaminoglycans	179-182	endogenous retrovirus group K member 20	Homo sapiens	97-100
27255605-4	2016	Transient active TGF-beta treatment consistently reproduces native compressive Young s modulus (EY) and glycosaminoglycan (GAG) content in constructs, but standard dosages of 10ng/mL exacerbate matrix heterogeneity.	Glycosaminoglycans	104-121	transforming growth factor beta 1	Homo sapiens	17-25
27255605-4	2016	Transient active TGF-beta treatment consistently reproduces native compressive Young s modulus (EY) and glycosaminoglycan (GAG) content in constructs, but standard dosages of 10ng/mL exacerbate matrix heterogeneity.	Glycosaminoglycans	123-126	transforming growth factor beta 1	Homo sapiens	17-25
27275929-7	2016	In addition, histologic analyses demonstrate that while BMP-9 does not increase mineralization, BMP-9 treatment results in an increase of sulfated glycosaminoglycans.	Glycosaminoglycans	147-165	growth differentiation factor 2	Homo sapiens	96-101
26847431-5	2016	Enhancement could be inhibited by mutations in PF4 that shift the oligomeric equilibrium toward the monomeric state, or by using soluble glycosaminoglycans (GAGs) to which tetrameric PF4 avidly binds.	Glycosaminoglycans	137-155	platelet factor 4	Homo sapiens	183-186
26847431-5	2016	Enhancement could be inhibited by mutations in PF4 that shift the oligomeric equilibrium toward the monomeric state, or by using soluble glycosaminoglycans (GAGs) to which tetrameric PF4 avidly binds.	Glycosaminoglycans	157-161	platelet factor 4	Homo sapiens	183-186
26847431-6	2016	We conclude that at physiologically relevant concentrations, oligomeric PF4 enhances infection by HIV-1 by interacting with the viral envelope protein as well as cell surface GAGs, enhancing virus attachment to the cell surface.	Glycosaminoglycans	175-179	platelet factor 4	Homo sapiens	72-75
27105565-6	2016	In this study, binding between GAGs from MPS I chondrocytes and fibroblast growth factor 2 (FGF2) was not significantly different from binding of FGF2 to GAGs from control chondrocytes.	Glycosaminoglycans	31-35	fibroblast growth factor 2	Mus musculus	92-96
27324118-11	2016	Biochemically, the fibrin and collagen gel dSRC groups were statistically improved in glycosaminoglycan and hydroxyproline content compared to the control.	Glycosaminoglycans	86-103	Src oncogene at 64B	Drosophila melanogaster	43-47
27170746-8	2016	Combined, these results suggest a stepwise model for viral cell-to-cell transmission wherein (i) Env-receptor interactions anchor target cells to infected cells, (ii) Env signals Gag"s recruitment to the cell-cell contact dependent on an intact Env CT and Gag MA, and (iii) Env CT and Gag MA, in conjunction with extracellular forces, combine to regulate VS stability and infectious outcomes.	Glycosaminoglycans	179-182	endogenous retrovirus group K member 20	Homo sapiens	167-170
27170746-8	2016	Combined, these results suggest a stepwise model for viral cell-to-cell transmission wherein (i) Env-receptor interactions anchor target cells to infected cells, (ii) Env signals Gag"s recruitment to the cell-cell contact dependent on an intact Env CT and Gag MA, and (iii) Env CT and Gag MA, in conjunction with extracellular forces, combine to regulate VS stability and infectious outcomes.	Glycosaminoglycans	179-182	endogenous retrovirus group K member 20	Homo sapiens	167-170
27170746-8	2016	Combined, these results suggest a stepwise model for viral cell-to-cell transmission wherein (i) Env-receptor interactions anchor target cells to infected cells, (ii) Env signals Gag"s recruitment to the cell-cell contact dependent on an intact Env CT and Gag MA, and (iii) Env CT and Gag MA, in conjunction with extracellular forces, combine to regulate VS stability and infectious outcomes.	Glycosaminoglycans	256-259	endogenous retrovirus group K member 20	Homo sapiens	167-170
27170746-8	2016	Combined, these results suggest a stepwise model for viral cell-to-cell transmission wherein (i) Env-receptor interactions anchor target cells to infected cells, (ii) Env signals Gag"s recruitment to the cell-cell contact dependent on an intact Env CT and Gag MA, and (iii) Env CT and Gag MA, in conjunction with extracellular forces, combine to regulate VS stability and infectious outcomes.	Glycosaminoglycans	256-259	endogenous retrovirus group K member 20	Homo sapiens	167-170
27170746-8	2016	Combined, these results suggest a stepwise model for viral cell-to-cell transmission wherein (i) Env-receptor interactions anchor target cells to infected cells, (ii) Env signals Gag"s recruitment to the cell-cell contact dependent on an intact Env CT and Gag MA, and (iii) Env CT and Gag MA, in conjunction with extracellular forces, combine to regulate VS stability and infectious outcomes.	Glycosaminoglycans	256-259	endogenous retrovirus group K member 20	Homo sapiens	167-170
27170746-8	2016	Combined, these results suggest a stepwise model for viral cell-to-cell transmission wherein (i) Env-receptor interactions anchor target cells to infected cells, (ii) Env signals Gag"s recruitment to the cell-cell contact dependent on an intact Env CT and Gag MA, and (iii) Env CT and Gag MA, in conjunction with extracellular forces, combine to regulate VS stability and infectious outcomes.	Glycosaminoglycans	179-182	endogenous retrovirus group K member 20	Homo sapiens	167-170
27280284-4	2016	Specifically, we show that Gag mutants with compromised interactions with ALIX and Tsg101, two early ESCRT factors, have an average budding delay of ~75 minutes and ~10 hours, respectively.	Glycosaminoglycans	27-30	programmed cell death 6 interacting protein	Homo sapiens	74-78
27699273-1	2016	Mucopolysaccharidosis type II (MPSII) is an X-linked lysosomal storage disease characterized by severe neurologic and somatic disease caused by deficiency of iduronate-2-sulfatase (IDS), an enzyme that catabolizes the glycosaminoglycans heparan and dermatan sulphate.	Glycosaminoglycans	218-236	iduronate 2-sulfatase	Mus musculus	158-179
27699273-1	2016	Mucopolysaccharidosis type II (MPSII) is an X-linked lysosomal storage disease characterized by severe neurologic and somatic disease caused by deficiency of iduronate-2-sulfatase (IDS), an enzyme that catabolizes the glycosaminoglycans heparan and dermatan sulphate.	Glycosaminoglycans	218-236	iduronate 2-sulfatase	Mus musculus	181-184
27280284-4	2016	Specifically, we show that Gag mutants with compromised interactions with ALIX and Tsg101, two early ESCRT factors, have an average budding delay of ~75 minutes and ~10 hours, respectively.	Glycosaminoglycans	27-30	tumor susceptibility 101	Homo sapiens	83-89
27331076-3	2016	We treated MPS IIIA mice at 1, 2, 3, 6, and 9 months of age with an intravenous injection of scAAV9-U1a-hSGSH vector, leading to restoration of SGSH activity and reduction of glycosaminoglycans (GAG) throughout the central nervous system (CNS) and somatic tissues at a dose of 5E12 vg/kg.	Glycosaminoglycans	175-193	N-sulfoglucosamine sulfohydrolase	Homo sapiens	104-109
27331076-3	2016	We treated MPS IIIA mice at 1, 2, 3, 6, and 9 months of age with an intravenous injection of scAAV9-U1a-hSGSH vector, leading to restoration of SGSH activity and reduction of glycosaminoglycans (GAG) throughout the central nervous system (CNS) and somatic tissues at a dose of 5E12 vg/kg.	Glycosaminoglycans	175-193	N-sulfoglucosamine sulfohydrolase (sulfamidase)	Mus musculus	105-109
27331076-3	2016	We treated MPS IIIA mice at 1, 2, 3, 6, and 9 months of age with an intravenous injection of scAAV9-U1a-hSGSH vector, leading to restoration of SGSH activity and reduction of glycosaminoglycans (GAG) throughout the central nervous system (CNS) and somatic tissues at a dose of 5E12 vg/kg.	Glycosaminoglycans	195-198	N-sulfoglucosamine sulfohydrolase	Homo sapiens	104-109
27273064-3	2016	In this process, the nucleocapsid (NC) domain of Gag binds to the packaging signal of gRNA which consists of a series of stem-loops (SL1-SL3) ensuring gRNA selection and packaging into virions.	Glycosaminoglycans	49-52	TATA-box binding protein associated factor, RNA polymerase I subunit A	Homo sapiens	133-140
27255651-2	2016	NT4 specifically binds to sulfated glycosaminoglycans on cancer cell membranes.	Glycosaminoglycans	35-53	neurotrophin 4	Homo sapiens	0-3
27255651-4	2016	We demonstrated here that the branched peptide NT4 binds sulfated glycosaminoglycans with high affinity and with preferential binding to heparan sulfate.	Glycosaminoglycans	66-84	neurotrophin 4	Homo sapiens	47-50
27255651-6	2016	Results obtained by taking advantage of the selective targeting of glycosaminoglycans chains by NT4, provide insights into the role of heparan sulfate proteoglycans in cancer cell adhesion and migration and suggest a determinant role of sulfated glycosaminoglycans in the control of cancer cell directional migration.	Glycosaminoglycans	67-85	neurotrophin 4	Homo sapiens	96-99
27255651-6	2016	Results obtained by taking advantage of the selective targeting of glycosaminoglycans chains by NT4, provide insights into the role of heparan sulfate proteoglycans in cancer cell adhesion and migration and suggest a determinant role of sulfated glycosaminoglycans in the control of cancer cell directional migration.	Glycosaminoglycans	246-264	neurotrophin 4	Homo sapiens	96-99
27155776-3	2016	PAPP-A binds tightly to glycosaminoglycans present on the surface of cells, thus functioning within tissues as a growth-promoting enzyme, releasing bioactive IGF in close proximity to the IGF receptor.	Glycosaminoglycans	24-42	pappalysin 1	Homo sapiens	0-6
27044744-9	2016	Along with previous work, these findings suggest that TSG-6 functions as a pluripotent regulator of chemokines by modulating chemokine/GAG interactions, which may be a major mechanism by which TSG-6 produces its anti-inflammatory effects in vivo.	Glycosaminoglycans	135-138	TNF alpha induced protein 6	Homo sapiens	54-59
27044744-9	2016	Along with previous work, these findings suggest that TSG-6 functions as a pluripotent regulator of chemokines by modulating chemokine/GAG interactions, which may be a major mechanism by which TSG-6 produces its anti-inflammatory effects in vivo.	Glycosaminoglycans	135-138	TNF alpha induced protein 6	Homo sapiens	193-198
26290588-10	2016	In vitro, agrin knockdown resulted in reduced glycosaminoglycan content, downregulation of the cartilage transcription factor SOX9 and other cartilage-specific ECM molecules.	Glycosaminoglycans	46-63	agrin	Mus musculus	10-15
27006333-0	2016	Glycan-deficient PrP stimulates VEGFR2 signaling via glycosaminoglycan.	Glycosaminoglycans	53-70	major prion protein	Cricetulus griseus	17-20
27006333-0	2016	Glycan-deficient PrP stimulates VEGFR2 signaling via glycosaminoglycan.	Glycosaminoglycans	53-70	vascular endothelial growth factor receptor 2	Cricetulus griseus	32-38
27006333-5	2016	Accordingly, CHO cells expressing glycan-deficient PrP lacking the GAG binding motif or cells treated with heparinase to remove GAG show diminished Akt signaling.	Glycosaminoglycans	67-70	major prion protein	Cricetulus griseus	51-54
26874675-5	2016	The inhibitory capacity of C1-INH for the CP is potentiated by heparin and other glycosaminoglycans, but no data exist for the LP and AP.	Glycosaminoglycans	81-99	serpin family G member 1	Homo sapiens	27-33
27091995-0	2016	Structural basis for oligomerization and glycosaminoglycan binding of CCL5 and CCL3.	Glycosaminoglycans	41-58	C-C motif chemokine ligand 5	Homo sapiens	70-74
27491210-1	2016	Mucopolysaccharidosis type IIIA (MPS-IIIA) is a childhood metabolic neuropathology caused by the inherited deficiency of the lysosomal enzyme sulfamidase and is characterized by the accumulation of undegraded glycosaminoglycans in the lysosomes of cells and tissues of affected patients.	Glycosaminoglycans	209-227	N-sulfoglucosamine sulfohydrolase	Homo sapiens	0-31
33440483-3	2016	Growth factor binding ability of the native sulfated glycosaminoglycans can be incorporated into the synthetic scaffold matrix through functionalization with specific chemical moieties.	Glycosaminoglycans	53-71	myotrophin	Rattus norvegicus	0-13
27232667-5	2016	BMP-2 and dexamethasone in combination with TGF-beta1 or TGF-beta3 excelled at inducing chondrogenesis on SMSCs, HFPSCs and chondrocytes, as measured by glycosaminoglycans and collagen type II staining of pellets, quantitative glycosaminoglycan expression, quantitative PCR of cartilage signature genes and electron microscopy.	Glycosaminoglycans	153-171	bone morphogenetic protein 2	Homo sapiens	0-5
27232667-5	2016	BMP-2 and dexamethasone in combination with TGF-beta1 or TGF-beta3 excelled at inducing chondrogenesis on SMSCs, HFPSCs and chondrocytes, as measured by glycosaminoglycans and collagen type II staining of pellets, quantitative glycosaminoglycan expression, quantitative PCR of cartilage signature genes and electron microscopy.	Glycosaminoglycans	153-171	transforming growth factor beta 1	Homo sapiens	44-53
27232667-5	2016	BMP-2 and dexamethasone in combination with TGF-beta1 or TGF-beta3 excelled at inducing chondrogenesis on SMSCs, HFPSCs and chondrocytes, as measured by glycosaminoglycans and collagen type II staining of pellets, quantitative glycosaminoglycan expression, quantitative PCR of cartilage signature genes and electron microscopy.	Glycosaminoglycans	153-171	transforming growth factor beta 3	Homo sapiens	57-66
27232667-5	2016	BMP-2 and dexamethasone in combination with TGF-beta1 or TGF-beta3 excelled at inducing chondrogenesis on SMSCs, HFPSCs and chondrocytes, as measured by glycosaminoglycans and collagen type II staining of pellets, quantitative glycosaminoglycan expression, quantitative PCR of cartilage signature genes and electron microscopy.	Glycosaminoglycans	153-170	bone morphogenetic protein 2	Homo sapiens	0-5
27232667-5	2016	BMP-2 and dexamethasone in combination with TGF-beta1 or TGF-beta3 excelled at inducing chondrogenesis on SMSCs, HFPSCs and chondrocytes, as measured by glycosaminoglycans and collagen type II staining of pellets, quantitative glycosaminoglycan expression, quantitative PCR of cartilage signature genes and electron microscopy.	Glycosaminoglycans	153-170	transforming growth factor beta 1	Homo sapiens	44-53
27232667-5	2016	BMP-2 and dexamethasone in combination with TGF-beta1 or TGF-beta3 excelled at inducing chondrogenesis on SMSCs, HFPSCs and chondrocytes, as measured by glycosaminoglycans and collagen type II staining of pellets, quantitative glycosaminoglycan expression, quantitative PCR of cartilage signature genes and electron microscopy.	Glycosaminoglycans	153-170	transforming growth factor beta 3	Homo sapiens	57-66
27223472-1	2016	In hematopoietic cells, serglycin proteoglycans mainly contribute to proper storage and secretion of inflammatory mediators via their negatively charged glycosaminoglycans.	Glycosaminoglycans	153-171	serglycin	Mus musculus	24-33
27091995-0	2016	Structural basis for oligomerization and glycosaminoglycan binding of CCL5 and CCL3.	Glycosaminoglycans	41-58	C-C motif chemokine ligand 3	Homo sapiens	79-83
27091995-7	2016	However, this motif is partially buried when CCL3, CCL4, and CCL5 are oligomerized; thus, the mechanism by which GAG binds these chemokine oligomers has been elusive.	Glycosaminoglycans	113-116	C-C motif chemokine ligand 3	Homo sapiens	45-49
27091995-7	2016	However, this motif is partially buried when CCL3, CCL4, and CCL5 are oligomerized; thus, the mechanism by which GAG binds these chemokine oligomers has been elusive.	Glycosaminoglycans	113-116	C-C motif chemokine ligand 4	Homo sapiens	51-55
27091995-7	2016	However, this motif is partially buried when CCL3, CCL4, and CCL5 are oligomerized; thus, the mechanism by which GAG binds these chemokine oligomers has been elusive.	Glycosaminoglycans	113-116	C-C motif chemokine ligand 5	Homo sapiens	61-65
27091995-8	2016	Our structures of GAG-bound CCL5 and CCL3 oligomers reveal that these chemokine oligomers have distinct GAG-binding mechanisms.	Glycosaminoglycans	18-21	C-C motif chemokine ligand 5	Homo sapiens	28-32
27091995-8	2016	Our structures of GAG-bound CCL5 and CCL3 oligomers reveal that these chemokine oligomers have distinct GAG-binding mechanisms.	Glycosaminoglycans	104-107	C-C motif chemokine ligand 5	Homo sapiens	28-32
27091995-8	2016	Our structures of GAG-bound CCL5 and CCL3 oligomers reveal that these chemokine oligomers have distinct GAG-binding mechanisms.	Glycosaminoglycans	104-107	C-C motif chemokine ligand 3	Homo sapiens	37-41
27091995-10	2016	However, residues from two partially buried BBXB motifs along with other residues combine to form a GAG-binding groove in the CCL3 oligomer.	Glycosaminoglycans	100-103	C-C motif chemokine ligand 3	Homo sapiens	126-130
27091995-12	2016	We also report an alternative CCL3 oligomer structure that reveals how conformational changes in CCL3 N termini profoundly alter its surface properties and dimer-dimer interactions to affect GAG binding and oligomerization.	Glycosaminoglycans	191-194	C-C motif chemokine ligand 3	Homo sapiens	30-34
27091995-12	2016	We also report an alternative CCL3 oligomer structure that reveals how conformational changes in CCL3 N termini profoundly alter its surface properties and dimer-dimer interactions to affect GAG binding and oligomerization.	Glycosaminoglycans	191-194	C-C motif chemokine ligand 3	Homo sapiens	97-101
26920026-4	2016	In the present study, we show that PRELP mediates cell adhesion by binding to cell-surface glycosaminoglycans (GAGs).	Glycosaminoglycans	91-109	proline and arginine rich end leucine rich repeat protein	Rattus norvegicus	35-40
26929154-3	2016	Lentivirus-mediated BMP7 over-expression induced differentiation of BMSCs into an NP phenotype, as indicated by expression of the NP markers collagen type II, aggrecan, SOX9 and keratins 8 and 19, increased the content of glycosaminoglycan, and up-regulated beta-1,3-glucuronosyl transferase 1, a regulator of chondroitin sulfate synthesis in NP cells.	Glycosaminoglycans	222-239	bone morphogenetic protein 7	Oryctolagus cuniculus	20-24
27018617-4	2016	In a micromass culture (muMass) system, BMP2 had a positive effect on glycosaminoglycan deposition at day 7 (p &lt; 0.001), which in combination with BMP6 synergistically enhanced cartilage-like tissue formation that displayed in vitro mineralization capacity at day 14 (p &lt; 0.001).	Glycosaminoglycans	70-87	bone morphogenetic protein 2	Homo sapiens	40-44
26873963-10	2016	GPER-induced attenuation of aortic remodeling was associated with a reduction in oxidative stress and decreased accumulation of glycosaminoglycans.	Glycosaminoglycans	128-146	G protein-coupled estrogen receptor 1	Rattus norvegicus	0-4
27079852-7	2016	Gene delivery of TGF-beta3 and BMP2 and subsequent cell-mediated expression of these therapeutic genes resulted in a significant increase in sulfated glycosaminoglycan and collagen production, particularly in the pTGF-beta3-pBMP2 codelivery group in comparison to the delivery of either pTGF-beta3 or pBMP2 in isolation.	Glycosaminoglycans	150-167	transforming growth factor beta 3	Homo sapiens	17-26
27079852-7	2016	Gene delivery of TGF-beta3 and BMP2 and subsequent cell-mediated expression of these therapeutic genes resulted in a significant increase in sulfated glycosaminoglycan and collagen production, particularly in the pTGF-beta3-pBMP2 codelivery group in comparison to the delivery of either pTGF-beta3 or pBMP2 in isolation.	Glycosaminoglycans	150-167	bone morphogenetic protein 2	Homo sapiens	31-35
27128502-9	2016	In accordance with previous findings, isolated Env FTR was associated with higher plasma HIV RNA and lower CD4 counts, while patients with both Gag and Env FTR also had higher Gag- and Env-specific proliferative CD8+ T cell responses.	Glycosaminoglycans	176-179	endogenous retrovirus group K member 20	Homo sapiens	152-155
27128502-9	2016	In accordance with previous findings, isolated Env FTR was associated with higher plasma HIV RNA and lower CD4 counts, while patients with both Gag and Env FTR also had higher Gag- and Env-specific proliferative CD8+ T cell responses.	Glycosaminoglycans	176-179	endogenous retrovirus group K member 20	Homo sapiens	152-155
27078017-1	2016	Arylsulfatase B (B-acetylgalactosamine 4-sulfatase; ARSB) is the enzyme that removes 4-sulfate groups from the non-reducing end of the glycosaminoglycans chondroitin 4-sulfate and dermatan sulfate.	Glycosaminoglycans	135-153	arylsulfatase B	Homo sapiens	0-15
26889021-6	2016	The epitope for group I MAbs was mapped to a region adjacent to the GAG binding site, a finding which suggests that group I MAbs could potentially interfere with the cellular adhesion of A27.	Glycosaminoglycans	68-71	immunoglobulin kappa variable 3-20	Homo sapiens	187-190
27078017-1	2016	Arylsulfatase B (B-acetylgalactosamine 4-sulfatase; ARSB) is the enzyme that removes 4-sulfate groups from the non-reducing end of the glycosaminoglycans chondroitin 4-sulfate and dermatan sulfate.	Glycosaminoglycans	135-153	arylsulfatase B	Homo sapiens	52-56
26636652-12	2016	Cartilage GAG release in either the presence or absence of IL-1alpha was unaltered by FGF-2 in both genotypes.	Glycosaminoglycans	10-13	interleukin 1 alpha	Mus musculus	59-68
26959357-0	2016	Subdominant Gag-specific anti-HIV efficacy in an HLA-B*57-positive elite controller.	Glycosaminoglycans	12-15	major histocompatibility complex, class I, B	Homo sapiens	49-54
26636652-13	2016	In cartilage cultures with FGF-18, IL-1alpha-stimulated GAG loss was significantly reduced only in Hspg2(Delta3-/Delta3-) mice, and this was associated with maintained expression of Fgfr3 mRNA and reduced expression of Mmp2/Mmp3 mRNA.	Glycosaminoglycans	56-59	fibroblast growth factor 18	Mus musculus	27-33
26636652-13	2016	In cartilage cultures with FGF-18, IL-1alpha-stimulated GAG loss was significantly reduced only in Hspg2(Delta3-/Delta3-) mice, and this was associated with maintained expression of Fgfr3 mRNA and reduced expression of Mmp2/Mmp3 mRNA.	Glycosaminoglycans	56-59	interleukin 1 alpha	Mus musculus	35-44
26636652-13	2016	In cartilage cultures with FGF-18, IL-1alpha-stimulated GAG loss was significantly reduced only in Hspg2(Delta3-/Delta3-) mice, and this was associated with maintained expression of Fgfr3 mRNA and reduced expression of Mmp2/Mmp3 mRNA.	Glycosaminoglycans	56-59	perlecan (heparan sulfate proteoglycan 2)	Mus musculus	119-121
26854388-7	2016	Both hFDM and hFDM/TGF-beta1 groups exhibited significantly more synthesis of glycosaminoglycan (GAG) and much better upregulation of chondrogenic markers expression.	Glycosaminoglycans	78-95	transforming growth factor beta 1	Homo sapiens	19-28
26854388-7	2016	Both hFDM and hFDM/TGF-beta1 groups exhibited significantly more synthesis of glycosaminoglycan (GAG) and much better upregulation of chondrogenic markers expression.	Glycosaminoglycans	97-100	transforming growth factor beta 1	Homo sapiens	19-28
26840742-9	2016	Treatment of ApoE(-/-) VSC chondrogenic cultures with interleukin (IL)-6 resulted in significantly increased glycosaminoglycan deposition and expression of characteristic chondrogenic genes at 21 days.	Glycosaminoglycans	109-126	apolipoprotein E	Mus musculus	13-17
26840742-9	2016	Treatment of ApoE(-/-) VSC chondrogenic cultures with interleukin (IL)-6 resulted in significantly increased glycosaminoglycan deposition and expression of characteristic chondrogenic genes at 21 days.	Glycosaminoglycans	109-126	interleukin 6	Mus musculus	54-72
27023704-7	2016	Gag fused to three different FPs (CFP, YFP, and RFP), assembled into viral-like particles and created punctate FRET signals that become visible on the cell surface when 3D-3Way FRET was applied to the data.	Glycosaminoglycans	0-3	complement factor properdin	Homo sapiens	34-37
27023704-7	2016	Gag fused to three different FPs (CFP, YFP, and RFP), assembled into viral-like particles and created punctate FRET signals that become visible on the cell surface when 3D-3Way FRET was applied to the data.	Glycosaminoglycans	0-3	tripartite motif containing 27	Homo sapiens	48-51
26836755-0	2016	Examination of Glycosaminoglycan Binding Sites on the XCL1 Dimer.	Glycosaminoglycans	15-32	X-C motif chemokine ligand 1	Homo sapiens	54-58
26986213-10	2016	CONCLUSIONS: Overexpression of lysosomal and proteasomal-related genes are expected responses to cellular stress induced by lysosomal storage in mucopolysaccharidosis type I. Upregulation of immunity-related genes implicates the potential involvement of glycosaminoglycan-induced inflammation in the pathogenesis of mucopolysaccharidosis-related arterial disease, for which clusterin represents a potential biomarker.	Glycosaminoglycans	254-271	clusterin	Canis lupus familiaris	374-383
27004850-3	2016	Moreover, to demonstrate the formation of GH amyloid in vitro, we studied various conditions (solvents, glycosaminoglycans, salts and metal ions) and found that in presence of zinc metal ions (Zn(II)), GH formed short curvy fibrils.	Glycosaminoglycans	104-122	growth hormone 1	Homo sapiens	42-44
27004850-3	2016	Moreover, to demonstrate the formation of GH amyloid in vitro, we studied various conditions (solvents, glycosaminoglycans, salts and metal ions) and found that in presence of zinc metal ions (Zn(II)), GH formed short curvy fibrils.	Glycosaminoglycans	104-122	growth hormone 1	Homo sapiens	202-204
26971438-4	2016	Digesting glycosaminoglycan side chains of CSPG with chondroitinase improved GRP migration on stripes of CSPG printed on cover glass, although GRPs were still responsive to the remaining repulsive signals of CSPG.	Glycosaminoglycans	10-27	galactosamine (N-acetyl)-6-sulfatase	Rattus norvegicus	53-67
26971438-4	2016	Digesting glycosaminoglycan side chains of CSPG with chondroitinase improved GRP migration on stripes of CSPG printed on cover glass, although GRPs were still responsive to the remaining repulsive signals of CSPG.	Glycosaminoglycans	10-27	gastrin releasing peptide	Rattus norvegicus	77-80
26836755-1	2016	Known for its distinct metamorphic behavior, XCL1 interconverts between a canonical chemokine folded monomer (XCL1mon) that interacts with the receptor, XCR1, and a unique dimer (XCL1dim) that interacts with glycosaminoglycans and inhibits HIV-1 activity.	Glycosaminoglycans	208-226	X-C motif chemokine ligand 1	Homo sapiens	45-49
26836755-5	2016	To assess the contributions of different GAG structures to XCL1 binding, we developed a solution fluorescence polarization assay and correlated affinity with the length and level of sulfation of heparan sulfate oligosaccharides.	Glycosaminoglycans	41-44	X-C motif chemokine ligand 1	Homo sapiens	59-63
26836755-6	2016	It was recently demonstrated that the XCL1 GAG binding form, XCL1dim, is responsible for preventing HIV-1 infection through interactions with gp120.	Glycosaminoglycans	43-46	X-C motif chemokine ligand 1	Homo sapiens	38-42
26836755-6	2016	It was recently demonstrated that the XCL1 GAG binding form, XCL1dim, is responsible for preventing HIV-1 infection through interactions with gp120.	Glycosaminoglycans	43-46	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	142-147
26450354-9	2016	Two patients, both with high baseline glycosaminoglycan levels in their urine and severe mutations in the arylsulfatase B gene, scored clearly lower than expected.	Glycosaminoglycans	38-55	arylsulfatase B	Homo sapiens	106-121
26939667-11	2016	In vitro caveolin-1 silencing decreased the CLC microaggregate glycosaminoglycan (GAG) content, which could be rescued by CSD treatment.	Glycosaminoglycans	63-80	caveolin 1, caveolae protein	Mus musculus	9-19
26939667-11	2016	In vitro caveolin-1 silencing decreased the CLC microaggregate glycosaminoglycan (GAG) content, which could be rescued by CSD treatment.	Glycosaminoglycans	63-80	Charcot-Leyden crystal protein	Mus musculus	44-47
26939667-11	2016	In vitro caveolin-1 silencing decreased the CLC microaggregate glycosaminoglycan (GAG) content, which could be rescued by CSD treatment.	Glycosaminoglycans	82-85	caveolin 1, caveolae protein	Mus musculus	9-19
26939667-11	2016	In vitro caveolin-1 silencing decreased the CLC microaggregate glycosaminoglycan (GAG) content, which could be rescued by CSD treatment.	Glycosaminoglycans	82-85	Charcot-Leyden crystal protein	Mus musculus	44-47
26939667-15	2016	Nevertheless, CSD enhanced CLC GAG deposition in vitro, and hence the increased caveolin-1 expression during IVD degeneration may also facilitate an ultimate attempt at repair.	Glycosaminoglycans	31-34	Charcot-Leyden crystal protein	Mus musculus	27-30
26559151-4	2016	OBJECTIVE: To examine whether MC-2 would bind glycosaminoglycans to decrease proinflammatory cytokines" influence in the liver, minimize organ edema, prevent liver injury, and improve hepatic perfusion.	Glycosaminoglycans	46-64	melanocortin 5 receptor	Homo sapiens	30-34
26559151-5	2016	MC-2, a synthetic octapeptide derived from the heparin-binding domain of murine interferon gamma (IFN-gamma), binds glycosaminoglycans to modulate serum and interstitial cytokine levels and activity.	Glycosaminoglycans	116-134	melanocortin 5 receptor	Homo sapiens	0-4
26559151-5	2016	MC-2, a synthetic octapeptide derived from the heparin-binding domain of murine interferon gamma (IFN-gamma), binds glycosaminoglycans to modulate serum and interstitial cytokine levels and activity.	Glycosaminoglycans	116-134	interferon gamma	Mus musculus	80-107
26729921-4	2016	Here we develop a dual-fluorescence reporter to specifically measure methionine misincorporation at glutamic acid codons GAA and GAG via tRNA(Glu) mismethionylation in human cells.	Glycosaminoglycans	129-132	mitochondrially encoded tRNA glycine	Homo sapiens	137-146
26721883-0	2016	CXCL1/MGSA Is a Novel Glycosaminoglycan (GAG)-binding Chemokine: STRUCTURAL EVIDENCE FOR TWO DISTINCT NON-OVERLAPPING BINDING DOMAINS.	Glycosaminoglycans	22-39	C-X-C motif chemokine ligand 1	Homo sapiens	0-5
26721883-0	2016	CXCL1/MGSA Is a Novel Glycosaminoglycan (GAG)-binding Chemokine: STRUCTURAL EVIDENCE FOR TWO DISTINCT NON-OVERLAPPING BINDING DOMAINS.	Glycosaminoglycans	22-39	C-X-C motif chemokine ligand 1	Homo sapiens	6-10
26721883-0	2016	CXCL1/MGSA Is a Novel Glycosaminoglycan (GAG)-binding Chemokine: STRUCTURAL EVIDENCE FOR TWO DISTINCT NON-OVERLAPPING BINDING DOMAINS.	Glycosaminoglycans	41-44	C-X-C motif chemokine ligand 1	Homo sapiens	0-5
26721883-0	2016	CXCL1/MGSA Is a Novel Glycosaminoglycan (GAG)-binding Chemokine: STRUCTURAL EVIDENCE FOR TWO DISTINCT NON-OVERLAPPING BINDING DOMAINS.	Glycosaminoglycans	41-44	C-X-C motif chemokine ligand 1	Homo sapiens	6-10
26721883-3	2016	However, very little is known regarding the structural basis underlying hCXCL1-GAG interactions.	Glycosaminoglycans	79-82	C-X-C motif chemokine ligand 1	Homo sapiens	72-78
26721883-5	2016	Binding experiments under conditions at which hCXCL1 exists as monomers and dimers indicate that the dimer is the high-affinity GAG ligand.	Glycosaminoglycans	128-131	C-X-C motif chemokine ligand 1	Homo sapiens	46-52
26721883-7	2016	One domain, consisting of N-loop and C-helical residues (defined as alpha-domain) has also been identified previously as the GAG-binding domain for the related chemokine CXCL8/IL-8.	Glycosaminoglycans	125-128	C-X-C motif chemokine ligand 8	Homo sapiens	170-175
26721883-7	2016	One domain, consisting of N-loop and C-helical residues (defined as alpha-domain) has also been identified previously as the GAG-binding domain for the related chemokine CXCL8/IL-8.	Glycosaminoglycans	125-128	C-X-C motif chemokine ligand 8	Homo sapiens	176-180
26721883-11	2016	We also show that the GAG-bound hCXCL1 completely occlude receptor binding.	Glycosaminoglycans	22-25	C-X-C motif chemokine ligand 1	Homo sapiens	32-38
26845288-1	2016	BACKGROUND: Mucopolysaccharidosis II, also known as Hunter syndrome, is a rare, X-linked disease caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase, which catalyses a step in the catabolism of glycosaminoglycans.	Glycosaminoglycans	211-229	iduronate 2-sulfatase	Homo sapiens	144-165
26879700-1	2016	BACKGROUND: von Willebrand factor (VWF) is a key load bearing domain for mamalian cell adhesion by binding various macromolecular ligands in extracellular matrix such as, collagens, elastin, and glycosaminoglycans.	Glycosaminoglycans	195-213	von Willebrand factor	Homo sapiens	12-33
26879700-1	2016	BACKGROUND: von Willebrand factor (VWF) is a key load bearing domain for mamalian cell adhesion by binding various macromolecular ligands in extracellular matrix such as, collagens, elastin, and glycosaminoglycans.	Glycosaminoglycans	195-213	von Willebrand factor	Homo sapiens	35-38
26845288-19	2016	Idursulfase antibodies were detected in 31.7% of participants at the end of the study and they were related to a smaller reduction in urine glycosaminoglycan levels.	Glycosaminoglycans	140-157	iduronate 2-sulfatase	Homo sapiens	0-11
26447927-1	2016	Mucopolysaccharidosis VII (MPS VII) is a lysosomal storage disease arising from mutations in beta-d-glucuronidase (GUSB), which results in glycosaminoglycan (GAG) accumulation and a variety of clinical manifestations including neurological disease.	Glycosaminoglycans	139-156	glucuronidase beta	Canis lupus familiaris	115-119
26849062-10	2016	Ad5-Gag antigen combined with Ad5-DeltaLMP1-MAVS enhanced control of vaccinia-gag replication in a mouse challenge model, with 4/5 animals showing undetectable virus following challenge.	Glycosaminoglycans	78-81	mitochondrial antiviral signaling protein	Mus musculus	44-48
26051019-1	2016	Mucopolysaccharidosis type II (MPS II) is an X-linked lysosomal storage disorder arising from deficiency of iduronate-2-sulfatase (IDS), which results in progressive accumulation of glycosaminoglycans (GAGs) in multiple tissues.	Glycosaminoglycans	182-200	iduronate 2-sulfatase	Homo sapiens	131-134
26447927-1	2016	Mucopolysaccharidosis VII (MPS VII) is a lysosomal storage disease arising from mutations in beta-d-glucuronidase (GUSB), which results in glycosaminoglycan (GAG) accumulation and a variety of clinical manifestations including neurological disease.	Glycosaminoglycans	158-161	glucuronidase beta	Canis lupus familiaris	115-119
26702127-4	2016	Sequential exogenous presentation of soluble transforming growth factor-beta1 (TGF-beta1) and bone morphogenetic protein-2 (BMP-2) at various defined time courses resulted in varying degrees of chondrogenesis and osteogenesis as demonstrated by glycosaminoglycan and calcium content.	Glycosaminoglycans	245-262	transforming growth factor beta 1	Homo sapiens	45-77
26828861-3	2016	Previous studies have shown that the extra cellular matrix (ECM) protein Hyaluronan and Proteoglycan Link Protein1a (Hapln1a) is molecularly and functionally downstream of Cx43, and that hapln1a knockdown leads to reduction of the glycosaminoglycan hyaluronan.	Glycosaminoglycans	231-248	hyaluronan and proteoglycan link protein 1a	Danio rerio	73-115
26828861-3	2016	Previous studies have shown that the extra cellular matrix (ECM) protein Hyaluronan and Proteoglycan Link Protein1a (Hapln1a) is molecularly and functionally downstream of Cx43, and that hapln1a knockdown leads to reduction of the glycosaminoglycan hyaluronan.	Glycosaminoglycans	231-248	hyaluronan and proteoglycan link protein 1a	Danio rerio	117-124
26828861-3	2016	Previous studies have shown that the extra cellular matrix (ECM) protein Hyaluronan and Proteoglycan Link Protein1a (Hapln1a) is molecularly and functionally downstream of Cx43, and that hapln1a knockdown leads to reduction of the glycosaminoglycan hyaluronan.	Glycosaminoglycans	231-248	gap junction protein alpha 1b	Danio rerio	172-176
26828861-3	2016	Previous studies have shown that the extra cellular matrix (ECM) protein Hyaluronan and Proteoglycan Link Protein1a (Hapln1a) is molecularly and functionally downstream of Cx43, and that hapln1a knockdown leads to reduction of the glycosaminoglycan hyaluronan.	Glycosaminoglycans	231-248	hyaluronan and proteoglycan link protein 1a	Danio rerio	187-194
26656789-1	2016	BACKGROUND: The enzyme Arylsulfatase B (ARSB; N-acetylgalactosamine 4-sulfatase), is required for degradation of sulfated glycosaminoglycans (GAGs) which accumulate in cystic fibrosis.	Glycosaminoglycans	122-140	arylsulfatase B	Homo sapiens	40-44
26702127-4	2016	Sequential exogenous presentation of soluble transforming growth factor-beta1 (TGF-beta1) and bone morphogenetic protein-2 (BMP-2) at various defined time courses resulted in varying degrees of chondrogenesis and osteogenesis as demonstrated by glycosaminoglycan and calcium content.	Glycosaminoglycans	245-262	transforming growth factor beta 1	Homo sapiens	79-88
26702127-4	2016	Sequential exogenous presentation of soluble transforming growth factor-beta1 (TGF-beta1) and bone morphogenetic protein-2 (BMP-2) at various defined time courses resulted in varying degrees of chondrogenesis and osteogenesis as demonstrated by glycosaminoglycan and calcium content.	Glycosaminoglycans	245-262	bone morphogenetic protein 2	Homo sapiens	94-122
26702127-4	2016	Sequential exogenous presentation of soluble transforming growth factor-beta1 (TGF-beta1) and bone morphogenetic protein-2 (BMP-2) at various defined time courses resulted in varying degrees of chondrogenesis and osteogenesis as demonstrated by glycosaminoglycan and calcium content.	Glycosaminoglycans	245-262	bone morphogenetic protein 2	Homo sapiens	124-129
26709853-3	2016	We present DNP-enhanced MAS NMR studies of tubular assemblies of CA and Gag CA-SP1 maturation intermediate and report 20-64-fold sensitivity enhancements due to DNP at 14.1 T. These sensitivity enhancements enabled direct observation of spacer peptide 1 (SP1) resonances in CA-SP1 by dipolar-based correlation experiments, unequivocally indicating that the SP1 peptide is unstructured in assembled CA-SP1 at cryogenic temperatures, corroborating our earlier results.	Glycosaminoglycans	72-75	caspase 1	Homo sapiens	76-82
26774171-3	2016	CypB has been shown to interact with the Gag protein of human immunodeficiency type 1 (HIV-1).	Glycosaminoglycans	41-44	peptidylprolyl isomerase B	Homo sapiens	0-4
26824799-8	2016	A different glycosaminoglycans amount between the TPS and its controls was detected, displaying a similar trend with respect to ALP activity.	Glycosaminoglycans	12-30	alkaline phosphatase, placental	Homo sapiens	128-131
26801396-5	2016	This inhibitory effect is specific for HSPG depletion and does not occur with pharmacological depletion of other glycosaminoglycan (GAG) family members.	Glycosaminoglycans	132-135	syndecan 1	Rattus norvegicus	39-43
26685054-0	2016	Nuclear Magnetic Resonance Insight into the Multiple Glycosaminoglycan Binding Modes of the Link Module from Human TSG-6.	Glycosaminoglycans	53-70	TNF alpha induced protein 6	Homo sapiens	115-120
26685054-2	2016	The Link module, one of the domains of TSG-6, is responsible for binding hyaluronan and other glycosaminoglycans found in the ECM.	Glycosaminoglycans	94-112	TNF alpha induced protein 6	Homo sapiens	39-44
26711999-1	2016	The matrix (MA) domain of HIV Gag has important functions in directing the trafficking of Gag to sites of assembly and mediating the incorporation of the envelope glycoprotein (Env) into assembling particles.	Glycosaminoglycans	30-33	endogenous retrovirus group K member 20	Homo sapiens	154-175
26711999-1	2016	The matrix (MA) domain of HIV Gag has important functions in directing the trafficking of Gag to sites of assembly and mediating the incorporation of the envelope glycoprotein (Env) into assembling particles.	Glycosaminoglycans	30-33	endogenous retrovirus group K member 20	Homo sapiens	177-180
26958319-5	2016	RESULTS: Following treatment with IL-1alpha, 2 mg/mL dose of GH pretreatment was associated with a reduction of glycosaminoglycan release, reduced generation of the pathological interglobular domain aggrecan catabolites, decreased mRNA levels of ADAMTS-4 and -5 and reduced activity of ADAMTS-4.	Glycosaminoglycans	112-129	interleukin 1 alpha	Bos taurus	34-43
26741651-6	2016	RESULTS: PLN-derived leukocytes from FIV-infected cats during the chronic asymptomatic phase demonstrated active viral gag transcription and FIV protein translation as determined by real-time RT-PCR, Western blot and in situ immunohistochemistry, whereas viral RNA in blood leukocytes was either undetectable or intermittently detectable and viral protein was not detected.	Glycosaminoglycans	119-122	phospholamban	Homo sapiens	9-12
27872853-5	2016	ELISA showed that HA-CS-IL-1Ra microspheres inhibited IL-1beta-induced inflammation by attenuating increases in NO2- and prostaglandin E2 levels as well as increase in glycosaminoglycan release.	Glycosaminoglycans	168-185	interleukin 1 receptor antagonist	Rattus norvegicus	24-30
27872853-5	2016	ELISA showed that HA-CS-IL-1Ra microspheres inhibited IL-1beta-induced inflammation by attenuating increases in NO2- and prostaglandin E2 levels as well as increase in glycosaminoglycan release.	Glycosaminoglycans	168-185	interleukin 1 beta	Rattus norvegicus	54-62
26340457-6	2016	GAG could significantly downregulate the expression level of tissue factor gene (P &lt; 0.05, P &lt; 0.01) and significantly upregulate the expression levels of tissue factor pathway inhibitor and thrombomodulin genes (P &lt; 0.05, P &lt; 0.01).	Glycosaminoglycans	0-3	coagulation factor III, tissue factor	Homo sapiens	61-74
26340457-6	2016	GAG could significantly downregulate the expression level of tissue factor gene (P &lt; 0.05, P &lt; 0.01) and significantly upregulate the expression levels of tissue factor pathway inhibitor and thrombomodulin genes (P &lt; 0.05, P &lt; 0.01).	Glycosaminoglycans	0-3	coagulation factor III, tissue factor	Homo sapiens	161-174
26767428-0	2016	The Structure-Activity Relationship of Glycosaminoglycans and Their Analogues with beta-Amyloid Peptide.	Glycosaminoglycans	39-57	amyloid beta precursor protein	Homo sapiens	83-103
26548632-4	2016	Here, we demonstrate that thrombin elicits dual transactivation-dependent signalling pathways to stimulate mRNA expression of glycosaminoglycan synthesizing enzymes chondroitin 4-O-sulfotransferase 1 and chondroitin sulfate synthase 1.	Glycosaminoglycans	126-143	coagulation factor II, thrombin	Homo sapiens	26-34
26548632-4	2016	Here, we demonstrate that thrombin elicits dual transactivation-dependent signalling pathways to stimulate mRNA expression of glycosaminoglycan synthesizing enzymes chondroitin 4-O-sulfotransferase 1 and chondroitin sulfate synthase 1.	Glycosaminoglycans	126-143	carbohydrate sulfotransferase 11	Homo sapiens	165-199
26548632-4	2016	Here, we demonstrate that thrombin elicits dual transactivation-dependent signalling pathways to stimulate mRNA expression of glycosaminoglycan synthesizing enzymes chondroitin 4-O-sulfotransferase 1 and chondroitin sulfate synthase 1.	Glycosaminoglycans	126-143	chondroitin sulfate synthase 1	Homo sapiens	204-234
26806351-3	2016	Here we describe a novel decoy protein consisting of a CCL2 mutant protein fused to human serum albumin (dnCCL2-HSA chimera) with enhanced binding affinity to glycosaminoglycans that was tested in vivo.	Glycosaminoglycans	159-177	chemokine (C-C motif) ligand 2	Mus musculus	55-59
26767428-6	2016	This review presents the conformational changes of Abeta in the presence of glycosaminoglycan, glycosaminoglycan oligosaccharides and analogues.	Glycosaminoglycans	76-93	amyloid beta precursor protein	Homo sapiens	51-56
26478015-5	2015	Our data demonstrate that the release of VEGF from the hydrogels is modulated in dependence on the GAG sulfation pattern.	Glycosaminoglycans	99-102	vascular endothelial growth factor A	Homo sapiens	41-45
26783399-5	2016	However, the combined TGF-beta3/HS treatment resulted in a significant increase in GAG synthesis, cartilage matrix protein secretion, and cartilage-specific gene expression compared to cells treated with TGF-beta3 alone.	Glycosaminoglycans	83-86	transforming growth factor beta 3	Homo sapiens	22-31
26659409-0	2015	A Sulfated Glycosaminoglycan Linkage Region is a Novel Type of Human Natural Killer-1 (HNK-1) Epitope Expressed on Aggrecan in Perineuronal Nets.	Glycosaminoglycans	11-28	beta-1,3-glucuronyltransferase 1	Homo sapiens	87-92
26656715-6	2015	Our results show that the breadth and magnitude of Gag-specific CD4(+) T cell responses were significantly higher in individuals with neutralizing antibodies than in those without neutralizing antibodies.	Glycosaminoglycans	51-54	CD4 molecule	Homo sapiens	64-67
26656715-7	2015	The breadth of Gag-specific CD4(+) T cell responses was positively correlated with the breadth of neutralizing antibody activity.	Glycosaminoglycans	15-18	CD4 molecule	Homo sapiens	28-31
26656715-9	2015	Together, these data suggest that robust Gag-specific CD4(+) T cells and, to a lesser extent, gp41-specific CD4(+) T cells may provide important intermolecular help to Env-specific B cells that promote the generation or maintenance of Env-specific neutralizing antibodies.	Glycosaminoglycans	41-44	CD4 molecule	Homo sapiens	54-57
26656715-9	2015	Together, these data suggest that robust Gag-specific CD4(+) T cells and, to a lesser extent, gp41-specific CD4(+) T cells may provide important intermolecular help to Env-specific B cells that promote the generation or maintenance of Env-specific neutralizing antibodies.	Glycosaminoglycans	41-44	endogenous retrovirus group K member 20	Homo sapiens	168-171
26656715-9	2015	Together, these data suggest that robust Gag-specific CD4(+) T cells and, to a lesser extent, gp41-specific CD4(+) T cells may provide important intermolecular help to Env-specific B cells that promote the generation or maintenance of Env-specific neutralizing antibodies.	Glycosaminoglycans	41-44	endogenous retrovirus group K member 20	Homo sapiens	235-238
26656715-14	2015	These associations suggest that Gag- and gp41-specific CD4(+) T cell responses may provide robust help to B cells for the generation or maintenance of neutralizing antibodies in natural HIV-infection.	Glycosaminoglycans	32-35	CD4 molecule	Homo sapiens	55-58
26440046-6	2015	Trophic factors FGF-2, BDNF, and IL10 bound with high affinity to CS-GAGs, and were significantly (p &lt; 0.05) enriched in CS-GAG hydrogels when compared to unsulfated hyaluronic acid (HA) hydrogels.	Glycosaminoglycans	69-72	fibroblast growth factor 2	Rattus norvegicus	16-21
26440046-8	2015	Finally, rat neurospheres in CS-GAG hydrogels conditioned with the mitogen FGF-2 demonstrated significantly (p &lt; 0.05) higher self-renewal when compared to neurospheres cultured in unconditioned hydrogels.	Glycosaminoglycans	32-35	fibroblast growth factor 2	Rattus norvegicus	75-80
26445237-0	2015	Cotransfected human chondrocytes: over-expression of IGF-I and SOX9 enhances the synthesis of cartilage matrix components collagen-II and glycosaminoglycans.	Glycosaminoglycans	138-156	insulin like growth factor 1	Homo sapiens	53-58
26626158-4	2015	NT4 selectively targets tumor cells by binding to membrane sulfated glycosaminoglycans (GAG) and to endocytic receptors, like LRP1 and LRP6, which are established tumor markers.	Glycosaminoglycans	68-86	neurotrophin 4	Homo sapiens	0-3
26626158-4	2015	NT4 selectively targets tumor cells by binding to membrane sulfated glycosaminoglycans (GAG) and to endocytic receptors, like LRP1 and LRP6, which are established tumor markers.	Glycosaminoglycans	88-91	neurotrophin 4	Homo sapiens	0-3
26646821-8	2015	CHST3 siRNA successfully inhibited the expression of CHST3 mRNA throughout the study and this was associated with significant reduction of GAGs and C6SPG.	Glycosaminoglycans	139-143	carbohydrate sulfotransferase 3	Mus musculus	0-5
26646821-8	2015	CHST3 siRNA successfully inhibited the expression of CHST3 mRNA throughout the study and this was associated with significant reduction of GAGs and C6SPG.	Glycosaminoglycans	139-143	carbohydrate sulfotransferase 3	Mus musculus	53-58
26445237-0	2015	Cotransfected human chondrocytes: over-expression of IGF-I and SOX9 enhances the synthesis of cartilage matrix components collagen-II and glycosaminoglycans.	Glycosaminoglycans	138-156	SRY-box transcription factor 9	Homo sapiens	63-67
26445237-4	2015	We evaluated the combined effect of IGF-I and SOX9 transgene expression on Col-II and GAG production by cultured human articular chondrocytes.	Glycosaminoglycans	86-89	SRY-box transcription factor 9	Homo sapiens	46-50
26318439-2	2015	Through computerized structural analysis, we found a marine-derived polysaccharide, holothurian glycosaminoglycan (hGAG), behaved as a ligand-competitive inhibitor of P-selectin, indicating its potential to disrupt the binding of P-selectin to cell surface receptor and activation of downstream regulators of tumor cell migration.	Glycosaminoglycans	96-113	selectin, platelet	Mus musculus	167-177
26303011-0	2015	PA401, a novel CXCL8-based biologic therapeutic with increased glycosaminoglycan binding, reduces bronchoalveolar lavage neutrophils and systemic inflammatory markers in a murine model of LPS-induced lung inflammation.	Glycosaminoglycans	63-80	C-X-C motif chemokine ligand 8	Homo sapiens	15-20
26303011-3	2015	CXCL8 exerts its chemotactic activity by binding to its GPCR receptors (CXCR1/R2) located on neutrophils, as well as through interactions with glycosaminoglycans (GAGs) on cell surfaces including those of the microvascular endothelium.	Glycosaminoglycans	143-161	C-X-C motif chemokine ligand 8	Homo sapiens	0-5
26303011-3	2015	CXCL8 exerts its chemotactic activity by binding to its GPCR receptors (CXCR1/R2) located on neutrophils, as well as through interactions with glycosaminoglycans (GAGs) on cell surfaces including those of the microvascular endothelium.	Glycosaminoglycans	163-167	C-X-C motif chemokine ligand 8	Homo sapiens	0-5
26303011-5	2015	METHODS: We have engineered increased GAG-binding affinity into human CXCL8, thereby obtaining a competitive inhibitor that displaces wild-type IL-8/CXCL8 from GAGs.	Glycosaminoglycans	160-164	melanoma antigen	Mus musculus	38-41
26303011-5	2015	METHODS: We have engineered increased GAG-binding affinity into human CXCL8, thereby obtaining a competitive inhibitor that displaces wild-type IL-8/CXCL8 from GAGs.	Glycosaminoglycans	160-164	C-X-C motif chemokine ligand 8	Homo sapiens	70-75
26303011-5	2015	METHODS: We have engineered increased GAG-binding affinity into human CXCL8, thereby obtaining a competitive inhibitor that displaces wild-type IL-8/CXCL8 from GAGs.	Glycosaminoglycans	160-164	C-X-C motif chemokine ligand 8	Homo sapiens	144-148
26303011-5	2015	METHODS: We have engineered increased GAG-binding affinity into human CXCL8, thereby obtaining a competitive inhibitor that displaces wild-type IL-8/CXCL8 from GAGs.	Glycosaminoglycans	160-164	C-X-C motif chemokine ligand 8	Homo sapiens	149-154
26465965-4	2015	Family with sequence similarity member 20-B (FAM20B) is a newly identified kinase that phosphorylates the xylose in the common linkage region connecting the GAG with the protein core of PGs.	Glycosaminoglycans	157-160	FAM20B, glycosaminoglycan xylosylkinase	Mus musculus	45-51
26318439-2	2015	Through computerized structural analysis, we found a marine-derived polysaccharide, holothurian glycosaminoglycan (hGAG), behaved as a ligand-competitive inhibitor of P-selectin, indicating its potential to disrupt the binding of P-selectin to cell surface receptor and activation of downstream regulators of tumor cell migration.	Glycosaminoglycans	96-113	selectin, platelet	Mus musculus	230-240
26623642-8	2015	The ratio of non-synonymous to synonymous substitutions in the env gene (0.7-0.75) was higher than the gag (0.26-0.34) or pol (0.21-0.26) genes.	Glycosaminoglycans	103-106	endogenous retrovirus group K member 20	Homo sapiens	63-66
26302421-0	2015	Engineering Metamorphic Chemokine Lymphotactin/XCL1 into the GAG-Binding, HIV-Inhibitory Dimer Conformation.	Glycosaminoglycans	61-64	X-C motif chemokine ligand 1	Homo sapiens	34-46
26608316-2	2016	Physiologically, the N-terminal polybasic region of residues 23 to 31 of PrP has been shown to be involved in its endocytic trafficking and interactions with glycosaminoglycans or putative ectodomains of membrane-associated proteins.	Glycosaminoglycans	158-176	prion protein	Mus musculus	73-76
26440575-4	2015	By identifying an IAPP derivative with a restricted conformational ensemble that co-assembles with IAPP, we observed that helical species were off-pathway in homogenous environment and in presence of lipid bilayers or glycosaminoglycans.	Glycosaminoglycans	218-236	islet amyloid polypeptide	Homo sapiens	18-22
26440575-4	2015	By identifying an IAPP derivative with a restricted conformational ensemble that co-assembles with IAPP, we observed that helical species were off-pathway in homogenous environment and in presence of lipid bilayers or glycosaminoglycans.	Glycosaminoglycans	218-236	islet amyloid polypeptide	Homo sapiens	99-103
26302421-0	2015	Engineering Metamorphic Chemokine Lymphotactin/XCL1 into the GAG-Binding, HIV-Inhibitory Dimer Conformation.	Glycosaminoglycans	61-64	X-C motif chemokine ligand 1	Homo sapiens	47-51
26269189-13	2015	HIV controllers maintain a large proportion of Gag-specific expandable memory CD8(+) T cells involved in ongoing viral suppression.	Glycosaminoglycans	47-50	CD8a molecule	Homo sapiens	78-81
26370074-4	2015	The major structural protein of MLV particles, Gag, frequently co-localized with Siglec-1, and trans-infection, primarily of surface-bound MLV particles, efficiently occurred.	Glycosaminoglycans	47-50	sialic acid binding Ig-like lectin 1, sialoadhesin	Mus musculus	81-89
26537682-5	2015	We found that Gag expression from integrated proviruses occurred in resting cells that lacked surface CD4, likely resulting from Nef- and Env-mediated receptor internalization.	Glycosaminoglycans	14-17	CD4 molecule	Homo sapiens	102-105
26537682-5	2015	We found that Gag expression from integrated proviruses occurred in resting cells that lacked surface CD4, likely resulting from Nef- and Env-mediated receptor internalization.	Glycosaminoglycans	14-17	S100 calcium binding protein B	Homo sapiens	129-132
26537682-5	2015	We found that Gag expression from integrated proviruses occurred in resting cells that lacked surface CD4, likely resulting from Nef- and Env-mediated receptor internalization.	Glycosaminoglycans	14-17	endogenous retrovirus group K member 20	Homo sapiens	138-141
26537682-12	2015	Gag(+) CD4(-) cells can also be detected in suppressed patients, suggesting that a subset of infected cells express proteins during ART.	Glycosaminoglycans	0-3	CD4 molecule	Homo sapiens	7-10
25895983-1	2015	BACKGROUND: Syndecan-4 is a transmembrane heparan sulfate proteoglycan expressed in a variety of cells, and glycosaminoglycan side chains of syndecan-4 bind to several proteins, suggesting several biological functions.	Glycosaminoglycans	108-125	syndecan 4	Homo sapiens	141-151
26512081-3	2016	A conserved late domain motif, Pro-Thr-Ala-Pro (PTAP), located in the p6 region of Gag (p6(Gag)), plays a central role in ESCRT recruitment to the site of virus budding.	Glycosaminoglycans	83-86	S100 calcium binding protein A12	Homo sapiens	88-95
27785363-1	2015	Glycosaminoglycans (GAGs) such as heparin are promising materials for growth factor delivery due to their ability to efficiently bind positively charged growth factors including bone morphogenetic protein-2 (BMP-2) through their negatively charged sulfate groups.	Glycosaminoglycans	0-18	bone morphogenetic protein 2	Mus musculus	178-206
25421491-10	2015	CONCLUSION: The short T1(Gd) centrally indicates degenerative cartilage changes consistent with loss of glycosaminoglycans.	Glycosaminoglycans	104-122	interleukin 1 receptor like 1	Homo sapiens	22-28
26363218-4	2015	Additional experiments demonstrated that the expression of the p55 Gag protein is sufficient for ADAR1 incorporation into virus-like particles (VLPs).	Glycosaminoglycans	67-70	adenosine deaminase RNA specific	Homo sapiens	97-102
27785363-1	2015	Glycosaminoglycans (GAGs) such as heparin are promising materials for growth factor delivery due to their ability to efficiently bind positively charged growth factors including bone morphogenetic protein-2 (BMP-2) through their negatively charged sulfate groups.	Glycosaminoglycans	0-18	bone morphogenetic protein 2	Mus musculus	208-213
26157071-6	2015	In contrast to ovalbumin and OVAY, OVAX interacts with heparin, a negatively charged glycosaminoglycan, via a positively charged domain exposed at the surface of the molecule.	Glycosaminoglycans	85-102	ovalbumin-related protein X (SERPINB14C)	Gallus gallus	35-39
26459242-10	2015	The glycosaminoglycan biosynthesis-heparin sulphate/heparin pathway is significantly enriched in the TOP2B gene ontology analysis, suggesting changes in this pathway in the absence of TOP2B may cause the axon guidance faults.	Glycosaminoglycans	4-21	DNA topoisomerase II beta	Homo sapiens	101-106
26459242-10	2015	The glycosaminoglycan biosynthesis-heparin sulphate/heparin pathway is significantly enriched in the TOP2B gene ontology analysis, suggesting changes in this pathway in the absence of TOP2B may cause the axon guidance faults.	Glycosaminoglycans	4-21	DNA topoisomerase II beta	Homo sapiens	184-189
26416734-6	2015	The ability to counteract SERINC5 was conserved in Nef encoded by diverse primate immunodeficiency viruses, as well as in the structurally unrelated glycosylated Gag from murine leukaemia virus.	Glycosaminoglycans	162-165	serine incorporator 5	Homo sapiens	26-33
26416734-6	2015	The ability to counteract SERINC5 was conserved in Nef encoded by diverse primate immunodeficiency viruses, as well as in the structurally unrelated glycosylated Gag from murine leukaemia virus.	Glycosaminoglycans	162-165	Nef	Human immunodeficiency virus 1	51-54
26342234-2	2015	Although, the precise mechanism remains elusive, interaction between Env and the matrix (MA) domain of Gag plays a central role.	Glycosaminoglycans	103-106	endogenous retrovirus group K member 20	Homo sapiens	69-72
26407983-1	2015	BACKGROUND: Mucopolysaccharidosis type I (MPS I) is caused by the deficiency of alpha-L-iduronidase (IDUA), which is involved in the degradation of glycosaminoglycans (GAGs), such as heparan sulfate and dermatan sulfate in the lysosome.	Glycosaminoglycans	148-166	iduronidase, alpha-L	Mus musculus	101-105
26388616-10	2015	NCCM from all species significantly increased the DNA and GAG content of the human CLC micro-aggregates.	Glycosaminoglycans	58-61	Charcot-Leyden crystal galectin	Homo sapiens	83-86
26347037-4	2015	Here we use different siRNAs targeting EXTL2 and EXTL3 genes, which are important for HS synthesis, as SRT in Sanfilippo C patients" fibroblasts in order to decrease glycosaminoglycan (GAG) storage inside the lysosomes.	Glycosaminoglycans	166-183	exostosin like glycosyltransferase 2	Homo sapiens	39-44
26347037-4	2015	Here we use different siRNAs targeting EXTL2 and EXTL3 genes, which are important for HS synthesis, as SRT in Sanfilippo C patients" fibroblasts in order to decrease glycosaminoglycan (GAG) storage inside the lysosomes.	Glycosaminoglycans	166-183	exostosin like glycosyltransferase 3	Homo sapiens	49-54
26347037-4	2015	Here we use different siRNAs targeting EXTL2 and EXTL3 genes, which are important for HS synthesis, as SRT in Sanfilippo C patients" fibroblasts in order to decrease glycosaminoglycan (GAG) storage inside the lysosomes.	Glycosaminoglycans	185-188	exostosin like glycosyltransferase 2	Homo sapiens	39-44
26347037-4	2015	Here we use different siRNAs targeting EXTL2 and EXTL3 genes, which are important for HS synthesis, as SRT in Sanfilippo C patients" fibroblasts in order to decrease glycosaminoglycan (GAG) storage inside the lysosomes.	Glycosaminoglycans	185-188	exostosin like glycosyltransferase 3	Homo sapiens	49-54
26347358-5	2015	However, polyfunctionality in HIV subjects was associated with an HIV Gag response of CD38+ T cells, whereas polyfunctionality for EUs was induced upon SEB stimulation by CD38- T cells.	Glycosaminoglycans	70-73	CD38 molecule	Homo sapiens	86-90
26196533-10	2015	In contrast, LNCaP cells grown in 3D secreted elevated levels of PSA, particularly on the scaffold composed of collagen and glycosaminoglycans.	Glycosaminoglycans	124-142	kallikrein related peptidase 3	Homo sapiens	65-68
25820496-2	2015	The present study was designed to investigate whether chondroitin sulfate E (CS-E), which is one of the sulfated glycosaminoglycans (GAGs), is involved in osteoactivin (OA) activity, and osteoclast differentiation.	Glycosaminoglycans	113-131	cystathionase (cystathionine gamma-lyase)	Mus musculus	77-81
25915185-5	2015	Tissues exposed to TGF-beta3 had significantly increased glycosaminoglycan and total collagen protein production along with upregulated cartilage-specific gene expression, resulting in tissues with a higher Young"s Modulus.	Glycosaminoglycans	57-74	transforming growth factor beta 3	Bos taurus	19-28
28649535-1	2015	Mucopolysaccharidosis type I (MPS I), is an autosomal recessive lysosomal storage disorder caused by a deficiency in the alpha-L-iduronidase enzyme, resulting in decreased enzymatic activity and accumulation of glycosaminoglycans.	Glycosaminoglycans	211-229	iduronidase, alpha-L	Mus musculus	121-140
26251846-8	2015	Moreover, the analyses indicate changes in multiple other pathways, including those relating to the metabolism of glycosaminoglycans, methionine, and coenzyme A, possibly reflecting downstream effects of URAT1 loss.	Glycosaminoglycans	114-132	solute carrier family 22 (organic anion/cation transporter), member 12	Mus musculus	204-209
26033936-4	2015	The aim of the present study was to understand if sulfated GAG could modulate HPSE, since the mechanisms that regulate HPSE have not been completely defined.	Glycosaminoglycans	59-62	heparanase	Cricetulus griseus	78-82
25998424-4	2015	Very low levels of oxygen (&lt;1%), acidosis (pH 6.2), and exposure to IL-1beta led to reductions in cell viability, increased GAG release, alterations in DeltaPsim and ROS levels, and reduced GSH:GSSG ratio.	Glycosaminoglycans	127-130	interleukin-1 beta	Equus caballus	71-79
26033936-8	2015	Total ablation of GAG with 4-MU in CHO-K1 inhibited HPSE expression, while the lack of sulfation had no effect.	Glycosaminoglycans	18-21	heparanase	Cricetulus griseus	52-56
26033936-11	2015	In view of our results, we can conclude that GAG are essential modulators of HPSE expression and location.	Glycosaminoglycans	45-48	heparanase	Cricetulus griseus	77-81
26033936-12	2015	Therefore, GAG profile could impact cell behavior mediated by the regulation of HPSE.	Glycosaminoglycans	11-14	heparanase	Cricetulus griseus	80-84
26343641-6	2015	Cell number and GAG content increased upon the addition of BMP3 in a dose-dependent manner.	Glycosaminoglycans	16-19	bone morphogenetic protein 3	Homo sapiens	59-63
26183778-4	2015	These peptides display high affinity for glycosaminoglycans (GAGs) and compete with functional intact chemokines for GAG binding, the longest peptide (CXCL9(74-103)) being the most potent.	Glycosaminoglycans	41-59	chemokine (C-X-C motif) ligand 9	Mus musculus	151-156
26085164-3	2015	HIV-1 inhibition by XCL1 requires access to the alternative all-beta conformation, which interacts with glycosaminoglycans (GAGs) but not with the specific XCL1 receptor, XCR1.	Glycosaminoglycans	104-122	X-C motif chemokine ligand 1	Homo sapiens	20-24
26085164-9	2015	Interestingly, the complement of residues involved in HIV-1 blockade is partially overlapping, but distinct from those involved in the GAG-binding function of XCL1.	Glycosaminoglycans	135-138	X-C motif chemokine ligand 1	Homo sapiens	159-163
26295701-6	2015	Deletion of Ext1 in the mesoderm induces a cardiac phenotype similar to that of a mutant with conditional deletion of UDP-glucose dehydrogenase, a key enzyme responsible for synthesis of all glycosaminoglycans.	Glycosaminoglycans	191-209	exostosin glycosyltransferase 1	Mus musculus	12-16
26295701-6	2015	Deletion of Ext1 in the mesoderm induces a cardiac phenotype similar to that of a mutant with conditional deletion of UDP-glucose dehydrogenase, a key enzyme responsible for synthesis of all glycosaminoglycans.	Glycosaminoglycans	191-209	UDP-glucose dehydrogenase	Mus musculus	118-143
26291824-6	2015	In addition, Gag-stimulated CD8+ T-cells and cytokine-stimulated NK cells were tested for cytotoxic activity.	Glycosaminoglycans	13-16	CD8a molecule	Homo sapiens	28-31
26347860-8	2015	The TGF-beta3 group also produced a collagen type II and glycosaminoglycan-rich extracellular matrix, detected by immunohistochemistry, Alcian blue staining, and Safranin O staining suggesting robust chondrogenesis within the scaffold.	Glycosaminoglycans	57-74	transforming growth factor beta 3	Homo sapiens	4-13
26223367-0	2015	Flexible Linker Modulates Glycosaminoglycan Affinity of Decorin Binding Protein A. Decorin binding protein A (DBPA) is a glycosaminoglycan (GAG)-binding adhesin found on the surface of the bacterium Borrelia burgdorferi (B. burgdorferi), the causative agent of Lyme disease.	Glycosaminoglycans	121-138	Y-box binding protein 3	Homo sapiens	110-114
26223367-0	2015	Flexible Linker Modulates Glycosaminoglycan Affinity of Decorin Binding Protein A. Decorin binding protein A (DBPA) is a glycosaminoglycan (GAG)-binding adhesin found on the surface of the bacterium Borrelia burgdorferi (B. burgdorferi), the causative agent of Lyme disease.	Glycosaminoglycans	140-143	Y-box binding protein 3	Homo sapiens	110-114
26223367-2	2015	Interestingly, DBPA from different strains (B31, N40, and PBr) show significant differences in GAG affinities, but the structural basis for the differences is not clear.	Glycosaminoglycans	95-98	Y-box binding protein 3	Homo sapiens	15-19
26223367-3	2015	In this study, we show that GAG affinity of N40 DBPA is modulated in part by flexible segments that control access to the GAG binding site, such that shortening of the linker leads to higher GAG affinity when analyzed using ELISA, gel mobility shift assay, solution NMR, and isothermal titration calorimetry.	Glycosaminoglycans	28-31	Y-box binding protein 3	Homo sapiens	48-52
26223367-3	2015	In this study, we show that GAG affinity of N40 DBPA is modulated in part by flexible segments that control access to the GAG binding site, such that shortening of the linker leads to higher GAG affinity when analyzed using ELISA, gel mobility shift assay, solution NMR, and isothermal titration calorimetry.	Glycosaminoglycans	122-125	Y-box binding protein 3	Homo sapiens	48-52
26223367-3	2015	In this study, we show that GAG affinity of N40 DBPA is modulated in part by flexible segments that control access to the GAG binding site, such that shortening of the linker leads to higher GAG affinity when analyzed using ELISA, gel mobility shift assay, solution NMR, and isothermal titration calorimetry.	Glycosaminoglycans	122-125	Y-box binding protein 3	Homo sapiens	48-52
25994595-6	2015	dGEMRIC and biochemical analyzes of the OC constructs showed a reduced glycosaminoglycan (GAG) contents upon IL-1beta administration.	Glycosaminoglycans	71-88	interleukin 1 beta	Homo sapiens	109-117
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
25872744-9	2015	Furthermore, we observed low genetic diversity in the gag region of the viral variants throughout the course of infection, which is indicative of low viral replication and corresponds to the low viral load observed in the HLA-B27-positive patients.	Glycosaminoglycans	54-57	major histocompatibility complex, class I, B	Homo sapiens	222-227
25943740-2	2015	In addition, the ARSB substrate chondroitin 4-sulfate (C4S) and total sulfated glycosaminoglycans increased.	Glycosaminoglycans	79-97	arylsulfatase B	Rattus norvegicus	17-21
26279273-5	2015	Glycosaminoglycan content was studied by micromass culture of chondrocytes of PKC-delta KO mice.	Glycosaminoglycans	0-17	protein kinase C, delta	Mus musculus	78-87
26279273-10	2015	Furthermore, in vitro culture of chondrocyte micromass showed a decreased alcian blue staining of chondrocyte micromass in the PKC-delta KO mice, indicative of a reduced level of glycosaminoglycan production.	Glycosaminoglycans	179-196	protein kinase C, delta	Mus musculus	127-136
26018465-3	2015	Previously, we showed that the magnitude of the HIV-2 gag-specific T-cell response is inversely correlated with plasma viral load, particularly when responses are directed against an epitope, 165 DRFYKSLRA173 , within the highly conserved Major Homology Region of gag-p26.	Glycosaminoglycans	54-57	transmembrane p24 trafficking protein 3	Homo sapiens	268-271
26018465-4	2015	We also showed that the presence of three proline residues, at positions 119, 159 and 178 of gag-p26, was significantly correlated with low viral load.	Glycosaminoglycans	93-96	transmembrane p24 trafficking protein 3	Homo sapiens	97-100
25937317-3	2015	Proteins enriched in lysine and other positively charged residues (histidine and arginine) as well as glycosaminoglycans and gangliosides bind Plg.	Glycosaminoglycans	102-120	plasminogen	Homo sapiens	143-146
25979873-7	2015	Herein, we demonstrate that FAP(+) CASCs are required for maintenance of the provisional tumor stroma because depletion of these cells, by adoptive transfer of FAP-targeted chimeric antigen receptor (CAR) T cells, reduced extracellular matrix proteins and glycosaminoglycans.	Glycosaminoglycans	256-274	fibroblast activation protein alpha	Homo sapiens	28-31
26158506-6	2015	Our structural, biophysical and cellular data, map Fz4 and putative Lrp5/6 binding sites to distinct patches on Norrin, and reveal a GAG binding site spanning Norrin and Fz4CRD.	Glycosaminoglycans	133-136	Norrie disease (pseudoglioma) (human)	Mus musculus	159-165
26258071-2	2015	Many lung cancers have changes in their microenvironment including upregulation of the extracellular matrix glycosaminoglycan, hyaluronan (HA), which we have previously demonstrated can regulate the activity of the extracellular serine protease, hyaluronan binding protein 2 (HABP2).	Glycosaminoglycans	108-125	hyaluronan binding protein 2	Homo sapiens	246-274
26258071-2	2015	Many lung cancers have changes in their microenvironment including upregulation of the extracellular matrix glycosaminoglycan, hyaluronan (HA), which we have previously demonstrated can regulate the activity of the extracellular serine protease, hyaluronan binding protein 2 (HABP2).	Glycosaminoglycans	108-125	hyaluronan binding protein 2	Homo sapiens	276-281
25893793-12	2015	Since the phenotype of the Nias patients differs from the Larsen-like syndrome described for patients with mutation p.(Arg277Gln), we suggest mutation B3GAT3:p.(Pro140Leu) to cause a different type of GAG linkeropathy showing no involvement of the heart.	Glycosaminoglycans	201-204	beta-1,3-glucuronyltransferase 3	Homo sapiens	151-157
25195511-0	2015	Transgenic 4-1BBL-engineered vaccine stimulates potent Gag-specific therapeutic and long-term immunity via increased priming of CD44(+)CD62L(high) IL-7R(+) CTLs with up- and downregulation of anti- and pro-apoptosis genes.	Glycosaminoglycans	55-58	tumor necrosis factor (ligand) superfamily, member 9	Mus musculus	11-17
25195511-0	2015	Transgenic 4-1BBL-engineered vaccine stimulates potent Gag-specific therapeutic and long-term immunity via increased priming of CD44(+)CD62L(high) IL-7R(+) CTLs with up- and downregulation of anti- and pro-apoptosis genes.	Glycosaminoglycans	55-58	CD44 antigen	Mus musculus	128-132
25195511-0	2015	Transgenic 4-1BBL-engineered vaccine stimulates potent Gag-specific therapeutic and long-term immunity via increased priming of CD44(+)CD62L(high) IL-7R(+) CTLs with up- and downregulation of anti- and pro-apoptosis genes.	Glycosaminoglycans	55-58	selectin, lymphocyte	Mus musculus	135-140
25195511-0	2015	Transgenic 4-1BBL-engineered vaccine stimulates potent Gag-specific therapeutic and long-term immunity via increased priming of CD44(+)CD62L(high) IL-7R(+) CTLs with up- and downregulation of anti- and pro-apoptosis genes.	Glycosaminoglycans	55-58	interleukin 7 receptor	Mus musculus	147-152
25195511-8	2015	Importantly, the Gag-specific Gag-Texo/4-1BBL vaccine also stimulates more efficient Gag-specific therapeutic and long-term immunity against HLA-A2/Gag-expressing B16 melanoma BL6-10Gag/A2 cells than the control Gag-Texo/Null vaccine in transgenic HLA-A2 mice.	Glycosaminoglycans	17-20	tumor necrosis factor (ligand) superfamily, member 9	Mus musculus	39-45
25195511-8	2015	Importantly, the Gag-specific Gag-Texo/4-1BBL vaccine also stimulates more efficient Gag-specific therapeutic and long-term immunity against HLA-A2/Gag-expressing B16 melanoma BL6-10Gag/A2 cells than the control Gag-Texo/Null vaccine in transgenic HLA-A2 mice.	Glycosaminoglycans	30-33	tumor necrosis factor (ligand) superfamily, member 9	Mus musculus	39-45
25195511-9	2015	Taken together, our novel Gag-Texo/4-1BBL vaccine, which is capable of stimulating potent Gag-specific therapeutic and long-term immunity, may represent a new immunotherapeutic vaccine for controlling HIV-1 infection.	Glycosaminoglycans	26-29	tumor necrosis factor (ligand) superfamily, member 9	Mus musculus	35-41
25195511-9	2015	Taken together, our novel Gag-Texo/4-1BBL vaccine, which is capable of stimulating potent Gag-specific therapeutic and long-term immunity, may represent a new immunotherapeutic vaccine for controlling HIV-1 infection.	Glycosaminoglycans	90-93	tumor necrosis factor (ligand) superfamily, member 9	Mus musculus	35-41
25936869-1	2015	BACKGROUND: Biglycan (BGN) is a proteoglycan composed of a 42-kDa core protein and two glycosaminoglycan (GAG) chains, and known to be involved in structural, space-filling functions and many physiological regulations in the skin.	Glycosaminoglycans	87-104	biglycan	Homo sapiens	12-20
25813774-4	2015	3D pellet cultures of transduced cells in the presence of TGFbeta-3 revealed increased pellet size and higher levels of total glycosaminoglycan in both Sox9 and Sox9+ OSKM co-transduced chondrocytes compared to untransduced and green fluorescent protein expressing controls.	Glycosaminoglycans	126-143	transforming growth factor beta 3	Canis lupus familiaris	58-67
25813774-4	2015	3D pellet cultures of transduced cells in the presence of TGFbeta-3 revealed increased pellet size and higher levels of total glycosaminoglycan in both Sox9 and Sox9+ OSKM co-transduced chondrocytes compared to untransduced and green fluorescent protein expressing controls.	Glycosaminoglycans	126-143	SRY-box transcription factor 9	Canis lupus familiaris	152-156
25813774-4	2015	3D pellet cultures of transduced cells in the presence of TGFbeta-3 revealed increased pellet size and higher levels of total glycosaminoglycan in both Sox9 and Sox9+ OSKM co-transduced chondrocytes compared to untransduced and green fluorescent protein expressing controls.	Glycosaminoglycans	126-143	SRY-box transcription factor 9	Canis lupus familiaris	161-165
25936869-1	2015	BACKGROUND: Biglycan (BGN) is a proteoglycan composed of a 42-kDa core protein and two glycosaminoglycan (GAG) chains, and known to be involved in structural, space-filling functions and many physiological regulations in the skin.	Glycosaminoglycans	87-104	biglycan	Homo sapiens	22-25
25936869-7	2015	UV irradiation also decreased mRNA expression levels of XYLT1 and 2, which are responsible for initiation of GAG chain synthesis.	Glycosaminoglycans	109-112	xylosyltransferase 1	Homo sapiens	56-67
25967551-4	2015	Heparan sulfate specifically modifies Shh processing at the cell surface, and purified glycosaminoglycans enhance the proteolytic removal of N- and C-terminal Shh peptides under cell-free conditions.	Glycosaminoglycans	87-105	sonic hedgehog signaling molecule	Homo sapiens	159-162
26123575-5	2015	Using a heat map method to highlight differences in the viral sequences between donor and recipient, we demonstrated that the majority of the recipient"s mutations outside of Env were within epitopes restricted by HLA-B*27:05 and HLA-B*57:01, including the well-studied Gag epitopes.	Glycosaminoglycans	270-273	major histocompatibility complex, class I, B	Homo sapiens	214-219
25866187-8	2015	The clinical potential of this approach is demonstrated in an explant defect model where EMT(+TGF) from aged MSCs synthesize de novo tissue containing sulfated glycosaminoglycans and type II collagen in situ.	Glycosaminoglycans	160-178	IL2 inducible T cell kinase	Homo sapiens	89-92
26151781-2	2015	As a group, the glycosaminoglycans provide mechanical strength to skin, as they can absorb water and occupy the space between elastin fibers and collagen.	Glycosaminoglycans	16-34	elastin	Homo sapiens	126-133
25886697-8	2015	Western blot analysis demonstrated that the ratio of glycosaminoglycan (GAG) decorated DCN to core DCN was reduced in P0 and 1 mo lum(-/-) hearts.	Glycosaminoglycans	53-70	zinc finger protein 185	Mus musculus	118-126
25886697-8	2015	Western blot analysis demonstrated that the ratio of glycosaminoglycan (GAG) decorated DCN to core DCN was reduced in P0 and 1 mo lum(-/-) hearts.	Glycosaminoglycans	53-70	lumican	Mus musculus	130-133
25886697-8	2015	Western blot analysis demonstrated that the ratio of glycosaminoglycan (GAG) decorated DCN to core DCN was reduced in P0 and 1 mo lum(-/-) hearts.	Glycosaminoglycans	72-75	zinc finger protein 185	Mus musculus	118-126
25886697-8	2015	Western blot analysis demonstrated that the ratio of glycosaminoglycan (GAG) decorated DCN to core DCN was reduced in P0 and 1 mo lum(-/-) hearts.	Glycosaminoglycans	72-75	lumican	Mus musculus	130-133
25712888-5	2015	These effects were also supported by the finding that spicatoside A (20 muM) reduced glycosaminoglycan release from IL-1alpha-treated rabbit joint cartilage culture to some degree.	Glycosaminoglycans	85-102	interleukin-1 alpha	Oryctolagus cuniculus	116-125
26059549-0	2015	Type II collagen and glycosaminoglycan expression induction in primary human chondrocyte by TGF-beta1.	Glycosaminoglycans	21-38	transforming growth factor beta 1	Homo sapiens	92-101
26059549-4	2015	The effect of modified TGF-beta1 on chondrocytes was evaluated based on the type II collagen mRNA levels and the amount of glycosaminoclycan (GAG) formed around chondrocytes, which are indicative markers of redifferentiated chondrocytes.	Glycosaminoglycans	142-145	transforming growth factor beta 1	Homo sapiens	23-32
26059549-8	2015	Type II collagen and GAG production were induced in hChonJ cells by TGF-beta1 secreted from the irradiated hChonJb#7 cells when the cells were co-cultured in micro-masses.	Glycosaminoglycans	21-24	transforming growth factor beta 1	Homo sapiens	68-77
26199949-12	2015	gag-specific T-cell responses were detected in 63% of participants by interferon-gamma enzyme-linked immunospot at the highest dose post boost.	Glycosaminoglycans	0-3	interferon gamma	Homo sapiens	70-86
25751597-2	2015	PF-ACE-AED approach allowed the possibility to distinguish weak and strong interactions of the binding processes between the most common apolipoprotein E protein isoforms (apoE2, apoE3, apoE4) of high density lipoprotein (HDL) and apoE-containing HDL2 with major glycosaminoglycan (GAG) chain of proteoglycans (PGs), chondroitin-6-sulfate (C6S).	Glycosaminoglycans	263-280	apolipoprotein E	Homo sapiens	137-153
25761450-1	2015	Mucopolysaccharidosis type II (MPS II) is a neuropathic lysosomal storage disorder caused by a deficiency of iduronate-2-sulfatase (IDS), which leads to the accumulation of glycosaminoglycans (GAGs).	Glycosaminoglycans	173-191	iduronate 2-sulfatase	Mus musculus	132-135
25827571-10	2015	Others contribute to O-glycan and in particular glycosaminoglycan biosynthesis, suggesting that Sppl3 function is not restricted to N-glycosylation, but also functions in other forms of protein glycosylation.	Glycosaminoglycans	48-65	signal peptide peptidase like 3	Homo sapiens	96-101
25267436-4	2015	When chondrogenic differentiation of ASCs was evaluated for both constructs, sulfated glycosaminoglycan (sGAG) content was significantly higher in the TGF-beta1-immobilized scaffold.	Glycosaminoglycans	86-103	transforming growth factor beta 1	Homo sapiens	151-160
25965995-12	2015	Biosynthesis of glycosaminoglycan (GAG) and aggrecan was increased in HSFs treated with BMP-2.	Glycosaminoglycans	16-33	bone morphogenetic protein 2	Cavia porcellus	88-93
25413299-4	2015	We demonstrated that coculture in collagen scaffolds of BM-MSC with Mf derived from monocytes polarized with M-CSF (M-Mf), but not with GM-CSF (GM-Mf) resulted in significantly higher glycosaminoglycan (GAG) content than what would be expected from an equal number of BM-MSC alone (defined as chondro-induction).	Glycosaminoglycans	184-201	colony stimulating factor 1	Homo sapiens	109-114
26030443-8	2015	Additional reduction in Gag cleavage efficiency was noted following the removal of p6* from between the two PRs.	Glycosaminoglycans	24-27	S100 calcium binding protein A12	Homo sapiens	83-86
25751597-2	2015	PF-ACE-AED approach allowed the possibility to distinguish weak and strong interactions of the binding processes between the most common apolipoprotein E protein isoforms (apoE2, apoE3, apoE4) of high density lipoprotein (HDL) and apoE-containing HDL2 with major glycosaminoglycan (GAG) chain of proteoglycans (PGs), chondroitin-6-sulfate (C6S).	Glycosaminoglycans	263-280	apolipoprotein E	Homo sapiens	172-177
25751597-2	2015	PF-ACE-AED approach allowed the possibility to distinguish weak and strong interactions of the binding processes between the most common apolipoprotein E protein isoforms (apoE2, apoE3, apoE4) of high density lipoprotein (HDL) and apoE-containing HDL2 with major glycosaminoglycan (GAG) chain of proteoglycans (PGs), chondroitin-6-sulfate (C6S).	Glycosaminoglycans	263-280	apolipoprotein E	Homo sapiens	172-176
25751597-2	2015	PF-ACE-AED approach allowed the possibility to distinguish weak and strong interactions of the binding processes between the most common apolipoprotein E protein isoforms (apoE2, apoE3, apoE4) of high density lipoprotein (HDL) and apoE-containing HDL2 with major glycosaminoglycan (GAG) chain of proteoglycans (PGs), chondroitin-6-sulfate (C6S).	Glycosaminoglycans	282-285	apolipoprotein E	Homo sapiens	137-153
25751597-2	2015	PF-ACE-AED approach allowed the possibility to distinguish weak and strong interactions of the binding processes between the most common apolipoprotein E protein isoforms (apoE2, apoE3, apoE4) of high density lipoprotein (HDL) and apoE-containing HDL2 with major glycosaminoglycan (GAG) chain of proteoglycans (PGs), chondroitin-6-sulfate (C6S).	Glycosaminoglycans	282-285	apolipoprotein E	Homo sapiens	172-177
25751597-2	2015	PF-ACE-AED approach allowed the possibility to distinguish weak and strong interactions of the binding processes between the most common apolipoprotein E protein isoforms (apoE2, apoE3, apoE4) of high density lipoprotein (HDL) and apoE-containing HDL2 with major glycosaminoglycan (GAG) chain of proteoglycans (PGs), chondroitin-6-sulfate (C6S).	Glycosaminoglycans	282-285	apolipoprotein E	Homo sapiens	172-176
25751597-6	2015	In addition, the affinity constant values determined could be compared with those obtained in our previous studies for the interactions between apoE isoforms and another important GAG chain of PGs - dermatan sulfate (DS).	Glycosaminoglycans	180-183	apolipoprotein E	Homo sapiens	144-148
25950566-7	2015	We suggest that binding to ligands as heparin or other glycosaminoglycans could be key events tuning the fine details of the interaction of apoA-I variants with the micro-environment, and probably eliciting the toxicity of these variants in hereditary amyloidoses.	Glycosaminoglycans	55-73	apolipoprotein A1	Homo sapiens	140-146
25736501-7	2015	When non-canonical BMPR signaling molecules were examined, ERK1/2 phosphorylation was found to be decreased in MC-GAG but elevated in Col-GAG.	Glycosaminoglycans	114-117	mitogen-activated protein kinase 3	Homo sapiens	59-65
25695518-2	2015	DBPA facilitates the bacteria"s colonization of human tissue by adhering to glycosaminoglycan (GAG), a sulfated polysaccharide.	Glycosaminoglycans	76-93	Y-box binding protein 3	Homo sapiens	0-4
25695518-2	2015	DBPA facilitates the bacteria"s colonization of human tissue by adhering to glycosaminoglycan (GAG), a sulfated polysaccharide.	Glycosaminoglycans	95-98	Y-box binding protein 3	Homo sapiens	0-4
25662098-6	2015	M-CSFR activation was analysed by Western blot after glycosaminoglycans abrasion, syndecan-1 overexpression or repression and addition of a blocking anti-syndecan antibody.	Glycosaminoglycans	53-71	colony stimulating factor 1 receptor	Homo sapiens	2-6
25695518-3	2015	Interestingly, DBPA sequence variation among different strains of Borrelia spirochetes is high, resulting in significant differences in their GAG affinities.	Glycosaminoglycans	142-145	Y-box binding protein 3	Homo sapiens	15-19
25541466-3	2015	Heparins, a heterogeneous mixture of glycosaminoglycans, can inhibit metastatic cascades by blocking P-selectin-mediated intercellular adhesion between tumor cells and PTs.	Glycosaminoglycans	37-55	selectin, platelet	Mus musculus	101-111
25695518-7	2015	In particular, the C-terminus of PBr DBPA, unlike C-termini from B31 and N40 DBPAs, is positioned away from the GAG-binding pocket and the linker between helices one and two of PBr DBPA is highly structured and retracted from the GAG-binding pocket.	Glycosaminoglycans	112-115	Y-box binding protein 3	Homo sapiens	37-41
25695518-7	2015	In particular, the C-terminus of PBr DBPA, unlike C-termini from B31 and N40 DBPAs, is positioned away from the GAG-binding pocket and the linker between helices one and two of PBr DBPA is highly structured and retracted from the GAG-binding pocket.	Glycosaminoglycans	230-233	Y-box binding protein 3	Homo sapiens	37-41
25695518-8	2015	The repositioning of the C-terminus allowed the formation of an extra GAG-binding epitope in PBr DBPA and the retracted linker gave GAG ligands more access to the GAG-binding epitopes than other DBPAs.	Glycosaminoglycans	70-73	Y-box binding protein 3	Homo sapiens	97-101
25954275-4	2015	The extracellular matrix glycosaminoglycan hyaluronic acid (HA) is the principle ligand of CD44.	Glycosaminoglycans	25-42	CD44 molecule (Indian blood group)	Homo sapiens	91-95
25762741-7	2015	Virions treated with protease inhibitors failed to release Vpx, indicating that Gag processing was required for Vpx release from the virion.	Glycosaminoglycans	80-83	vpx protein	Simian immunodeficiency virus	112-115
25882933-12	2015	DMMB quantitative determination of GAG showed that GAG amount of chondrocytes in 100 mug/L BMP-7 groups was significantly higher than those in the other groups (P&lt;0.05).	Glycosaminoglycans	35-38	bone morphogenetic protein 7	Oryctolagus cuniculus	91-96
25882933-12	2015	DMMB quantitative determination of GAG showed that GAG amount of chondrocytes in 100 mug/L BMP-7 groups was significantly higher than those in the other groups (P&lt;0.05).	Glycosaminoglycans	51-54	bone morphogenetic protein 7	Oryctolagus cuniculus	91-96
25655827-2	2015	The biosynthesis of GAG chains is initiated by xylosylation of the core protein followed by galactosylation by the galactosyltransferase beta4GalT7.	Glycosaminoglycans	20-23	beta-1,4-galactosyltransferase 7	Homo sapiens	137-147
25857450-8	2015	The serum MBL levels were significantly higher in the DI-exposed subjects (both the DI-OA patients and AECs) carrying ht1 [GAG] (P=0.028).	Glycosaminoglycans	123-126	mannose binding lectin 2	Homo sapiens	10-13
25897103-3	2015	Beta-glucuronidase (GLU) is a lysosomal exoglycosidase involved in degradation of glycosaminoglycans of the cell membranes and extracellular matrix of normal and cancerous colon tissues.	Glycosaminoglycans	82-100	glucuronidase beta	Homo sapiens	0-18
25897103-3	2015	Beta-glucuronidase (GLU) is a lysosomal exoglycosidase involved in degradation of glycosaminoglycans of the cell membranes and extracellular matrix of normal and cancerous colon tissues.	Glycosaminoglycans	82-100	glucuronidase beta	Homo sapiens	20-23
24663337-7	2015	CXCL4-induced up-regulation of both MMP7 and S100A8 was curbed in the presence of heparin, which binds to CXCL4 and glycosaminoglycans, most likely representing the macrophage receptor for CXCL4.	Glycosaminoglycans	116-134	platelet factor 4	Homo sapiens	0-5
24663337-7	2015	CXCL4-induced up-regulation of both MMP7 and S100A8 was curbed in the presence of heparin, which binds to CXCL4 and glycosaminoglycans, most likely representing the macrophage receptor for CXCL4.	Glycosaminoglycans	116-134	matrix metallopeptidase 7	Homo sapiens	36-40
24663337-7	2015	CXCL4-induced up-regulation of both MMP7 and S100A8 was curbed in the presence of heparin, which binds to CXCL4 and glycosaminoglycans, most likely representing the macrophage receptor for CXCL4.	Glycosaminoglycans	116-134	S100 calcium binding protein A8	Homo sapiens	45-51
25134498-1	2015	Hurler syndrome is a disorder of mucopolysaccharide metabolism caused due to inherited deficiencies of lysosomal alpha-l-iduronidase activity.	Glycosaminoglycans	33-51	alpha-L-iduronidase	Homo sapiens	113-132
25517798-5	2015	Cells expressing the p21 shRNA demonstrated higher proliferative potential during monolayer expansion and increased synthesis of glycosaminoglycans (GAGs) in pellet cultures.	Glycosaminoglycans	129-147	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	21-24
25517798-5	2015	Cells expressing the p21 shRNA demonstrated higher proliferative potential during monolayer expansion and increased synthesis of glycosaminoglycans (GAGs) in pellet cultures.	Glycosaminoglycans	149-153	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	21-24
25863062-4	2015	Upon investigating the specific interaction between the unique hydrophilic domain (HD) of the human cell-surface sulfatase Sulf1 against its physiological glycosaminoglycan (GAG) target heparan sulfate (HS) by single molecule force spectroscopy (SMFS), we found clear evidence of catch bond behavior in this system.	Glycosaminoglycans	155-172	sulfatase 1	Homo sapiens	123-128
25863062-4	2015	Upon investigating the specific interaction between the unique hydrophilic domain (HD) of the human cell-surface sulfatase Sulf1 against its physiological glycosaminoglycan (GAG) target heparan sulfate (HS) by single molecule force spectroscopy (SMFS), we found clear evidence of catch bond behavior in this system.	Glycosaminoglycans	174-177	sulfatase 1	Homo sapiens	123-128
25945286-11	2015	The role played by chondroitin sulfate glycosaminoglycan (GAG) chains on the ability of sdc1 to associate with its ligands needs further investigation.	Glycosaminoglycans	58-61	syndecan 1	Homo sapiens	88-92
25945286-12	2015	At wound sites heparanase can cleave the HS GAG chains of sdc1, alter its ability to bind cytokines, and induce shedding of the ectodomain.	Glycosaminoglycans	44-47	syndecan 1	Homo sapiens	58-62
25568325-1	2015	Among glycosaminoglycan (GAG) biosynthetic enzymes, the human beta1,4-galactosyltransferase 7 (hbeta4GalT7) is characterized by its unique capacity to take over xyloside derivatives linked to a hydrophobic aglycone as substrates and/or inhibitors.	Glycosaminoglycans	6-23	beta-1,4-galactosyltransferase 7	Homo sapiens	62-93
25655827-3	2015	Some beta-d-xylosides, such as 2-naphthyl beta-d-xylopyranoside, can induce GAG synthesis by serving as acceptor substrates for beta4GalT7 and by that also compete with the GAG synthesis on core proteins.	Glycosaminoglycans	76-79	beta-1,4-galactosyltransferase 7	Homo sapiens	128-138
25568325-1	2015	Among glycosaminoglycan (GAG) biosynthetic enzymes, the human beta1,4-galactosyltransferase 7 (hbeta4GalT7) is characterized by its unique capacity to take over xyloside derivatives linked to a hydrophobic aglycone as substrates and/or inhibitors.	Glycosaminoglycans	25-28	beta-1,4-galactosyltransferase 7	Homo sapiens	62-93
25589788-4	2015	Here, we demonstrate that FXIIa utilizes cell membrane-bound glycosaminoglycans to interact with the cell surface of human lung fibroblasts (HLF).	Glycosaminoglycans	61-79	HLF transcription factor, PAR bZIP family member	Homo sapiens	141-144
25548284-2	2015	Heparanase is an endoglycosidase that specifically degrades the unbranched glycosaminoglycan side chains of HSPGs.	Glycosaminoglycans	75-92	heparanase	Mus musculus	0-10
25731175-6	2015	Structural analyses reveal glycosaminoglycan binding sites on Notum, which probably help Notum to co-localize with Wnt proteins.	Glycosaminoglycans	27-44	notum, palmitoleoyl-protein carboxylesterase	Homo sapiens	62-67
25731175-6	2015	Structural analyses reveal glycosaminoglycan binding sites on Notum, which probably help Notum to co-localize with Wnt proteins.	Glycosaminoglycans	27-44	notum, palmitoleoyl-protein carboxylesterase	Homo sapiens	89-94
25295378-4	2015	Hence, in this study we also examined whether these patients had increased seroreactivity to the aforementioned HRES-1 Gag peptides.	Glycosaminoglycans	119-122	HTLV-1 related endogenous sequence	Homo sapiens	112-118
25689358-2	2015	We describe a case wherein the use of the Molt mouth gag significantly facilitated airway control using fiberoptic tracheal intubation.	Glycosaminoglycans	53-56	transmembrane protein 132D	Homo sapiens	42-46
25497737-6	2015	Ca(2+) flux, chemotaxis, and heparin binding assays showed that the monomer form of XCL2 is responsible for G protein-coupled receptor activation while the dimeric form is important for GAG binding.	Glycosaminoglycans	186-189	X-C motif chemokine ligand 2	Homo sapiens	84-88
25476526-1	2015	We investigated whether expression of xylosyltransferase-1 (XT-1), a key enzyme in glycosaminoglycan biosynthesis, is responsive to disk degeneration and to inhibition by the inflammatory cytokines tumor necrosis factor alpha and IL-1beta in nucleus pulposus (NP) cells.	Glycosaminoglycans	83-100	xylosyltransferase 1	Homo sapiens	38-58
25476526-1	2015	We investigated whether expression of xylosyltransferase-1 (XT-1), a key enzyme in glycosaminoglycan biosynthesis, is responsive to disk degeneration and to inhibition by the inflammatory cytokines tumor necrosis factor alpha and IL-1beta in nucleus pulposus (NP) cells.	Glycosaminoglycans	83-100	xylosyltransferase 1	Homo sapiens	60-64
25480151-2	2015	Fgf2 requires glycosaminoglycans, like chondroitin and dermatan sulfates (hereafter denoted CS/DS) as co-receptors.	Glycosaminoglycans	14-32	fibroblast growth factor 2	Cricetulus griseus	0-4
25453468-2	2015	Glycosaminoglycans (GAGs) possess the ability to influence the chemokine profile of the CF lung by binding CXCL8 and protecting it from proteolytic degradation.	Glycosaminoglycans	0-18	C-X-C motif chemokine ligand 8	Homo sapiens	107-112
25373459-7	2015	When co-cultured with chondrocytes, the ADSCs on three-dimensional PRP scaffolds were able to form neocartilage, with positive staining of safranine O, which indicated the production of glycosaminoglycan, and type II collagen.	Glycosaminoglycans	186-203	complement component 4 binding protein alpha	Homo sapiens	67-70
25453468-13	2015	CONCLUSION: PA401 can disrupt CXCL8:GAG complexes, rendering the chemokine susceptible to proteolytic degradation.	Glycosaminoglycans	36-39	C-X-C motif chemokine ligand 8	Homo sapiens	30-35
25608886-5	2015	RESULTS: CCL2 neutralization potently reduced the number of p24 Gag+ cells during the course of either productive or single cycle infection with HIV-1.	Glycosaminoglycans	64-67	C-C motif chemokine ligand 2	Homo sapiens	9-13
25541102-1	2015	Mucopolysaccharidosis type I (MPS I) is due to deficient alpha-L-iduronidase (IDUA) which leads to storage of undegraded glycosaminoglycans (GAG).	Glycosaminoglycans	121-139	iduronidase, alpha-L	Mus musculus	57-76
25541102-1	2015	Mucopolysaccharidosis type I (MPS I) is due to deficient alpha-L-iduronidase (IDUA) which leads to storage of undegraded glycosaminoglycans (GAG).	Glycosaminoglycans	121-139	iduronidase, alpha-L	Mus musculus	78-82
25541102-1	2015	Mucopolysaccharidosis type I (MPS I) is due to deficient alpha-L-iduronidase (IDUA) which leads to storage of undegraded glycosaminoglycans (GAG).	Glycosaminoglycans	141-144	iduronidase, alpha-L	Mus musculus	57-76
25541102-1	2015	Mucopolysaccharidosis type I (MPS I) is due to deficient alpha-L-iduronidase (IDUA) which leads to storage of undegraded glycosaminoglycans (GAG).	Glycosaminoglycans	141-144	iduronidase, alpha-L	Mus musculus	78-82
25559179-1	2015	Mucopolysaccharidosis (MPS) VII is a lysosomal storage disorder caused by the deficiency of the enzyme beta-glucuronidase (Gusb(-/-)) and results in glycosaminoglycan (GAG) accumulation.	Glycosaminoglycans	149-166	glucuronidase, beta	Mus musculus	103-121
25559179-1	2015	Mucopolysaccharidosis (MPS) VII is a lysosomal storage disorder caused by the deficiency of the enzyme beta-glucuronidase (Gusb(-/-)) and results in glycosaminoglycan (GAG) accumulation.	Glycosaminoglycans	149-166	glucuronidase, beta	Mus musculus	123-127
25559179-1	2015	Mucopolysaccharidosis (MPS) VII is a lysosomal storage disorder caused by the deficiency of the enzyme beta-glucuronidase (Gusb(-/-)) and results in glycosaminoglycan (GAG) accumulation.	Glycosaminoglycans	168-171	glucuronidase, beta	Mus musculus	103-121
25559179-1	2015	Mucopolysaccharidosis (MPS) VII is a lysosomal storage disorder caused by the deficiency of the enzyme beta-glucuronidase (Gusb(-/-)) and results in glycosaminoglycan (GAG) accumulation.	Glycosaminoglycans	168-171	glucuronidase, beta	Mus musculus	123-127
25605972-10	2015	Thus, heparin and perhaps related glycosaminoglycans function as ligands for ALK, revealing a potential mechanism for the regulation of ALK activity in vivo and suggesting an approach for developing ALK-targeted therapies for cancer.	Glycosaminoglycans	34-52	ALK receptor tyrosine kinase	Homo sapiens	77-80
25605972-10	2015	Thus, heparin and perhaps related glycosaminoglycans function as ligands for ALK, revealing a potential mechanism for the regulation of ALK activity in vivo and suggesting an approach for developing ALK-targeted therapies for cancer.	Glycosaminoglycans	34-52	ALK receptor tyrosine kinase	Homo sapiens	136-139
25605972-10	2015	Thus, heparin and perhaps related glycosaminoglycans function as ligands for ALK, revealing a potential mechanism for the regulation of ALK activity in vivo and suggesting an approach for developing ALK-targeted therapies for cancer.	Glycosaminoglycans	34-52	ALK receptor tyrosine kinase	Homo sapiens	136-139
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
26682223-3	2015	The glutathione concentration is determined by the number of GAG repeats in gamma-glutamylcysteine synthetase.	Glycosaminoglycans	61-64	glutamate-cysteine ligase catalytic subunit	Homo sapiens	76-109
25622168-2	2015	Mucopolysaccharidosis type II (MPS II) is an X-linked recessive disorder characterized by a deficiency of the enzyme iduronate-2-sulfatase leading to a multisystem involvement by tissue accumulation of glycosaminoglycans heparan and dermatan sulfate.	Glycosaminoglycans	202-220	iduronate 2-sulfatase	Homo sapiens	117-138
26279449-14	2015	GAG synthesis and type II collagen were decreased in both the IL-1beta groups and the Osthole groups, and significantly reduced by Osthole plus IL-1beta.	Glycosaminoglycans	0-3	interleukin 1 beta	Rattus norvegicus	62-70
26236728-2	2015	Mentioned glycosaminoglycans chains are covalently O-linked to serine residues within the core proteins creating heparan sulfate/heparin proteoglycans (HSPG).	Glycosaminoglycans	10-28	syndecan 2	Homo sapiens	152-156
26356269-1	2015	BACKGROUND/AIMS: Chondroitin sulfate synthase 1 (CHSY1) is a glycosyltransferases involved in the biosynthesis of chondroitin and dermatan sulfate glycosaminoglycan (GAG).	Glycosaminoglycans	166-169	chondroitin sulfate synthase 1	Rattus norvegicus	17-47
26356269-1	2015	BACKGROUND/AIMS: Chondroitin sulfate synthase 1 (CHSY1) is a glycosyltransferases involved in the biosynthesis of chondroitin and dermatan sulfate glycosaminoglycan (GAG).	Glycosaminoglycans	166-169	chondroitin sulfate synthase 1	Rattus norvegicus	49-54
26356269-2	2015	TGF-beta can stimulate sulfated GAG production in nucleus pulposus cells; however, the underlying mechanisms are poorly understood.	Glycosaminoglycans	32-35	transforming growth factor, beta 1	Rattus norvegicus	0-8
26279449-14	2015	GAG synthesis and type II collagen were decreased in both the IL-1beta groups and the Osthole groups, and significantly reduced by Osthole plus IL-1beta.	Glycosaminoglycans	0-3	interleukin 1 beta	Rattus norvegicus	144-152
25524633-6	2014	By targeting miR-95 in cells from MSD patients, we can effectively increase residual SUMF1 expression, allowing for reactivation of sulfatase activity and increased clearance of sulfated GAGs.	Glycosaminoglycans	187-191	microRNA 95	Homo sapiens	13-19
25535477-5	2015	Further, GDF/F4 also inhibited the glycosaminoglycan release from interleukin-1alpha-treated rabbit cartilage culture (30.6% inhibition at 30 mug/mL).	Glycosaminoglycans	35-52	interleukin-1 alpha	Oryctolagus cuniculus	66-84
25325940-2	2015	One example, the extensively studied heparin pentasaccharide sequence-which binds antithrombin-III, inducing a conformational change that increases its serpin protease activity by 1,000-fold-is unique in that no other specific GAG-protein structure-function relations have been described to the same degree.	Glycosaminoglycans	227-230	serpin family C member 1	Homo sapiens	82-98
25750456-8	2015	In addition, we will briefly review PGC analysis approaches for glycopeptides, glycosaminoglycans (GAGs) and human milk oligosaccharides (HMOs).	Glycosaminoglycans	79-97	progastricsin	Homo sapiens	36-39
26495958-0	2015	Heparin and LPS-induced COX-2 expression in airway cells: a link between its anti-inflammatory effects and GAG sulfation.	Glycosaminoglycans	107-110	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	24-29
26125521-0	2015	Dose-dependent inhibition of Gag cellular immunity by Env in SIV/HIV DNA vaccinated macaques.	Glycosaminoglycans	29-32	endogenous retrovirus group K member 20	Homo sapiens	54-57
26125521-5	2015	In contrast, under high env:gag DNA plasmid ratio, the development of Gag cellular responses was significantly reduced by either SIV or HIV Env, whereas Gag humoral responses were not affected.	Glycosaminoglycans	70-73	endogenous retrovirus group K member 20	Homo sapiens	24-27
26125521-5	2015	In contrast, under high env:gag DNA plasmid ratio, the development of Gag cellular responses was significantly reduced by either SIV or HIV Env, whereas Gag humoral responses were not affected.	Glycosaminoglycans	70-73	endogenous retrovirus group K member 20	Homo sapiens	140-143
26447809-2	2015	We have previously reported that high molecular weight hyaluronan (HMW-HA), a major glycosaminoglycan in the body, promotes rapid signal transduction in human pulmonary microvascular endothelial cells (HPMVEC) leading to barrier enhancement.	Glycosaminoglycans	84-101	cilia and flagella associated protein 97	Homo sapiens	67-70
25577208-0	2015	Bioactive IGF-1 release from collagen-GAG scaffold to enhance cartilage repair in vitro.	Glycosaminoglycans	38-41	insulin like growth factor 1	Homo sapiens	10-15
25320314-4	2015	We investigated and characterized at the molecular level the process of ICAM-1 incorporation using initially a Pr55(Gag)-based virus-like particle (VLP) model.	Glycosaminoglycans	116-119	intercellular adhesion molecule 1	Homo sapiens	72-78
25524633-6	2014	By targeting miR-95 in cells from MSD patients, we can effectively increase residual SUMF1 expression, allowing for reactivation of sulfatase activity and increased clearance of sulfated GAGs.	Glycosaminoglycans	187-191	sulfatase modifying factor 1	Homo sapiens	85-90
25526200-5	2014	The second codon position after the initiation codon was generally selected to be GAG, which has lower tRNA abundance in pigs than its synonymous member (GAA).	Glycosaminoglycans	82-85	alpha glucosidase	Sus scrofa	154-157
25674472-1	2014	A single GAG codon deletion in the gene encoding torsinA is linked to most cases of early-onset torsion dystonia.	Glycosaminoglycans	9-12	torsin family 1 member A	Homo sapiens	49-56
26914760-9	2014	Glycosaminoglycan content for discs injected with IL-1beta alone was significantly lower than for intact controls.	Glycosaminoglycans	0-17	interleukin 1 beta	Rattus norvegicus	50-58
25422423-4	2014	Cathepsin K is organized into elongated C-shaped protease dimers that reveal a putative collagen-binding interface aided by glycosaminoglycans.	Glycosaminoglycans	124-142	cathepsin K	Homo sapiens	0-11
25422423-9	2014	We propose that one cathepsin K molecule binds to collagen-bound glycosaminoglycans at the gap region and recruits a second protease molecule that provides an unfolding and cleavage mechanism for triple helical collagen.	Glycosaminoglycans	65-83	cathepsin K	Homo sapiens	20-31
25422423-10	2014	Removal of collagen-associated glycosaminoglycans prevents cathepsin K binding and subsequently fiber hydrolysis.	Glycosaminoglycans	31-49	cathepsin K	Homo sapiens	59-70
25142140-1	2014	Mucopolysaccharidosis type IIIA (MPS-IIIA) or Sanfilippo A syndrome is a lysosomal storage genetic disease that results from the deficiency of the N-sulfoglucosamine sulfohydrolase (SGSH) protein, a sulfamidase required for the degradation of heparan sulfate glycosaminoglycans (GAGs).	Glycosaminoglycans	279-283	N-sulfoglucosamine sulfohydrolase (sulfamidase)	Mus musculus	182-186
25142140-5	2014	Hydrodynamic delivery of SGSH-encoding pFAR4 into MPS-IIIA diseased mice led to high serum levels of sulfamidase protein that was efficiently taken up by neighboring organs, as shown by the correction of GAG accumulation.	Glycosaminoglycans	204-207	N-sulfoglucosamine sulfohydrolase (sulfamidase)	Mus musculus	25-29
24497431-4	2014	Results demonstrated that a resilient, hydrophilic hydrogel which displays a unique "shape-memory" sponge characteristic could be formed from a blend of soluble elastin aggregates, chondroitin-6-sulfate, hyaluronic acid and collagen following freeze-drying, stabilization with a carbodiimide and penta-galloyl glucose-based fixative, and subsequent partial degradation with glycosaminoglycan degrading enzymes.	Glycosaminoglycans	374-391	elastin	Homo sapiens	161-168
25454870-9	2014	This was accompanied by a significant reduction in expression of CD38 on CD4 T cells (p=0.0194), significantly increased IFN-gamma and IL-2 production in response to Gag (p=0.0122) and elevated IFN-gamma production in response to Tat (p=0.041) at week 48 compared to baseline.	Glycosaminoglycans	166-169	interferon gamma	Homo sapiens	121-130
25454870-9	2014	This was accompanied by a significant reduction in expression of CD38 on CD4 T cells (p=0.0194), significantly increased IFN-gamma and IL-2 production in response to Gag (p=0.0122) and elevated IFN-gamma production in response to Tat (p=0.041) at week 48 compared to baseline.	Glycosaminoglycans	166-169	interleukin 2	Homo sapiens	135-139
26914760-10	2014	For discs injected with IL-1beta along with IL-1ra microspheres, glycosaminoglycan content was not significantly different from intact controls.	Glycosaminoglycans	65-82	interleukin 1 beta	Rattus norvegicus	24-32
26914760-10	2014	For discs injected with IL-1beta along with IL-1ra microspheres, glycosaminoglycan content was not significantly different from intact controls.	Glycosaminoglycans	65-82	interleukin 1 receptor antagonist	Rattus norvegicus	44-50
25280972-8	2014	Gene expression for Cx43 and COX-2 was enhanced by tensile strain leading to increased PGE2 release and GAG levels in PAM and CAM when compared to unstrained controls.	Glycosaminoglycans	104-107	gap junction protein alpha 1	Homo sapiens	20-24
25280972-8	2014	Gene expression for Cx43 and COX-2 was enhanced by tensile strain leading to increased PGE2 release and GAG levels in PAM and CAM when compared to unstrained controls.	Glycosaminoglycans	104-107	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	29-34
25504019-6	2014	Direct sequencing of all 20 exons of the TCIRG1 gene revealed a single nucleotide change in exon 11 (c1305 G &gt; T), which causes the substitution of Asp (GAT) for Glu (GAG) at position 435, and a two-nucleotide deletion in exon 16 (c1952-1953 del CA), causing a frame-shift mutation.	Glycosaminoglycans	170-173	T cell immune regulator 1, ATPase H+ transporting V0 subunit a3	Homo sapiens	41-47
24873753-4	2014	Microsphere and TGF-beta1 loading concentrations were identified that resulted in glycosaminoglycan (GAG) production comparable to those of control aggregates cultured in TGF-beta1-containing medium.	Glycosaminoglycans	82-99	transforming growth factor beta 1	Homo sapiens	16-25
24873753-4	2014	Microsphere and TGF-beta1 loading concentrations were identified that resulted in glycosaminoglycan (GAG) production comparable to those of control aggregates cultured in TGF-beta1-containing medium.	Glycosaminoglycans	101-104	transforming growth factor beta 1	Homo sapiens	16-25
25504019-6	2014	Direct sequencing of all 20 exons of the TCIRG1 gene revealed a single nucleotide change in exon 11 (c1305 G &gt; T), which causes the substitution of Asp (GAT) for Glu (GAG) at position 435, and a two-nucleotide deletion in exon 16 (c1952-1953 del CA), causing a frame-shift mutation.	Glycosaminoglycans	170-173	glycine-N-acyltransferase	Homo sapiens	156-159
28649518-1	2015	Mutations in B3GALT6, encoding the galactosyltransferase II (GalT-II) involved in the synthesis of the glycosaminoglycan (GAG) linkage region of proteoglycans (PGs), have recently been associated with a spectrum of connective tissue disorders, including spondyloepimetaphyseal dysplasia with joint laxity type 1 (SEMDJL1) and Ehlers-Danlos-like syndrome.	Glycosaminoglycans	103-120	beta-1,3-galactosyltransferase 6	Homo sapiens	13-20
28649518-1	2015	Mutations in B3GALT6, encoding the galactosyltransferase II (GalT-II) involved in the synthesis of the glycosaminoglycan (GAG) linkage region of proteoglycans (PGs), have recently been associated with a spectrum of connective tissue disorders, including spondyloepimetaphyseal dysplasia with joint laxity type 1 (SEMDJL1) and Ehlers-Danlos-like syndrome.	Glycosaminoglycans	103-120	beta-1,3-galactosyltransferase 6	Homo sapiens	35-59
28649518-5	2015	The key role of GalT-II in GAG synthesis and the crucial biological functions of PGs are consistent with the perturbation of many physiological functions that are critical for the correct architecture and homeostasis of various connective tissues, including skin, bone, cartilage, tendons, and ligaments, and generates the wide phenotypic spectrum of GalT-II-deficient patients.	Glycosaminoglycans	27-30	beta-1,3-galactosyltransferase 6	Homo sapiens	16-23
28649518-1	2015	Mutations in B3GALT6, encoding the galactosyltransferase II (GalT-II) involved in the synthesis of the glycosaminoglycan (GAG) linkage region of proteoglycans (PGs), have recently been associated with a spectrum of connective tissue disorders, including spondyloepimetaphyseal dysplasia with joint laxity type 1 (SEMDJL1) and Ehlers-Danlos-like syndrome.	Glycosaminoglycans	103-120	beta-1,3-galactosyltransferase 6	Homo sapiens	61-68
25331875-3	2014	We show that the atypical secretory kinase family with sequence similarity 20, member B (Fam20B) phosphorylates the initiating xylose residue in the proteoglycan tetrasaccharide linkage region, and that this event functions as a molecular switch to regulate subsequent glycosaminoglycan assembly.	Glycosaminoglycans	269-286	FAM20B glycosaminoglycan xylosylkinase	Homo sapiens	89-95
25015527-0	2014	Importance of the polarity of the glycosaminoglycan chain on the interaction with FGF-1.	Glycosaminoglycans	34-51	fibroblast growth factor 1	Homo sapiens	82-87
25016280-0	2014	Photopatterning of vascular endothelial growth factor within collagen-glycosaminoglycan scaffolds can induce a spatially confined response in human umbilical vein endothelial cells.	Glycosaminoglycans	69-87	vascular endothelial growth factor A	Homo sapiens	19-53
25122554-5	2014	TNF-alpha induced syndecan 4 (SDC4) mRNA up-regulation by 2.5-fold, whereas cell surface SDC4 and heparan sulfate (HS) were reduced by 36 and 30%, respectively, and SDC4 and sulfated glycosaminoglycan in the culture medium were increased by 52 and 65%, respectively, indicating TNF-alpha-induced shedding.	Glycosaminoglycans	183-200	tumor necrosis factor	Homo sapiens	0-9
25397470-14	2014	Gp120 Mn and Bal, nef and p55-gag treatment had no effect on OC differentiation.	Glycosaminoglycans	30-33	H3 histone pseudogene 44	Homo sapiens	26-29
25360552-7	2014	Single genome amplification characterized the infections of 2 unprotected animals in the gag-env immunized group, both of which had reduced acute plasma viral loads that ended as transient infections indicating partial immune control.	Glycosaminoglycans	89-92	endogenous retrovirus group K member 20	Homo sapiens	93-96
25459762-1	2014	Human alpha-L-iduronidase (IDUA) is a member of glycoside hydrolase family and is involved in the catabolism of glycosaminoglycans (GAGs), heparan sulfate (HS) and dermatan sulfate (DS).	Glycosaminoglycans	112-130	alpha-L-iduronidase	Homo sapiens	6-25
25459762-1	2014	Human alpha-L-iduronidase (IDUA) is a member of glycoside hydrolase family and is involved in the catabolism of glycosaminoglycans (GAGs), heparan sulfate (HS) and dermatan sulfate (DS).	Glycosaminoglycans	112-130	alpha-L-iduronidase	Homo sapiens	27-31
25199049-10	2014	Overexpression of PN-1 lacking either its antiprotease activity or its binding capacity to glycosaminoglycans had no effect on fibronectin expression.	Glycosaminoglycans	91-109	serpin family E member 2	Homo sapiens	18-22
24659483-7	2014	Allosteric inhibitors of plasmin have also been designed including small molecule lysine analogs that bind to plasmin"s kringle domain(s) and sulfated glycosaminoglycan mimetics that bind to plasmin"s catalytic domain.	Glycosaminoglycans	151-168	plasminogen	Homo sapiens	25-32
25360552-8	2014	Four of 6 rhesus were infected in the gag-env + GM-CSF group which demonstrated that GM-CSF abrogated protection.	Glycosaminoglycans	38-41	endogenous retrovirus group K member 20	Homo sapiens	42-45
25360552-8	2014	Four of 6 rhesus were infected in the gag-env + GM-CSF group which demonstrated that GM-CSF abrogated protection.	Glycosaminoglycans	38-41	colony stimulating factor 2	Homo sapiens	85-91
25360552-12	2014	Because there were only 2 infected animals in the gag-env vaccinated rhesus compared to 10 infected rhesus in the other 2 groups, the significance of finding single env variants in the gag-env vaccinated group could not be established.	Glycosaminoglycans	50-53	endogenous retrovirus group K member 20	Homo sapiens	54-57
27379277-6	2014	It was found that interleukin-1beta increased the release of sulfated glycosaminoglycans and hyaluronan from the explants into the culture media consistently with the decrease in uronic acid and collagen content in the cartilage explants.	Glycosaminoglycans	70-88	interleukin-1 beta	Equus caballus	18-35
27896125-1	2014	Mucopolysaccharidosis type I (MPSI) is a rare autosomal recessive disorder caused by mutations in the gene encoding the lysosomal enzyme alpha-l-iduronidase (IDUA), which is instrumental in the hydrolysis of the glycosaminoglycans, dermatan and heparan sulfate.	Glycosaminoglycans	212-230	alpha-L-iduronidase	Homo sapiens	137-156
27896125-1	2014	Mucopolysaccharidosis type I (MPSI) is a rare autosomal recessive disorder caused by mutations in the gene encoding the lysosomal enzyme alpha-l-iduronidase (IDUA), which is instrumental in the hydrolysis of the glycosaminoglycans, dermatan and heparan sulfate.	Glycosaminoglycans	212-230	alpha-L-iduronidase	Homo sapiens	158-162
25176127-2	2014	TIMP-3 binds to sulfated ECM glycosaminoglycans or is endocytosed by cells via low-density lipoprotein receptor-related protein 1 (LRP-1).	Glycosaminoglycans	29-47	TIMP metallopeptidase inhibitor 3	Homo sapiens	0-6
25267637-1	2014	Patients with mucopolysaccharidosis type I (MPS I), a genetic deficiency of the lysosomal enzyme alpha-l-iduronidase (IDUA), exhibit accumulation of glycosaminoglycans in tissues, with resulting diverse clinical manifestations including neurological, ocular, skeletal, and cardiac disease.	Glycosaminoglycans	149-167	alpha-L-iduronidase	Homo sapiens	97-116
25267637-1	2014	Patients with mucopolysaccharidosis type I (MPS I), a genetic deficiency of the lysosomal enzyme alpha-l-iduronidase (IDUA), exhibit accumulation of glycosaminoglycans in tissues, with resulting diverse clinical manifestations including neurological, ocular, skeletal, and cardiac disease.	Glycosaminoglycans	149-167	alpha-L-iduronidase	Homo sapiens	118-122
25122765-10	2014	We conclude that docking of ADAMTS5 with two N-terminal GAG chains of versican-V1 via its ancillary domain is required for versican processing at Glu(441)-Ala(442).	Glycosaminoglycans	56-59	ADAM metallopeptidase with thrombospondin type 1 motif 5	Homo sapiens	28-35
25122765-11	2014	V1 proteolysis by ADAMTS1 demonstrated a similar requirement for the N-terminal GAG chains and Glu(441).	Glycosaminoglycans	80-83	ADAM metallopeptidase with thrombospondin type 1 motif 1	Homo sapiens	18-25
24880028-6	2014	CD8+ T cells are vital for clearance of WNF infected cells from the CNS, whereas TLR-3 and TLR-7 mediated anti-virus response through increased serum inflammatory cytokines to disrupt the BBB providing infected leucocytes and free virus access to the CNS (so called Trojan horse) Cellular virus attachment factors, promoting FV cell entry are widely distributed and include DC-SIGN (that detects complex carbohydrate molecules); Glycosamino glycans (GAG), Heparan sulphate(HSPG) Semaphorin 7A, Low Density Lipid receptors (LDLR); these are not FV specific virus entry receptors.	Glycosaminoglycans	429-448	toll like receptor 3	Equus caballus	81-86
24352367-5	2014	A new computational model, based on the mechano-electrochemical mixture theory, was developed to describe competitive binding kinetics of IGF-1 with IGFBP and CSR, and associated glycosaminoglycan (GAG) biosynthesis.	Glycosaminoglycans	179-196	insulin like growth factor 1	Homo sapiens	138-143
24352367-5	2014	A new computational model, based on the mechano-electrochemical mixture theory, was developed to describe competitive binding kinetics of IGF-1 with IGFBP and CSR, and associated glycosaminoglycan (GAG) biosynthesis.	Glycosaminoglycans	198-201	insulin like growth factor 1	Homo sapiens	138-143
24352367-9	2014	Results indicated that the lower ratio of IGF-1 to IGFBP found in obese population reduces cartilage GAG concentration up to 18 % when compared to normal population.	Glycosaminoglycans	101-104	insulin like growth factor 1	Homo sapiens	42-47
25295005-3	2014	These findings led to the development of potential anti-amyloid therapies, and among them homotaurine, a glycosaminoglycan mimetic designed to interfere with the actions of Abeta early in the cascade of amyloidogenic events, and by its gamma-aminobutyric acid type (GABA) A receptor affinity.	Glycosaminoglycans	105-122	amyloid beta precursor protein	Homo sapiens	173-178
25400736-3	2014	In the present study, we examined the inhibitory effects of cordycepin on interleukin-1 beta (IL-1beta)-induced glycosaminoglycan (GAG) release, nitric oxide production as well as gene expressions of inflammatory and catabolic mediators in human cartilage and chondrocytes.	Glycosaminoglycans	112-129	interleukin 1 beta	Homo sapiens	74-92
25400736-3	2014	In the present study, we examined the inhibitory effects of cordycepin on interleukin-1 beta (IL-1beta)-induced glycosaminoglycan (GAG) release, nitric oxide production as well as gene expressions of inflammatory and catabolic mediators in human cartilage and chondrocytes.	Glycosaminoglycans	112-129	interleukin 1 beta	Homo sapiens	94-102
25400736-8	2014	We found that cordycepin suppressed IL-1beta-stimulated GAG release.	Glycosaminoglycans	56-59	interleukin 1 beta	Homo sapiens	36-44
25202993-8	2014	It tuned out that the promoted GAG synthesis and USSs gene expression induced by APS-3c was mediated by the stimulated IGF1 and IGF1R gene expression, but not through directly activation of IGF1R signaling pathway.	Glycosaminoglycans	31-34	insulin like growth factor 1	Homo sapiens	119-123
25202993-8	2014	It tuned out that the promoted GAG synthesis and USSs gene expression induced by APS-3c was mediated by the stimulated IGF1 and IGF1R gene expression, but not through directly activation of IGF1R signaling pathway.	Glycosaminoglycans	31-34	insulin like growth factor 1 receptor	Homo sapiens	128-133
25192337-11	2014	TGF-beta expression and macrophage infiltration were prevented by the GAG treatments, and podocyte damage was halted.	Glycosaminoglycans	70-73	transforming growth factor, beta 1	Rattus norvegicus	0-8
24931141-1	2014	A three-nucleotide (GAG) deletion (DeltaE) in TorsinA (TOR1A) has been identified as the most common cause of dominantly inherited early-onset torsion dystonia (DYT1).	Glycosaminoglycans	20-23	torsin family 1 member A	Homo sapiens	161-165
25151041-8	2014	Our observations suggest that (i) IL-4 cell-signalling in the absence of IL-13 retarded gag-specific antibody isotype class switching, or (ii) IL-13Ralpha2 signalling was involved in inducing good gag-specific B cell immunity.	Glycosaminoglycans	88-91	interleukin 4	Homo sapiens	34-38
25151041-8	2014	Our observations suggest that (i) IL-4 cell-signalling in the absence of IL-13 retarded gag-specific antibody isotype class switching, or (ii) IL-13Ralpha2 signalling was involved in inducing good gag-specific B cell immunity.	Glycosaminoglycans	197-200	interleukin 4	Homo sapiens	34-38
25151041-8	2014	Our observations suggest that (i) IL-4 cell-signalling in the absence of IL-13 retarded gag-specific antibody isotype class switching, or (ii) IL-13Ralpha2 signalling was involved in inducing good gag-specific B cell immunity.	Glycosaminoglycans	197-200	interleukin 13 receptor subunit alpha 2	Homo sapiens	143-155
25107907-0	2014	Overexpression of Galnt3 in chondrocytes resulted in dwarfism due to the increase of mucin-type O-glycans and reduction of glycosaminoglycans.	Glycosaminoglycans	123-141	polypeptide N-acetylgalactosaminyltransferase 3	Mus musculus	18-24
25107907-9	2014	These findings indicate that overexpression of Galnt3 in chondrocytes caused dwarfism due to the increase of mucin-type O-glycans and the reduction of GAGs, probably through competition with xylosyltransferases, which initiate GAG chains by attaching O-linked xylose to serine residues, suggesting a negative effect of Galnt family proteins on Acan deposition in addition to the positive effect of Galnt3 on chondrocyte maturation.	Glycosaminoglycans	151-154	polypeptide N-acetylgalactosaminyltransferase 3	Mus musculus	47-53
25231261-1	2014	BACKGROUND: Hunter Syndrome is an X-linked lysosomal storage disorder due to the deficit of iduronate 2-sulfatase, an enzyme catalysing the degradation of the glycosaminoglycans (GAG) dermatan- and heparan-sulfate.	Glycosaminoglycans	159-177	iduronate 2-sulfatase	Homo sapiens	92-113
25198673-2	2014	We also examined mucosal expression of IL-6, which stimulates excess GAG synthesis in disorders such as Grave"s ophthalmopathy.	Glycosaminoglycans	69-72	interleukin 6	Homo sapiens	39-43
24931141-1	2014	A three-nucleotide (GAG) deletion (DeltaE) in TorsinA (TOR1A) has been identified as the most common cause of dominantly inherited early-onset torsion dystonia (DYT1).	Glycosaminoglycans	20-23	torsin family 1 member A	Homo sapiens	55-60
24699889-3	2014	Genistein has been shown previously to inhibit GAG synthesis in MPS fibroblasts, presumably through inhibition of tyrosine kinase activity of the epidermal growth factor receptor (EGFR).	Glycosaminoglycans	47-50	epidermal growth factor receptor	Homo sapiens	146-178
24699889-7	2014	This suggests that GAG synthesis is not exclusively regulated through the tyrosine kinase activity of the EGFR.	Glycosaminoglycans	19-22	epidermal growth factor receptor	Homo sapiens	106-110
24880028-6	2014	CD8+ T cells are vital for clearance of WNF infected cells from the CNS, whereas TLR-3 and TLR-7 mediated anti-virus response through increased serum inflammatory cytokines to disrupt the BBB providing infected leucocytes and free virus access to the CNS (so called Trojan horse) Cellular virus attachment factors, promoting FV cell entry are widely distributed and include DC-SIGN (that detects complex carbohydrate molecules); Glycosamino glycans (GAG), Heparan sulphate(HSPG) Semaphorin 7A, Low Density Lipid receptors (LDLR); these are not FV specific virus entry receptors.	Glycosaminoglycans	429-448	toll like receptor 7	Equus caballus	91-96
24880028-6	2014	CD8+ T cells are vital for clearance of WNF infected cells from the CNS, whereas TLR-3 and TLR-7 mediated anti-virus response through increased serum inflammatory cytokines to disrupt the BBB providing infected leucocytes and free virus access to the CNS (so called Trojan horse) Cellular virus attachment factors, promoting FV cell entry are widely distributed and include DC-SIGN (that detects complex carbohydrate molecules); Glycosamino glycans (GAG), Heparan sulphate(HSPG) Semaphorin 7A, Low Density Lipid receptors (LDLR); these are not FV specific virus entry receptors.	Glycosaminoglycans	450-453	toll like receptor 3	Equus caballus	81-86
24880028-6	2014	CD8+ T cells are vital for clearance of WNF infected cells from the CNS, whereas TLR-3 and TLR-7 mediated anti-virus response through increased serum inflammatory cytokines to disrupt the BBB providing infected leucocytes and free virus access to the CNS (so called Trojan horse) Cellular virus attachment factors, promoting FV cell entry are widely distributed and include DC-SIGN (that detects complex carbohydrate molecules); Glycosamino glycans (GAG), Heparan sulphate(HSPG) Semaphorin 7A, Low Density Lipid receptors (LDLR); these are not FV specific virus entry receptors.	Glycosaminoglycans	450-453	toll like receptor 7	Equus caballus	91-96
25008926-8	2014	This VRC difference was reflected by a significantly higher frequency in the Barbados cohort of HLA-B*27/57/58:01/81:01-associated Gag escape mutations previously shown to incur a fitness cost on the virus (P = 0.004), a difference between the two cohorts that remained statistically significant even in subjects not expressing these protective alleles (P = 0.01).	Glycosaminoglycans	131-134	major histocompatibility complex, class I, B	Homo sapiens	96-101
24970887-2	2014	Because matrix glycosaminoglycan (GAG) is known to be important for these functions, we characterized the structural features of human beta-defensin 6 (hBD6) and GAG interaction using a combination of structural and in silico analyses.	Glycosaminoglycans	15-32	defensin beta 106B	Homo sapiens	135-150
25228841-7	2014	RESULTS: SKI306X and PV inhibited IL-1beta-induced GAG release from cartilage explants, and SKI306X, CM, PV, and TK inhibited IL-1beta-induced MMP gene expression.	Glycosaminoglycans	51-54	interleukin 1 beta	Homo sapiens	34-42
25196597-7	2014	Synovium derived mesenchymal stem cells harboring the SEMD mutation exhibited lower glycosaminoglycan content than those of WT MATN3 in response to TGF-beta.	Glycosaminoglycans	84-101	transforming growth factor beta 1	Homo sapiens	148-156
24970887-2	2014	Because matrix glycosaminoglycan (GAG) is known to be important for these functions, we characterized the structural features of human beta-defensin 6 (hBD6) and GAG interaction using a combination of structural and in silico analyses.	Glycosaminoglycans	15-32	defensin beta 106B	Homo sapiens	152-156
24970887-2	2014	Because matrix glycosaminoglycan (GAG) is known to be important for these functions, we characterized the structural features of human beta-defensin 6 (hBD6) and GAG interaction using a combination of structural and in silico analyses.	Glycosaminoglycans	34-37	defensin beta 106B	Homo sapiens	135-150
24970887-2	2014	Because matrix glycosaminoglycan (GAG) is known to be important for these functions, we characterized the structural features of human beta-defensin 6 (hBD6) and GAG interaction using a combination of structural and in silico analyses.	Glycosaminoglycans	34-37	defensin beta 106B	Homo sapiens	152-156
25345098-3	2014	(1) The absence of GUSB activity leads to the progressive accumulation of undegraded glycosaminoglycans (GAGs) in many tissues of the body.	Glycosaminoglycans	85-103	glucuronidase, beta	Mus musculus	19-23
25345098-3	2014	(1) The absence of GUSB activity leads to the progressive accumulation of undegraded glycosaminoglycans (GAGs) in many tissues of the body.	Glycosaminoglycans	105-109	glucuronidase, beta	Mus musculus	19-23
24958728-2	2014	Evidence exists that the collagenase activity of CatK is promoted by chondroitin sulfate (CS), a sulfated glycosaminoglycan.	Glycosaminoglycans	106-123	cathepsin K	Homo sapiens	49-53
24970887-3	2014	Our results showed that GAG model compounds, a pentasaccharide (fondaparinux, FX) and an octasaccharide heparin derivative (dp8) bind to the alpha-helix and in the loops between the beta2 and beta3 strands, inducing the formation of a ternary complex with a 2:1 hBD6:FX stoichiometry.	Glycosaminoglycans	24-27	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	182-197
24970887-3	2014	Our results showed that GAG model compounds, a pentasaccharide (fondaparinux, FX) and an octasaccharide heparin derivative (dp8) bind to the alpha-helix and in the loops between the beta2 and beta3 strands, inducing the formation of a ternary complex with a 2:1 hBD6:FX stoichiometry.	Glycosaminoglycans	24-27	defensin beta 106B	Homo sapiens	262-266
24970887-8	2014	Despite the similarity to chemokines and hBD2, our data indicate different properties for the hBD6-GAG complex.	Glycosaminoglycans	99-102	defensin beta 106B	Homo sapiens	94-98
24708339-8	2014	Since binding to glycosaminoglycans (GAG) modulates the function of CXCL12, binding to heparin was analyzed.	Glycosaminoglycans	17-35	C-X-C motif chemokine ligand 12	Homo sapiens	68-74
24708339-8	2014	Since binding to glycosaminoglycans (GAG) modulates the function of CXCL12, binding to heparin was analyzed.	Glycosaminoglycans	37-40	C-X-C motif chemokine ligand 12	Homo sapiens	68-74
25035928-7	2014	Also, induction of chondrogenesis was more effective in rRV-TGFB-transduced hSD-MSCs as shown by RT-PCR for chondrogenic markers, toluidine blue staining and glycosaminoglycan (GAG)/DNA ratio.	Glycosaminoglycans	158-175	transforming growth factor beta 1	Homo sapiens	60-64
25035928-7	2014	Also, induction of chondrogenesis was more effective in rRV-TGFB-transduced hSD-MSCs as shown by RT-PCR for chondrogenic markers, toluidine blue staining and glycosaminoglycan (GAG)/DNA ratio.	Glycosaminoglycans	177-180	transforming growth factor beta 1	Homo sapiens	60-64
24741089-0	2014	Induction of Gag-specific CD4 T cell responses during acute HIV infection is associated with improved viral control.	Glycosaminoglycans	13-16	CD4 molecule	Homo sapiens	26-29
24658508-1	2014	Hyaluronan (HA) is a glycosaminoglycan synthesized directly into the extracellular matrix by three hyaluronan synthases (HAS1, HAS2, and HAS3).	Glycosaminoglycans	21-38	hyaluronan synthase 3	Homo sapiens	137-141
24547725-9	2014	Both tofacitinib (JAK-inhibitor) and oxozeaenol (TAK1 inhibitor) significantly increased the GAG content of the pellets in osteoarthritis (OA)-like conditions.	Glycosaminoglycans	93-96	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	49-53
26344746-12	2014	In the HIV-infected adults, increased CD8+ T-cell responses to Gag, RT and viral protease peptides were detected.	Glycosaminoglycans	63-66	CD8a molecule	Homo sapiens	38-41
24891401-9	2014	Treatment of fibroblasts with heparinase and chondroitinase to cleave glycosaminoglycan chains abrogated the inhibitory effects of CXCL10 on cell migration.	Glycosaminoglycans	70-87	chemokine (C-X-C motif) ligand 10	Mus musculus	131-137
25000564-3	2014	Glycosaminoglycans and certain negatively charged phospholipids, like phosphatidylserine, bind to PCI and modulate its activity.	Glycosaminoglycans	0-18	serpin family A member 5	Homo sapiens	98-101
25610529-7	2014	The chondroprotective effects of kartogenin on IL-1beta-induced release of sulfated glycosaminoglycans from articular cartilage explants, reduction in safranin O staining of neocartilage discs as well as a reduction in aggrecan G1-ITEGE neoepitope in chondrocyte and explant cartilage cultures were observed.	Glycosaminoglycans	84-102	interleukin 1 beta	Homo sapiens	47-55
25101330-2	2014	GALNS is essential for breakdown of glycosaminoglycans.	Glycosaminoglycans	36-54	galactosamine (N-acetyl)-6-sulfatase	Homo sapiens	0-5
24741089-8	2014	Interestingly the induction of Gag-specific CD4 T cell responses in acute HIV infection was significantly inversely correlated with viral set point in chronic HIV infection (R = -0.5; P = 0.03), while the cumulative contribution of Env-specific CD4 T cell responses showed the reverse effect.	Glycosaminoglycans	31-34	CD4 molecule	Homo sapiens	44-47
24741089-8	2014	Interestingly the induction of Gag-specific CD4 T cell responses in acute HIV infection was significantly inversely correlated with viral set point in chronic HIV infection (R = -0.5; P = 0.03), while the cumulative contribution of Env-specific CD4 T cell responses showed the reverse effect.	Glycosaminoglycans	31-34	endogenous retrovirus group K member 20	Homo sapiens	232-235
24741089-8	2014	Interestingly the induction of Gag-specific CD4 T cell responses in acute HIV infection was significantly inversely correlated with viral set point in chronic HIV infection (R = -0.5; P = 0.03), while the cumulative contribution of Env-specific CD4 T cell responses showed the reverse effect.	Glycosaminoglycans	31-34	CD4 molecule	Homo sapiens	245-248
24456068-7	2014	The subsequent 3-day CTGF treatment further enhanced the cellular production of TNC and DCN, whereas CTGF treatment alone without the vibratory preconditioning significantly promoted the synthesis of collagen I (Col 1) and sulfated glycosaminoglycans (sGAGs).	Glycosaminoglycans	232-250	cellular communication network factor 2	Homo sapiens	101-105
24589453-6	2014	Lack of TSP-4 in medial soleus, red skeletal muscle with predominant oxidative metabolism, is associated with decreased levels of several specific glycosaminoglycan modifications, decreased expression of a TGFbeta receptor beta-glycan, decreased activity of lipoprotein lipase, which associates with vascular cell surfaces by binding to glycosaminoglycans, and decreased uptake of VLDL.	Glycosaminoglycans	337-355	tumor suppressor region 4	Mus musculus	8-13
24837770-0	2014	Group M consensus Gag and Nef peptides are as efficient at detecting clade A1 and D cross-subtype T-cell functions as subtype-specific consensus peptides.	Glycosaminoglycans	18-21	immunoglobulin kappa variable 2D-30	Homo sapiens	75-83
24239005-5	2014	After 56 days, MSC-laden constructs underwent a marked reversal in their growth trajectory, with significant declines in glycosaminoglycan content and mechanical properties.	Glycosaminoglycans	121-138	musculin	Homo sapiens	15-18
24284199-8	2014	Transient TGF-beta3 produced the highest GAG synthesis rate, highest GAG retention ratio, and the highest binding affinity; collagen synthesis was elevated in TGF-beta3 supplementation groups over control, with the highest binding affinity observed in the transient supplementation group; both COMP synthesis and retention were lower than those for GAG and collagen.	Glycosaminoglycans	41-44	transforming growth factor beta 3	Homo sapiens	10-19
24284199-8	2014	Transient TGF-beta3 produced the highest GAG synthesis rate, highest GAG retention ratio, and the highest binding affinity; collagen synthesis was elevated in TGF-beta3 supplementation groups over control, with the highest binding affinity observed in the transient supplementation group; both COMP synthesis and retention were lower than those for GAG and collagen.	Glycosaminoglycans	69-72	transforming growth factor beta 3	Homo sapiens	10-19
24284199-8	2014	Transient TGF-beta3 produced the highest GAG synthesis rate, highest GAG retention ratio, and the highest binding affinity; collagen synthesis was elevated in TGF-beta3 supplementation groups over control, with the highest binding affinity observed in the transient supplementation group; both COMP synthesis and retention were lower than those for GAG and collagen.	Glycosaminoglycans	69-72	transforming growth factor beta 3	Homo sapiens	10-19
24290139-7	2014	GAG contents and elasticity of pellets decreased (1.4- and 2.6-fold, respectively, p&lt;0.05) following IL-1beta stimulation.	Glycosaminoglycans	0-3	interleukin 1 beta	Homo sapiens	104-112
25071396-2	2014	Hunter syndrome is a genetic disorder where iduronate-2-sulfatase (I2S), an enzyme that degrades glycosaminoglycans, is absent or deficient.	Glycosaminoglycans	97-115	iduronate 2-sulfatase	Homo sapiens	44-65
24790092-2	2014	ZG16p has been reported to bind both to glycosaminoglycans and mannose.	Glycosaminoglycans	40-58	zymogen granule protein 16	Homo sapiens	0-5
24412195-8	2014	Differences in transcript expression of NDST1, HS6ST2 and HS6ST3, three heparan sulfate biosynthetic enzymes, within splanchnic mesoderm cells compared to H9 cells correlate to changes in glycosaminoglycan structure.	Glycosaminoglycans	188-205	N-deacetylase and N-sulfotransferase 1	Homo sapiens	40-45
24412195-8	2014	Differences in transcript expression of NDST1, HS6ST2 and HS6ST3, three heparan sulfate biosynthetic enzymes, within splanchnic mesoderm cells compared to H9 cells correlate to changes in glycosaminoglycan structure.	Glycosaminoglycans	188-205	heparan sulfate 6-O-sulfotransferase 2	Homo sapiens	47-53
24412195-8	2014	Differences in transcript expression of NDST1, HS6ST2 and HS6ST3, three heparan sulfate biosynthetic enzymes, within splanchnic mesoderm cells compared to H9 cells correlate to changes in glycosaminoglycan structure.	Glycosaminoglycans	188-205	heparan sulfate 6-O-sulfotransferase 3	Homo sapiens	58-64
25071396-2	2014	Hunter syndrome is a genetic disorder where iduronate-2-sulfatase (I2S), an enzyme that degrades glycosaminoglycans, is absent or deficient.	Glycosaminoglycans	97-115	iduronate 2-sulfatase	Homo sapiens	67-70
25071396-8	2014	Idursulfase (recombinant I2S) (Elaprase( ), Shire) enzyme replacement therapy (ERT), designed to address the underlying enzyme deficiency, is approved treatment and improves walking capacity and respiratory function, and reduces spleen and liver size and urinary glycosaminoglycan levels.	Glycosaminoglycans	263-280	iduronate 2-sulfatase	Homo sapiens	0-11
25071396-8	2014	Idursulfase (recombinant I2S) (Elaprase( ), Shire) enzyme replacement therapy (ERT), designed to address the underlying enzyme deficiency, is approved treatment and improves walking capacity and respiratory function, and reduces spleen and liver size and urinary glycosaminoglycan levels.	Glycosaminoglycans	263-280	iduronate 2-sulfatase	Homo sapiens	25-28
24114722-2	2014	Gag-specific responses were measured by IFN-gamma ELISpot.	Glycosaminoglycans	0-3	interferon gamma	Homo sapiens	40-49
25190157-16	2014	Both the radiological findings and increased urine GAG are important clues to diagnose MPS VI.Large decrease or absence of ARSB activity is diagnostic for MPS VI.Four novel mutations of ARSB gene were identified.	Glycosaminoglycans	51-54	arylsulfatase B	Homo sapiens	186-190
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
24671416-3	2014	In a previous work, we showed that glycosaminoglycan-induced GAPDH prefibrillar species accelerate the conversion of alpha-synuclein to fibrils.	Glycosaminoglycans	35-52	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	61-66
24671416-3	2014	In a previous work, we showed that glycosaminoglycan-induced GAPDH prefibrillar species accelerate the conversion of alpha-synuclein to fibrils.	Glycosaminoglycans	35-52	synuclein alpha	Homo sapiens	117-132
24671416-9	2014	Because GAPDH can be secreted outside the cell where glycosaminoglycans are present, it seems plausible that GAPDH protofibrils could be assembled in the extracellular space kidnapping alpha-synuclein toxic oligomers.	Glycosaminoglycans	53-71	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	8-13
24671416-9	2014	Because GAPDH can be secreted outside the cell where glycosaminoglycans are present, it seems plausible that GAPDH protofibrils could be assembled in the extracellular space kidnapping alpha-synuclein toxic oligomers.	Glycosaminoglycans	53-71	synuclein alpha	Homo sapiens	185-200
24834918-0	2014	ALIX is recruited temporarily into HIV-1 budding sites at the end of gag assembly.	Glycosaminoglycans	69-72	programmed cell death 6 interacting protein	Homo sapiens	0-4
24740510-4	2014	Single-genome sequencing was performed to detect viral mutations (variants) within seven HLA-B*5701-restricted epitopes in Gag (n = 4) and Nef (n = 3) in six untreated HLA-B*5701 subjects followed from early infection up to 7 y.	Glycosaminoglycans	123-126	major histocompatibility complex, class I, B	Homo sapiens	89-94
24740510-4	2014	Single-genome sequencing was performed to detect viral mutations (variants) within seven HLA-B*5701-restricted epitopes in Gag (n = 4) and Nef (n = 3) in six untreated HLA-B*5701 subjects followed from early infection up to 7 y.	Glycosaminoglycans	123-126	major histocompatibility complex, class I, B	Homo sapiens	168-173
24010680-6	2014	We observed that C-clade-infected individuals with HLA-B*07:02 target a broader range of Gag epitopes, and to higher magnitudes, than do individuals infected with B-clade infection.	Glycosaminoglycans	89-92	major histocompatibility complex, class I, B	Homo sapiens	51-56
24010680-10	2014	These data support earlier studies suggesting that increased breadth of the Gag-specific CD8(+) T cell response may contribute to improved HIV immune control irrespective of the particular HLA molecules expressed.	Glycosaminoglycans	76-79	CD8a molecule	Homo sapiens	89-92
24889233-4	2014	Nine new CD4(+) T cell epitopes were identified, 3 encoded by gag, 1 by pol, and 5 by env.	Glycosaminoglycans	62-65	CD4 antigen	Mus musculus	9-12
24501417-10	2014	We demonstrate functional constraints imposed by HIV clade relating to the residue at Gag 173 that explain the differential clade-specific escape patterns in HLA-B*57:03 subjects.	Glycosaminoglycans	86-89	major histocompatibility complex, class I, B	Homo sapiens	158-163
23900850-10	2014	We analyzed the electrostatic potential of the zCXL1 structure and identified the likely heparin-binding site for glycosaminoglycans (GAGs).	Glycosaminoglycans	114-132	CX chemokine ligand 34b, duplicate 11	Danio rerio	47-52
24500857-4	2014	Twenty-seven individuals had mutations in THAP1-most with the founder indel mutation-but two had different THAP1 mutations, 8 had mutations in GNAL, and 1 had a de novo GAG deletion in torsin 1A (TOR1A) (dystonia 1 [DYT1]).	Glycosaminoglycans	169-172	torsin family 1 member A	Homo sapiens	185-194
24176719-0	2014	EXTL2 controls liver regeneration and aortic calcification through xylose kinase-dependent regulation of glycosaminoglycan biosynthesis.	Glycosaminoglycans	105-122	exostosin-like glycosyltransferase 2	Mus musculus	0-5
24654599-0	2014	The ability of insulin to inhibit the formation of amyloid by pro-islet amyloid polypeptide processing intermediates is significantly reduced in the presence of sulfated glycosaminoglycans.	Glycosaminoglycans	170-188	insulin	Homo sapiens	15-22
24654599-4	2014	Here we show that insulin is a much less effective amyloid inhibitor of both IAPP and proIAPP processing intermediates in vitro in the presence of model glycosaminoglycans, but does inhibit the formation of amyloid by proIAPP processing intermediates in a homogeneous solution.	Glycosaminoglycans	153-171	insulin	Homo sapiens	18-25
24713822-7	2014	Hence, HCS mutations in Gag-p24 are likely to be severely deleterious in different HIV-1 subtype B backgrounds; however, some HCS mutations in both Gag-p24 and Env-gp120 fragments can be well tolerated.	Glycosaminoglycans	24-27	holocarboxylase synthetase	Homo sapiens	7-10
24713822-7	2014	Hence, HCS mutations in Gag-p24 are likely to be severely deleterious in different HIV-1 subtype B backgrounds; however, some HCS mutations in both Gag-p24 and Env-gp120 fragments can be well tolerated.	Glycosaminoglycans	148-151	holocarboxylase synthetase	Homo sapiens	7-10
24713822-7	2014	Hence, HCS mutations in Gag-p24 are likely to be severely deleterious in different HIV-1 subtype B backgrounds; however, some HCS mutations in both Gag-p24 and Env-gp120 fragments can be well tolerated.	Glycosaminoglycans	148-151	holocarboxylase synthetase	Homo sapiens	126-129
24577103-5	2014	Fgf18 was the extracellular and secreted factor that decreased glycosaminoglycan release and depletion from the cartilage, and enhanced proliferation of articular chondrocytes.	Glycosaminoglycans	63-80	fibroblast growth factor 18	Rattus norvegicus	0-5
24429370-5	2014	Gag-specific CD4(+) and CD8(+) T cells were also detectable in foreskin of SIV- and SHIV-infected animals and were at least comparable in magnitude to those in peripheral blood.	Glycosaminoglycans	0-3	CD4 molecule	Homo sapiens	13-16
24491910-7	2014	Enhanced accumulation of cartilage-associated glycosaminoglycans by hMSCs incubated with TGF-beta3-loaded microspheres was seen and positive staining for collagen type II and proteoglycan confirmed successful in vitro chondrogenesis.	Glycosaminoglycans	46-64	transforming growth factor beta 3	Homo sapiens	89-98
24706838-10	2014	The combined structural and functional studies provide mechanistic insights into the pathogenic contribution of glycosaminoglycan in SAA1.1-mediated AA amyloid formation.	Glycosaminoglycans	112-129	serum amyloid A1	Homo sapiens	133-137
24338203-8	2014	Real-time-quantitative PCR showed that sesamin promoted the expression of the genes encoding the core protein (ACAN) of the major CS-PG aggrecan and the biosynthetic enzymes (XYLT1, XYLT2, CHSY1 and CHPF) required for the synthesis of CS-GAG side chains.	Glycosaminoglycans	238-241	aggrecan	Homo sapiens	111-115
24496449-6	2014	Specifically, we show that, in addition to interacting with Wnt, GPC3 and Frizzled interact directly through the glycosaminoglycan chains of GPC3, indicating that this glypican stimulates the formation of signaling complexes between Wnt and Frizzled.	Glycosaminoglycans	113-130	glypican 3	Homo sapiens	65-69
24496449-6	2014	Specifically, we show that, in addition to interacting with Wnt, GPC3 and Frizzled interact directly through the glycosaminoglycan chains of GPC3, indicating that this glypican stimulates the formation of signaling complexes between Wnt and Frizzled.	Glycosaminoglycans	113-130	glypican 3	Homo sapiens	141-145
24176719-0	2014	EXTL2 controls liver regeneration and aortic calcification through xylose kinase-dependent regulation of glycosaminoglycan biosynthesis.	Glycosaminoglycans	105-122	FAM20B, glycosaminoglycan xylosylkinase	Mus musculus	67-80
24176719-13	2014	Taken together, these results indicated that the EXTL2-dependent mechanism that regulates GAG biosynthesis is important for the maintenance of tissue homeostasis under pathological conditions, that is, lack of EXTL2 causes GAG overproduction and structural changes of GAGs associated with pathological processes.	Glycosaminoglycans	90-93	exostosin-like glycosyltransferase 2	Mus musculus	49-54
24176719-13	2014	Taken together, these results indicated that the EXTL2-dependent mechanism that regulates GAG biosynthesis is important for the maintenance of tissue homeostasis under pathological conditions, that is, lack of EXTL2 causes GAG overproduction and structural changes of GAGs associated with pathological processes.	Glycosaminoglycans	90-93	exostosin-like glycosyltransferase 2	Mus musculus	210-215
24176719-13	2014	Taken together, these results indicated that the EXTL2-dependent mechanism that regulates GAG biosynthesis is important for the maintenance of tissue homeostasis under pathological conditions, that is, lack of EXTL2 causes GAG overproduction and structural changes of GAGs associated with pathological processes.	Glycosaminoglycans	223-226	exostosin-like glycosyltransferase 2	Mus musculus	49-54
24176719-13	2014	Taken together, these results indicated that the EXTL2-dependent mechanism that regulates GAG biosynthesis is important for the maintenance of tissue homeostasis under pathological conditions, that is, lack of EXTL2 causes GAG overproduction and structural changes of GAGs associated with pathological processes.	Glycosaminoglycans	223-226	exostosin-like glycosyltransferase 2	Mus musculus	210-215
24343103-3	2014	At the cellular level, deficiency in beta-glu activity leads to abnormal accumulation of glycosaminoglycans (GAGs), and secondary accumulation of GM2 and GM3 gangliosides, which have been linked to neuroinflammation.	Glycosaminoglycans	89-107	glucuronidase beta	Canis lupus familiaris	37-45
24744753-2	2014	However, Vpr and homologous HIV-2, and SIV Vpx are the only viral auxiliary proteins specifically incorporated into virus particles through direct interaction with the Gag precursor, indicating that this presence in the core of the mature virions is mainly required for optimal establishment of the early steps of the virus life cycle in the newly infected cell.	Glycosaminoglycans	168-171	Vpr	Human immunodeficiency virus 1	9-12
24127863-8	2014	Forced expression of TGF-beta1 in vivo enhanced versican, XT-I, GlcAT-I, and C4ST-I expression and PG-GAG deposition in rat lungs.	Glycosaminoglycans	102-105	transforming growth factor, beta 1	Rattus norvegicus	21-30
24462977-4	2014	Drosophila mutant embryos deficient for UDP-glucose dehydrogenase activity (Ugdh, required for GAG synthesis) exhibit abnormal Fgf, Wnt and TGFss signaling and die during gastrulation, indicating a broad and critical role for proteoglycans during early embryonic development (Lin et al., 1999; Lin and Perrimon 2000) (Hacker et al., 1997).	Glycosaminoglycans	95-98	UDP-glucose dehydrogenase	Mus musculus	76-80
24462977-4	2014	Drosophila mutant embryos deficient for UDP-glucose dehydrogenase activity (Ugdh, required for GAG synthesis) exhibit abnormal Fgf, Wnt and TGFss signaling and die during gastrulation, indicating a broad and critical role for proteoglycans during early embryonic development (Lin et al., 1999; Lin and Perrimon 2000) (Hacker et al., 1997).	Glycosaminoglycans	95-98	branchless	Drosophila melanogaster	127-130
24046088-0	2014	Structural requirements of glycosaminoglycans for their interaction with HIV-1 envelope glycoprotein gp120.	Glycosaminoglycans	27-45	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	101-106
24046088-2	2014	We aimed to determine the general structural features of glycosaminoglycans that enable their binding to gp120, by surface plasmon resonance.	Glycosaminoglycans	57-75	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	105-110
24266751-6	2014	Glycosaminoglycan storage was reduced by 60% (P&lt;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
24403584-0	2014	The Nef-like effect of murine leukemia virus glycosylated gag on HIV-1 infectivity is mediated by its cytoplasmic domain and depends on the AP-2 adaptor complex.	Glycosaminoglycans	58-61	Nef	Human immunodeficiency virus 1	4-7
24150207-5	2014	The increases induced by CCT diet in the plasma levels of cholesterol, triglycerides, high-density lipoprotein, very-low-density lipoprotein, and low-density lipoprotein were completely attenuated with GAG treatment.	Glycosaminoglycans	202-205	FLVCR heme transporter 2	Rattus norvegicus	25-28
24150207-6	2014	Consistently, alterations induced by CCT diet in the levels of plasma lecithin cholesterol acyltransferase and lipoprotein lipase activities were restored to baseline levels with GAG treatment.	Glycosaminoglycans	179-182	FLVCR heme transporter 2	Rattus norvegicus	37-40
24150207-6	2014	Consistently, alterations induced by CCT diet in the levels of plasma lecithin cholesterol acyltransferase and lipoprotein lipase activities were restored to baseline levels with GAG treatment.	Glycosaminoglycans	179-182	lecithin cholesterol acyltransferase	Rattus norvegicus	70-106
24150207-6	2014	Consistently, alterations induced by CCT diet in the levels of plasma lecithin cholesterol acyltransferase and lipoprotein lipase activities were restored to baseline levels with GAG treatment.	Glycosaminoglycans	179-182	lipoprotein lipase	Rattus norvegicus	111-129
24150207-7	2014	Coherently, histology revealed a decrease associated with GAG treatment in the CCT-diet-induced foam cells (in aorta), tubular damages (kidney), and lipid accumulations (liver).	Glycosaminoglycans	58-61	FLVCR heme transporter 2	Rattus norvegicus	79-82
24326668-10	2014	Overexpression of Hs3st1 in MST-10H cells resulted in a change in the composition of heparan sulfate (HS)/HP and CS/dermatan sulfate (DS) glycosaminoglycans.	Glycosaminoglycans	138-156	heparan sulfate (glucosamine) 3-O-sulfotransferase 1	Mus musculus	18-24
24501198-4	2014	In this study, we have shown that TSG-6 inhibits chemokine-stimulated transendothelial migration of neutrophils via a direct interaction (KD, ~ 25 nM) between TSG-6 and the glycosaminoglycan binding site of CXCL8, which antagonizes the association of CXCL8 with heparin.	Glycosaminoglycans	173-190	TNF alpha induced protein 6	Homo sapiens	34-39
24501198-4	2014	In this study, we have shown that TSG-6 inhibits chemokine-stimulated transendothelial migration of neutrophils via a direct interaction (KD, ~ 25 nM) between TSG-6 and the glycosaminoglycan binding site of CXCL8, which antagonizes the association of CXCL8 with heparin.	Glycosaminoglycans	173-190	TNF alpha induced protein 6	Homo sapiens	159-164
24501198-4	2014	In this study, we have shown that TSG-6 inhibits chemokine-stimulated transendothelial migration of neutrophils via a direct interaction (KD, ~ 25 nM) between TSG-6 and the glycosaminoglycan binding site of CXCL8, which antagonizes the association of CXCL8 with heparin.	Glycosaminoglycans	173-190	C-X-C motif chemokine ligand 8	Homo sapiens	207-212
24501198-4	2014	In this study, we have shown that TSG-6 inhibits chemokine-stimulated transendothelial migration of neutrophils via a direct interaction (KD, ~ 25 nM) between TSG-6 and the glycosaminoglycan binding site of CXCL8, which antagonizes the association of CXCL8 with heparin.	Glycosaminoglycans	173-190	C-X-C motif chemokine ligand 8	Homo sapiens	251-256
24501198-5	2014	Furthermore, we found that TSG-6 impairs the binding of CXCL8 to cell surface glycosaminoglycans and the transport of CXCL8 across an endothelial cell monolayer.	Glycosaminoglycans	78-96	TNF alpha induced protein 6	Homo sapiens	27-32
24501198-5	2014	Furthermore, we found that TSG-6 impairs the binding of CXCL8 to cell surface glycosaminoglycans and the transport of CXCL8 across an endothelial cell monolayer.	Glycosaminoglycans	78-96	C-X-C motif chemokine ligand 8	Homo sapiens	56-61
24611521-7	2014	One highly overexpressed gene in the JCTM in both arrays, that for heparan sulfate 3-O-sulfotransferase-1 precursor, is thought to be somewhat unique, and could affect the glycosaminoglycan functionality in the extracellular matrix (ECM).	Glycosaminoglycans	172-189	heparan sulfate-glucosamine 3-sulfotransferase 1	Homo sapiens	67-105
24371068-2	2014	Here, we investigated the reversion kinetics of Gag(181-189)CM9 CD8(TL) escape-associated compensatory mutations in simian immunodeficiency virus (SIV)-infected macaques.	Glycosaminoglycans	48-51	CD8a molecule	Homo sapiens	64-67
24505475-6	2014	However, the ability of moDC transduced with ubiquitinated gag gene to upregulate co-stimulatory molecules was reduced, whilst no difference in moDC maturation was observed with a control ubiquitinated and non-ubiquitinated MART gene.	Glycosaminoglycans	59-62	septin 4	Homo sapiens	224-228
24411223-4	2014	alpha-L-iduronidase participates in glycosaminoglycan (GAG) catabolism and its insufficiency causes progressive GAG accumulation and onset of the MPS I-H phenotype, which consists of multiple somatic and neurological defects.	Glycosaminoglycans	55-58	alpha-L-iduronidase	Homo sapiens	0-19
24411223-6	2014	We previously showed that 2-week treatment with the designer aminoglycoside NB84 restored enough alpha-L-iduronidase function via PTC suppression to reduce tissue GAG accumulation in the Idua(tm1Kmke) MPS I-H mouse model, which carries a PTC homologous to the human IDUA-W402X nonsense mutation.	Glycosaminoglycans	163-166	alpha-L-iduronidase	Homo sapiens	187-191
24586357-1	2014	The hyaluronic acid receptor for endocytosis Stabilin-2/HARE mediates systemic clearance of multiple glycosaminoglycans from the vascular and lymphatic circulations.	Glycosaminoglycans	101-119	stabilin 2	Danio rerio	45-55
24384406-8	2014	The MMP-13 inhibitory effect was also supported by the finding that ginsenosides F4 and Rg3 reduced glycosaminoglycan release from IL-1alpha-treated rabbit joint cartilage culture to some degree.	Glycosaminoglycans	100-117	matrix metallopeptidase 13	Homo sapiens	4-7
24384406-8	2014	The MMP-13 inhibitory effect was also supported by the finding that ginsenosides F4 and Rg3 reduced glycosaminoglycan release from IL-1alpha-treated rabbit joint cartilage culture to some degree.	Glycosaminoglycans	100-117	interleukin-1 alpha	Oryctolagus cuniculus	131-140
24505475-7	2014	Furthermore moDC transduced with ubiquitinated gag produced more IL-10 than transduction with unmodified gag.	Glycosaminoglycans	47-50	interleukin 10	Homo sapiens	65-70
24505475-8	2014	Thus failure of gag ubiquitination to enhance CD8 responses may be caused by suppression of moDC maturation.	Glycosaminoglycans	16-19	CD8a molecule	Homo sapiens	46-49
23639078-2	2014	This allele is identical to DPB1*17:01 except for a single nucleotide substitution (GAC GAG) at position 57, which changes the encoded amino acid from Asp to Glu.	Glycosaminoglycans	88-91	major histocompatibility complex, class II, DP beta 1	Homo sapiens	28-32
24280245-6	2014	RESULTS: BMP-4/-7 treatment resulted in stronger collagen type-II staining and significantly enhanced glycosaminoglycan (GAG) deposition (3.2-fold; *P &lt; 0.01) correlating with improved hardness (~1.7-fold; *P = 0.001) reaching 83% of native cartilage values after 28 days, a value not reached before 9 weeks without stimulation.	Glycosaminoglycans	102-119	bone morphogenetic protein 4	Homo sapiens	9-14
24280245-6	2014	RESULTS: BMP-4/-7 treatment resulted in stronger collagen type-II staining and significantly enhanced glycosaminoglycan (GAG) deposition (3.2-fold; *P &lt; 0.01) correlating with improved hardness (~1.7-fold; *P = 0.001) reaching 83% of native cartilage values after 28 days, a value not reached before 9 weeks without stimulation.	Glycosaminoglycans	121-124	bone morphogenetic protein 4	Homo sapiens	9-14
24535856-6	2014	Compared with the control group, hCDMP1 gene-transfected BMSCs had enhanced secretory abilities of Col II, GAG, and other cartilage-specific matrices, with a trend of promoting cartilage differentiation.	Glycosaminoglycans	107-110	growth differentiation factor 5	Homo sapiens	33-39
24465991-3	2014	Importantly, boosting CE-primed macaques with DNA expressing full-length p55(gag) increased both magnitude of CE responses and breadth of Gag immunity, demonstrating alteration of the hierarchy of epitope recognition in the presence of pre-existing CE-specific responses.	Glycosaminoglycans	138-141	H3 histone pseudogene 44	Homo sapiens	73-76
24573064-5	2014	One of the most studied eNOS gene polymorphisms is a c.894G&gt;T polymorphism that results in the conversion of Glu (GAG) to Asp (GAT) at position 298.	Glycosaminoglycans	117-120	nitric oxide synthase 3	Homo sapiens	24-28
24573064-5	2014	One of the most studied eNOS gene polymorphisms is a c.894G&gt;T polymorphism that results in the conversion of Glu (GAG) to Asp (GAT) at position 298.	Glycosaminoglycans	117-120	glycine-N-acyltransferase	Homo sapiens	130-133
24416431-11	2014	In contrast, patients with high RAC to both Env and Gag (n = 8) had higher annual CD4 loss (p = 0.034) and lower CD8 counts (p = 0.014).	Glycosaminoglycans	52-55	AKT serine/threonine kinase 1	Homo sapiens	32-35
24315874-1	2014	Surfen (bis-2-methyl-4-amino-quinolyl-6-carbamide) binds to glycosaminoglycans (GAGs) and has been shown to influence their function, and the function of proteoglycans (complexes of GAGs linked to a core protein).	Glycosaminoglycans	60-78	beta-carboline-induced seizures 2	Mus musculus	8-13
24399699-1	2014	BACKGROUND: Mucopolysaccharidosis II, also known as Hunter syndrome, is a rare, X-linked disease caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase, which catalyses a step in the catabolism of glycosaminoglycans.	Glycosaminoglycans	211-229	iduronate 2-sulfatase	Homo sapiens	144-165
24399699-18	2014	Idursulfase antibodies were detected in 31.7% of patients at the end of the study and they were related to a smaller reduction in urine glycosaminoglycan levels.	Glycosaminoglycans	136-153	iduronate 2-sulfatase	Homo sapiens	0-11
24416431-11	2014	In contrast, patients with high RAC to both Env and Gag (n = 8) had higher annual CD4 loss (p = 0.034) and lower CD8 counts (p = 0.014).	Glycosaminoglycans	52-55	CD4 molecule	Homo sapiens	82-85
24416431-11	2014	In contrast, patients with high RAC to both Env and Gag (n = 8) had higher annual CD4 loss (p = 0.034) and lower CD8 counts (p = 0.014).	Glycosaminoglycans	52-55	CD8a molecule	Homo sapiens	113-116
24949445-9	2014	Characteristic GAG deletion in DYT1 consistently with the diagnosis of torsion dystonia was confirmed in 1 case.	Glycosaminoglycans	15-18	torsin family 1 member A	Homo sapiens	31-35
24443026-5	2014	D4ST1-deficient EDS is caused by mutations in CHST14, which encodes an enzyme responsible for post-translational modification of GAG.	Glycosaminoglycans	129-132	carbohydrate sulfotransferase 14	Homo sapiens	0-5
24443026-5	2014	D4ST1-deficient EDS is caused by mutations in CHST14, which encodes an enzyme responsible for post-translational modification of GAG.	Glycosaminoglycans	129-132	carbohydrate sulfotransferase 14	Homo sapiens	46-52
25587532-3	2014	A major role in modulating cathepsin activities play glycosaminoglycans, which were found not only to facilitate their autocatalytic activation including at neutral pH, but also to critically modulate their activities such as in the case of the collagenolytic activity of cathepsin K.	Glycosaminoglycans	53-71	cathepsin K	Homo sapiens	272-283
25036482-1	2014	Sulfated glycosaminoglycans and sulfated lipids are involved in the biological functions of human matrix metalloproteinase 7 (MMP-7).	Glycosaminoglycans	9-27	matrix metallopeptidase 7	Homo sapiens	98-124
24158117-4	2014	Three doses (0.1, 0.4 and 1.6 mg/kg) of glycosaminoglycan were intravenously injected via mice tail, resulting in an extremely significant increase of activated partial thromboplastin time (APTT) and thrombin time (TT) (P &lt; 0.01), no significant change of prothrombin time (PT) (P &gt; 0.05), and a weaker anticoagulant effect than that of heparin sodium.	Glycosaminoglycans	40-57	coagulation factor II	Mus musculus	200-208
24158117-4	2014	Three doses (0.1, 0.4 and 1.6 mg/kg) of glycosaminoglycan were intravenously injected via mice tail, resulting in an extremely significant increase of activated partial thromboplastin time (APTT) and thrombin time (TT) (P &lt; 0.01), no significant change of prothrombin time (PT) (P &gt; 0.05), and a weaker anticoagulant effect than that of heparin sodium.	Glycosaminoglycans	40-57	coagulation factor II	Mus musculus	259-270
25036482-1	2014	Sulfated glycosaminoglycans and sulfated lipids are involved in the biological functions of human matrix metalloproteinase 7 (MMP-7).	Glycosaminoglycans	9-27	matrix metallopeptidase 7	Homo sapiens	126-131
23934400-6	2014	All three of these TFs specifically bind the GCC box-like element of the GAG motif required for MeJA-induced transcription of NtPMT1a, a gene encoding putrescine N-methyltransferase, the first committed step in the synthesis of the nicotine pyrrolidine ring.	Glycosaminoglycans	73-76	putrescine N-methyltransferase 1	Nicotiana tabacum	151-181
23844733-5	2014	CXC chemokines (such as interleukin-8) are bound to glycosaminoglycans on the endothelial surface and activate captured neutrophils, inducing expression of integrins.	Glycosaminoglycans	52-70	C-X-C motif chemokine ligand 8	Homo sapiens	24-37
24161523-10	2014	We show that the pug mutation disrupts Xylt1 activity and subcellular localization, leading to a reduction in GAG chains in pug mutants.	Glycosaminoglycans	110-113	xylosyltransferase 1	Homo sapiens	39-44
24850234-3	2014	Mucopolysaccharidosis IVA and VII (MPS IVA and VII) are caused by the deficiency of N-acetylgalactosamine-6-sulfate sulfatase and beta-D-glucuronidase, respectively, resulting in accumulation of C6S and other GAG(s).	Glycosaminoglycans	209-212	glucuronidase beta	Homo sapiens	130-150
25059704-1	2014	Mucopolysaccharidosis type II (Hunter syndrome, MPS II) is an X-linked lysosomal storage disorder caused by the deficit of iduronate 2-sulfatase (IDS), an enzyme involved in the glycosaminoglycans (GAGs) degradation.	Glycosaminoglycans	178-196	iduronate 2-sulfatase	Homo sapiens	146-149
24371208-4	2014	Here, we report a new treatment where neomycin and pentagalloyl glucose (PGG) were incorporated into glutaraldehyde cross-linking neomycin-PGG-Glutaraldehyde (NPG) to stabilize both glycosaminoglycans and elastin in porcine aortic valves.	Glycosaminoglycans	182-200	elastin	Rattus norvegicus	205-212
24334460-9	2014	A known GUSB function is the prevention of lysosomal accumulation of glycosaminoglycans (GAGs).	Glycosaminoglycans	69-87	glucuronidase, beta	Mus musculus	8-12
24059751-0	2014	Core functional sequence of C-terminal GAG-binding domain directs cellular uptake of IGFBP-3-derived peptides.	Glycosaminoglycans	39-42	insulin-like growth factor-binding protein 3	Cricetulus griseus	85-92
24059751-1	2014	The current study clarifies the role of the Glycosaminoglycan (GAG)-binding domain of insulin-like growth factor binding protein-3 (IGFBP-3) in cell penetration.	Glycosaminoglycans	44-61	insulin-like growth factor-binding protein 3	Cricetulus griseus	86-130
24059751-1	2014	The current study clarifies the role of the Glycosaminoglycan (GAG)-binding domain of insulin-like growth factor binding protein-3 (IGFBP-3) in cell penetration.	Glycosaminoglycans	44-61	insulin-like growth factor-binding protein 3	Cricetulus griseus	132-139
24059751-1	2014	The current study clarifies the role of the Glycosaminoglycan (GAG)-binding domain of insulin-like growth factor binding protein-3 (IGFBP-3) in cell penetration.	Glycosaminoglycans	63-66	insulin-like growth factor-binding protein 3	Cricetulus griseus	86-130
24059751-1	2014	The current study clarifies the role of the Glycosaminoglycan (GAG)-binding domain of insulin-like growth factor binding protein-3 (IGFBP-3) in cell penetration.	Glycosaminoglycans	63-66	insulin-like growth factor-binding protein 3	Cricetulus griseus	132-139
24059751-2	2014	The cell penetration function of IGFBP-3 has been mapped to an 18-residue GAG-binding domain in the C-terminal region that mobilizes cellular uptake and nuclear localization of unrelated proteins.	Glycosaminoglycans	74-77	insulin-like growth factor-binding protein 3	Cricetulus griseus	33-40
24145510-3	2013	We show that upon HIV-1 infection of primary human macrophages, Gag is recruited to preexisting compartments containing the scavenger receptor CD36, which then become VCCs.	Glycosaminoglycans	64-67	CD36 molecule	Homo sapiens	143-147
24426297-5	2013	The current internationally accepted test for diagnosis of EIA is the agar gel immune-diffusion test (AGID), which detects antibodies to the major gag gene (p26) product.	Glycosaminoglycans	147-150	transmembrane p24 trafficking protein 3	Homo sapiens	157-160
24089560-6	2013	In contrast, intracellular levels of Gag, Env, or Tax protein are affected by IFN-alpha treatment in T cells, primary lymphocytes, or 293T cells transfected with HTLV-1 or HTLV-2 molecular clones, demonstrating that IFN-alpha acts during the late stages of infection.	Glycosaminoglycans	37-40	interferon alpha 1	Homo sapiens	78-87
24089560-6	2013	In contrast, intracellular levels of Gag, Env, or Tax protein are affected by IFN-alpha treatment in T cells, primary lymphocytes, or 293T cells transfected with HTLV-1 or HTLV-2 molecular clones, demonstrating that IFN-alpha acts during the late stages of infection.	Glycosaminoglycans	37-40	interferon alpha 1	Homo sapiens	216-225
24252269-14	2013	CONCLUSIONS: Our data demonstrate that HERV-K(HML-2) release is predominantly mediated through a consensus PTAP motif and two auxiliary YPX(n)L motifs in the p15 protein of the Gag precursor.	Glycosaminoglycans	177-180	cyclin dependent kinase inhibitor 2B	Homo sapiens	158-161
23839780-10	2013	In the culture with SB216763 + TGF-beta3, significantly more GAG was deposited (P &lt; 0.05).	Glycosaminoglycans	61-64	transforming growth factor beta 3	Homo sapiens	31-40
24169120-9	2013	In the intermediate-dose group, there was also a marginal Gag p15 response increase from baseline to week 17 [2859 (1867-56,933), P = 0.06], and this change was significantly greater than in the placebo group [0 (-713 to 297), P = 0.016].	Glycosaminoglycans	58-61	cyclin dependent kinase inhibitor 2B	Homo sapiens	62-65
23860311-1	2013	Mucopolysaccharidosis VII (MPS VII) is due to deficient activity of the lysosomal enzyme beta-glucuronidase (GUSB) and results in the accumulation of glycosaminoglycans (GAGs).	Glycosaminoglycans	150-168	glucuronidase beta	Canis lupus familiaris	109-113
24014069-9	2013	The experiment revealed the BMP peptide as a robust stimulant for GAG production.	Glycosaminoglycans	66-69	bone morphogenetic protein 1	Homo sapiens	28-31
23897063-5	2013	Depletion of HIV-specific CD8(+) IL-10(+) cells from PBMCs led to upregulation of CD38 on CD14(+) monocytes together with increased IL-6 production, in response to gag stimulation.	Glycosaminoglycans	164-167	interleukin 10	Homo sapiens	33-38
23897063-5	2013	Depletion of HIV-specific CD8(+) IL-10(+) cells from PBMCs led to upregulation of CD38 on CD14(+) monocytes together with increased IL-6 production, in response to gag stimulation.	Glycosaminoglycans	164-167	CD38 molecule	Homo sapiens	82-86
23897063-5	2013	Depletion of HIV-specific CD8(+) IL-10(+) cells from PBMCs led to upregulation of CD38 on CD14(+) monocytes together with increased IL-6 production, in response to gag stimulation.	Glycosaminoglycans	164-167	CD14 molecule	Homo sapiens	90-94
23897063-5	2013	Depletion of HIV-specific CD8(+) IL-10(+) cells from PBMCs led to upregulation of CD38 on CD14(+) monocytes together with increased IL-6 production, in response to gag stimulation.	Glycosaminoglycans	164-167	interleukin 6	Homo sapiens	132-136
24970196-3	2013	Herein is the first report of a tetrameric assembly of the human chemokine CCL11, which was shown bound to the GAG Arixtra .	Glycosaminoglycans	111-114	C-C motif chemokine ligand 11	Homo sapiens	75-80
23994438-1	2013	In chick eyes, exogenous insulin prevents the choroidal thickening caused by wearing positive lenses and increases ocular elongation and scleral glycosaminoglycan (GAG) synthesis, an indicator of eye growth.	Glycosaminoglycans	145-162	insulin	Gallus gallus	25-32
23994438-1	2013	In chick eyes, exogenous insulin prevents the choroidal thickening caused by wearing positive lenses and increases ocular elongation and scleral glycosaminoglycan (GAG) synthesis, an indicator of eye growth.	Glycosaminoglycans	164-167	insulin	Gallus gallus	25-32
23994438-15	2013	Insulin increased scleral GAG synthesis in both RCS and CS eye-cups, having a greater effect in the CS eye-cups.	Glycosaminoglycans	26-29	insulin	Homo sapiens	0-7
23994438-20	2013	In vitro, as in vivo, insulin prevents choroidal thickening and increases scleral GAG synthesis.	Glycosaminoglycans	82-85	insulin	Homo sapiens	22-29
23994438-22	2013	Insulin might also cause the choroid to produce secondary signals that affect scleral GAG synthesis.	Glycosaminoglycans	86-89	insulin	Homo sapiens	0-7
23832854-6	2013	The CA4+ CECT attenuation was strongly and positively correlated with the GAG content of the meniscus regions (R(2)  = 0.89, p &lt; 0.001) at low concentrations (12 mgI/ml), while the Ioxaglate CECT attenuation was moderately and negatively correlated with the GAG content (R(2)  = 0.51, p = 0.03) at 60 mgI/ml.	Glycosaminoglycans	74-77	carbonic anhydrase 4	Bos taurus	4-7
23832854-6	2013	The CA4+ CECT attenuation was strongly and positively correlated with the GAG content of the meniscus regions (R(2)  = 0.89, p &lt; 0.001) at low concentrations (12 mgI/ml), while the Ioxaglate CECT attenuation was moderately and negatively correlated with the GAG content (R(2)  = 0.51, p = 0.03) at 60 mgI/ml.	Glycosaminoglycans	261-264	carbonic anhydrase 4	Bos taurus	4-7
23832854-7	2013	CECT can image ex vivo menisci, and the CA4+, compared to Ioxaglate, enhanced attenuation strongly correlates with the GAG content and distribution in bovine meniscus.	Glycosaminoglycans	119-122	carbonic anhydrase 4	Bos taurus	40-43
24048477-5	2013	The Capsid region of the viral Gag protein dictates susceptibility to MX2, and the block to infection occurs at a late post-entry step, with both the nuclear accumulation and chromosomal integration of nascent viral complementary DNA suppressed.	Glycosaminoglycans	31-34	MX dynamin like GTPase 2	Homo sapiens	70-73
24205138-9	2013	Interestingly, over-expression of serglycin lacking the glycosaminoglycan attachment sites failed to promote these cellular functions, suggesting that glycanation of serglycin is a pre-requisite for its oncogenic properties.	Glycosaminoglycans	56-73	serglycin	Homo sapiens	34-43
24156636-5	2013	Sequencing analysis of a conserved region of the gag gene showed that proviral expression in ESCs and iPSCs represents at least 11 of the 66 nearly full length HERV-K(HML-2) loci, with slightly varying patterns in individual cell lines.	Glycosaminoglycans	49-52	C-type lectin domain containing 10A	Homo sapiens	167-172
24167632-3	2013	To lower its effective dose, we precomplexed BMP-2 with the glycosaminoglycans (GAGs) dermatan sulfate (DS) or heparin (HP), prior to loading it into a hyaluronic acid (HA) hydrogel.	Glycosaminoglycans	60-78	bone morphogenetic protein 2	Rattus norvegicus	45-50
24167632-7	2013	Ectopic bone formation assays at subcutaneous sites in rats demonstrated that HA hydrogel-delivered BMP-2 precomplexed with GAG induced twice the volume of bone compared with BMP-2 delivered uncomplexed to GAG.	Glycosaminoglycans	124-127	bone morphogenetic protein 2	Rattus norvegicus	100-105
24167632-7	2013	Ectopic bone formation assays at subcutaneous sites in rats demonstrated that HA hydrogel-delivered BMP-2 precomplexed with GAG induced twice the volume of bone compared with BMP-2 delivered uncomplexed to GAG.	Glycosaminoglycans	206-209	bone morphogenetic protein 2	Rattus norvegicus	100-105
23777290-6	2013	Preconditioning with Wnt3a improved transforming growth factor-beta1 mediated chondrogenesis (30% more glycosaminoglycans/cell in average).	Glycosaminoglycans	103-121	Wnt family member 3A	Homo sapiens	21-26
23597573-6	2013	Further, G-CSF controlled T. cruzi-induced extracellular-matrix alterations of collagens (Col I and Col llI), hydroxyproline, and glycosaminoglycan contents and promoted compensatory cardiac remodeling; however, these responses were not sufficient to control T. cruzi-induced cardiomyocyte atrophy.	Glycosaminoglycans	130-147	colony stimulating factor 3 (granulocyte)	Mus musculus	9-14
23871542-8	2013	Increasing GAG sulfation improved equine tenocyte metabolic activity in normal serum (10% FBS), low serum (1% FBS), and IGF-1 supplemented media conditions.	Glycosaminoglycans	11-14	insulin like growth factor 1	Equus caballus	120-125
23707661-6	2013	RESULTS: MPO binds to the ECM proteins collagen IV and fibronectin, and this association is enhanced by the pre-incubation of these proteins with glycosaminoglycans.	Glycosaminoglycans	146-164	myeloperoxidase	Homo sapiens	9-12
23707661-6	2013	RESULTS: MPO binds to the ECM proteins collagen IV and fibronectin, and this association is enhanced by the pre-incubation of these proteins with glycosaminoglycans.	Glycosaminoglycans	146-164	fibronectin 1	Homo sapiens	55-66
23707661-7	2013	Correspondingly, an excess of glycosaminoglycans in solution during incubation inhibits the binding of MPO to collagen IV and fibronectin.	Glycosaminoglycans	30-48	myeloperoxidase	Homo sapiens	103-106
23707661-7	2013	Correspondingly, an excess of glycosaminoglycans in solution during incubation inhibits the binding of MPO to collagen IV and fibronectin.	Glycosaminoglycans	30-48	fibronectin 1	Homo sapiens	126-137
23871542-9	2013	Notably, previously reported dose-dependent changes in tenocyte bioactivity to soluble IGF-1 within the CG scaffold were replicated by using a single dose of soluble IGF-1 in scaffolds containing increasingly sulfated GAGs.	Glycosaminoglycans	218-222	insulin like growth factor 1	Equus caballus	166-171
23940048-12	2013	Our results confirm the interaction of Sema3A with CS-E containing glycosaminoglycans in the dense extracellular matrix of rat brain.	Glycosaminoglycans	67-85	semaphorin 3A	Rattus norvegicus	39-45
22610501-5	2013	GAG repeat genotype (4, 7, 8, 9, and 10 repeat alleles) was determined by capillary electrophoresis of PCR products from the repeat region of the GCL catalytic subunit (GCLC).	Glycosaminoglycans	0-3	glutamate-cysteine ligase catalytic subunit	Homo sapiens	146-149
22610501-5	2013	GAG repeat genotype (4, 7, 8, 9, and 10 repeat alleles) was determined by capillary electrophoresis of PCR products from the repeat region of the GCL catalytic subunit (GCLC).	Glycosaminoglycans	0-3	glutamate-cysteine ligase catalytic subunit	Homo sapiens	169-173
23777470-3	2013	beta-Glucuronidase (GUSB) is an important lysosomal enzyme involved in the degradation of glucuronate-containing glycosaminoglycan.	Glycosaminoglycans	113-130	glucuronidase beta	Homo sapiens	0-18
23777470-3	2013	beta-Glucuronidase (GUSB) is an important lysosomal enzyme involved in the degradation of glucuronate-containing glycosaminoglycan.	Glycosaminoglycans	113-130	glucuronidase beta	Homo sapiens	20-24
23917744-1	2013	Mucopolysaccharidosis type-I is caused by a deficiency of the lysosomal enzyme alpha-L-iduronidase, resulting in gradual deposition of glycosaminoglycans in multiple body organs, affecting physical appearance and system functioning.	Glycosaminoglycans	135-153	alpha-L-iduronidase	Homo sapiens	79-98
24065103-4	2013	In this study, we demonstrate that the binding of EDN to cells requires cell surface glycosaminoglycans (GAGs), and the binding strength between EDN and GAGs depends on the sulfation levels of GAGs.	Glycosaminoglycans	85-103	ribonuclease A family member 2	Homo sapiens	50-53
24065103-4	2013	In this study, we demonstrate that the binding of EDN to cells requires cell surface glycosaminoglycans (GAGs), and the binding strength between EDN and GAGs depends on the sulfation levels of GAGs.	Glycosaminoglycans	85-103	ribonuclease A family member 2	Homo sapiens	145-148
24027021-0	2013	Inhibition of oncostatin M in osteoarthritic synovial fluid enhances GAG production in osteoarthritic cartilage repair.	Glycosaminoglycans	69-72	oncostatin M	Homo sapiens	14-26
23531422-2	2013	METHODS: To improve our understanding of ECM protein-conducting polymer interactions, we have used Atomic Force Microscopy (AFM) to elucidate the interactions of fibronectin (FN) on polypyrrole (PPy) doped with different glycosaminoglycans.	Glycosaminoglycans	221-239	fibronectin 1	Homo sapiens	162-173
24107440-2	2013	Dysfunctional ARSB causes lysosomal accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	52-70	arylsulfatase B	Homo sapiens	14-18
24107440-2	2013	Dysfunctional ARSB causes lysosomal accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	72-75	arylsulfatase B	Homo sapiens	14-18
23707223-1	2013	Hunter disease or mucopolysaccharidosis type II (MPS II) is an X-linked recessive lysosomal disorder caused by the deficit of the enzyme iduronate-2-sulfatase (IDS), involved in the catabolism of the glycosaminoglycans heparan and dermatan sulfate.	Glycosaminoglycans	200-218	iduronate 2-sulfatase	Homo sapiens	137-158
23707223-1	2013	Hunter disease or mucopolysaccharidosis type II (MPS II) is an X-linked recessive lysosomal disorder caused by the deficit of the enzyme iduronate-2-sulfatase (IDS), involved in the catabolism of the glycosaminoglycans heparan and dermatan sulfate.	Glycosaminoglycans	200-218	iduronate 2-sulfatase	Homo sapiens	160-163
23531422-2	2013	METHODS: To improve our understanding of ECM protein-conducting polymer interactions, we have used Atomic Force Microscopy (AFM) to elucidate the interactions of fibronectin (FN) on polypyrrole (PPy) doped with different glycosaminoglycans.	Glycosaminoglycans	221-239	fibronectin 1	Homo sapiens	175-177
23726270-5	2013	Enzyme replacement therapy (ERT) using idursulfase (Elaprase ) was conducted to the patient and it improved hepatosplenomegaly, white blood cells and platelets number, and decreased the level of urinary glycosaminoglycan.	Glycosaminoglycans	203-220	iduronate 2-sulfatase	Homo sapiens	39-50
24908534-1	2013	Mucopolysaccharidosis Type II (Hunter syndrome) is a rare X-linked recessive storage disorder caused by deficiency of lysosomal enzyme iduronate-2-sulfatase, causing excess accumulation of glycosaminoglycans in the lysosomes resulting in cellular damage, organ failure and death.	Glycosaminoglycans	189-207	iduronate 2-sulfatase	Homo sapiens	135-156
23985378-5	2013	Overexpression of glycosaminoglycans in the aorta enhanced aortic calcification in chronic kidney disease in EXTL2 knockout mice.	Glycosaminoglycans	18-36	exostosin-like glycosyltransferase 2	Mus musculus	109-114
23985378-7	2013	Furthermore, removal of glycosaminoglycans in EXTL2 knockout and wild-type mice-derived vascular smooth muscle cells effectively suppressed calcium deposition in a high-phosphate environment.	Glycosaminoglycans	24-42	exostosin-like glycosyltransferase 2	Mus musculus	46-51
23357408-6	2013	The surface-bound glycocalyx glycosaminoglycan constituent heparan sulfate is crucial for CFH binding and function, both in recognition of host tissue and prevention of spontaneous complement activation via the alternative pathway.	Glycosaminoglycans	29-46	complement factor H	Homo sapiens	90-93
23939434-2	2013	Reduced glycosaminoglycan, in endothelial HSPGs syndecan and perlecan, is associated with diabetic cardiovascular complications but changes in core protein remain controversial.	Glycosaminoglycans	8-25	syndecan 1	Homo sapiens	48-56
23734945-3	2013	We have demonstrated that EXTL2 terminates chain elongation of GAGs (glycosaminoglycans), and thereby regulates GAG biosynthesis.	Glycosaminoglycans	69-87	exostosin-like glycosyltransferase 2	Mus musculus	26-31
23734945-3	2013	We have demonstrated that EXTL2 terminates chain elongation of GAGs (glycosaminoglycans), and thereby regulates GAG biosynthesis.	Glycosaminoglycans	69-87	melanoma antigen	Mus musculus	63-66
23820243-5	2013	The GAG Indel polymorphism led to deletion of E (glutamic) amino acid (aa) in the IGF1R of Egyptian water buffaloes compared with Indian buffalo.	Glycosaminoglycans	4-7	IGF1R	Bubalus bubalis	82-87
23951310-8	2013	We propose that CCL18 has regulatory properties inhibiting chemokine function when GAG-mediated presentation plays a role in receptor activation.	Glycosaminoglycans	83-86	C-C motif chemokine ligand 18	Homo sapiens	16-21
23597636-4	2013	In the present study, we characterized the developmental time course of the formation of PNNs in the mouse primary visual cortex, using the specific antibodies against the two PNN component proteins aggrecan and tenascin-R, or the lectin Wisteria floribunda agglutinin (WFA) that directly binds to glycosaminoglycan chains of chondroitin sulfate proteoglycans (CSPGs).	Glycosaminoglycans	298-315	pinin	Mus musculus	89-92
23702148-8	2013	Defects treated with PTHrP at the 4-6 weeks time window exhibited better regeneration (reconstitution of cartilage and subchondral bone) with minimal terminal differentiation (hypertrophy, ossification and matrix degradation), as well as enhanced chondrogenesis (cell shape, Col2 and GAG accumulation) compared with treatment at other time windows.	Glycosaminoglycans	284-287	parathyroid hormone-related protein	Oryctolagus cuniculus	21-26
23507659-0	2013	HIV-1-infected individuals in antiretroviral therapy react specifically with polyfunctional T-cell responses to Gag p24.	Glycosaminoglycans	112-115	transmembrane p24 trafficking protein 2	Homo sapiens	116-119
23507659-6	2013	The Gag p24 response was more polyfunctional than corresponding responses observed in viremic individuals.	Glycosaminoglycans	4-7	transmembrane p24 trafficking protein 2	Homo sapiens	8-11
23740989-2	2013	It is proposed that Gag targeting is superior because of very early Gag epitope presentation, allowing early killing of infected cells before Nef-mediated downregulation of human leukocyte antigen class I (HLA-I).	Glycosaminoglycans	20-23	S100 calcium binding protein B	Homo sapiens	142-145
23863627-3	2013	Mucopolysaccharidosis type IIIA (MPS IIIA) is an autosomic recessive LSD caused by a deficiency in sulfamidase, a sulfatase involved in the stepwise degradation of glycosaminoglycan (GAG) heparan sulfate.	Glycosaminoglycans	164-187	N-sulfoglucosamine sulfohydrolase	Homo sapiens	0-31
23525031-0	2013	HLA-A*68:02-restricted Gag-specific cytotoxic T lymphocyte responses can drive selection pressure on HIV but are subdominant and ineffective.	Glycosaminoglycans	23-26	major histocompatibility complex, class I, A	Homo sapiens	0-5
23517781-1	2013	Hypochlorous acid and its acid-base counterpart, hypochlorite ions, produced under inflammatory conditions, may produce chloramides of glycosaminoglycans, perhaps through the binding of myeloperoxidase directly to the glycosaminoglycans.	Glycosaminoglycans	135-153	myeloperoxidase	Homo sapiens	186-201
23517781-1	2013	Hypochlorous acid and its acid-base counterpart, hypochlorite ions, produced under inflammatory conditions, may produce chloramides of glycosaminoglycans, perhaps through the binding of myeloperoxidase directly to the glycosaminoglycans.	Glycosaminoglycans	218-236	myeloperoxidase	Homo sapiens	186-201
23899094-6	2013	Aggregates co-transduced with Ad.IGF-1/Ad.FGF-2 showed a selective expression of proteoglycans and collagen II, with limited expression of collagens I and x demonstrated by histological analyses, and had significantly greater glycosaminoglycan and collagen production than the positive control (P &lt;=0.001).	Glycosaminoglycans	226-243	insulin like growth factor 1	Homo sapiens	33-38
23899094-6	2013	Aggregates co-transduced with Ad.IGF-1/Ad.FGF-2 showed a selective expression of proteoglycans and collagen II, with limited expression of collagens I and x demonstrated by histological analyses, and had significantly greater glycosaminoglycan and collagen production than the positive control (P &lt;=0.001).	Glycosaminoglycans	226-243	fibroblast growth factor 2	Homo sapiens	42-47
23883591-8	2013	There was strong parallelism in the actions of CNP on cGMP induction resulting in enhanced GAG synthesis and reduction of NO and PGE2 release induced by IL-1beta.	Glycosaminoglycans	91-94	natriuretic peptide C	Homo sapiens	47-50
23883591-12	2013	In contrast, the presence of the Npr3 agonist had the opposite effect and increased GAG synthesis and cGMP levels in response to mechanical loading and reduced NO and PGE2 release comparable to control samples.	Glycosaminoglycans	84-87	natriuretic peptide receptor 3	Homo sapiens	33-37
23525031-9	2013	CONCLUSION: This study is consistent with previous data showing that HLA-A-restricted Gag-specific responses can impose selection pressure on HIV.	Glycosaminoglycans	86-89	major histocompatibility complex, class I, A	Homo sapiens	69-74
23525031-10	2013	In the case of HLA-A*68:02 the Gag response is subdominant, and apparently has little impact in natural infection.	Glycosaminoglycans	31-34	major histocompatibility complex, class I, A	Homo sapiens	15-20
23632323-2	2013	Here we present a therapeutic strategy to harness the activity of endogenously produced BMP-2 by delivery of an affinity-matched heparan sulfate (HS) glycos aminoglycan biomaterial that increases the bioavailability, bioactivity and half-life of this growth factor.	Glycosaminoglycans	150-168	bone morphogenetic protein 2	Oryctolagus cuniculus	88-93
23874339-0	2013	The Activity of CCL18 is Principally Mediated through Interaction with Glycosaminoglycans.	Glycosaminoglycans	71-89	C-C motif chemokine ligand 18	Homo sapiens	16-21
23874339-9	2013	Both heparin binding and binding to PBLs are considerably abrogated by mutation of the BBXB motif in the 40s loop suggesting an essential role of the CCL18-glycosaminoglycan interaction.	Glycosaminoglycans	156-173	C-C motif chemokine ligand 18	Homo sapiens	150-155
23861967-0	2013	Human Ubc9 is involved in intracellular HIV-1 Env stability after trafficking out of the trans-Golgi network in a Gag dependent manner.	Glycosaminoglycans	114-117	ubiquitin conjugating enzyme E2 I	Homo sapiens	6-10
23861967-0	2013	Human Ubc9 is involved in intracellular HIV-1 Env stability after trafficking out of the trans-Golgi network in a Gag dependent manner.	Glycosaminoglycans	114-117	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	46-49
23747722-6	2013	XT-I catalyzes the initial step of glycosaminoglycan biosynthesis.	Glycosaminoglycans	35-52	xylosyltransferase 1	Homo sapiens	0-4
23664118-0	2013	Defective initiation of glycosaminoglycan synthesis due to B3GALT6 mutations causes a pleiotropic Ehlers-Danlos-syndrome-like connective tissue disorder.	Glycosaminoglycans	24-41	beta-1,3-galactosyltransferase 6	Homo sapiens	59-66
23374084-5	2013	The majority of Gag-specific T-cell responses in the female genital tract were monofunctional, although low frequencies of HIV Gag-specific polyfunctional CD8(+) T cells were detected at the cervix in 81 3% (13/16) of women.	Glycosaminoglycans	127-130	CD8a molecule	Homo sapiens	155-158
23374084-6	2013	The ability of CD8(+) T cells at both the cervix and in blood to express CD107a and to exhibit polyfunctional responses (two or more functions) following Gag stimulation was inversely associated with plasma viral load and positively associated with blood CD4 counts, suggesting that clinical status impacted on the functionality of HIV-specific T cells at the mucosa, in a similar way to blood.	Glycosaminoglycans	154-157	CD8a molecule	Homo sapiens	15-18
23374084-6	2013	The ability of CD8(+) T cells at both the cervix and in blood to express CD107a and to exhibit polyfunctional responses (two or more functions) following Gag stimulation was inversely associated with plasma viral load and positively associated with blood CD4 counts, suggesting that clinical status impacted on the functionality of HIV-specific T cells at the mucosa, in a similar way to blood.	Glycosaminoglycans	154-157	CD4 molecule	Homo sapiens	255-258
23388029-4	2013	The supplementation of chondrogenic MSC pellets with the recombinant human GDF-5 protein significantly enhanced MSC chondrogenic differentiation, as demonstrated by enhanced collagen type II and sulfated glycosaminoglycan (GAG) incorporation into the extracellular matrix.	Glycosaminoglycans	204-221	growth differentiation factor 5	Homo sapiens	75-80
23388029-4	2013	The supplementation of chondrogenic MSC pellets with the recombinant human GDF-5 protein significantly enhanced MSC chondrogenic differentiation, as demonstrated by enhanced collagen type II and sulfated glycosaminoglycan (GAG) incorporation into the extracellular matrix.	Glycosaminoglycans	223-226	growth differentiation factor 5	Homo sapiens	75-80
23389888-7	2013	Importantly, we demonstrated that treatment of accelerated aging Ercc1(-/Delta) mice, previously established to be a useful in vivo model to study age-related intervertebral disc degeneration (IDD), also resulted in improved disc total glycosaminoglycan content and proteoglycan synthesis.	Glycosaminoglycans	236-253	excision repair cross-complementing rodent repair deficiency, complementation group 1	Mus musculus	65-70
23616666-0	2013	Early Gag immunodominance of the HIV-specific T-cell response during acute/early infection is associated with higher CD8+ T-cell antiviral activity and correlates with preservation of the CD4+ T-cell compartment.	Glycosaminoglycans	6-9	CD8a molecule	Homo sapiens	117-120
23616666-0	2013	Early Gag immunodominance of the HIV-specific T-cell response during acute/early infection is associated with higher CD8+ T-cell antiviral activity and correlates with preservation of the CD4+ T-cell compartment.	Glycosaminoglycans	6-9	CD4 molecule	Homo sapiens	188-191
23616666-9	2013	The advantage of Gag-specific cells may result from their enhanced ability to mediate lysis of infected cells (evidenced by a higher capacity to degranulate and to mediate VIA) and to simultaneously produce IFN-gamma.	Glycosaminoglycans	17-20	interferon gamma	Homo sapiens	207-216
23616666-10	2013	Finally, Gag immunodominance was associated with elevated plasma levels of interleukin 2 (IL-2) and macrophage inflammatory protein 1beta (MIP-1beta).	Glycosaminoglycans	9-12	interleukin 2	Homo sapiens	75-88
23616666-10	2013	Finally, Gag immunodominance was associated with elevated plasma levels of interleukin 2 (IL-2) and macrophage inflammatory protein 1beta (MIP-1beta).	Glycosaminoglycans	9-12	interleukin 2	Homo sapiens	90-94
23616666-10	2013	Finally, Gag immunodominance was associated with elevated plasma levels of interleukin 2 (IL-2) and macrophage inflammatory protein 1beta (MIP-1beta).	Glycosaminoglycans	9-12	C-C motif chemokine ligand 4	Homo sapiens	100-137
23616666-10	2013	Finally, Gag immunodominance was associated with elevated plasma levels of interleukin 2 (IL-2) and macrophage inflammatory protein 1beta (MIP-1beta).	Glycosaminoglycans	9-12	C-C motif chemokine ligand 4	Homo sapiens	139-148
23616666-11	2013	All together, this study underscores the importance of CD8(+) T-cell specificity in the improved control of disease progression, which was related to the capacity of Gag-specific cells to mediate both lytic and nonlytic antiviral mechanisms at early time points postinfection.	Glycosaminoglycans	166-169	CD8a molecule	Homo sapiens	55-58
23637402-5	2013	We found that Gag assembly induced the aggregation of small Env clusters into larger domains and that these domains were completely immobile.	Glycosaminoglycans	14-17	endogenous retrovirus group K member 20	Homo sapiens	60-63
23637402-6	2013	Truncation of the cytoplasmic tail (CT) of Env abrogated Gag"s ability to induce Env clustering and restored Env mobility at assembly sites, both of which correlated with increased Env-induced fusion of infected and uninfected cells.	Glycosaminoglycans	57-60	endogenous retrovirus group K member 20	Homo sapiens	43-46
23637402-6	2013	Truncation of the cytoplasmic tail (CT) of Env abrogated Gag"s ability to induce Env clustering and restored Env mobility at assembly sites, both of which correlated with increased Env-induced fusion of infected and uninfected cells.	Glycosaminoglycans	57-60	endogenous retrovirus group K member 20	Homo sapiens	81-84
23637402-6	2013	Truncation of the cytoplasmic tail (CT) of Env abrogated Gag"s ability to induce Env clustering and restored Env mobility at assembly sites, both of which correlated with increased Env-induced fusion of infected and uninfected cells.	Glycosaminoglycans	57-60	endogenous retrovirus group K member 20	Homo sapiens	81-84
23637402-6	2013	Truncation of the cytoplasmic tail (CT) of Env abrogated Gag"s ability to induce Env clustering and restored Env mobility at assembly sites, both of which correlated with increased Env-induced fusion of infected and uninfected cells.	Glycosaminoglycans	57-60	endogenous retrovirus group K member 20	Homo sapiens	81-84
23637402-7	2013	Hence, while Env trapping by Gag secures Env incorporation into viral particles, Env clustering and its sequestration at assembly sites likely also leads to the repression of its fusion function, and thus, by preventing the formation of syncytia, Gag helps to secure efficient transfer of viral particles to target cells.	Glycosaminoglycans	29-32	endogenous retrovirus group K member 20	Homo sapiens	13-16
23637402-7	2013	Hence, while Env trapping by Gag secures Env incorporation into viral particles, Env clustering and its sequestration at assembly sites likely also leads to the repression of its fusion function, and thus, by preventing the formation of syncytia, Gag helps to secure efficient transfer of viral particles to target cells.	Glycosaminoglycans	29-32	endogenous retrovirus group K member 20	Homo sapiens	41-44
23637402-7	2013	Hence, while Env trapping by Gag secures Env incorporation into viral particles, Env clustering and its sequestration at assembly sites likely also leads to the repression of its fusion function, and thus, by preventing the formation of syncytia, Gag helps to secure efficient transfer of viral particles to target cells.	Glycosaminoglycans	29-32	endogenous retrovirus group K member 20	Homo sapiens	41-44
23664118-2	2013	They consist of glycosaminoglycan chains attached to a core protein via a tetrasaccharide linkage, whereby the addition of the third residue is catalyzed by galactosyltransferase II (beta3GalT6), encoded by B3GALT6.	Glycosaminoglycans	16-33	beta-1,3-galactosyltransferase 6	Homo sapiens	183-193
23664118-7	2013	A strong reduction in heparan sulfate level was also observed, indicating that beta3GalT6 deficiency alters synthesis of both main types of glycosaminoglycans.	Glycosaminoglycans	140-158	beta-1,3-galactosyltransferase 6	Homo sapiens	79-89
23628461-1	2013	Mucopolysaccharidosis (MPS) VII is a lysosomal storage disease due to deficient activity of beta-glucuronidase (GUSB), and results in glycosaminoglycan accumulation.	Glycosaminoglycans	134-151	glucuronidase beta	Canis lupus familiaris	92-110
23474328-8	2013	Immunohistochemistry for TGFbeta3/DPSC constructs (n = 5/group) showed cartilage-like matrix formation with glycosaminoglycans.	Glycosaminoglycans	108-126	transforming growth factor beta 3	Homo sapiens	25-33
22829115-3	2013	In this study, a recombinant baculovirus containing the gag gene p24 was constructed and the protein, used as antigen, analyzed by western blot and an indirect in-house rp24-ELISA test.	Glycosaminoglycans	56-59	transmembrane p24 trafficking protein 2	Homo sapiens	65-68
23628461-1	2013	Mucopolysaccharidosis (MPS) VII is a lysosomal storage disease due to deficient activity of beta-glucuronidase (GUSB), and results in glycosaminoglycan accumulation.	Glycosaminoglycans	134-151	glucuronidase beta	Canis lupus familiaris	112-116
23336980-2	2013	The most common inherited primary dystonia is DYT1 dystonia, which is due to loss of a GAG codon in the TOR1A gene that encodes torsinA.	Glycosaminoglycans	87-90	torsin family 1, member A (torsin A)	Mus musculus	46-50
23336980-2	2013	The most common inherited primary dystonia is DYT1 dystonia, which is due to loss of a GAG codon in the TOR1A gene that encodes torsinA.	Glycosaminoglycans	87-90	torsin family 1, member A (torsin A)	Mus musculus	104-109
23336980-2	2013	The most common inherited primary dystonia is DYT1 dystonia, which is due to loss of a GAG codon in the TOR1A gene that encodes torsinA.	Glycosaminoglycans	87-90	torsin family 1, member A (torsin A)	Mus musculus	128-135
23289669-16	2013	However, BMP-2 overexpression consistently resulted in a trend toward decreased GAG/DNA ratios in both mechanical stimulated and unloaded groups.	Glycosaminoglycans	80-83	bone morphogenetic protein 2	Homo sapiens	9-14
23530034-8	2013	Last, knockdown of CCN2 in NP cells results in a significant decrease in GAG synthesis and expression of AGGRECAN and COLLAGEN II.	Glycosaminoglycans	73-76	cellular communication network factor 2	Homo sapiens	19-23
23360441-5	2013	After 4 weeks of culture, IGF-I treatment significantly improved mechanical and biochemical properties, while maintaining DNA content, with a 26-fold increase in glycosaminoglycan (GAG) content and 10-fold increase in collagen content compared to 0-week controls, and a 3-fold increase in the equilibrium modulus at 2 weeks compared to controls.	Glycosaminoglycans	162-179	IGFI	Bos taurus	26-31
23360441-5	2013	After 4 weeks of culture, IGF-I treatment significantly improved mechanical and biochemical properties, while maintaining DNA content, with a 26-fold increase in glycosaminoglycan (GAG) content and 10-fold increase in collagen content compared to 0-week controls, and a 3-fold increase in the equilibrium modulus at 2 weeks compared to controls.	Glycosaminoglycans	181-184	IGFI	Bos taurus	26-31
23360441-6	2013	IGF-I-treated menisci had ~60% of the GAG content of native tissue and the compressive equilibrium modulus matched native properties by 2 weeks of culture.	Glycosaminoglycans	38-41	IGFI	Bos taurus	0-5
23734081-10	2013	The increasing level of HS or sulfated glycosaminoglycan in the vitreous was associated with its increased inhibitory effect on interaction between VEGF and surface heparin in vitro (p=0.014, R2=0.377).	Glycosaminoglycans	39-56	vascular endothelial growth factor A	Homo sapiens	148-152
23614643-0	2013	Dimerized glycosaminoglycan chains increase FGF signaling during zebrafish development.	Glycosaminoglycans	10-27	fibroblast growth factor 8a	Danio rerio	44-47
23614643-10	2013	On the basis of these in vivo findings, we propose a new model for GAG/FGF/FGFR interactions in which dimerized GAG chains can activate FGF-mediated signal transduction pathways.	Glycosaminoglycans	67-70	fibroblast growth factor 8a	Danio rerio	71-74
23614643-10	2013	On the basis of these in vivo findings, we propose a new model for GAG/FGF/FGFR interactions in which dimerized GAG chains can activate FGF-mediated signal transduction pathways.	Glycosaminoglycans	67-70	fibroblast growth factor 8a	Danio rerio	75-78
23536183-3	2013	CONCLUSION: The alternative helix conformation enhances the anti-angiogenic activity of CXCL4L1 by reducing the glycosaminoglycan binding ability.	Glycosaminoglycans	112-129	platelet factor 4 variant 1	Homo sapiens	88-95
23705972-4	2013	It has been long established that the gp41-CT interacts with the Gag precursor protein to ensure Env incorporation into the virion.	Glycosaminoglycans	65-68	endogenous retrovirus group K member 20	Homo sapiens	97-100
23529876-1	2013	Mucopolysaccharidosis type II (MPS II), also known as Hunter syndrome (OMIM 309900), is a rare, X-linked lysosomal storage disorder caused by a deficiency of iduronate-2-sulfatase (IDS; EC 3.1.6.13), which is involved in the lysosomal degradation of glycosaminoglycans (GAG).	Glycosaminoglycans	250-268	iduronate 2-sulfatase	Mus musculus	158-179
23529876-4	2013	The results showed that the group treated with 12 microg/day doses of rh-IDS demonstrated decreased GAG concentrations compared to the untreated KO mice group (P = 0.003).	Glycosaminoglycans	100-103	iduronate 2-sulfatase	Mus musculus	73-76
23238867-5	2013	The production of glycoaminoglycans (GAG) in the BMP-2-treated TDSCs was assessed by alcian blue staining.	Glycosaminoglycans	37-40	bone morphogenetic protein 2	Rattus norvegicus	49-54
22724470-0	2013	Glycosaminoglycan sulodexide inhibition of MMP-9 gelatinase secretion and activity: possible pharmacological role against collagen degradation in vascular chronic diseases.	Glycosaminoglycans	0-17	matrix metallopeptidase 9	Homo sapiens	43-48
23360476-0	2013	Glycosaminoglycans are functional ligands for receptor for advanced glycation end-products in tumors.	Glycosaminoglycans	0-18	advanced glycosylation end product-specific receptor	Mus musculus	46-90
23077084-8	2013	Highest amount of glycosaminoglycan contents of rBMSCs on GAM concluded that BMP6 gene-activated chitosan scaffold has a potential in the application of cartilage regeneration.	Glycosaminoglycans	18-35	bone morphogenetic protein 6	Rattus norvegicus	77-81
23508903-4	2013	Interestingly, this cluster is one of the two glycosaminoglycan binding sites of the native HLf involved in its antiviral activity; however, the mechanism of the HLP1-23 action was different from that of the full-length protein, the peptide inhibiting HBV infection when pre-incubated with the virus, while no effect was observed on the target cells.	Glycosaminoglycans	46-63	HLF transcription factor, PAR bZIP family member	Homo sapiens	92-95
22983812-1	2013	Mucopolysaccharidosis I (MPS I) is a lysosomal storage disease due to alpha-L-iduronidase (IDUA) deficiency that results in the accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	144-162	iduronidase, alpha-L	Mus musculus	70-89
22983812-1	2013	Mucopolysaccharidosis I (MPS I) is a lysosomal storage disease due to alpha-L-iduronidase (IDUA) deficiency that results in the accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	144-162	iduronidase, alpha-L	Mus musculus	91-95
22983812-1	2013	Mucopolysaccharidosis I (MPS I) is a lysosomal storage disease due to alpha-L-iduronidase (IDUA) deficiency that results in the accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	164-167	iduronidase, alpha-L	Mus musculus	70-89
22983812-1	2013	Mucopolysaccharidosis I (MPS I) is a lysosomal storage disease due to alpha-L-iduronidase (IDUA) deficiency that results in the accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	164-167	iduronidase, alpha-L	Mus musculus	91-95
23351479-7	2013	Although abnormal gag reflexes have been reported in cases of glossopharyngeal schwannoma and neurofibroma in patients with neurofibromatosis-1, a gag reflex has not been reported previously as a complication of IM in the head and neck.	Glycosaminoglycans	18-21	neurofibromin 1	Homo sapiens	124-143
23238867-8	2013	GAG production and Acan increased while Dcn, Bgn, and Fmod decreased in TDSCs after BMP-2 stimulation.	Glycosaminoglycans	0-3	bone morphogenetic protein 2	Rattus norvegicus	84-89
23418755-7	2013	This indicates possible interactions of the testican-3 core protein with components of the extracellular matrix which are blocked by addition of the glycosaminoglycan chains.	Glycosaminoglycans	149-166	sparc/osteonectin, cwcv and kazal-like domains proteoglycan 3	Mus musculus	44-54
23238867-9	2013	In conclusion, BMP-2 promoted GAG deposition, aggrecan expression, and enhanced non-tenocyte differentiation of TDSCs in vitro.	Glycosaminoglycans	30-33	bone morphogenetic protein 2	Rattus norvegicus	15-20
23613843-2	2013	In the present study, we found that the loss of virus infectivity as a result of envelope (Env) incorporation defect caused by a Gag matrix (MA) mutation (L30E) was significantly alleviated by introducing a start codon mutation in vpu.	Glycosaminoglycans	129-132	endogenous retrovirus group K member 20	Homo sapiens	91-94
23675305-4	2013	In addition, PFV Gag interacts with the FV Envelope (Env) protein to facilitate budding of infectious particles.	Glycosaminoglycans	17-20	endogenous retrovirus group K member 20	Homo sapiens	43-46
23675305-7	2013	We present the crystal structure of a dimeric amino terminal domain from PFV, Gag-NtD, both free and in complex with the leader peptide of PFV Env.	Glycosaminoglycans	78-81	fuzzy planar cell polarity protein	Homo sapiens	82-85
23675305-7	2013	We present the crystal structure of a dimeric amino terminal domain from PFV, Gag-NtD, both free and in complex with the leader peptide of PFV Env.	Glycosaminoglycans	78-81	endogenous retrovirus group K member 20	Homo sapiens	143-146
23675305-9	2013	Furthermore, we present structural, biochemical and virological data that reveal the molecular details of the essential Gag-Env interaction and in addition we also examine the specificity of Trim5alpha restriction of PFV.	Glycosaminoglycans	120-123	endogenous retrovirus group K member 20	Homo sapiens	124-127
23357641-3	2013	Here, we examined the binding of nephronectin to a panel of glycosaminoglycan (GAG) chains.	Glycosaminoglycans	60-77	nephronectin	Mus musculus	33-45
23357641-3	2013	Here, we examined the binding of nephronectin to a panel of glycosaminoglycan (GAG) chains.	Glycosaminoglycans	79-82	nephronectin	Mus musculus	33-45
23618494-10	2013	Pull-down assays, using proteins of mammalian and prokaryotic origin, support the previous hypothesis of a direct interaction of both PFV proteins without requirement for cellular cofactors and suggest a potential direct contact of Env through this N-terminal Gag domain.	Glycosaminoglycans	260-263	endogenous retrovirus group K member 20	Homo sapiens	232-235
23613843-2	2013	In the present study, we found that the loss of virus infectivity as a result of envelope (Env) incorporation defect caused by a Gag matrix (MA) mutation (L30E) was significantly alleviated by introducing a start codon mutation in vpu.	Glycosaminoglycans	129-132	Vpu	Human immunodeficiency virus 1	231-234
23180184-4	2013	Nine subjects were found to have the GAG deletion in TOR1A gene.	Glycosaminoglycans	37-40	torsin family 1 member A	Homo sapiens	53-58
22770546-2	2013	It is an autosomal dominantly inherited disorder caused by deletion of a GAG triplet in exon 5 of the DYT1 gene.	Glycosaminoglycans	73-76	torsin family 1 member A	Homo sapiens	102-106
22770546-9	2013	CONCLUSION: In children with dystonia; if brain imaging is unremarkable and when there is no history of CNS disorders such as perinatal asphyxia, infections, drug exposure or trauma; genetic analysis for GAG deletion of DYT-1 gene may be performed even if dystonia starts at a very young age or it spreads to involve oromandibular muscles.	Glycosaminoglycans	204-207	torsin family 1 member A	Homo sapiens	220-225
23593225-5	2013	Idua encodes alpha-L-iduronidase, an enzyme required for degradation of the glycosaminoglycans (GAGs) heparan sulfate and dermatan sulfate.	Glycosaminoglycans	76-94	iduronidase, alpha-L	Mus musculus	0-4
23593225-5	2013	Idua encodes alpha-L-iduronidase, an enzyme required for degradation of the glycosaminoglycans (GAGs) heparan sulfate and dermatan sulfate.	Glycosaminoglycans	76-94	iduronidase, alpha-L	Mus musculus	13-32
22886070-1	2013	Recently, we demonstrated that the human xylosyltransferase II (XT-II) has enzymatic activity and is able to catalyze the initial and rate-limiting step in the biosynthesis of glycosaminoglycans (GAGs) like chondroitin and dermatan sulfate, as well as heparan sulfate and heparin.	Glycosaminoglycans	176-194	xylosyltransferase 2	Homo sapiens	41-62
22886070-1	2013	Recently, we demonstrated that the human xylosyltransferase II (XT-II) has enzymatic activity and is able to catalyze the initial and rate-limiting step in the biosynthesis of glycosaminoglycans (GAGs) like chondroitin and dermatan sulfate, as well as heparan sulfate and heparin.	Glycosaminoglycans	176-194	xylosyltransferase 2	Homo sapiens	64-69
22886070-8	2013	Our results provide an insight into transcriptional regulation of the XYLT2 gene and may contribute to understanding the manifold GAG-involving processes in health and disease.	Glycosaminoglycans	130-133	xylosyltransferase 2	Homo sapiens	70-75
23412898-6	2013	Interestingly, protein levels of three key enzymes responsible for decorin GAG chain synthesis were also increased after AB, two of them gradually declining after DB.	Glycosaminoglycans	75-78	decorin	Mus musculus	67-74
23745018-9	2013	The data confirms previous findings on the importance for efficacious binding, of an arginine residue at the 2(nd) position of the gag SL9 epitope, and extends this principle to other epitopes which interacts with HLA B*27.	Glycosaminoglycans	131-134	major histocompatibility complex, class I, B	Homo sapiens	214-219
23395820-10	2013	These results indicate that EXTL2 functions to suppress GAG biosynthesis that is enhanced by a xylose kinase and that the EXTL2-dependent mechanism that regulates GAG biosynthesis might be a "quality control system" for proteoglycans.	Glycosaminoglycans	56-59	exostosin-like glycosyltransferase 2	Mus musculus	28-33
23395820-10	2013	These results indicate that EXTL2 functions to suppress GAG biosynthesis that is enhanced by a xylose kinase and that the EXTL2-dependent mechanism that regulates GAG biosynthesis might be a "quality control system" for proteoglycans.	Glycosaminoglycans	163-166	exostosin-like glycosyltransferase 2	Mus musculus	122-127
23801937-1	2013	Mucopolysaccharidosis type II (MPS II), also known as Hunter syndrome, is a rare, X-linked disease caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase, which catalyses a step in the catabolism of glycosaminoglycans resulting in accumulation of heparan and dermatan sulfate in many organs and tissues.	Glycosaminoglycans	213-231	iduronate 2-sulfatase	Homo sapiens	146-167
23395820-0	2013	EXTL2, a member of the EXT family of tumor suppressors, controls glycosaminoglycan biosynthesis in a xylose kinase-dependent manner.	Glycosaminoglycans	65-82	exostosin-like glycosyltransferase 2	Mus musculus	0-5
23395820-2	2013	EXTL2, one of three EXT-like genes in the human genome that are homologous to EXT1 and EXT2, encodes a transferase that adds not only GlcNAc but also N-acetylgalactosamine to the glycosaminoglycan (GAG)-protein linkage region via an alpha1,4-linkage.	Glycosaminoglycans	179-196	exostosin like glycosyltransferase 2	Homo sapiens	0-5
23395820-2	2013	EXTL2, one of three EXT-like genes in the human genome that are homologous to EXT1 and EXT2, encodes a transferase that adds not only GlcNAc but also N-acetylgalactosamine to the glycosaminoglycan (GAG)-protein linkage region via an alpha1,4-linkage.	Glycosaminoglycans	179-196	exostosin glycosyltransferase 1	Homo sapiens	78-82
23395820-2	2013	EXTL2, one of three EXT-like genes in the human genome that are homologous to EXT1 and EXT2, encodes a transferase that adds not only GlcNAc but also N-acetylgalactosamine to the glycosaminoglycan (GAG)-protein linkage region via an alpha1,4-linkage.	Glycosaminoglycans	179-196	exostosin glycosyltransferase 2	Homo sapiens	87-91
23395820-2	2013	EXTL2, one of three EXT-like genes in the human genome that are homologous to EXT1 and EXT2, encodes a transferase that adds not only GlcNAc but also N-acetylgalactosamine to the glycosaminoglycan (GAG)-protein linkage region via an alpha1,4-linkage.	Glycosaminoglycans	198-201	exostosin like glycosyltransferase 2	Homo sapiens	0-5
23395820-2	2013	EXTL2, one of three EXT-like genes in the human genome that are homologous to EXT1 and EXT2, encodes a transferase that adds not only GlcNAc but also N-acetylgalactosamine to the glycosaminoglycan (GAG)-protein linkage region via an alpha1,4-linkage.	Glycosaminoglycans	198-201	exostosin glycosyltransferase 1	Homo sapiens	78-82
23395820-2	2013	EXTL2, one of three EXT-like genes in the human genome that are homologous to EXT1 and EXT2, encodes a transferase that adds not only GlcNAc but also N-acetylgalactosamine to the glycosaminoglycan (GAG)-protein linkage region via an alpha1,4-linkage.	Glycosaminoglycans	198-201	exostosin glycosyltransferase 2	Homo sapiens	87-91
23314954-0	2013	Rapid binding of electrostatically stabilized iron oxide nanoparticles to THP-1 monocytic cells via interaction with glycosaminoglycans.	Glycosaminoglycans	117-135	GLI family zinc finger 2	Homo sapiens	74-79
23497128-4	2013	Since Gag protein is known to interact with membrane lipid phosphatidylinositol (4,5) bisphosphate [PI(4,5)P2] and one of the known binding partners of NS3, cellular protein p11 also interacts with annexin a PI(4,5)P2 interacting protein, this study was designed to understand the role of this negatively charged membrane lipid in BTV assembly and maturation.	Glycosaminoglycans	6-9	KRAS proto-oncogene, GTPase	Homo sapiens	152-155
23140171-0	2013	Targeting of conserved gag-epitopes in early HIV infection is associated with lower plasma viral load and slower CD4(+) T cell depletion.	Glycosaminoglycans	23-26	CD4 molecule	Homo sapiens	113-116
23579467-9	2013	Glycosaminoglycans contents were increased 217% by TGF-beta3 and 220% by BMP-6.	Glycosaminoglycans	0-18	transforming growth factor beta 3	Homo sapiens	51-60
23261552-7	2013	In addition, elastin could stimulate cryopreserved chondrocytes to synthesize more glycosaminoglycans and collagen than poly-L-lysine.	Glycosaminoglycans	83-101	elastin	Homo sapiens	13-20
23325685-2	2013	Genetic and biochemical data indicate that the matrix (MA) domain of Gag and the cytoplasmic tail of the transmembrane glycoprotein gp41 play an important role in coordinating Env incorporation; however, the molecular mechanism and possible role of host factors in this process remain to be defined.	Glycosaminoglycans	69-72	endogenous retrovirus group K member 20	Homo sapiens	176-179
23579467-9	2013	Glycosaminoglycans contents were increased 217% by TGF-beta3 and 220% by BMP-6.	Glycosaminoglycans	0-18	bone morphogenetic protein 6	Homo sapiens	73-78
23235146-5	2013	Bound GAG proved to be biologically active, rescuing the neural differentiation capacity of heparan sulfate-deficient mouse embryonic stem cells and functioning in concert with FGF4 to facilitate the formation of extensive neural processes across the scaffold surface.	Glycosaminoglycans	6-9	fibroblast growth factor 4	Mus musculus	177-181
22550062-1	2013	The enzyme Arylsulfatase B (ARSB; N-acetylgalactosamine-4-sulfatase) removes 4-sulfate groups from chondroitin-4-sulfate and dermatan sulfate and is required for the degradation of these sulfated glycosaminoglycans (sGAGs).	Glycosaminoglycans	196-214	arylsulfatase B	Homo sapiens	11-26
22550062-1	2013	The enzyme Arylsulfatase B (ARSB; N-acetylgalactosamine-4-sulfatase) removes 4-sulfate groups from chondroitin-4-sulfate and dermatan sulfate and is required for the degradation of these sulfated glycosaminoglycans (sGAGs).	Glycosaminoglycans	196-214	arylsulfatase B	Homo sapiens	28-32
22550062-1	2013	The enzyme Arylsulfatase B (ARSB; N-acetylgalactosamine-4-sulfatase) removes 4-sulfate groups from chondroitin-4-sulfate and dermatan sulfate and is required for the degradation of these sulfated glycosaminoglycans (sGAGs).	Glycosaminoglycans	196-214	arylsulfatase B	Homo sapiens	34-67
25049774-6	2013	A real-time PCR analysis showed that the expression levels of pluripotency (Oct 4), cell growth (Glut 5), and anti-apoptosis (Bax inhibitor) genes were significantly higher in embryos derived from HA- or HP-treated sperm than in control or other treatment groups, while pro-apoptotic gene expression (caspase-3) was significantly lower in all GAG treatment groups (p&lt;0.05).	Glycosaminoglycans	343-346	BCL2 associated X, apoptosis regulator	Bos taurus	126-129
22915292-7	2013	Glycosaminoglycan content was decreased in both ApoE KO annulus fibrosus (AF) and nucleus pulposus (NP) cells.	Glycosaminoglycans	0-17	apolipoprotein E	Mus musculus	48-52
22718137-1	2013	Natural glycosaminoglycans (GAGs) and chemically modified GAG derivatives are known to support osteogenic differentiation of mesenchymal stromal cells (MSC).	Glycosaminoglycans	8-26	musculin	Homo sapiens	152-155
22718137-1	2013	Natural glycosaminoglycans (GAGs) and chemically modified GAG derivatives are known to support osteogenic differentiation of mesenchymal stromal cells (MSC).	Glycosaminoglycans	28-31	musculin	Homo sapiens	152-155
23172685-5	2013	Interestingly, Gag-specific DN T-cell responses were found in 3/13 (23%) HIV-exposed seronegative individuals (Group A), involving both DN/alphabeta(+) and DN/gammadelta(+) T-cells through MIP1beta and IFNgamma production.	Glycosaminoglycans	15-18	C-C motif chemokine ligand 4	Homo sapiens	189-197
23172685-5	2013	Interestingly, Gag-specific DN T-cell responses were found in 3/13 (23%) HIV-exposed seronegative individuals (Group A), involving both DN/alphabeta(+) and DN/gammadelta(+) T-cells through MIP1beta and IFNgamma production.	Glycosaminoglycans	15-18	interferon gamma	Homo sapiens	202-210
23223231-1	2013	Xylosyltransferase I (XT-I) is an essential enzyme of proteoglycan (PG) biosynthesis pathway catalyzing the initial and rate-limiting step in glycosaminoglycan chain assembly.	Glycosaminoglycans	142-159	xylosyltransferase 1	Homo sapiens	0-20
23025322-0	2013	Insights into the glycosaminoglycan-mediated cytotoxic mechanism of eosinophil cationic protein revealed by NMR.	Glycosaminoglycans	18-35	ribonuclease A family member 3	Homo sapiens	68-95
23025322-2	2013	Eosinophil cationic protein (ECP) is a cytotoxic ribonuclease that interacts with glycosaminoglycans at the cell surface; this promotes the destabilization of the cellular membrane and triggers ECP"s toxic activity.	Glycosaminoglycans	82-100	ribonuclease A family member 3	Homo sapiens	0-27
23025322-2	2013	Eosinophil cationic protein (ECP) is a cytotoxic ribonuclease that interacts with glycosaminoglycans at the cell surface; this promotes the destabilization of the cellular membrane and triggers ECP"s toxic activity.	Glycosaminoglycans	82-100	ribonuclease A family member 3	Homo sapiens	29-32
23025322-2	2013	Eosinophil cationic protein (ECP) is a cytotoxic ribonuclease that interacts with glycosaminoglycans at the cell surface; this promotes the destabilization of the cellular membrane and triggers ECP"s toxic activity.	Glycosaminoglycans	82-100	ribonuclease A family member 3	Homo sapiens	194-197
23468635-4	2013	Distinctive HIV-1 Gag assembly sites were readily detected and were associated with Env clusters that always extended beyond the actual Gag assembly site and often showed enrichment at the periphery and surrounding the assembly site.	Glycosaminoglycans	18-21	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	84-87
23468635-4	2013	Distinctive HIV-1 Gag assembly sites were readily detected and were associated with Env clusters that always extended beyond the actual Gag assembly site and often showed enrichment at the periphery and surrounding the assembly site.	Glycosaminoglycans	136-139	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	84-87
23468635-8	2013	The observed Env accumulation surrounding Gag assemblies, with a lower density on the actual bud, could facilitate viral spread in vivo.	Glycosaminoglycans	42-45	endogenous retrovirus group K member 20	Homo sapiens	13-16
22834895-8	2013	Expansion in FGF-2, followed by differentiation at 5% oxygen tension, was observed to synergistically enhance subsequent sulfated glycosaminoglycan (sGAG) accumulation after chondrogenic induction.	Glycosaminoglycans	130-147	fibroblast growth factor 2	Homo sapiens	13-18
23327652-14	2013	CONCLUSIONS: IDCs show alterations in the expression of HSPG genes; principally the expression and localization of proteoglycans and the sulfation patterns of glycosaminoglycan chains, depending on the metastatic nature of the tumor.	Glycosaminoglycans	159-176	syndecan 2	Homo sapiens	56-60
23223231-1	2013	Xylosyltransferase I (XT-I) is an essential enzyme of proteoglycan (PG) biosynthesis pathway catalyzing the initial and rate-limiting step in glycosaminoglycan chain assembly.	Glycosaminoglycans	142-159	xylosyltransferase 1	Homo sapiens	22-26
23148226-1	2013	The ability to interact with cell surface glycosaminoglycans (GAGs) is essential to the cell migration properties of chemokines, but association with soluble GAGs induces the oligomerization of most chemokines including CXCL12.	Glycosaminoglycans	158-162	C-X-C motif chemokine ligand 12	Rattus norvegicus	220-226
23172228-2	2013	This observation led us to investigate whether chondroadherin interacts via this C-terminal heparin-binding domain with glycosaminoglycan chains of proteoglycans at the cell surface.	Glycosaminoglycans	120-137	chondroadherin	Homo sapiens	47-61
23148226-9	2013	These results clarify the structural basis for GAG recognition by CXCL12 and lend insight into the development of CXCL12-based therapeutics.	Glycosaminoglycans	47-50	C-X-C motif chemokine ligand 12	Rattus norvegicus	66-72
23148226-9	2013	These results clarify the structural basis for GAG recognition by CXCL12 and lend insight into the development of CXCL12-based therapeutics.	Glycosaminoglycans	47-50	C-X-C motif chemokine ligand 12	Rattus norvegicus	114-120
23983782-6	2013	Results showed that the hyperglycemia-induced GAG alterations in the cell surface perlecan as well as in the ECM indeed upregulated the expressions of IL-6, IL-8, and MCP-1 and the activities of MMP-2 and MMP-9 and downregulated the expressions of TIMP-2.	Glycosaminoglycans	46-49	interleukin 6	Homo sapiens	151-155
24373218-15	2013	Overall, during the two time courses, GAG release was 58.67% +- 10.91% (SD) for IL-1beta versus 52.91% +- 9.35% (SD) with carprofen + IL-1beta.	Glycosaminoglycans	38-41	interleukin-1 beta	Equus caballus	80-88
23079801-0	2013	Poor HIV control in HLA-B*27 and B*57/58 noncontrollers is associated with limited number of polyfunctional Gag p24-specific CD8+ T cells.	Glycosaminoglycans	108-111	major histocompatibility complex, class I, B	Homo sapiens	20-25
23079801-8	2013	Moreover, the absolute number of high functional quality Gag p24-specific CD8 T cells was significantly in a negative correlation with pVL (r = -0.6984, P = 0.0006) and also in a positive correlation with CD4 T-cell count (r = 0.5648, P = 0.0095).	Glycosaminoglycans	57-60	transmembrane p24 trafficking protein 2	Homo sapiens	61-64
23079801-9	2013	CONCLUSION: We concluded that an adequate number of high functional quality Gag p24-specific CD8 T cells is strongly associated with a natural HIV controller status.	Glycosaminoglycans	76-79	transmembrane p24 trafficking protein 2	Homo sapiens	80-83
23983782-6	2013	Results showed that the hyperglycemia-induced GAG alterations in the cell surface perlecan as well as in the ECM indeed upregulated the expressions of IL-6, IL-8, and MCP-1 and the activities of MMP-2 and MMP-9 and downregulated the expressions of TIMP-2.	Glycosaminoglycans	46-49	C-X-C motif chemokine ligand 8	Homo sapiens	157-161
23983782-6	2013	Results showed that the hyperglycemia-induced GAG alterations in the cell surface perlecan as well as in the ECM indeed upregulated the expressions of IL-6, IL-8, and MCP-1 and the activities of MMP-2 and MMP-9 and downregulated the expressions of TIMP-2.	Glycosaminoglycans	46-49	C-C motif chemokine ligand 2	Homo sapiens	167-172
23983782-6	2013	Results showed that the hyperglycemia-induced GAG alterations in the cell surface perlecan as well as in the ECM indeed upregulated the expressions of IL-6, IL-8, and MCP-1 and the activities of MMP-2 and MMP-9 and downregulated the expressions of TIMP-2.	Glycosaminoglycans	46-49	matrix metallopeptidase 2	Homo sapiens	195-200
23983782-6	2013	Results showed that the hyperglycemia-induced GAG alterations in the cell surface perlecan as well as in the ECM indeed upregulated the expressions of IL-6, IL-8, and MCP-1 and the activities of MMP-2 and MMP-9 and downregulated the expressions of TIMP-2.	Glycosaminoglycans	46-49	matrix metallopeptidase 9	Homo sapiens	205-210
23983782-6	2013	Results showed that the hyperglycemia-induced GAG alterations in the cell surface perlecan as well as in the ECM indeed upregulated the expressions of IL-6, IL-8, and MCP-1 and the activities of MMP-2 and MMP-9 and downregulated the expressions of TIMP-2.	Glycosaminoglycans	46-49	TIMP metallopeptidase inhibitor 2	Homo sapiens	248-254
23215760-0	2013	Incidence of the Hb E [beta26(B8)Glu Lys, GAG&gt;AAG] variant in Totos, one of the smallest primitive tribes in the world.	Glycosaminoglycans	42-45	hemoglobin subunit epsilon 1	Homo sapiens	17-21
23018968-3	2013	METHODS: This review acknowledges the importance of dysregulated transforming growth factor-beta (TGF-beta) in TAADs and offers a complementary hypothesis that increased TGF-beta could contribute to the accumulation of glycosaminoglycans in the media of the proximal thoracic aorta.	Glycosaminoglycans	219-237	transforming growth factor beta 1	Homo sapiens	170-178
21926150-12	2013	Also, collagen production was increased significantly after 4 and 6 weeks of culture compared to cultures without TGF-beta and also more GAG staining was found after 4 and 6 weeks in the sections of the TGF-beta stimulated cultures.	Glycosaminoglycans	137-140	transforming growth factor beta-1 proprotein	Capra hircus	203-211
23437288-5	2013	Results show TFP (1 ng/mL TGF-beta1, 5 ng/mL bFGF, 10 ng/mL PDGF) supplementation of serum-free chondrogenic expansion medium enhances the post-expansion chondrogenic potential of costochondral cells, evidenced by increased glycosaminoglycan content, decreased type I/II collagen ratio, and enhanced compressive properties.	Glycosaminoglycans	224-241	inhibitor of carbonic anhydrase pseudogene	Homo sapiens	13-16
23123544-0	2013	Gag-CA Q110D mutation elicits TRIM5-independent enhancement of HIV-1mt replication in macaque cells.	Glycosaminoglycans	0-3	tripartite motif containing 5	Homo sapiens	30-35
23069857-4	2013	GAG and LDH release and numbers of CN increased whereas NO production and mRNA levels of matrix metalloproteinase (MMP)-2, -3 and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4 decreased strain-dependently after compression.	Glycosaminoglycans	0-3	ADAM metallopeptidase with thrombospondin type 1 motif 4	Bos taurus	171-203
23457456-7	2013	E10.5 FVB/N KLF2-/- hearts have reduced glycosaminoglycans in the cardiac jelly, correlating with the reduced EMT.	Glycosaminoglycans	40-58	Kruppel-like factor 2 (lung)	Mus musculus	12-16
22752444-0	2012	RANTES/CCL5-induced pro-angiogenic effects depend on CCR1, CCR5 and glycosaminoglycans.	Glycosaminoglycans	68-86	C-C motif chemokine ligand 5	Rattus norvegicus	0-6
23301025-7	2013	FGF-2 enhanced the BMP-2-induced increase in metachromatic staining for glycosaminoglycans (GAGs) only when it was present during the first week of culturing alone.	Glycosaminoglycans	72-90	fibroblast growth factor 2	Bos taurus	0-5
23301025-7	2013	FGF-2 enhanced the BMP-2-induced increase in metachromatic staining for glycosaminoglycans (GAGs) only when it was present during the first week of culturing alone.	Glycosaminoglycans	72-90	bone morphogenetic protein 2	Bos taurus	19-24
24454406-8	2013	Furthermore, GDF5 transfected MCS injected into an IVD papain degeneration organ culture model showed a partial recovery of the GAG/DNA ratio after 7 days.	Glycosaminoglycans	128-131	growth differentiation factor 5	Homo sapiens	13-17
23109338-8	2012	This may be explained by our demonstrated N6L interaction with sulfated glycosaminoglycans and consequently the controlled bioavailability of glycosaminoglycan-bound TIMP-3.	Glycosaminoglycans	72-90	TIMP metallopeptidase inhibitor 3	Homo sapiens	166-172
23109338-8	2012	This may be explained by our demonstrated N6L interaction with sulfated glycosaminoglycans and consequently the controlled bioavailability of glycosaminoglycan-bound TIMP-3.	Glycosaminoglycans	72-89	TIMP metallopeptidase inhibitor 3	Homo sapiens	166-172
23058565-1	2012	BACKGROUND: The deletion mutation of glutamate codon (GAG) in the TOR1A gene is a major cause of primary generalized dystonia.	Glycosaminoglycans	54-57	torsin family 1 member A	Homo sapiens	66-71
23206933-9	2012	Adding IL-6 increased GAG production by healthy chondrocytes and decreased GAG release by osteoarthritic chondrocytes (P &lt; 0.05).	Glycosaminoglycans	22-25	interleukin 6	Homo sapiens	7-11
23206933-9	2012	Adding IL-6 increased GAG production by healthy chondrocytes and decreased GAG release by osteoarthritic chondrocytes (P &lt; 0.05).	Glycosaminoglycans	75-78	interleukin 6	Homo sapiens	7-11
23206933-10	2012	Inhibition of IL-6 present in osteoarthritic synovial fluid showed a trend towards decreased GAG content of the explants (P = 0.06).	Glycosaminoglycans	93-96	interleukin 6	Homo sapiens	14-18
22752444-0	2012	RANTES/CCL5-induced pro-angiogenic effects depend on CCR1, CCR5 and glycosaminoglycans.	Glycosaminoglycans	68-86	C-C motif chemokine ligand 5	Rattus norvegicus	7-11
23134572-9	2012	When the Vpr-defective virus life cycle was compared with the WT virus life cycle in the semi-permissive cells, it was found that the Vpr-defective virus could enter the cell and produce virions containing properly processed Gag and Env proteins, but these virions showed much less efficiency for reverse transcription during the next-round of infection.	Glycosaminoglycans	225-228	Vpr	Human immunodeficiency virus 1	9-12
22978549-8	2012	RESULTS: Co-immunoprecipitation analyses and live cell tri-molecular fluorescence complementation assays revealed that interactions between EAP30 and Gag and another between EAP30 and Staufen1 occur in mammalian cells.	Glycosaminoglycans	150-153	SNF8 subunit of ESCRT-II	Homo sapiens	140-145
22992945-9	2012	S1P dose-dependently inhibited IL-1beta-induced NF-kappaB p65, cyclooxygenase (COX)-2, MMP-1, MMP-3, MMP-13 and MMP-14 mRNA expression in human chondrocytes and IL-1beta-induced PGE2 synthesis and GAG degradation in human cartilage explants.	Glycosaminoglycans	197-200	interleukin 1 beta	Homo sapiens	31-39
22973023-0	2012	Differential clade-specific HLA-B*3501 association with HIV-1 disease outcome is linked to immunogenicity of a single Gag epitope.	Glycosaminoglycans	118-121	major histocompatibility complex, class I, B	Homo sapiens	28-33
22981647-0	2012	Natural deletion of L35Y36 in p6 gag eliminate LYPXnL/ALIX auxiliary virus release pathway in HIV-1 subtype C. Natural loss of L35Y36 residues in ALIX binding site of HIV-1 subtype C was found to prevent the p6 gag-ALIX interaction.	Glycosaminoglycans	33-36	programmed cell death 6 interacting protein	Homo sapiens	54-58
22981647-0	2012	Natural deletion of L35Y36 in p6 gag eliminate LYPXnL/ALIX auxiliary virus release pathway in HIV-1 subtype C. Natural loss of L35Y36 residues in ALIX binding site of HIV-1 subtype C was found to prevent the p6 gag-ALIX interaction.	Glycosaminoglycans	33-36	programmed cell death 6 interacting protein	Homo sapiens	146-150
22981647-0	2012	Natural deletion of L35Y36 in p6 gag eliminate LYPXnL/ALIX auxiliary virus release pathway in HIV-1 subtype C. Natural loss of L35Y36 residues in ALIX binding site of HIV-1 subtype C was found to prevent the p6 gag-ALIX interaction.	Glycosaminoglycans	33-36	programmed cell death 6 interacting protein	Homo sapiens	146-150
23005914-5	2012	By tailoring the peptide displayed to cells and the substrate mechanical properties, a hydrogel was generated that binds hES cell surface glycosaminoglycans (GAGs) and functions robustly in a defined culture medium to support long-term hES cell self-renewal.	Glycosaminoglycans	138-156	ribosome binding protein 1	Homo sapiens	121-124
23005914-5	2012	By tailoring the peptide displayed to cells and the substrate mechanical properties, a hydrogel was generated that binds hES cell surface glycosaminoglycans (GAGs) and functions robustly in a defined culture medium to support long-term hES cell self-renewal.	Glycosaminoglycans	138-156	ribosome binding protein 1	Homo sapiens	236-239
23005914-5	2012	By tailoring the peptide displayed to cells and the substrate mechanical properties, a hydrogel was generated that binds hES cell surface glycosaminoglycans (GAGs) and functions robustly in a defined culture medium to support long-term hES cell self-renewal.	Glycosaminoglycans	158-162	ribosome binding protein 1	Homo sapiens	121-124
23005914-5	2012	By tailoring the peptide displayed to cells and the substrate mechanical properties, a hydrogel was generated that binds hES cell surface glycosaminoglycans (GAGs) and functions robustly in a defined culture medium to support long-term hES cell self-renewal.	Glycosaminoglycans	158-162	ribosome binding protein 1	Homo sapiens	236-239
23131037-7	2012	Further, we demonstrate that the Gag p27CA-specific CD4+ T cells exhibited cytolytic activity and that SIV bearing the Gag D205E mutation escapes this CD4+ T cell effector function ex vivo.	Glycosaminoglycans	33-36	CD4 molecule	Homo sapiens	52-55
23131037-7	2012	Further, we demonstrate that the Gag p27CA-specific CD4+ T cells exhibited cytolytic activity and that SIV bearing the Gag D205E mutation escapes this CD4+ T cell effector function ex vivo.	Glycosaminoglycans	119-122	CD4 molecule	Homo sapiens	151-154
23121099-7	2012	Biochemical assay and histology showed that GDF-5 can obviously enhance GAG, Cx43 and type II collagen expressions.	Glycosaminoglycans	72-75	growth differentiation factor 5	Homo sapiens	44-49
23121099-9	2012	Furthermore, real-time polymerase chain reaction showed that GDF-5 enhanced GAG and type II collagen transcription while 1-heptanol reduced them, but was affectless on Cx43 transcription.	Glycosaminoglycans	76-79	growth differentiation factor 5	Homo sapiens	61-66
23055560-2	2012	Proteolysis of its main structural component, Gag, is required for morphological maturation and infectivity and leads to release of four functional domains and the spacer peptides SP1 and SP2.	Glycosaminoglycans	46-49	Sp2 transcription factor	Homo sapiens	188-191
22765926-5	2012	Cells cultured with &gt;=100 mug/mL of the peptide produced 74% of the GAG content that cells cultured with BMP-2 produced.	Glycosaminoglycans	71-74	bone morphogenetic protein 2	Homo sapiens	108-113
22765926-6	2012	Comparable levels of GAG production were promoted by the peptide and BMP-2 over 4 weeks of culture.	Glycosaminoglycans	21-24	bone morphogenetic protein 2	Homo sapiens	69-74
23134572-9	2012	When the Vpr-defective virus life cycle was compared with the WT virus life cycle in the semi-permissive cells, it was found that the Vpr-defective virus could enter the cell and produce virions containing properly processed Gag and Env proteins, but these virions showed much less efficiency for reverse transcription during the next-round of infection.	Glycosaminoglycans	225-228	Vpr	Human immunodeficiency virus 1	134-137
22933280-4	2012	Recent studies have shown that human chromosome region maintenance 1 (hCRM1) stimulates Gag release from rodent cells.	Glycosaminoglycans	88-91	exportin 1	Homo sapiens	70-75
22895561-4	2012	In the present study, we explored the potential role of the GAG chains of BGN in promoting BMP-4-induced osteoblast differentiation.	Glycosaminoglycans	60-63	bone morphogenetic protein 4	Mus musculus	91-96
22895561-9	2012	Our study demonstrated that a mutant BGN lacking GAG chains decreased BGN-assisted BMP-4 signaling and osteoblast differentiation and that the expression of this mutant BGN in biglycan knockout (BGN-KO) calvarial osteoblasts could not rescue its differentiation deficiency as efficiently as wild-type (WT) BGN.	Glycosaminoglycans	49-52	bone morphogenetic protein 4	Mus musculus	83-88
22895561-10	2012	These results strongly suggest that the GAG chains of BGN promote BGN-assisted BMP-4 function.	Glycosaminoglycans	40-43	bone morphogenetic protein 4	Mus musculus	79-84
22896606-7	2012	HLA-B*42:01, which presents multiple Gag epitopes, is associated with a 0.52 log(10) lower viral-load set point than HLA-B*42:02 (P = 0.02), which presents no p24 Gag epitopes.	Glycosaminoglycans	37-40	major histocompatibility complex, class I, B	Homo sapiens	0-5
22896606-7	2012	HLA-B*42:01, which presents multiple Gag epitopes, is associated with a 0.52 log(10) lower viral-load set point than HLA-B*42:02 (P = 0.02), which presents no p24 Gag epitopes.	Glycosaminoglycans	163-166	major histocompatibility complex, class I, B	Homo sapiens	0-5
22933291-8	2012	These results provide in vivo evidence of the detrimental impact of B*81:01-mediated viral evolution, in a single Gag p24 epitope, on the control of viremia.	Glycosaminoglycans	114-117	transmembrane p24 trafficking protein 2	Homo sapiens	118-121
22698876-4	2012	The initial annealing by Gag is assisted by the architecture of an early viral assembly intermediate we term the "tRNA(Lys3) annealing complex" whose composition includes Gag, GagPol, viral RNA, lysyl-tRNA synthetase (LysRS), and the tRNA(Lys) isoacceptors.	Glycosaminoglycans	25-28	mitochondrially encoded tRNA glycine	Homo sapiens	114-123
22809835-6	2012	RESULTS: Hylan G-F 20 retained GAG in IL-1beta-exposed bovine and human cartilage explants and abrogated IL-1beta-mediated increases in MMP-1, -3, and -13 in human explant culture.	Glycosaminoglycans	31-34	interleukin 1 beta	Bos taurus	38-46
22698876-4	2012	The initial annealing by Gag is assisted by the architecture of an early viral assembly intermediate we term the "tRNA(Lys3) annealing complex" whose composition includes Gag, GagPol, viral RNA, lysyl-tRNA synthetase (LysRS), and the tRNA(Lys) isoacceptors.	Glycosaminoglycans	25-28	lysyl-tRNA synthetase 1	Homo sapiens	195-216
22698876-4	2012	The initial annealing by Gag is assisted by the architecture of an early viral assembly intermediate we term the "tRNA(Lys3) annealing complex" whose composition includes Gag, GagPol, viral RNA, lysyl-tRNA synthetase (LysRS), and the tRNA(Lys) isoacceptors.	Glycosaminoglycans	25-28	lysyl-tRNA synthetase 1	Homo sapiens	218-223
22674034-1	2012	OBJECTIVE: To study the regulation of expression of beta-1,3-glucuronosyltransferase 1 (GlcAT-1), an important regulator of glycosaminoglycan (GAG) synthesis, by Smad3 in nucleus pulposus (NP) cells.	Glycosaminoglycans	124-141	SMAD family member 3	Rattus norvegicus	162-167
23095131-2	2012	The signaling of FGF-2, a growth factor involved in this mechanism, is regulated by glycosaminoglycans.	Glycosaminoglycans	84-102	fibroblast growth factor 2	Homo sapiens	17-22
22674034-11	2012	Lentiviral transduction of NP cells with short hairpin RNA Smad3 resulted in a decrease in GlcAT-1 expression and accumulation of GAG.	Glycosaminoglycans	130-133	SMAD family member 3	Rattus norvegicus	59-64
22674034-16	2012	However, an altered responsiveness to TGFbeta during disc degeneration may compromise GAG synthesis.	Glycosaminoglycans	86-89	transforming growth factor, beta 1	Rattus norvegicus	38-45
22795539-6	2012	Also, the specific extracellular matrix of glycosaminoglycan (GAG) production of hMSCs adhered onto SOX9 gene plus heparinized TGF-beta 3 coated dexamethasone loaded PLGA microspheres increased more 2.5 times than control group.	Glycosaminoglycans	43-60	SRY-box transcription factor 9	Homo sapiens	100-104
22795539-6	2012	Also, the specific extracellular matrix of glycosaminoglycan (GAG) production of hMSCs adhered onto SOX9 gene plus heparinized TGF-beta 3 coated dexamethasone loaded PLGA microspheres increased more 2.5 times than control group.	Glycosaminoglycans	43-60	transforming growth factor beta 3	Homo sapiens	127-137
22795539-6	2012	Also, the specific extracellular matrix of glycosaminoglycan (GAG) production of hMSCs adhered onto SOX9 gene plus heparinized TGF-beta 3 coated dexamethasone loaded PLGA microspheres increased more 2.5 times than control group.	Glycosaminoglycans	62-65	SRY-box transcription factor 9	Homo sapiens	100-104
22749061-4	2012	Additionally, we identified an intronic splicing regulatory element within the p17-instability element of the Gag-ORF enhancing D1-activation.	Glycosaminoglycans	110-113	family with sequence similarity 72 member B	Homo sapiens	79-82
22795539-6	2012	Also, the specific extracellular matrix of glycosaminoglycan (GAG) production of hMSCs adhered onto SOX9 gene plus heparinized TGF-beta 3 coated dexamethasone loaded PLGA microspheres increased more 2.5 times than control group.	Glycosaminoglycans	62-65	transforming growth factor beta 3	Homo sapiens	127-137
22877511-3	2012	Mutations in decorin or alterations in the post-translational modifications of the glycosaminoglycan (GAG) chain lead to connective tissue disorders such as the congenital stromal corneal dystrophy and the Ehlers-Danlos syndrome.	Glycosaminoglycans	83-100	decorin	Homo sapiens	13-20
22877511-3	2012	Mutations in decorin or alterations in the post-translational modifications of the glycosaminoglycan (GAG) chain lead to connective tissue disorders such as the congenital stromal corneal dystrophy and the Ehlers-Danlos syndrome.	Glycosaminoglycans	102-105	decorin	Homo sapiens	13-20
22877511-4	2012	The summarized data reveal that decorin has a large impact on biological processes also because of the complex structure of the GAG chain.	Glycosaminoglycans	128-131	decorin	Homo sapiens	32-39
22877511-7	2012	Since defects in the biosynthesis of either the protein core or the GAG chain lead to structural alterations in the extracellular matrix and changes in the protein expression profile of the cells embedded in the matrix, this review focuses on the insights of structural function of decorin and includes data about dermatan sulfate.	Glycosaminoglycans	68-71	decorin	Homo sapiens	282-289
22797723-5	2012	Glycosaminoglycan-modified and -unmodified APLP2, and particularly APLP2 C-terminal fragments, also demonstrated increased expression in oncogene-transformed pancreatic ductal cells.	Glycosaminoglycans	0-17	amyloid beta precursor like protein 2	Homo sapiens	43-48
22659308-2	2012	The most common of the inherited dystonias is DYT1 dystonia, which is due to deletion of a single GAG codon (DeltaE) in the TOR1A gene that encodes torsinA.	Glycosaminoglycans	98-101	torsin family 1, member A (torsin A)	Mus musculus	46-50
22714108-6	2012	In pellet cultures of MSCs, TGF-beta1 successfully induced chondrogenic differentiation and glycosaminoglycan synthesis.	Glycosaminoglycans	92-109	transforming growth factor beta 1	Gallus gallus	28-37
22714108-7	2012	Addition of CNP into the TGF-beta1 supplemented chondrogenic differentiation medium further induced the glycosaminoglycan synthesis and hypertrophy of differentiated chondrocytes in these pellets.	Glycosaminoglycans	104-121	natriuretic peptide C	Homo sapiens	12-15
22714108-7	2012	Addition of CNP into the TGF-beta1 supplemented chondrogenic differentiation medium further induced the glycosaminoglycan synthesis and hypertrophy of differentiated chondrocytes in these pellets.	Glycosaminoglycans	104-121	transforming growth factor beta 1	Gallus gallus	25-34
22714108-9	2012	In conclusion, CNP-3/NPR-B signaling may strongly be involved in synthesis of glycosaminoglycans of the chondrogenic matrix and hypertrophy of differentiated chondrocytes during TGF-beta1 induced chondrogenic differentiation of MSCs.	Glycosaminoglycans	78-96	C-type natriuretic peptide 3	Gallus gallus	15-20
22659308-2	2012	The most common of the inherited dystonias is DYT1 dystonia, which is due to deletion of a single GAG codon (DeltaE) in the TOR1A gene that encodes torsinA.	Glycosaminoglycans	98-101	torsin family 1, member A (torsin A)	Mus musculus	124-129
22659308-2	2012	The most common of the inherited dystonias is DYT1 dystonia, which is due to deletion of a single GAG codon (DeltaE) in the TOR1A gene that encodes torsinA.	Glycosaminoglycans	98-101	torsin family 1, member A (torsin A)	Mus musculus	148-155
22265686-4	2012	Novel method for enrichment analysis of GAG-primed PGIs by combined use of anti-FITC antibody and LC/mass spectrometry was established.	Glycosaminoglycans	40-43	prostaglandin I2 synthase	Homo sapiens	51-55
22718867-10	2012	TNF inhibited GAG deposition in both RA and OA samples similarly.	Glycosaminoglycans	14-17	tumor necrosis factor	Homo sapiens	0-3
23007908-3	2012	Low doses of IL-1beta (50 pg/mL) enhanced colony-forming units-fibroblastic (CFU-f) and -osteoblastic (CFU-o) number (up to 1.5-fold) and size (1.2-fold) in the absence of further supplements and glycosaminoglycan accumulation (1.4-fold) upon BM-MSC chondrogenic induction.	Glycosaminoglycans	196-213	interleukin 1 beta	Homo sapiens	13-21
22265686-6	2012	It was demonstrated that PGIs become good substrates for GAG biosynthesis within the cells and high molecular weight GAGs primed by PGIs is chondroitin sulfate involving N-acetyl-d-galactosamine residues substituted by 4-O-sulfate or 6-O-sulfate group as major components.	Glycosaminoglycans	57-60	prostaglandin I2 synthase	Homo sapiens	25-29
22265686-8	2012	CONCLUSION: Synthetic serglycin-type PGIs allow for live cell imaging during proteoglycan biosynthesis and structural characterization of GAG-primed PGIs by an antibody-based enrichment protocol.	Glycosaminoglycans	138-141	prostaglandin I2 synthase	Homo sapiens	37-41
22265686-8	2012	CONCLUSION: Synthetic serglycin-type PGIs allow for live cell imaging during proteoglycan biosynthesis and structural characterization of GAG-primed PGIs by an antibody-based enrichment protocol.	Glycosaminoglycans	138-141	prostaglandin I2 synthase	Homo sapiens	149-153
22718819-7	2012	Cotransfection of RPL4 cDNA with Moloney murine leukemia proviral DNA results in Gag processing defects and a reduction of viral particle formation, presumably caused by the RPL4-dependent alteration of the Gag-to-Gag-Pol ratio required for virion assembly and release.	Glycosaminoglycans	81-84	ribosomal protein L4	Mus musculus	18-22
22721770-3	2012	Xylosyltransferase-1 (XT-1) is the enzyme that initiates GAG-chain formation.	Glycosaminoglycans	57-60	xylosyltransferase 1	Homo sapiens	0-20
22721770-3	2012	Xylosyltransferase-1 (XT-1) is the enzyme that initiates GAG-chain formation.	Glycosaminoglycans	57-60	xylosyltransferase 1	Homo sapiens	22-26
22580564-4	2012	CD4 T-cell responses focused primarily on Gag, whereas CD8 T-cell responses were broadly directed against Gag, gp41, and Nef VIP sets.	Glycosaminoglycans	42-45	CD4 molecule	Homo sapiens	0-3
22687758-2	2012	Heparin (HP), a highly sulfated glycosaminoglycan (GAG) that avidly binds BMP-2, has inherent biological properties that may circumvent these limitations.	Glycosaminoglycans	32-49	bone morphogenetic protein 2	Rattus norvegicus	74-79
22687758-2	2012	Heparin (HP), a highly sulfated glycosaminoglycan (GAG) that avidly binds BMP-2, has inherent biological properties that may circumvent these limitations.	Glycosaminoglycans	51-54	bone morphogenetic protein 2	Rattus norvegicus	74-79
22759308-6	2012	In addition, the 5"-UTR regulates expression in an RNA concentration-dependent manner, with a high concentration of RNA triggering specific reduction of full-length Gag p55 production.	Glycosaminoglycans	165-168	H3 histone pseudogene 44	Homo sapiens	169-172
22922259-6	2012	In particular, GAG-specific TFH cells were detected at significantly higher levels in the lymph nodes compared with those of GP120-specific TFH cells and showed preferential secretion of the helper cytokine IL-21.	Glycosaminoglycans	15-18	interleukin 21	Homo sapiens	207-212
22704483-1	2012	Mucopolysaccharidosis type II (MPS II), or Hunter syndrome, is a lysosomal storage disorder caused by a deficiency of iduronate-2-sulfatase (IDS) and is characterized by the accumulation of glycosaminoglycans (GAGs).	Glycosaminoglycans	190-208	iduronate 2-sulfatase	Mus musculus	141-144
22798665-3	2012	We observed that Gag stimulation of macaque PBMCs induced subset-specific NK cell responses in SIV-controlling but not SIV-noncontrolling animals, as well as that circulatory NK cell responses were dependent on Ag-specific IL-2 production by CD4(+) central memory T cells.	Glycosaminoglycans	17-20	interleukin 2	Homo sapiens	223-227
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
22902520-1	2012	Mucopolysaccharidosis (MPS) type VII is a lysosomal storage disease caused by deficiency of the lysosomal enzyme beta-glucuronidase (GUS), leading to accumulation of glycosaminoglycans (GAGs).	Glycosaminoglycans	166-184	glucuronidase, beta	Mus musculus	133-136
22704650-4	2012	With the porcine cartilage explant, IL-1beta induced release of sulfated-glycosaminoglycan (s-GAG) and hydroxyproline release, and this induction was significantly inhibited by sesamin.	Glycosaminoglycans	94-97	interleukin 1 beta	Rattus norvegicus	36-44
22146554-2	2012	In articular cartilage, xylosyltransferase 1 (Xylt1) is the key enzyme that initiates glycosaminoglycan (GAG) chain synthesis by transferring the first sugar residue to the PG core protein.	Glycosaminoglycans	86-103	xylosyltransferase 1	Mus musculus	24-44
22146554-2	2012	In articular cartilage, xylosyltransferase 1 (Xylt1) is the key enzyme that initiates glycosaminoglycan (GAG) chain synthesis by transferring the first sugar residue to the PG core protein.	Glycosaminoglycans	86-103	xylosyltransferase 1	Mus musculus	46-51
22146554-2	2012	In articular cartilage, xylosyltransferase 1 (Xylt1) is the key enzyme that initiates glycosaminoglycan (GAG) chain synthesis by transferring the first sugar residue to the PG core protein.	Glycosaminoglycans	105-108	xylosyltransferase 1	Mus musculus	24-44
22146554-2	2012	In articular cartilage, xylosyltransferase 1 (Xylt1) is the key enzyme that initiates glycosaminoglycan (GAG) chain synthesis by transferring the first sugar residue to the PG core protein.	Glycosaminoglycans	105-108	xylosyltransferase 1	Mus musculus	46-51
22660841-1	2012	Syndecan-4 is a cell membrane proteoglycan composed of a transmembrane core protein and substituted glycosaminoglycan (GAG) and N-linked glycosylated (N-glycosylated) chains.	Glycosaminoglycans	119-122	syndecan-4	Meleagris gallopavo	0-10
22863285-7	2012	IL-1ra released from microspheres attenuated the degradative effects of IL-1beta as defined by mechanical properties, glycosaminoglycans (GAG) content, nitric oxide production and mRNA expression of inflammatory mediators for 7 days, and continued to limit functional degradation for up to 20 days.	Glycosaminoglycans	118-136	interleukin 1 receptor antagonist	Homo sapiens	0-6
22863285-7	2012	IL-1ra released from microspheres attenuated the degradative effects of IL-1beta as defined by mechanical properties, glycosaminoglycans (GAG) content, nitric oxide production and mRNA expression of inflammatory mediators for 7 days, and continued to limit functional degradation for up to 20 days.	Glycosaminoglycans	138-141	interleukin 1 receptor antagonist	Homo sapiens	0-6
22539336-8	2012	To further define function of CANT1, we studied proteoglycan synthesis in CANT1 mutated patient fibroblasts, and found significant reduced GAG synthesis in presence of beta-D-xyloside, suggesting that CANT1 plays a role in proteoglycan metabolism.	Glycosaminoglycans	139-142	calcium activated nucleotidase 1	Homo sapiens	30-35
22813851-0	2012	Plasma biomarkers of oxidative and AGE-mediated damage of proteins and glycosaminoglycans during healthy ageing: a possible association with ECM metabolism.	Glycosaminoglycans	71-89	multimerin 1	Homo sapiens	141-144
22618708-7	2012	The crystal structures suggest a unique 2-step mechanism of thrombin recognition involving rapid electrostatics-driven association to form an initial glycosaminoglycan-bridged complex, followed by a large conformational rearrangement to form the productive Michaelis complex.	Glycosaminoglycans	150-167	coagulation factor II, thrombin	Homo sapiens	60-68
22444322-0	2012	The influence of glycosaminoglycans on IL-8-mediated functions of neutrophils.	Glycosaminoglycans	17-35	C-X-C motif chemokine ligand 8	Homo sapiens	39-43
23016426-3	2012	The results showed that having been induced with bFGF, the BMSCs could differentiate into fibroblast-like cells, which could synthesize GAG and collagen type I matrix.	Glycosaminoglycans	136-139	fibroblast growth factor 2	Homo sapiens	49-53
22498748-4	2012	These mutations do not modify the folding or secretion of the protein, but abolish the glycosaminoglycan-induced activation of antithrombin by affecting the heparin-binding domain.	Glycosaminoglycans	87-104	serpin family C member 1	Homo sapiens	127-139
22817660-6	2012	RESULTS: IHH, TGF-beta1 and BMP-2 genes were equipotent inducers of chondrogenesis in primary MSCs, as evidenced by strong staining for proteoglycans, collagen type II, increased levels of glycosaminoglycan synthesis, and expression of mRNAs associated with chondrogenesis.	Glycosaminoglycans	189-206	Indian hedgehog signaling molecule	Homo sapiens	9-12
22817660-6	2012	RESULTS: IHH, TGF-beta1 and BMP-2 genes were equipotent inducers of chondrogenesis in primary MSCs, as evidenced by strong staining for proteoglycans, collagen type II, increased levels of glycosaminoglycan synthesis, and expression of mRNAs associated with chondrogenesis.	Glycosaminoglycans	189-206	bone morphogenetic protein 2	Homo sapiens	28-33
22618708-3	2012	Rather, PN1 is expressed by multiple cell types, including macrophages, smooth muscle cells, and platelets, and it is on the surface of these cells, bound to glycosaminoglycans, that PN1 inhibits the signaling functions of thrombin.	Glycosaminoglycans	158-176	serpin family E member 2	Homo sapiens	8-11
22618708-3	2012	Rather, PN1 is expressed by multiple cell types, including macrophages, smooth muscle cells, and platelets, and it is on the surface of these cells, bound to glycosaminoglycans, that PN1 inhibits the signaling functions of thrombin.	Glycosaminoglycans	158-176	serpin family E member 2	Homo sapiens	183-186
22618708-3	2012	Rather, PN1 is expressed by multiple cell types, including macrophages, smooth muscle cells, and platelets, and it is on the surface of these cells, bound to glycosaminoglycans, that PN1 inhibits the signaling functions of thrombin.	Glycosaminoglycans	158-176	coagulation factor II, thrombin	Homo sapiens	223-231
22414620-12	2012	Most importantly, intra-articular treatment with either PTH(1-34) (0.1-100 nM) 3 days/injection or PTH/PLGA microspheres (15 days/injection) for 5 weeks revealed the similar effect on suppressing papain-induced OA changes (decreasing GAG and Col II and increasing Col X) in rat knee cartilage.	Glycosaminoglycans	234-237	parathyroid hormone	Rattus norvegicus	56-59
22613796-4	2012	Whereas Gag-specific CTLs generally were less susceptible to Nef than those targeting other proteins, this was determined by the ability to eliminate infected cells before de novo synthesis of viral proteins, which was also observed for CTLs targeting a Nef epitope.	Glycosaminoglycans	8-11	S100 calcium binding protein B	Homo sapiens	254-257
22613796-6	2012	These results suggest that whereas Gag-specific CTLs are more likely to recognize infected cells before Nef-mediated HLA-I down-regulation, this varies depending on the specific epitope and virus inoculum.	Glycosaminoglycans	35-38	S100 calcium binding protein B	Homo sapiens	104-107
22613796-7	2012	Reduced susceptibility to Nef therefore may contribute to the overall association of Gag-specific CTL responses to better immune control if a sufficient multiplicity of infection is attained in vivo, but this property is not unique to Gag.	Glycosaminoglycans	85-88	S100 calcium binding protein B	Homo sapiens	26-29
22613796-7	2012	Reduced susceptibility to Nef therefore may contribute to the overall association of Gag-specific CTL responses to better immune control if a sufficient multiplicity of infection is attained in vivo, but this property is not unique to Gag.	Glycosaminoglycans	235-238	S100 calcium binding protein B	Homo sapiens	26-29
22613796-4	2012	Whereas Gag-specific CTLs generally were less susceptible to Nef than those targeting other proteins, this was determined by the ability to eliminate infected cells before de novo synthesis of viral proteins, which was also observed for CTLs targeting a Nef epitope.	Glycosaminoglycans	8-11	S100 calcium binding protein B	Homo sapiens	61-64
22764251-4	2012	We identify a 15 aa domain containing an arginine-lysine doublet (RK peptide) within Otx2, bearing prototypic traits of a glycosaminoglycan (GAG) binding sequence that mediates Otx2 binding to PNNs, and specifically to chondroitin sulfate D and E, with high affinity.	Glycosaminoglycans	122-139	orthodenticle homeobox 2	Mus musculus	85-89
22764251-4	2012	We identify a 15 aa domain containing an arginine-lysine doublet (RK peptide) within Otx2, bearing prototypic traits of a glycosaminoglycan (GAG) binding sequence that mediates Otx2 binding to PNNs, and specifically to chondroitin sulfate D and E, with high affinity.	Glycosaminoglycans	122-139	orthodenticle homeobox 2	Mus musculus	177-181
22764251-4	2012	We identify a 15 aa domain containing an arginine-lysine doublet (RK peptide) within Otx2, bearing prototypic traits of a glycosaminoglycan (GAG) binding sequence that mediates Otx2 binding to PNNs, and specifically to chondroitin sulfate D and E, with high affinity.	Glycosaminoglycans	141-144	orthodenticle homeobox 2	Mus musculus	85-89
22764251-4	2012	We identify a 15 aa domain containing an arginine-lysine doublet (RK peptide) within Otx2, bearing prototypic traits of a glycosaminoglycan (GAG) binding sequence that mediates Otx2 binding to PNNs, and specifically to chondroitin sulfate D and E, with high affinity.	Glycosaminoglycans	141-144	orthodenticle homeobox 2	Mus musculus	177-181
22764251-10	2012	The pharmacological use of the Otx2 GAG binding domain offers a novel, potent therapeutic tool with which to restore cortical plasticity in the mature brain.	Glycosaminoglycans	36-39	orthodenticle homeobox 2	Mus musculus	31-35
22414620-12	2012	Most importantly, intra-articular treatment with either PTH(1-34) (0.1-100 nM) 3 days/injection or PTH/PLGA microspheres (15 days/injection) for 5 weeks revealed the similar effect on suppressing papain-induced OA changes (decreasing GAG and Col II and increasing Col X) in rat knee cartilage.	Glycosaminoglycans	234-237	parathyroid hormone	Rattus norvegicus	99-102
22644958-6	2012	After 4 weeks, the wet weight and GAG content in Exp.	Glycosaminoglycans	34-37	muscleblind like splicing regulator 1	Homo sapiens	49-52
22471560-3	2012	To elucidate the molecular mechanism of binding of FH to glycosaminoglycans, we performed ultracentrifugation, X-ray scattering and surface plasmon resonance with FH and glycosaminoglycan fragments.	Glycosaminoglycans	57-75	complement factor H	Homo sapiens	51-53
23507865-4	2012	Regulatory aspects of the interplay between IL-8 and heparan sulfate, the most abundant glycosaminoglycan, are highlighted.	Glycosaminoglycans	88-105	C-X-C motif chemokine ligand 8	Homo sapiens	44-48
23507865-5	2012	In this field, the large natural heterogeneity of glycosaminoglycans represents a great challenge that impedes the modeling of IL-8 functions.	Glycosaminoglycans	50-68	C-X-C motif chemokine ligand 8	Homo sapiens	127-131
22579681-11	2012	The results reveal the structural basis for the high affinity of ECP for glycosaminoglycans and can assist in structure-based drug design of inhibitors of the protein cytotoxicity to host tissues during inflammation.	Glycosaminoglycans	73-91	ribonuclease A family member 3	Homo sapiens	65-68
22835945-12	2012	These results suggest that SAGs bind to the extracellular matrix proteoglycans decorin and biglycan, with interaction mediated by the conjugated glycosaminoglycan chain.	Glycosaminoglycans	145-162	biglycan	Homo sapiens	91-99
22471560-3	2012	To elucidate the molecular mechanism of binding of FH to glycosaminoglycans, we performed ultracentrifugation, X-ray scattering and surface plasmon resonance with FH and glycosaminoglycan fragments.	Glycosaminoglycans	57-74	complement factor H	Homo sapiens	51-53
22410212-5	2012	Consistent with the inhibition of sulfatase activity, following exposure to carrageenan, GAG content increased significantly and showed marked differences in disaccharide composition.	Glycosaminoglycans	89-92	arylsulfatase family member H	Homo sapiens	34-43
22410212-8	2012	Study results suggest that carrageenan inhibition of sulfatase activity leads to re-distribution of the cellular GAG composition with increase in di-sulfated CS and with potential consequences for cell structure and function.	Glycosaminoglycans	113-116	arylsulfatase family member H	Homo sapiens	53-62
22491464-9	2012	Gag-specific CD8(+) T-cell responses were efficiently induced in A(+) animals, while Nef-specific CD8(+) T-cell responses were in A(+), E(+), and B(+) animals.	Glycosaminoglycans	0-3	CD8a molecule	Homo sapiens	13-16
22121037-9	2012	There was a heterogenous attenuation of PNN components, including glycosaminoglycans, indicating the elaborate molecular organization of the PNN components.	Glycosaminoglycans	66-84	pinin	Mus musculus	141-144
22493510-0	2012	Receptor for advanced glycation end products (RAGE) functions as receptor for specific sulfated glycosaminoglycans, and anti-RAGE antibody or sulfated glycosaminoglycans delivered in vivo inhibit pulmonary metastasis of tumor cells.	Glycosaminoglycans	96-114	advanced glycosylation end product-specific receptor	Mus musculus	46-50
22493510-0	2012	Receptor for advanced glycation end products (RAGE) functions as receptor for specific sulfated glycosaminoglycans, and anti-RAGE antibody or sulfated glycosaminoglycans delivered in vivo inhibit pulmonary metastasis of tumor cells.	Glycosaminoglycans	151-169	advanced glycosylation end product-specific receptor	Mus musculus	46-50
22245318-6	2012	In addition, elastin-modified constructs yielded higher quantities of secreted glycosaminoglycans and produced collagen than poly-L-lysine-modified constructs.	Glycosaminoglycans	79-97	elastin	Bos taurus	13-20
22226333-0	2012	The GAG deletion in Tor1A (DYT1) is a rare cause of complex musician"s dystonia.	Glycosaminoglycans	4-7	torsin family 1 member A	Homo sapiens	20-25
22226333-0	2012	The GAG deletion in Tor1A (DYT1) is a rare cause of complex musician"s dystonia.	Glycosaminoglycans	4-7	torsin family 1 member A	Homo sapiens	27-31
22593947-0	2004	N"-Fluorescein-N""-[4-O-(beta-d-glucopyranuronic acid)-3-difluoromethylphenyl]-S-methylthiourea (FITC-TrapG) and N"-(p-aminophenyl)thioether of IR-820-N""-[4-O-(beta-d-glucopyranuronic acid)-3-difluoromethylphenyl]-S-methylthiourea (NIR-TrapG) The beta-glucuronidase (betaG; EC 3.2.1.31) is a lysosomal enzyme that catalyzes the hydrolysis of beta-glucuronic acid residues from the cell-surface glycosaminoglycans for normal reconstruction of the extracellular matrix (ECM) (1), and the enzyme is believed to participate in the processes of angiogenesis, cancer metastasis, and inflammation (2).	Glycosaminoglycans	395-413	signal sequence receptor, gamma	Mus musculus	102-107
22272563-3	2012	The N-glycosylated chains and GAG chains are required for S4 to regulate turkey myogenic satellite cell proliferation.	Glycosaminoglycans	30-33	syndecan-4	Meleagris gallopavo	58-60
22272563-5	2012	S4 mutants with only one or without any N-glycosylated chains attached to the core protein with or without GAG chains were generated to study the function of N-glycosylated chains and the interaction between N-glycosylated chains and GAG chains.	Glycosaminoglycans	107-110	syndecan-4	Meleagris gallopavo	0-2
22245318-8	2012	The staining images revealed that elastin induced larger amounts of regenerated bovine knee chondrocytes, glycosaminoglycans, and type II collagen in the constructs than poly-L-lysine.	Glycosaminoglycans	106-124	elastin	Bos taurus	34-41
22366163-13	2012	Thus, absence of sulfatase activity increases sulfated GAG deposition in the lungs causing deregulation of TGFbeta signaling and arrest of alveolarization.	Glycosaminoglycans	55-58	transforming growth factor, beta 1	Mus musculus	107-114
22643054-0	2012	A novel synthetic derivative of human erythropoietin designed to bind to glycosaminoglycans.	Glycosaminoglycans	73-91	erythropoietin	Homo sapiens	38-52
22419810-8	2012	Remarkably, both the frequency and the number of Gag CM9-specific public clonotypes were strongly correlated with VIA mediated by EM CD8(+) T cells.	Glycosaminoglycans	49-52	CD8a molecule	Homo sapiens	133-136
22107247-4	2012	BMP-2 in the atelocollagen with the supplement of insulin and T3 in the medium could not only produce a greater GAG matrix in a shorter period but also sustain cell viability with lower mortality.	Glycosaminoglycans	112-115	bone morphogenetic protein 2	Homo sapiens	0-5
22402327-1	2012	Previous work shows that MPS I dogs receiving enzyme replacement with recombinant human alpha-l-iduronidase into the cisterna magna showed normal brain glycosaminoglycan (GAG) storage after three or four doses.	Glycosaminoglycans	152-169	alpha-L-iduronidase	Homo sapiens	88-107
22107247-4	2012	BMP-2 in the atelocollagen with the supplement of insulin and T3 in the medium could not only produce a greater GAG matrix in a shorter period but also sustain cell viability with lower mortality.	Glycosaminoglycans	112-115	insulin	Homo sapiens	50-57
22351761-10	2012	Importantly, the loops are evolutionarily conserved in vertebrate glypican-1, and one of them is involved in glycosaminoglycan class determination.	Glycosaminoglycans	109-126	glypican 1	Homo sapiens	66-76
21736424-6	2012	Our results demonstrated that when the individual Gag, Pol, or Env gene products were coimmunized with the whole repertoire of nonstructural proteins, the Gag-specific CD8(+) T response was greatly enhanced, while the Env- and Pol-specific CD8(+) T responses were significantly reduced.	Glycosaminoglycans	50-53	endogenous retrovirus group K member 20	Homo sapiens	218-221
22383528-2	2012	This was reversed by transfection with the Smpd3 gene, suggesting a connection between sphingolipid and glycosaminoglycan metabolism.	Glycosaminoglycans	104-121	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	43-48
22520214-0	2012	Treatment of adult MPSI mouse brains with IDUA-expressing mesenchymal stem cells decreases GAG deposition and improves exploratory behavior.	Glycosaminoglycans	91-94	iduronidase, alpha-L	Mus musculus	42-46
22520214-1	2012	BACKGROUND: Mucopolysaccharidosis type I (MPSI) is caused by a deficiency in alpha-L iduronidase (IDUA), which leads to lysosomal accumulation of the glycosaminoglycans (GAGs) dermatan and heparan sulfate.	Glycosaminoglycans	150-168	iduronidase, alpha-L	Mus musculus	98-102
22520214-1	2012	BACKGROUND: Mucopolysaccharidosis type I (MPSI) is caused by a deficiency in alpha-L iduronidase (IDUA), which leads to lysosomal accumulation of the glycosaminoglycans (GAGs) dermatan and heparan sulfate.	Glycosaminoglycans	170-174	iduronidase, alpha-L	Mus musculus	98-102
22520214-3	2012	Based on the neuroprotective and tissue regenerative properties of mesenchymal stem cells (MSCs), we hypothesized that the administration of MSCs transduced with a murine leukemia virus (MLV) vector expressing IDUA to IDUA KO mouse brains could reduce GAG deposition in the brain and, as a result, improve neurofunctionality, as measured by exploratory activity.	Glycosaminoglycans	252-255	iduronidase, alpha-L	Mus musculus	210-214
22520214-10	2012	Overall, these results indicate that while the initial level of IDUA was not sustainable for a month, it was enough to reduce and maintain low GAG deposition and improve the exploratory activity for months.	Glycosaminoglycans	143-146	iduronidase, alpha-L	Mus musculus	64-68
22351752-9	2012	In addition, we found that although syndecan-1 interacts exclusively through its glycosaminoglycan chains, syndecan-4 binding relies on both its core protein and its heparan sulfate chains.	Glycosaminoglycans	81-98	syndecan 1	Homo sapiens	36-46
21736424-6	2012	Our results demonstrated that when the individual Gag, Pol, or Env gene products were coimmunized with the whole repertoire of nonstructural proteins, the Gag-specific CD8(+) T response was greatly enhanced, while the Env- and Pol-specific CD8(+) T responses were significantly reduced.	Glycosaminoglycans	155-158	endogenous retrovirus group K member 20	Homo sapiens	63-66
22455987-7	2012	In addition, the PlnD1-HA/BMP2-treated knees had higher mRNA levels encoding for type II collagen, proteoglycans and xylosyltransferase 1, a rate-limiting anabolic enzyme involved in the biosynthesis of glycosaminoglycan chains, relative to control knees (PlnD1-HA).	Glycosaminoglycans	203-220	bone morphogenetic protein 2	Mus musculus	26-30
22455987-7	2012	In addition, the PlnD1-HA/BMP2-treated knees had higher mRNA levels encoding for type II collagen, proteoglycans and xylosyltransferase 1, a rate-limiting anabolic enzyme involved in the biosynthesis of glycosaminoglycan chains, relative to control knees (PlnD1-HA).	Glycosaminoglycans	203-220	xylosyltransferase 1	Mus musculus	117-137
22320434-6	2012	Thickening and plaque deposits made by smooth muscle alpha actin- and vimentin-positive cells in a glycosaminoglycan matrix were observed.	Glycosaminoglycans	99-116	vimentin	Homo sapiens	70-78
22357927-4	2012	2-OST-deficient embryos have reduced GAG chain sulfation and are refractory to exogenous Wnt8 overexpression.	Glycosaminoglycans	37-40	heparan sulfate 2-O-sulfotransferase 1a	Danio rerio	0-5
22234688-4	2012	It has a high affinity for glycosaminoglycans, such as heparan sulfates, which potentiate its activity toward thrombin and target it to the pericellular space.	Glycosaminoglycans	27-45	coagulation factor II	Mus musculus	110-118
22289416-4	2012	A colorimetric assay for total sulfated glycosaminoglycan (GAG) quantification, comparing human keratinocytes (CCD1106 KERTr) expressing wild type and mutant recombinant GalNAc4-ST1, revealed decreased levels of total sulfated GAGs in cells expressing mutant GalNAc4-ST1, suggesting loss of function.	Glycosaminoglycans	40-57	carbohydrate sulfotransferase 8	Homo sapiens	170-181
23960993-6	2012	CONCLUSIONS: The most useful stains in ruling out SCC in a suspected case of MECC were shown to be mucicarmine and the glycosaminoglycan (GAG) stains.	Glycosaminoglycans	119-136	serpin family B member 3	Homo sapiens	50-53
23960993-6	2012	CONCLUSIONS: The most useful stains in ruling out SCC in a suspected case of MECC were shown to be mucicarmine and the glycosaminoglycan (GAG) stains.	Glycosaminoglycans	138-141	serpin family B member 3	Homo sapiens	50-53
22326778-4	2012	Immunization with EDAp24 fusion protein together with poly(I:C) adjuvant induced a specific p24 IFN-gamma production (Th1 profile) as well as protection against a Lm-Gag challenge, suggesting an additive or synergistic effect between both adjuvants.	Glycosaminoglycans	166-169	transmembrane p24 trafficking protein 2	Homo sapiens	21-24
22331468-4	2012	These effects do not require the antiprotease activity of PN-1 but involve PN-1 binding to glycosaminoglycans.	Glycosaminoglycans	91-109	serine (or cysteine) peptidase inhibitor, clade E, member 2	Mus musculus	75-79
22298772-7	2012	Mitogenic assays in cultured cells showed an age-dependent decrease of the elderly GAG capacities to potentiate FGF-2 whereas the potentiating effect on VEGF(165) was increased, as confirmed by augmented angiogenic cell proliferation in Matrigel plugs.	Glycosaminoglycans	83-86	fibroblast growth factor 2	Rattus norvegicus	112-117
22100386-6	2012	Sheets incorporated with fast-degrading microspheres containing TGF-beta1 produced significantly more GAG and GAG per DNA than all other groups tested and stained more intensely for type II collagen.	Glycosaminoglycans	102-105	transforming growth factor beta 1	Homo sapiens	64-73
22100386-6	2012	Sheets incorporated with fast-degrading microspheres containing TGF-beta1 produced significantly more GAG and GAG per DNA than all other groups tested and stained more intensely for type II collagen.	Glycosaminoglycans	110-113	transforming growth factor beta 1	Homo sapiens	64-73
22100438-0	2012	Tat(48-60) peptide amino acid sequence is not unique in its cell penetrating properties and cell-surface glycosaminoglycans inhibit its cellular uptake.	Glycosaminoglycans	105-123	tyrosine aminotransferase	Homo sapiens	0-3
22100438-9	2012	Cell uptake of Tat peptide was unspecific, took place either by phagocytosis or pinocytosis, and was inhibited by cell-surface glycosaminoglycans.	Glycosaminoglycans	127-145	tyrosine aminotransferase	Homo sapiens	15-18
22100438-11	2012	In conclusion, we show that Tat-related peptides enter cells on the basis of their cationic charge following different endocytosis pathways and that glycosaminoglycans on the cell surface negatively affect their uptake.	Glycosaminoglycans	149-167	tyrosine aminotransferase	Homo sapiens	28-31
21702696-3	2012	We show that the three amino acid deletion in gag p17 previously described from these LTS is not real and was a result of an alignment error.	Glycosaminoglycans	46-49	family with sequence similarity 72 member B	Homo sapiens	50-53
22320225-10	2012	Thus, potentially disease-related functional distinctions between mutants, and between FH and FH-related 1, may manifest in the presence of specific glycosaminoglycans.	Glycosaminoglycans	149-167	complement factor H	Homo sapiens	87-89
22406547-3	2012	We found that NgR1 and NgR3 bind with high affinity to the glycosaminoglycan moiety of proteoglycans and participate in CSPG inhibition in cultured neurons.	Glycosaminoglycans	59-76	reticulon 4 receptor	Mus musculus	14-18
22406547-3	2012	We found that NgR1 and NgR3 bind with high affinity to the glycosaminoglycan moiety of proteoglycans and participate in CSPG inhibition in cultured neurons.	Glycosaminoglycans	59-76	reticulon 4 receptor like 1	Homo sapiens	23-27
22394585-14	2012	CONCLUSION: TGF-beta maintains biomechanical properties and regulates expression of Papss2 and sulfation of glycosaminoglycans in mouse articular cartilage.	Glycosaminoglycans	108-126	transforming growth factor, beta 1	Mus musculus	12-20
22158871-5	2012	Compared with heparan sulfate, a well known glycosaminoglycan capable of forming a complex with FGF2, polySia formed a larger complex with distinct properties in facilitating oligomerization of FGF2, as well as in binding to FGF receptors.	Glycosaminoglycans	44-61	fibroblast growth factor 2	Mus musculus	96-100
22189147-6	2012	SOX trio-co-transduction significantly increased GAG contents as well as type II collagen gene and protein expression.	Glycosaminoglycans	49-52	quiescin sulfhydryl oxidase 1	Rattus norvegicus	0-3
21360690-3	2012	The chondrogenic potential, evaluated in three-dimensional (3D) cell aggregates, showed that FGF-2 and FGF-6, when used in combination with TGFbeta2 increased the size and glycosaminoglycan content of the cell aggregates without increasing cell number.	Glycosaminoglycans	172-189	fibroblast growth factor 2	Homo sapiens	93-98
21360690-3	2012	The chondrogenic potential, evaluated in three-dimensional (3D) cell aggregates, showed that FGF-2 and FGF-6, when used in combination with TGFbeta2 increased the size and glycosaminoglycan content of the cell aggregates without increasing cell number.	Glycosaminoglycans	172-189	fibroblast growth factor 6	Homo sapiens	103-108
21360690-3	2012	The chondrogenic potential, evaluated in three-dimensional (3D) cell aggregates, showed that FGF-2 and FGF-6, when used in combination with TGFbeta2 increased the size and glycosaminoglycan content of the cell aggregates without increasing cell number.	Glycosaminoglycans	172-189	transforming growth factor beta 2	Homo sapiens	140-148
22370795-6	2012	At low concentrations of TGF-beta3 (1 ng/mL), HP acted to enhance chondrogenesis of both SDSCs and FPSCs, as evident by a 3-fold increase in Sox9 expression and a significant increase in glycosaminoglycan accumulation.	Glycosaminoglycans	187-204	transforming growth factor beta 3	Homo sapiens	25-34
22147696-9	2012	MMP processing of CCL16-(1-97) in its extended carboxyl terminus yields two products, CCL16-(8-77) and CCL16-(8-85), with both showing unexpected enhanced glycosaminoglycan binding.	Glycosaminoglycans	155-172	C-C motif chemokine ligand 16	Homo sapiens	18-23
22147696-9	2012	MMP processing of CCL16-(1-97) in its extended carboxyl terminus yields two products, CCL16-(8-77) and CCL16-(8-85), with both showing unexpected enhanced glycosaminoglycan binding.	Glycosaminoglycans	155-172	C-C motif chemokine ligand 16	Homo sapiens	86-91
22147696-9	2012	MMP processing of CCL16-(1-97) in its extended carboxyl terminus yields two products, CCL16-(8-77) and CCL16-(8-85), with both showing unexpected enhanced glycosaminoglycan binding.	Glycosaminoglycans	155-172	C-C motif chemokine ligand 16	Homo sapiens	86-91
21890503-8	2012	In general, a functional association was found between the glycosaminoglycan and N-glycosylated chains attached to the central core proteins of syndecan-4 and glypican-1 affecting their regulation of muscle cell proliferation, differentiation, and FGF2 responsiveness.	Glycosaminoglycans	59-76	syndecan 4	Homo sapiens	144-154
21890503-8	2012	In general, a functional association was found between the glycosaminoglycan and N-glycosylated chains attached to the central core proteins of syndecan-4 and glypican-1 affecting their regulation of muscle cell proliferation, differentiation, and FGF2 responsiveness.	Glycosaminoglycans	59-76	glypican 1	Homo sapiens	159-169
21890503-8	2012	In general, a functional association was found between the glycosaminoglycan and N-glycosylated chains attached to the central core proteins of syndecan-4 and glypican-1 affecting their regulation of muscle cell proliferation, differentiation, and FGF2 responsiveness.	Glycosaminoglycans	59-76	fibroblast growth factor 2	Homo sapiens	248-252
21866573-4	2012	TGFbeta3 + Dex stimulated degenerated human NP cells to proliferate and exhibit an anti-catabolic gene expression profile (with a decrease in ADAMTS5 and MMP1 compared to basal, and an increase in SOX9, decrease in ADAMTS5, MMP1, collagen I and collagen III compared to day 0), while NCA stimulated the greatest GAG per cell.	Glycosaminoglycans	312-315	transforming growth factor beta 3	Homo sapiens	0-8
21866573-5	2012	We conclude that degenerated human NP cells exhibit regenerative potential, and that an optimal treatment will likely require treatments, such as TGFbeta3 + Dex, which were able to increase cell metabolism and reduce catabolism, as well as treatments with factors found in NC conditioned medium, that were able to produce high amounts of GAG per cell.	Glycosaminoglycans	338-341	transforming growth factor beta 3	Homo sapiens	146-154
22158871-5	2012	Compared with heparan sulfate, a well known glycosaminoglycan capable of forming a complex with FGF2, polySia formed a larger complex with distinct properties in facilitating oligomerization of FGF2, as well as in binding to FGF receptors.	Glycosaminoglycans	44-61	fibroblast growth factor 2	Mus musculus	96-99
22315264-3	2012	UFH is a heterogeneous mixture of glycosaminoglycans that bind to antithrombin via a unique pentasaccharide sequence and catalyze the inactivation of thrombin, factor Xa, and other clotting enzymes.	Glycosaminoglycans	34-52	serpin family C member 1	Homo sapiens	66-78
22315264-3	2012	UFH is a heterogeneous mixture of glycosaminoglycans that bind to antithrombin via a unique pentasaccharide sequence and catalyze the inactivation of thrombin, factor Xa, and other clotting enzymes.	Glycosaminoglycans	34-52	coagulation factor II, thrombin	Homo sapiens	70-78
22315264-3	2012	UFH is a heterogeneous mixture of glycosaminoglycans that bind to antithrombin via a unique pentasaccharide sequence and catalyze the inactivation of thrombin, factor Xa, and other clotting enzymes.	Glycosaminoglycans	34-52	coagulation factor X	Homo sapiens	160-169
21948871-6	2012	An overlay binding assay revealed that ZG16p binds specifically to heparan sulfate PGs by recognizing their GAG chains.	Glycosaminoglycans	108-111	zymogen granule protein 16	Rattus norvegicus	39-44
22115678-1	2012	Syndecan-4 is composed of a core protein and covalently attached glycosaminoglycan (GAG) and N-linked glycosylated (N-glycosylated) chains.	Glycosaminoglycans	65-82	syndecan-4	Meleagris gallopavo	0-10
22115678-1	2012	Syndecan-4 is composed of a core protein and covalently attached glycosaminoglycan (GAG) and N-linked glycosylated (N-glycosylated) chains.	Glycosaminoglycans	84-87	syndecan-4	Meleagris gallopavo	0-10
22068049-4	2012	The optimal binding ratio of His-tagged Green Fluorescent Protein (His-GFP) and His-tagged HIV-1 Gag p41 (His-Gag p41) to the Ni-NCs was 1:221 and 1:480 w/w, respectively.	Glycosaminoglycans	97-100	erythrocyte membrane protein band 4.1	Mus musculus	101-104
22068049-4	2012	The optimal binding ratio of His-tagged Green Fluorescent Protein (His-GFP) and His-tagged HIV-1 Gag p41 (His-Gag p41) to the Ni-NCs was 1:221 and 1:480 w/w, respectively.	Glycosaminoglycans	110-113	erythrocyte membrane protein band 4.1	Mus musculus	114-117
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	10-13	erythrocyte membrane protein band 4.1	Mus musculus	14-17
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	10-13	erythrocyte membrane protein band 4.1	Mus musculus	111-114
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	10-13	erythrocyte membrane protein band 4.1	Mus musculus	111-114
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	10-13	erythrocyte membrane protein band 4.1	Mus musculus	111-114
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	107-110	erythrocyte membrane protein band 4.1	Mus musculus	14-17
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	107-110	erythrocyte membrane protein band 4.1	Mus musculus	111-114
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	107-110	erythrocyte membrane protein band 4.1	Mus musculus	111-114
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	107-110	erythrocyte membrane protein band 4.1	Mus musculus	111-114
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	107-110	erythrocyte membrane protein band 4.1	Mus musculus	14-17
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	107-110	erythrocyte membrane protein band 4.1	Mus musculus	111-114
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	107-110	erythrocyte membrane protein band 4.1	Mus musculus	111-114
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	107-110	erythrocyte membrane protein band 4.1	Mus musculus	111-114
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	107-110	erythrocyte membrane protein band 4.1	Mus musculus	14-17
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	107-110	erythrocyte membrane protein band 4.1	Mus musculus	111-114
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	107-110	erythrocyte membrane protein band 4.1	Mus musculus	111-114
22068049-8	2012	Serum His-Gag p41-specific antibody levels were found to be significantly higher at 1 and 0.5 mug doses of Gag p41-His-Ni-NCs (His-Gag p41 equivalent) compared with His-Gag p41 (1 mug) adjuvanted with aluminum hydroxide (AH).	Glycosaminoglycans	107-110	erythrocyte membrane protein band 4.1	Mus musculus	111-114
22068049-9	2012	The serum IgG2a levels induced by Gag p41-His-Ni-NCs (1 mug) were significantly higher than AH adjuvanted His-Gag p41.	Glycosaminoglycans	34-37	immunoglobulin heavy variable V1-9	Mus musculus	10-15
22068049-9	2012	The serum IgG2a levels induced by Gag p41-His-Ni-NCs (1 mug) were significantly higher than AH adjuvanted His-Gag p41.	Glycosaminoglycans	34-37	erythrocyte membrane protein band 4.1	Mus musculus	38-41
22184056-1	2012	BACKGROUND: Hyaluronan is a crucial glycosaminoglycan of the vertebrate embryonic extracellular matrix able to influence cell behaviour, both by assembling the pericellular matrices and by activating signal transducing receptors such as CD44.	Glycosaminoglycans	36-53	CD44 molecule (Indian blood group)	Homo sapiens	237-241
21902467-8	2012	HNC-based constructs exhibited a more efficient recovery upon IL-1beta withdrawal, resulting in a higher accumulation of GAG (up to 2.6-fold) compared to the corresponding HAC-based tissues.	Glycosaminoglycans	121-124	interleukin 1 beta	Homo sapiens	62-70
21246269-5	2012	While proteinase 3 binds heavily to surface targets on vital PMNs, cathepsin G and elastase interact preferentially with sulphated glycosaminoglycans.	Glycosaminoglycans	131-149	cathepsin G	Homo sapiens	67-91
22052369-2	2012	The glycosaminoglycan (GAG) layer at the bladder surface             non-specifically blocks the adherence of bacteria, ions and molecules to the bladder             epithelium and bladder cancer cells express CD44 that binds GAG.	Glycosaminoglycans	4-21	CD44 molecule (Indian blood group)	Homo sapiens	210-214
22052369-2	2012	The glycosaminoglycan (GAG) layer at the bladder surface             non-specifically blocks the adherence of bacteria, ions and molecules to the bladder             epithelium and bladder cancer cells express CD44 that binds GAG.	Glycosaminoglycans	23-26	CD44 molecule (Indian blood group)	Homo sapiens	210-214
22052369-2	2012	The glycosaminoglycan (GAG) layer at the bladder surface             non-specifically blocks the adherence of bacteria, ions and molecules to the bladder             epithelium and bladder cancer cells express CD44 that binds GAG.	Glycosaminoglycans	226-229	CD44 molecule (Indian blood group)	Homo sapiens	210-214
22377305-5	2012	A striking feature is the very efficient and polyfunctional CD8 T cell response of these patients, which exhibits a high avidity against the gag protein of the virus.	Glycosaminoglycans	141-144	CD8a molecule	Homo sapiens	60-63
22001376-1	2012	Biglycan (BGN) is a small proteoglycan that consists of a protein core containing leucine-rich repeat regions and two glycosaminoglycan (GAG) chains of either chondroitin sulfate (CS) or dermatan sulfate (DS) type.	Glycosaminoglycans	118-135	biglycan	Homo sapiens	0-8
22001376-1	2012	Biglycan (BGN) is a small proteoglycan that consists of a protein core containing leucine-rich repeat regions and two glycosaminoglycan (GAG) chains of either chondroitin sulfate (CS) or dermatan sulfate (DS) type.	Glycosaminoglycans	118-135	biglycan	Homo sapiens	10-13
22001376-1	2012	Biglycan (BGN) is a small proteoglycan that consists of a protein core containing leucine-rich repeat regions and two glycosaminoglycan (GAG) chains of either chondroitin sulfate (CS) or dermatan sulfate (DS) type.	Glycosaminoglycans	137-140	biglycan	Homo sapiens	0-8
22001376-1	2012	Biglycan (BGN) is a small proteoglycan that consists of a protein core containing leucine-rich repeat regions and two glycosaminoglycan (GAG) chains of either chondroitin sulfate (CS) or dermatan sulfate (DS) type.	Glycosaminoglycans	137-140	biglycan	Homo sapiens	10-13
23106140-5	2012	IL-26 forms homodimers and adheres to glycosaminoglycans on cell surfaces, presumably due to its positive charge.	Glycosaminoglycans	38-56	interleukin 26	Homo sapiens	0-5
22041899-5	2012	Furthermore, Ser(13) is exposed in the tetrameric structure of CXCL10, which is consistent with our finding that the scFvs are able to bind to CXCL9 and CXCL10 immobilized on glycosaminoglycans.	Glycosaminoglycans	175-193	C-X-C motif chemokine ligand 10	Homo sapiens	63-69
22041899-5	2012	Furthermore, Ser(13) is exposed in the tetrameric structure of CXCL10, which is consistent with our finding that the scFvs are able to bind to CXCL9 and CXCL10 immobilized on glycosaminoglycans.	Glycosaminoglycans	175-193	C-X-C motif chemokine ligand 9	Homo sapiens	143-148
22041899-5	2012	Furthermore, Ser(13) is exposed in the tetrameric structure of CXCL10, which is consistent with our finding that the scFvs are able to bind to CXCL9 and CXCL10 immobilized on glycosaminoglycans.	Glycosaminoglycans	175-193	C-X-C motif chemokine ligand 10	Homo sapiens	153-159
21966936-2	2012	However, the structure of its glycosaminoglycan chain has not been well characterized, and this study was undertaken to investigate the structure of the glycosaminoglycan chain that decorated lubricin in human synovial fluid to provide insight into its biological role.	Glycosaminoglycans	153-170	proteoglycan 4	Homo sapiens	192-200
22040724-2	2012	The potentiation of C1-INH by heparin and other glycosaminoglycans (GAGs) regulates a broad spectrum of C1-INH activities in vivo both in normal and disease states.	Glycosaminoglycans	48-66	serpin family G member 1	Homo sapiens	20-26
22040724-2	2012	The potentiation of C1-INH by heparin and other glycosaminoglycans (GAGs) regulates a broad spectrum of C1-INH activities in vivo both in normal and disease states.	Glycosaminoglycans	48-66	serpin family G member 1	Homo sapiens	104-110
21959004-6	2012	Further investigation showed that applying transforming growth factor beta1 (TGF-beta1) or bone morphogenetic protein 2 (BMP-2) to DIAS constructs caused increased sulfated glycosaminoglycan content.	Glycosaminoglycans	173-190	transforming growth factor beta 1	Homo sapiens	43-75
21959004-6	2012	Further investigation showed that applying transforming growth factor beta1 (TGF-beta1) or bone morphogenetic protein 2 (BMP-2) to DIAS constructs caused increased sulfated glycosaminoglycan content.	Glycosaminoglycans	173-190	transforming growth factor beta 1	Homo sapiens	77-86
21959004-6	2012	Further investigation showed that applying transforming growth factor beta1 (TGF-beta1) or bone morphogenetic protein 2 (BMP-2) to DIAS constructs caused increased sulfated glycosaminoglycan content.	Glycosaminoglycans	173-190	bone morphogenetic protein 2	Homo sapiens	91-119
21959004-6	2012	Further investigation showed that applying transforming growth factor beta1 (TGF-beta1) or bone morphogenetic protein 2 (BMP-2) to DIAS constructs caused increased sulfated glycosaminoglycan content.	Glycosaminoglycans	173-190	bone morphogenetic protein 2	Homo sapiens	121-126
22506762-10	2012	The decorin protein was found in the tissue, the DS glycosaminoglycan chain was removed with thrombin digestion, and there was no change in the mechanical properties of the tissue due to the thrombin digestion relative to controls.	Glycosaminoglycans	52-69	coagulation factor II, thrombin	Homo sapiens	93-101
21939780-10	2012	These data indicated that the syndecan-4 cytoplasmic domain and the GAG and N-glycosylated chains are critical in syndecan-4 regulating satellite cell proliferation, responsiveness to FGF2, and PKCalpha cell membrane localization.	Glycosaminoglycans	68-71	syndecan-4	Meleagris gallopavo	114-124
22031937-6	2012	In particular, CD4 T cell responses targeting Gag were robustly associated with lower levels of viremia (P = 0.0002, R = -0.45).	Glycosaminoglycans	46-49	CD4 molecule	Homo sapiens	15-18
21939780-10	2012	These data indicated that the syndecan-4 cytoplasmic domain and the GAG and N-glycosylated chains are critical in syndecan-4 regulating satellite cell proliferation, responsiveness to FGF2, and PKCalpha cell membrane localization.	Glycosaminoglycans	68-71	fibroblast growth factor 2	Meleagris gallopavo	184-188
23018676-2	2012	It is caused by a GAG deletion in the Tor1A gene located on chromosome 9.	Glycosaminoglycans	18-21	torsin family 1, member A (torsin A)	Mus musculus	38-43
22611399-1	2012	Most cases of early onset DYT1 dystonia in humans are caused by a GAG deletion in the TOR1A gene leading to loss of a glutamic acid (DeltaE) in the torsinA protein, which underlies a movement disorder associated with neuronal dysfunction without apparent neurodegeneration.	Glycosaminoglycans	66-69	torsin family 1 member A	Homo sapiens	26-30
22611399-1	2012	Most cases of early onset DYT1 dystonia in humans are caused by a GAG deletion in the TOR1A gene leading to loss of a glutamic acid (DeltaE) in the torsinA protein, which underlies a movement disorder associated with neuronal dysfunction without apparent neurodegeneration.	Glycosaminoglycans	66-69	torsin family 1 member A	Homo sapiens	86-91
22611399-1	2012	Most cases of early onset DYT1 dystonia in humans are caused by a GAG deletion in the TOR1A gene leading to loss of a glutamic acid (DeltaE) in the torsinA protein, which underlies a movement disorder associated with neuronal dysfunction without apparent neurodegeneration.	Glycosaminoglycans	66-69	torsin family 1 member A	Homo sapiens	148-155
22079829-8	2012	In addition, HGF-MSCs also significantly decreased neurocan expression and glycosaminoglycan chain deposition around hemisection lesions.	Glycosaminoglycans	75-92	hepatocyte growth factor	Homo sapiens	13-16
22031937-8	2012	Furthermore, Gag/Env ratios were a potent marker of viral control, with a high frequency and magnitude of Gag responses and low proportion of Env responses associated with effective immune control.	Glycosaminoglycans	13-16	endogenous retrovirus group K member 20	Homo sapiens	142-145
22031937-8	2012	Furthermore, Gag/Env ratios were a potent marker of viral control, with a high frequency and magnitude of Gag responses and low proportion of Env responses associated with effective immune control.	Glycosaminoglycans	106-109	endogenous retrovirus group K member 20	Homo sapiens	17-20
22275804-10	2012	While digestion was more pronounced in the WT group, double digestion with Keratanase I and Chondroitinase ABC removed 88% of the GAG filaments in the WT, compared to 72% of those in the P2X(7) (-/-) mice, indicating that there are more heparan sulfate proteoglycans in the latter.	Glycosaminoglycans	130-133	galactosamine (N-acetyl)-6-sulfate sulfatase	Mus musculus	75-106
22252637-1	2012	Serglycin is a proteoglycan composed of a relatively small (~17 kDa) core protein to which sulfated glycosaminoglycans of either heparin, heparan sulfate or chondroitin sulfate types are attached.	Glycosaminoglycans	100-118	serglycin	Mus musculus	0-9
22252645-8	2012	Transfection of chondrocytes or cartilage explants by the expression vector for the glycosyltransferase beta-1,3-glucuronosyltransferase-I (GlcAT-I) enhanced PG synthesis and deposition in the ECM by promoting the synthesis of chondroitin sulfate GAG chains of the cartilage matrix.	Glycosaminoglycans	247-250	beta-1,3-glucuronyltransferase 3	Homo sapiens	84-138
22252645-8	2012	Transfection of chondrocytes or cartilage explants by the expression vector for the glycosyltransferase beta-1,3-glucuronosyltransferase-I (GlcAT-I) enhanced PG synthesis and deposition in the ECM by promoting the synthesis of chondroitin sulfate GAG chains of the cartilage matrix.	Glycosaminoglycans	247-250	beta-1,3-glucuronyltransferase 3	Homo sapiens	140-147
23430900-0	2012	Plasmatic and Urinary Glycosaminoglycans Characterization in Mucopolysaccharidosis II Patient Treated with Enzyme-Replacement Therapy with Idursulfase.	Glycosaminoglycans	22-40	iduronate 2-sulfatase	Homo sapiens	139-150
22056610-9	2012	NB84 treatment restored enough functional alpha-L-iduronidase activity to partially reverse abnormal GAG accumulation and lysosomal abundance in mouse embryonic fibroblasts derived from the Idua-W392X mouse.	Glycosaminoglycans	101-104	iduronidase, alpha-L	Mus musculus	42-61
22056610-10	2012	Finally, in vivo administration of NB84 to Idua-W392X mice significantly reduced urine GAG excretion and tissue GAG storage.	Glycosaminoglycans	87-90	iduronidase, alpha-L	Mus musculus	43-47
22056610-10	2012	Finally, in vivo administration of NB84 to Idua-W392X mice significantly reduced urine GAG excretion and tissue GAG storage.	Glycosaminoglycans	112-115	iduronidase, alpha-L	Mus musculus	43-47
22289849-1	2012	INTRODUCTION: Mucopolysaccharidosis VI (MPS-VI) is caused by a deficiency in N-acetylgalactosamine-4-sulfatase activity, resulting in lysosomal accumulation of partially degraded glycosaminoglycans (GAGs).	Glycosaminoglycans	179-197	arylsulfatase B	Homo sapiens	77-110
22355269-0	2012	Mechanisms regulating the secretion of the promalignancy chemokine CCL5 by breast tumor cells: CCL5"s 40s loop and intracellular glycosaminoglycans.	Glycosaminoglycans	129-147	C-C motif chemokine 5	Cricetulus griseus	67-71
22355269-6	2012	Based on the studies showing that the 40s loop of CCL5 mediates its binding to glycosaminoglycans (GAG), we analyzed the roles of GAG in regulating CCL5 secretion.	Glycosaminoglycans	79-97	C-C motif chemokine 5	Cricetulus griseus	50-54
22355269-6	2012	Based on the studies showing that the 40s loop of CCL5 mediates its binding to glycosaminoglycans (GAG), we analyzed the roles of GAG in regulating CCL5 secretion.	Glycosaminoglycans	99-102	C-C motif chemokine 5	Cricetulus griseus	50-54
22355269-7	2012	TRKN-mutated CCL5 had lower propensity for colocalization with GAG in the Golgi compared to the WT chemokine.	Glycosaminoglycans	63-66	C-C motif chemokine 5	Cricetulus griseus	13-17
22355269-8	2012	Secretion of WT CCL5 was significantly reduced in CHO mutant cells deficient in GAG synthesis, and the WT chemokine acquired an ER-like distribution in these cells, similar to that of TRKN-mutated CCL5 in GAG-expressing cells.	Glycosaminoglycans	80-83	C-C motif chemokine 5	Cricetulus griseus	16-20
22355269-8	2012	Secretion of WT CCL5 was significantly reduced in CHO mutant cells deficient in GAG synthesis, and the WT chemokine acquired an ER-like distribution in these cells, similar to that of TRKN-mutated CCL5 in GAG-expressing cells.	Glycosaminoglycans	205-208	C-C motif chemokine 5	Cricetulus griseus	197-201
22355269-9	2012	The release of WT CCL5 was also reduced after inhibition of GAG presence/synthesis by intracellular expression of heparanase, inhibition of GAG sulfation, and sulfate deprivation.	Glycosaminoglycans	60-63	C-C motif chemokine 5	Cricetulus griseus	18-22
22355269-9	2012	The release of WT CCL5 was also reduced after inhibition of GAG presence/synthesis by intracellular expression of heparanase, inhibition of GAG sulfation, and sulfate deprivation.	Glycosaminoglycans	140-143	C-C motif chemokine 5	Cricetulus griseus	18-22
22355269-10	2012	The need for a (43)TRKN(46) motif and for a GAG-mediated process in CCL5 secretion may enable the future design of modalities that prevent CCL5 release by breast tumor cells.	Glycosaminoglycans	44-47	C-C motif chemokine 5	Cricetulus griseus	68-72
22355269-10	2012	The need for a (43)TRKN(46) motif and for a GAG-mediated process in CCL5 secretion may enable the future design of modalities that prevent CCL5 release by breast tumor cells.	Glycosaminoglycans	44-47	C-C motif chemokine 5	Cricetulus griseus	139-143
22811910-1	2012	Together with the Gag protein, the Env glycoprotein is a major retroviral structural protein and is essential for forming infectious virus particles.	Glycosaminoglycans	18-21	endogenous retrovirus group K member 20	Homo sapiens	35-38
22166420-3	2012	DYT1 is caused by a GAG deletion in the TOR1A gene.	Glycosaminoglycans	20-23	torsin family 1 member A	Homo sapiens	0-4
22166420-3	2012	DYT1 is caused by a GAG deletion in the TOR1A gene.	Glycosaminoglycans	20-23	torsin family 1 member A	Homo sapiens	40-45
22428001-7	2012	Hypoxia, like ARSB silencing, significantly increased the total cellular sulfated glycosaminoglycans and chondroitin-4-sulfate (C4S) content.	Glycosaminoglycans	82-100	arylsulfatase B	Homo sapiens	14-18
22792193-10	2012	In addition, the predicted Gag peptides were found to induce broader polyfunctional CD4+ T cell responses compared to the commonly used Gag-p55 peptide pool.	Glycosaminoglycans	27-30	H3 histone pseudogene 44	Homo sapiens	140-143
22479506-0	2012	Xylosyltransferase-I regulates glycosaminoglycan synthesis during the pathogenic process of human osteoarthritis.	Glycosaminoglycans	31-48	xylosyltransferase 1	Homo sapiens	0-20
22479506-2	2012	However, the mechanism of GAG loss and the role of xylosyltransferase-I (XT-I) that initiates GAG biosynthesis onto PG molecules in the pathogenic process of human OA are unknown.	Glycosaminoglycans	94-97	xylosyltransferase 1	Homo sapiens	51-71
22479506-2	2012	However, the mechanism of GAG loss and the role of xylosyltransferase-I (XT-I) that initiates GAG biosynthesis onto PG molecules in the pathogenic process of human OA are unknown.	Glycosaminoglycans	94-97	xylosyltransferase 1	Homo sapiens	73-77
22479506-6	2012	Importantly, XT-I inhibition by shRNA or forced-expression with a pCMV-XT-I construct correlated with the modulation of GAG anabolism in human cartilage explants.	Glycosaminoglycans	120-123	xylosyltransferase 1	Homo sapiens	13-17
22479506-6	2012	Importantly, XT-I inhibition by shRNA or forced-expression with a pCMV-XT-I construct correlated with the modulation of GAG anabolism in human cartilage explants.	Glycosaminoglycans	120-123	xylosyltransferase 1	Homo sapiens	71-75
22479506-7	2012	The observation that XT-I gene expression was down-regulated by IL-1beta and up-regulated by TGF-beta1 indicates that these cytokines may play a role in regulating GAG content in human OA.	Glycosaminoglycans	164-167	xylosyltransferase 1	Homo sapiens	21-25
22479506-7	2012	The observation that XT-I gene expression was down-regulated by IL-1beta and up-regulated by TGF-beta1 indicates that these cytokines may play a role in regulating GAG content in human OA.	Glycosaminoglycans	164-167	transforming growth factor beta 1	Homo sapiens	93-102
23152789-4	2012	The availability of multiple co-crystal structures facilitates a structural analysis that challenges the long-held belief that the GAG binding sites in antithrombin and thrombin are essentially similar with high solvent exposure and shallow surface characteristics.	Glycosaminoglycans	131-134	serpin family C member 1	Homo sapiens	152-164
23152789-4	2012	The availability of multiple co-crystal structures facilitates a structural analysis that challenges the long-held belief that the GAG binding sites in antithrombin and thrombin are essentially similar with high solvent exposure and shallow surface characteristics.	Glycosaminoglycans	131-134	coagulation factor II, thrombin	Homo sapiens	156-164
22912852-2	2012	In such regards, a protein scaffold based on the HIV p24 CA protein is a highly attractive approach, providing also Gag epitopes for eliciting HIV non-neutralizing protective antibodies and specific CD4(+) and CD8(+) T cell responses.	Glycosaminoglycans	116-119	transmembrane p24 trafficking protein 2	Homo sapiens	53-56
22511961-5	2012	Overexpression of wild-type Nkx3.2 (WT-Nkx3.2) upregulated glycosaminoglycan (GAG) production and expression of type II collagen alpha1 (Col2a1) mRNA, and these effects were evident before WT-Nkx3.2-mediated upregulation of Sox9.	Glycosaminoglycans	59-76	NK3 homeobox 2	Mus musculus	28-34
22511961-5	2012	Overexpression of wild-type Nkx3.2 (WT-Nkx3.2) upregulated glycosaminoglycan (GAG) production and expression of type II collagen alpha1 (Col2a1) mRNA, and these effects were evident before WT-Nkx3.2-mediated upregulation of Sox9.	Glycosaminoglycans	59-76	NK3 homeobox 2	Mus musculus	39-45
22511961-5	2012	Overexpression of wild-type Nkx3.2 (WT-Nkx3.2) upregulated glycosaminoglycan (GAG) production and expression of type II collagen alpha1 (Col2a1) mRNA, and these effects were evident before WT-Nkx3.2-mediated upregulation of Sox9.	Glycosaminoglycans	59-76	NK3 homeobox 2	Mus musculus	39-45
22511961-5	2012	Overexpression of wild-type Nkx3.2 (WT-Nkx3.2) upregulated glycosaminoglycan (GAG) production and expression of type II collagen alpha1 (Col2a1) mRNA, and these effects were evident before WT-Nkx3.2-mediated upregulation of Sox9.	Glycosaminoglycans	78-81	NK3 homeobox 2	Mus musculus	28-34
22511961-5	2012	Overexpression of wild-type Nkx3.2 (WT-Nkx3.2) upregulated glycosaminoglycan (GAG) production and expression of type II collagen alpha1 (Col2a1) mRNA, and these effects were evident before WT-Nkx3.2-mediated upregulation of Sox9.	Glycosaminoglycans	78-81	NK3 homeobox 2	Mus musculus	39-45
22511961-5	2012	Overexpression of wild-type Nkx3.2 (WT-Nkx3.2) upregulated glycosaminoglycan (GAG) production and expression of type II collagen alpha1 (Col2a1) mRNA, and these effects were evident before WT-Nkx3.2-mediated upregulation of Sox9.	Glycosaminoglycans	78-81	NK3 homeobox 2	Mus musculus	39-45
22355381-3	2012	The LAMP/gag DNA chimeric vaccine encodes the HIV-1 p55gag fused to the lysosome-associated membrane protein-1 (LAMP-1) and has been shown to enhance anti-Gag antibody (Ab) and cellular immune responses in adult and neonatal mice; such a vaccine represents a new concept in antigen presentation.	Glycosaminoglycans	9-12	lysosomal-associated membrane protein 3	Mus musculus	4-8
22511961-6	2012	RNAi-mediated inhibition of Nkx3.2 abolished GAG production and expression of Col2a1 mRNA.	Glycosaminoglycans	45-48	NK3 homeobox 2	Mus musculus	28-34
22511961-8	2012	In addition, WT-Nkx3.2 partially restored downregulation of GAG production, Col2 protein expression, and Col2a1 mRNA expression induced by Sox9 RNAi.	Glycosaminoglycans	60-63	NK3 homeobox 2	Mus musculus	16-22
22511961-8	2012	In addition, WT-Nkx3.2 partially restored downregulation of GAG production, Col2 protein expression, and Col2a1 mRNA expression induced by Sox9 RNAi.	Glycosaminoglycans	60-63	SRY (sex determining region Y)-box 9	Mus musculus	139-143
22355381-3	2012	The LAMP/gag DNA chimeric vaccine encodes the HIV-1 p55gag fused to the lysosome-associated membrane protein-1 (LAMP-1) and has been shown to enhance anti-Gag antibody (Ab) and cellular immune responses in adult and neonatal mice; such a vaccine represents a new concept in antigen presentation.	Glycosaminoglycans	9-12	lysosomal associated membrane protein 1	Homo sapiens	112-118
22355381-7	2012	When offspring were immunized with LAMP/gag DNA, the anti-Gag Ab response and the Gag-specific IFN-gamma-secreting cells were decreased.	Glycosaminoglycans	40-43	lysosomal associated membrane protein 3	Homo sapiens	35-39
22151889-9	2011	Furthermore depletion of glycosaminoglycan from cartilage explants by IL-1beta and TNF-alpha was significantly enhanced by FTY720-P in an MMP-3 dependent manner.	Glycosaminoglycans	25-42	interleukin 1 beta	Bos taurus	70-78
23196519-5	2012	DYT1, a primary dystonia, is well known as early-onset torsion dystonia with dominantly inherited generalized dystonia caused by a GAG deletion in the TOR1A gene located at 9q34.11.	Glycosaminoglycans	131-134	torsin family 1 member A	Homo sapiens	0-4
23196519-5	2012	DYT1, a primary dystonia, is well known as early-onset torsion dystonia with dominantly inherited generalized dystonia caused by a GAG deletion in the TOR1A gene located at 9q34.11.	Glycosaminoglycans	131-134	torsin family 1 member A	Homo sapiens	151-156
22924029-1	2012	The sickle hemoglobin is an abnormal hemoglobin due to point mutation (GAG   GTG) in exon 1 of the beta globin gene resulting in the substitution of glutamic acid by valine at position 6 of the beta globin polypeptide chain.	Glycosaminoglycans	71-74	hemoglobin subunit beta	Homo sapiens	99-110
22924029-1	2012	The sickle hemoglobin is an abnormal hemoglobin due to point mutation (GAG   GTG) in exon 1 of the beta globin gene resulting in the substitution of glutamic acid by valine at position 6 of the beta globin polypeptide chain.	Glycosaminoglycans	71-74	hemoglobin subunit beta	Homo sapiens	194-205
22279584-8	2012	Lumbar administration of recombinant I2S to enzyme deficient animals reduced the storage of glycosaminoglycans in both superficial and deep brain tissues, with concurrent morphological improvements.	Glycosaminoglycans	92-110	iduronate 2-sulfatase	Mus musculus	37-40
22242148-7	2012	Furthermore, a binding assay revealed that hepatocyte growth factor dose-dependently binds to SRPX2 protein, and a ligand-glycosaminoglycans interaction was speculated to be likely in proteoglycans.	Glycosaminoglycans	122-140	hepatocyte growth factor	Homo sapiens	43-67
22911005-0	2012	Directly infected resting CD4+T cells can produce HIV Gag without spreading infection in a model of HIV latency.	Glycosaminoglycans	54-57	CD4 molecule	Homo sapiens	26-29
22151889-9	2011	Furthermore depletion of glycosaminoglycan from cartilage explants by IL-1beta and TNF-alpha was significantly enhanced by FTY720-P in an MMP-3 dependent manner.	Glycosaminoglycans	25-42	tumor necrosis factor	Bos taurus	83-92
22151889-9	2011	Furthermore depletion of glycosaminoglycan from cartilage explants by IL-1beta and TNF-alpha was significantly enhanced by FTY720-P in an MMP-3 dependent manner.	Glycosaminoglycans	25-42	stromelysin-1	Bos taurus	138-143
21994463-5	2011	Here, we used pyrosequencing to investigate the kinetics and patterns of mutations surrounding the Mamu-A1*00101-bound Gag(181-189)CM9 CD8+ T cell epitope.	Glycosaminoglycans	119-122	CD8a molecule	Homo sapiens	135-138
22093831-8	2011	Over-expression of exogenous Nkx3.2 promoted glycosaminoglycan (GAG) production and inhibited Runx2 mRNA expression and, based on a dual luciferase assay, Runx2 promoter activity.	Glycosaminoglycans	45-62	NK3 homeobox 2	Mus musculus	29-35
22093831-8	2011	Over-expression of exogenous Nkx3.2 promoted glycosaminoglycan (GAG) production and inhibited Runx2 mRNA expression and, based on a dual luciferase assay, Runx2 promoter activity.	Glycosaminoglycans	64-67	NK3 homeobox 2	Mus musculus	29-35
22093831-9	2011	Interestingly, downregulation of Nkx3.2 using RNAi abolished hypoxia-dependent GAG production and restored Runx2 mRNA expression and promoter activity.	Glycosaminoglycans	79-82	NK3 homeobox 2	Mus musculus	33-39
22030348-1	2011	Mucopolysaccharidosis I (MPS I) is a lysosomal storage disease due to an alpha-L-iduronidase deficiency, which leads to an accumulation of glycosaminoglycans in the lysosomes of most cells, resulting in tissue and organ dysfunction.	Glycosaminoglycans	139-157	alpha-L-iduronidase	Homo sapiens	73-92
21965007-0	2011	Genomic instability in blood cells from murine model of mucopolysaccharidosis type I. Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of alfa-iduronidase (IDUA), which leads to intralysosomal accumulation of glycosaminoglycans.	Glycosaminoglycans	223-241	iduronidase, alpha-L	Mus musculus	152-168
21963080-10	2011	CONCLUSION: C-IMT in MPS patients is increased compared to matched controls, likely reflective of arterial intima-medial glycosaminoglycan accumulation.	Glycosaminoglycans	121-138	CIMT	Homo sapiens	12-17
21930407-1	2011	Mucopolysaccharidosis type VI (MPS VI) is a progressive, multisystem autosomal recessive lysosomal disorder resulting from deficient N-acetylgalactosamine-4-sulphatase (ASB) and the consequent accumulation of glycosaminoglycan (GAG).	Glycosaminoglycans	209-226	arylsulfatase B	Homo sapiens	169-172
21930407-1	2011	Mucopolysaccharidosis type VI (MPS VI) is a progressive, multisystem autosomal recessive lysosomal disorder resulting from deficient N-acetylgalactosamine-4-sulphatase (ASB) and the consequent accumulation of glycosaminoglycan (GAG).	Glycosaminoglycans	228-231	arylsulfatase B	Homo sapiens	169-172
22122911-8	2011	CONCLUSION: The HBMs of DBPs that bind to DARC have similar heparin binding affinities as some V3 loop peptides and chemokines, are responsible for specific sulfated polysaccharide inhibition of parasite binding and invasion of red blood cells, and are more likely to bind to negative charges on the receptor than cell surface glycosaminoglycans.	Glycosaminoglycans	327-345	atypical chemokine receptor 1 (Duffy blood group)	Homo sapiens	42-46
21707438-9	2011	CDM supplemented with TGF-beta3 resulted in significantly higher glycosaminoglycan content (762.69+-220.79 ng/mg wet weight) and type II collagen (COL II) content (6.25+-1.64 ng/mg wet weight) at day 21 compared with untreated samples.	Glycosaminoglycans	65-82	transforming growth factor beta 3	Homo sapiens	22-31
22194689-8	2011	Glycosylated-Gag from MoMLV substituted for Nef in conferring resistance to 2F5 and 4E10, indicating that this activity is conserved in a retrovirus that does not encode Nef.	Glycosaminoglycans	13-16	S100 calcium binding protein B	Homo sapiens	170-173
21875359-5	2011	Histological, immunohistochemical, and biochemistry analyses indicated that the constructs generated from predifferentiated hMSCs induced by GDF-5 (Group D2) exhibited up-regulated glycosaminoglycan (GAG) and type II collagen expression and contained higher amounts of GAG and total collagen than any other group.	Glycosaminoglycans	181-198	growth differentiation factor 5	Homo sapiens	141-146
21875359-5	2011	Histological, immunohistochemical, and biochemistry analyses indicated that the constructs generated from predifferentiated hMSCs induced by GDF-5 (Group D2) exhibited up-regulated glycosaminoglycan (GAG) and type II collagen expression and contained higher amounts of GAG and total collagen than any other group.	Glycosaminoglycans	200-203	growth differentiation factor 5	Homo sapiens	141-146
21875359-5	2011	Histological, immunohistochemical, and biochemistry analyses indicated that the constructs generated from predifferentiated hMSCs induced by GDF-5 (Group D2) exhibited up-regulated glycosaminoglycan (GAG) and type II collagen expression and contained higher amounts of GAG and total collagen than any other group.	Glycosaminoglycans	269-272	growth differentiation factor 5	Homo sapiens	141-146
22093708-0	2011	Human HERC5 restricts an early stage of HIV-1 assembly by a mechanism correlating with the ISGylation of Gag.	Glycosaminoglycans	105-108	HECT and RLD domain containing E3 ubiquitin protein ligase 5	Homo sapiens	6-11
22093708-4	2011	The E3 ligase activity of HERC5 was required for blocking HIV-1 Gag particle production and correlated with the post-translational modification of Gag with ISG15.	Glycosaminoglycans	147-150	HECT and RLD domain containing E3 ubiquitin protein ligase 5	Homo sapiens	26-31
22093708-4	2011	The E3 ligase activity of HERC5 was required for blocking HIV-1 Gag particle production and correlated with the post-translational modification of Gag with ISG15.	Glycosaminoglycans	64-67	HECT and RLD domain containing E3 ubiquitin protein ligase 5	Homo sapiens	26-31
22093708-8	2011	Moreover, HERC5 restricted murine leukemia virus (MLV) Gag particle production, showing that HERC5 is effective in restricting Gag particle production of an evolutionarily divergent retrovirus.	Glycosaminoglycans	55-58	HECT and RLD domain containing E3 ubiquitin protein ligase 5	Homo sapiens	10-15
22093708-8	2011	Moreover, HERC5 restricted murine leukemia virus (MLV) Gag particle production, showing that HERC5 is effective in restricting Gag particle production of an evolutionarily divergent retrovirus.	Glycosaminoglycans	55-58	HECT and RLD domain containing E3 ubiquitin protein ligase 5	Homo sapiens	93-98
21904187-3	2011	METHODS: In four patients, we analysed by clonal analysis the viral population in gag cleavage site (p17/p24, p24/p2, p2/p7, p7/p1, p1/p6(gag)), in p6(gag), in gag-pol frameshift [p1/transframe protein (TFP)/p6(pol)] and in protease-coding region.	Glycosaminoglycans	82-85	family with sequence similarity 72 member B	Homo sapiens	101-104
22093708-8	2011	Moreover, HERC5 restricted murine leukemia virus (MLV) Gag particle production, showing that HERC5 is effective in restricting Gag particle production of an evolutionarily divergent retrovirus.	Glycosaminoglycans	127-130	HECT and RLD domain containing E3 ubiquitin protein ligase 5	Homo sapiens	10-15
22093708-8	2011	Moreover, HERC5 restricted murine leukemia virus (MLV) Gag particle production, showing that HERC5 is effective in restricting Gag particle production of an evolutionarily divergent retrovirus.	Glycosaminoglycans	127-130	HECT and RLD domain containing E3 ubiquitin protein ligase 5	Homo sapiens	93-98
22093708-9	2011	CONCLUSIONS: HERC5 represents a potential new host factor that blocks an early stage of retroviral Gag particle assembly.	Glycosaminoglycans	99-102	HECT and RLD domain containing E3 ubiquitin protein ligase 5	Homo sapiens	13-18
22256598-0	2011	[Regulation of Wnt-3a signaling and diffusion by sulfated glycosaminoglycans].	Glycosaminoglycans	58-76	Wnt family member 3A	Homo sapiens	15-21
21778119-5	2011	The majority of Gag-responsive CD8 T cells were CD103+ in both blood and at the cervix.	Glycosaminoglycans	16-19	CD8a molecule	Homo sapiens	31-34
21778119-5	2011	The majority of Gag-responsive CD8 T cells were CD103+ in both blood and at the cervix.	Glycosaminoglycans	16-19	integrin subunit alpha E	Homo sapiens	48-53
21778119-6	2011	Despite this, the magnitude of Gag-specific IFN-gamma responses by CD103+CD8+ T cells in blood did not predict similar Gag-specific responses at the cervix.	Glycosaminoglycans	31-34	integrin subunit alpha E	Homo sapiens	67-72
21778119-6	2011	Despite this, the magnitude of Gag-specific IFN-gamma responses by CD103+CD8+ T cells in blood did not predict similar Gag-specific responses at the cervix.	Glycosaminoglycans	31-34	CD8a molecule	Homo sapiens	73-76
21865377-4	2011	The CD4(+) T cell responses were predominantly Env directed, whereas the CD8(+) T cell responses were similarly distributed against Env, Gag, and GPN.	Glycosaminoglycans	137-140	CD8a molecule	Homo sapiens	73-76
22071845-1	2011	BACKGROUND: Mucopolysaccharidosis II, also known as Hunter syndrome, is a rare, X-linked disease caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase, which catalyses a step in the catabolism of glycosaminoglycans.	Glycosaminoglycans	211-229	iduronate 2-sulfatase	Homo sapiens	144-165
22071845-17	2011	Idursulfase antibodies were detected in 31.7% of patients at the end of the study and they were related to a smaller reduction in urine glycosaminoglycan levels.	Glycosaminoglycans	136-153	iduronate 2-sulfatase	Homo sapiens	0-11
21885201-7	2011	ChABC is a protein heavily glycosylated structurally, and it was reported that inhibiting the glycosylation of xylosyltransferase-1 with a DNA enzyme could reduce GAG chains in the lesion of spinal cord.	Glycosaminoglycans	163-166	xylosyltransferase 1	Homo sapiens	111-131
22163342-10	2011	As expected, the addition or insertion of myr-signals that allowed Env-independent budding of FFV SVPs also retargeted Gag to plasma membrane-proximal sites and other intracellular membrane compartments.	Glycosaminoglycans	119-122	endogenous retrovirus group K member 20	Homo sapiens	67-70
21957261-3	2011	These residues have been implicated in several biological functions of PrP, including endocytic trafficking and binding of glycosaminoglycans.	Glycosaminoglycans	123-141	prion protein	Mus musculus	71-74
21792913-9	2011	The addition of TGF-beta to chondrogenic pellet cultures significantly enhanced glycosaminoglycan accumulation, but caused no significant effect on cellular oxygen consumption.	Glycosaminoglycans	80-97	transforming growth factor beta 1	Homo sapiens	16-24
21689719-0	2011	Substrate specificity of kallikrein-related peptidase 13 activated by salts or glycosaminoglycans and a search for natural substrate candidates.	Glycosaminoglycans	79-97	kallikrein related peptidase 13	Homo sapiens	25-56
21689719-2	2011	We report the activation of KLK13 by kosmotropic salts and glycosaminoglycans and its substrate specificity by employing a series of five substrates derived from the fluorescence resonance energy transfer (FRET) peptide Abz-KLRSSKQ-EDDnp.	Glycosaminoglycans	59-77	kallikrein related peptidase 13	Homo sapiens	28-33
21689719-7	2011	In conclusion, the observed hydrolytic activities of KLK13 and its co-localization with its activators, glycosaminoglycans in the salivary gland and high concentration of sodium citrate in male reproductive tissues, indicates that KLK13 may play a role in the defense of the upper digestive apparatus and in male reproductive organs.	Glycosaminoglycans	104-122	kallikrein related peptidase 13	Homo sapiens	53-58
21689719-7	2011	In conclusion, the observed hydrolytic activities of KLK13 and its co-localization with its activators, glycosaminoglycans in the salivary gland and high concentration of sodium citrate in male reproductive tissues, indicates that KLK13 may play a role in the defense of the upper digestive apparatus and in male reproductive organs.	Glycosaminoglycans	104-122	kallikrein related peptidase 13	Homo sapiens	231-236
21792394-2	2011	As a consequence of the conversion of chondroitin sulfate (CS) to dermatan sulfate (DS), the glycosaminoglycans become more flexible and enable DS to perform more sophisticated signaling functions.	Glycosaminoglycans	93-111	colony stimulating factor 1	Homo sapiens	59-61
21957261-7	2011	However, we find that mutant PrP toxicity is potently inhibited by application of exogenous glycosaminoglycans, suggesting that the latter molecules block an essential interaction between the N terminus of PrP and a membrane-associated target site.	Glycosaminoglycans	92-110	prion protein	Mus musculus	29-32
21957261-7	2011	However, we find that mutant PrP toxicity is potently inhibited by application of exogenous glycosaminoglycans, suggesting that the latter molecules block an essential interaction between the N terminus of PrP and a membrane-associated target site.	Glycosaminoglycans	92-110	prion protein	Mus musculus	206-209
22117415-0	2011	[Translational analysis of the Grp gene, a genomic homologue of the Gag gene of the gypsy retrotransposon of Drosophila melanogaster].	Glycosaminoglycans	68-71	Gag-related	Drosophila melanogaster	31-34
21772054-5	2011	Formation of these complexes occurs at a specific molar ratio of PF4 to glycosaminoglycan.	Glycosaminoglycans	72-89	platelet factor 4	Homo sapiens	65-68
21707907-7	2011	Furthermore, RP-2ms mainly depended on cell surface glycosaminoglycans for viral binding and it became vimentin-dependent only when binding to glycosaminoglycans was blocked.	Glycosaminoglycans	143-161	vimentin	Homo sapiens	103-111
21724848-9	2011	Budding and infectivity defects due to overexpression of ITCH and SMURF-1 were correlated with higher than normal ubiquitination of Gag.	Glycosaminoglycans	132-135	itchy E3 ubiquitin protein ligase	Homo sapiens	57-61
21724848-9	2011	Budding and infectivity defects due to overexpression of ITCH and SMURF-1 were correlated with higher than normal ubiquitination of Gag.	Glycosaminoglycans	132-135	SMAD specific E3 ubiquitin protein ligase 1	Homo sapiens	66-73
21880179-1	2011	Serglycin belongs to a family of small proteoglycans with Ser-Gly dipeptide repeats, and it is modified with different types of glycosaminoglycan side chains.	Glycosaminoglycans	128-145	serglycin	Homo sapiens	0-9
21451580-5	2011	The amino-terminus of BlaM was fused to the myristoylation signal of lyn, which was placed upstream of the amino-terminus of Gag (BlaM-gag-pol).	Glycosaminoglycans	125-128	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	69-72
24956304-10	2011	Fibril diameters did not change with TGF-b1 stimulation or cell lineage; however, highly sulfated glycosaminoglycans associated with the collagen fibrils significantly increased with TGF-b1.	Glycosaminoglycans	98-116	transforming growth factor beta 1	Homo sapiens	183-189
21867964-10	2011	Moreover, we clarified that zebrafish Ngb interacts with negatively charged cell-surface glycosaminoglycan.	Glycosaminoglycans	89-106	neuroglobin	Danio rerio	38-41
21752903-0	2011	High-functional-avidity cytotoxic T lymphocyte responses to HLA-B-restricted Gag-derived epitopes associated with relative HIV control.	Glycosaminoglycans	77-80	major histocompatibility complex, class I, B	Homo sapiens	60-65
21752914-7	2011	The intracellular HIV-1 Gag half-life was shorter in cells containing A3G complexes than in those lacking complexes.	Glycosaminoglycans	24-27	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	70-73
24159460-6	2011	Gag p24 antigen production in ingenol-treated MT4 cells was reduced by 24.5% on day 6 post-infection.	Glycosaminoglycans	0-3	transmembrane p24 trafficking protein 2	Homo sapiens	4-7
22393785-1	2011	HIV-1 matrix protein (MA) is multifunctional structural protein located on N-terminus of Gag precursor p55 and responsible for its transport to plasma membrane, the site of virus assembly.	Glycosaminoglycans	89-92	H3 histone pseudogene 44	Homo sapiens	103-106
21253856-1	2011	Hurler syndrome (MPS IH) is caused by a mutation in the gene encoding alpha-L-iduronidase (IDUA) and leads to the accumulation of partially degraded glycosaminoglycans (GAGs).	Glycosaminoglycans	149-167	iduronidase, alpha-L	Mus musculus	91-95
21854562-8	2011	Supporting these gene expression results, IL-1beta-induced cartilage matrix breakdown, as evidenced by GAG release from cartilage explants, was also significantly blocked (p &lt; 0.05).	Glycosaminoglycans	103-106	interleukin 1 beta	Homo sapiens	42-50
21832969-4	2011	These two single nucleotide polymorphisms (SNPs) in exon 11 of the DBP gene, at codons 416 (GAT&gt;GAG; Asp&gt;Glu) and 420 (ACG&gt;AAG; Thr&gt;Lys), have been previously suggested to play roles in the etiology of other autoimmune diseases.	Glycosaminoglycans	99-102	D-box binding PAR bZIP transcription factor	Homo sapiens	67-70
21683796-6	2011	RESULTS: Direct delivery of Ad-BMP-6 demonstrated delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) and histologic evidence of greater Glycosaminoglycan (GAG) content in repair tissue at 12 weeks, while Ad-BMP-2 had greater non-mineral cartilage at the surface at 52 weeks (p&lt;0.04).	Glycosaminoglycans	140-157	bone morphogenetic protein 6	Homo sapiens	31-36
21866614-20	2004	UFH is a heterogeneous mixture of glycosaminoglycans that bind to the enzyme inhibitor antithrombin III via the pentasaccharide.	Glycosaminoglycans	34-52	serpin family C member 1	Homo sapiens	87-103
21860600-1	2011	A mixture of glycosaminoglycan (GAG) chains from a plasma proteoglycan bikunin was fractionated using native, continuous-elution polyacrylamide gel electrophoresis, and the resulting fractions were analyzed by electrospray ionization Fourier transform mass spectrometry (ESI FTMS).	Glycosaminoglycans	32-35	alpha-1-microglobulin/bikunin precursor	Homo sapiens	71-78
21600196-3	2011	Sulfation of the GAG chain is key as evidenced by the renal agenesis phenotype in mice deficient in the HS biosynthetic enzyme, heparan sulfate 2-O sulfotransferase (Hs2st; an enzyme which catalyzes the 2-O-sulfation of uronic acids in heparan sulfate).	Glycosaminoglycans	17-20	heparan sulfate 2-O-sulfotransferase 1	Mus musculus	166-171
21549206-8	2011	CONCLUSION: Electrostatic attraction of CA4+ allowed effective imaging of the GAG components of articular cartilage at 50% lower molar concentration than Ioxaglate and 20-fold lower molar concentration than Gadopentetate.	Glycosaminoglycans	78-81	carbonic anhydrase 4	Bos taurus	40-43
21549206-9	2011	The CA4+ contrast agent exhibited a significant correlation between CT attenuation and GAG content in ex vivo bovine osteochondral plugs.	Glycosaminoglycans	87-90	carbonic anhydrase 4	Bos taurus	4-7
21843316-10	2011	In contrast, in-frame PFV Gag-Pol fusion with C-terminal Gag ORF truncations or non-removable Gag peptide addition to Pol displayed wildtype particle release, but reduced particle infectivity.	Glycosaminoglycans	57-60	Gag-Pol	Human immunodeficiency virus 1	26-33
21749451-1	2011	Intrathecal (IT) recombinant human alpha-l-iduronidase (rhIDU) has been shown to reduce mean brain glycosaminoglycans (GAGs) to normal levels in mucopolysaccharidosis I (MPS I) dogs.	Glycosaminoglycans	99-117	alpha-L-iduronidase	Homo sapiens	35-54
21749451-1	2011	Intrathecal (IT) recombinant human alpha-l-iduronidase (rhIDU) has been shown to reduce mean brain glycosaminoglycans (GAGs) to normal levels in mucopolysaccharidosis I (MPS I) dogs.	Glycosaminoglycans	119-123	alpha-L-iduronidase	Homo sapiens	35-54
21813902-10	2011	Recombinant human arylsulfatase B significantly improves endurance and reduces urinary glycosaminoglycan excretion.	Glycosaminoglycans	87-104	arylsulfatase B	Homo sapiens	18-33
21520049-8	2011	Furthermore, GFOGER integrin blocking peptide, MEK inhibitor and JNK inhibitor, not p38 inhibitor, significantly reduced the type II collagen-induced GAG deposition level.	Glycosaminoglycans	150-153	mitogen-activated protein kinase kinase 7	Homo sapiens	47-50
21520049-8	2011	Furthermore, GFOGER integrin blocking peptide, MEK inhibitor and JNK inhibitor, not p38 inhibitor, significantly reduced the type II collagen-induced GAG deposition level.	Glycosaminoglycans	150-153	mitogen-activated protein kinase 8	Homo sapiens	65-68
21683796-6	2011	RESULTS: Direct delivery of Ad-BMP-6 demonstrated delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) and histologic evidence of greater Glycosaminoglycan (GAG) content in repair tissue at 12 weeks, while Ad-BMP-2 had greater non-mineral cartilage at the surface at 52 weeks (p&lt;0.04).	Glycosaminoglycans	159-162	bone morphogenetic protein 6	Homo sapiens	31-36
21505295-7	2011	During treatment interruption, gag-specific CD4(+) T cells were not lost, although the frequency of HIV-specific CD8(+) cells increased.	Glycosaminoglycans	31-34	CD4 molecule	Homo sapiens	44-47
21505295-8	2011	Most gag-specific CD4(+) T cells were potentially cytotoxic (CD107a(+)) and were not influenced by pVL or by HAART.	Glycosaminoglycans	5-8	CD4 molecule	Homo sapiens	18-21
21505295-8	2011	Most gag-specific CD4(+) T cells were potentially cytotoxic (CD107a(+)) and were not influenced by pVL or by HAART.	Glycosaminoglycans	5-8	lysosomal associated membrane protein 1	Homo sapiens	61-67
21653700-0	2011	Sulfated glycosaminoglycans are required for specific and sensitive fibroblast growth factor (FGF) 19 signaling via FGF receptor 4 and betaKlotho.	Glycosaminoglycans	9-27	fibroblast growth factor receptor 4	Homo sapiens	116-130
21653700-0	2011	Sulfated glycosaminoglycans are required for specific and sensitive fibroblast growth factor (FGF) 19 signaling via FGF receptor 4 and betaKlotho.	Glycosaminoglycans	9-27	klotho beta	Homo sapiens	135-145
21653700-3	2011	Here we report that hFGF19 at picomolar levels require sulfated glycosaminoglycans (sGAGs), such as heparan sulfate, heparin, and chondroitin sulfates, for its signaling via human FGFR4 in the presence of human betaKlotho.	Glycosaminoglycans	64-82	fibroblast growth factor 19	Homo sapiens	20-26
21653700-3	2011	Here we report that hFGF19 at picomolar levels require sulfated glycosaminoglycans (sGAGs), such as heparan sulfate, heparin, and chondroitin sulfates, for its signaling via human FGFR4 in the presence of human betaKlotho.	Glycosaminoglycans	64-82	fibroblast growth factor receptor 4	Homo sapiens	180-185
21596823-1	2011	PURPOSE: Versican is a large proteoglycan with numerous chondroitin sulfate (CS) glycosaminoglycan (GAG) side chains attached.	Glycosaminoglycans	81-98	versican	Homo sapiens	9-17
21762808-5	2011	In this regard, we hypothesized that a likely interaction of MAPK/ERK-2 with Gag(p55) may enable its packaging into virus particles.	Glycosaminoglycans	77-80	mitogen-activated protein kinase 1	Homo sapiens	66-71
21762808-5	2011	In this regard, we hypothesized that a likely interaction of MAPK/ERK-2 with Gag(p55) may enable its packaging into virus particles.	Glycosaminoglycans	77-80	phosphoinositide-3-kinase regulatory subunit 3	Homo sapiens	81-84
21762808-7	2011	We further show that MAPK/ERK-2 interacts specifically with the poly-proline motif present in the capsid region of Gag(p55).	Glycosaminoglycans	115-118	mitogen-activated protein kinase 1	Homo sapiens	26-31
21762808-7	2011	We further show that MAPK/ERK-2 interacts specifically with the poly-proline motif present in the capsid region of Gag(p55).	Glycosaminoglycans	115-118	phosphoinositide-3-kinase regulatory subunit 3	Homo sapiens	119-122
21762808-8	2011	Utilizing virus-like particles directed by Gag, we have shown that the exchange of conserved proline residues within capsid of Gag(p55) resulted in impaired incorporation of MAPK/ERK-2.	Glycosaminoglycans	43-46	phosphoinositide-3-kinase regulatory subunit 3	Homo sapiens	131-134
21762808-8	2011	Utilizing virus-like particles directed by Gag, we have shown that the exchange of conserved proline residues within capsid of Gag(p55) resulted in impaired incorporation of MAPK/ERK-2.	Glycosaminoglycans	43-46	mitogen-activated protein kinase 1	Homo sapiens	179-184
21762808-8	2011	Utilizing virus-like particles directed by Gag, we have shown that the exchange of conserved proline residues within capsid of Gag(p55) resulted in impaired incorporation of MAPK/ERK-2.	Glycosaminoglycans	127-130	phosphoinositide-3-kinase regulatory subunit 3	Homo sapiens	131-134
21762808-8	2011	Utilizing virus-like particles directed by Gag, we have shown that the exchange of conserved proline residues within capsid of Gag(p55) resulted in impaired incorporation of MAPK/ERK-2.	Glycosaminoglycans	127-130	mitogen-activated protein kinase 1	Homo sapiens	179-184
21762808-9	2011	In addition, the deletion of a domain comprising amino acids 201 to 255 within host cell MAPK/ERK-2 abrogates its interaction with Gag(p55).	Glycosaminoglycans	131-134	mitogen-activated protein kinase 1	Homo sapiens	94-99
21762808-9	2011	In addition, the deletion of a domain comprising amino acids 201 to 255 within host cell MAPK/ERK-2 abrogates its interaction with Gag(p55).	Glycosaminoglycans	131-134	phosphoinositide-3-kinase regulatory subunit 3	Homo sapiens	135-138
21596823-1	2011	PURPOSE: Versican is a large proteoglycan with numerous chondroitin sulfate (CS) glycosaminoglycan (GAG) side chains attached.	Glycosaminoglycans	100-103	versican	Homo sapiens	9-17
21400477-5	2011	Procatabolic responses to IL-1beta and TNFalpha, such as release of glycosaminoglycan, nitric oxide, and matrix metalloproteinases 3 and 13 were determined by dimethylmethylene blue assay, Griess reaction, and Western blotting, respectively, in cartilage explants and chondrocytes with and without knockdown of AMPKalpha by small interfering RNA.	Glycosaminoglycans	68-85	interleukin 1 beta	Homo sapiens	26-34
21718840-10	2011	Importantly, enhanced 5HTR responsiveness due to increased 5HTR2A and 2B expression results in a significantly greater response in remodeling endpoints (proliferation, collagen, and GAG production) to 5HT in the presence of 5HT transporter blockade.	Glycosaminoglycans	182-185	solute carrier family 6 member 4	Homo sapiens	224-239
21400477-5	2011	Procatabolic responses to IL-1beta and TNFalpha, such as release of glycosaminoglycan, nitric oxide, and matrix metalloproteinases 3 and 13 were determined by dimethylmethylene blue assay, Griess reaction, and Western blotting, respectively, in cartilage explants and chondrocytes with and without knockdown of AMPKalpha by small interfering RNA.	Glycosaminoglycans	68-85	tumor necrosis factor	Homo sapiens	39-47
21400481-1	2011	OBJECTIVE: To determine whether hypoxia and hypoxia-inducible factor (HIF) proteins regulate expression of beta-1,3-glucuronyltransferase 1 (GlcAT-1), a key enzyme in glycosaminoglycan synthesis in nucleus pulposus cells.	Glycosaminoglycans	167-184	beta-1,3-glucuronyltransferase 1	Rattus norvegicus	107-139
21613398-5	2011	Cytotoxic T-lymphocyte (CTL) responses during acute infection predominantly targeted the TW10 and KF9 epitopes in p24(Gag) and Nef, respectively.	Glycosaminoglycans	118-121	transmembrane p24 trafficking protein 2	Homo sapiens	114-117
21510821-9	2011	Nitrite production, GAG expression, and GFP-TAT transduction were significantly attenuated by inhibitors of JNK, p38, or ERK.	Glycosaminoglycans	20-23	mitogen-activated protein kinase 8	Homo sapiens	108-111
21510821-9	2011	Nitrite production, GAG expression, and GFP-TAT transduction were significantly attenuated by inhibitors of JNK, p38, or ERK.	Glycosaminoglycans	20-23	mitogen-activated protein kinase 1	Homo sapiens	121-124
21507971-3	2011	Vpx and the related accessory protein Vpr are packaged into virions through a virus-specific interaction with the p6 carboxy-terminal domain of Gag.	Glycosaminoglycans	144-147	vpx protein	Simian immunodeficiency virus	0-3
21444626-0	2011	A GAG trinucleotide-repeat polymorphism in the gene for glutathione biosynthetic enzyme, GCLC, affects gene expression through translation.	Glycosaminoglycans	2-5	glutamate-cysteine ligase catalytic subunit	Homo sapiens	89-93
21444626-1	2011	A guanine-adenine-guanine (GAG) repeat polymorphism with 5 different alleles (4, 7, 8, 9, and 10 repeats) in the 5" untranslated region (UTR) of GCLC has been associated with altered GCL activity and glutathione (GSH) levels.	Glycosaminoglycans	27-30	glutamate-cysteine ligase catalytic subunit	Homo sapiens	145-149
21444626-1	2011	A guanine-adenine-guanine (GAG) repeat polymorphism with 5 different alleles (4, 7, 8, 9, and 10 repeats) in the 5" untranslated region (UTR) of GCLC has been associated with altered GCL activity and glutathione (GSH) levels.	Glycosaminoglycans	27-30	glutamate-cysteine ligase catalytic subunit	Homo sapiens	145-148
21444626-6	2011	A similar association of GAG repeat with GCLC phenotype was observed in vivo in healthy adults, as individuals with GAG-7/7 genotype had lower GCL activity and GSH levels in lymphocytes compared to those with GAG-9/9 (P&lt;0.05).	Glycosaminoglycans	25-28	glutamate-cysteine ligase catalytic subunit	Homo sapiens	41-45
21444626-6	2011	A similar association of GAG repeat with GCLC phenotype was observed in vivo in healthy adults, as individuals with GAG-7/7 genotype had lower GCL activity and GSH levels in lymphocytes compared to those with GAG-9/9 (P&lt;0.05).	Glycosaminoglycans	25-28	glutamate-cysteine ligase catalytic subunit	Homo sapiens	41-44
21444626-6	2011	A similar association of GAG repeat with GCLC phenotype was observed in vivo in healthy adults, as individuals with GAG-7/7 genotype had lower GCL activity and GSH levels in lymphocytes compared to those with GAG-9/9 (P&lt;0.05).	Glycosaminoglycans	116-119	glutamate-cysteine ligase catalytic subunit	Homo sapiens	41-45
21444626-6	2011	A similar association of GAG repeat with GCLC phenotype was observed in vivo in healthy adults, as individuals with GAG-7/7 genotype had lower GCL activity and GSH levels in lymphocytes compared to those with GAG-9/9 (P&lt;0.05).	Glycosaminoglycans	116-119	glutamate-cysteine ligase catalytic subunit	Homo sapiens	41-44
21444626-6	2011	A similar association of GAG repeat with GCLC phenotype was observed in vivo in healthy adults, as individuals with GAG-7/7 genotype had lower GCL activity and GSH levels in lymphocytes compared to those with GAG-9/9 (P&lt;0.05).	Glycosaminoglycans	116-119	glutamate-cysteine ligase catalytic subunit	Homo sapiens	41-45
21444626-6	2011	A similar association of GAG repeat with GCLC phenotype was observed in vivo in healthy adults, as individuals with GAG-7/7 genotype had lower GCL activity and GSH levels in lymphocytes compared to those with GAG-9/9 (P&lt;0.05).	Glycosaminoglycans	116-119	glutamate-cysteine ligase catalytic subunit	Homo sapiens	41-44
21444626-7	2011	Higher GCL activity and GSH levels observed in red blood cells (RBCs) from individuals with GAG-7/7 compared to GAG-9/9 are likely due to differences in GCL regulation in RBCs.	Glycosaminoglycans	92-95	glutamate-cysteine ligase catalytic subunit	Homo sapiens	7-10
21444626-7	2011	Higher GCL activity and GSH levels observed in red blood cells (RBCs) from individuals with GAG-7/7 compared to GAG-9/9 are likely due to differences in GCL regulation in RBCs.	Glycosaminoglycans	92-95	glutamate-cysteine ligase catalytic subunit	Homo sapiens	153-156
21444626-7	2011	Higher GCL activity and GSH levels observed in red blood cells (RBCs) from individuals with GAG-7/7 compared to GAG-9/9 are likely due to differences in GCL regulation in RBCs.	Glycosaminoglycans	112-115	glutamate-cysteine ligase catalytic subunit	Homo sapiens	7-10
21444626-7	2011	Higher GCL activity and GSH levels observed in red blood cells (RBCs) from individuals with GAG-7/7 compared to GAG-9/9 are likely due to differences in GCL regulation in RBCs.	Glycosaminoglycans	112-115	glutamate-cysteine ligase catalytic subunit	Homo sapiens	153-156
21444626-8	2011	Altogether, these results suggest that GAG polymorphism affects GCLC expression via translation, and thus may be associated with altered risk for GSH-related diseases and toxicities.	Glycosaminoglycans	39-42	glutamate-cysteine ligase catalytic subunit	Homo sapiens	64-68
21555785-1	2011	We characterized the interaction of amylin with heparin fragments of defined length, which model the glycosaminoglycan chains associated with amyloid deposits found in type 2 diabetes.	Glycosaminoglycans	101-118	islet amyloid polypeptide	Mus musculus	36-42
21525359-6	2011	Although IAP mRNA localized to P bodies, Gag was targeted to the endoplasmic reticulum (ER), from which IAP buds.	Glycosaminoglycans	41-44	alkaline phosphatase, intestinal	Homo sapiens	104-107
21624346-8	2011	GAG release induced by IL-1alpha in the explants, and severity of arthritis were greater in GlcNAc6ST-1(-/-) mice than their WT littermates.	Glycosaminoglycans	0-3	carbohydrate sulfotransferase 2	Mus musculus	92-103
21624346-4	2011	We examined, in culture, the difference between GlcNAc6ST-1(-/-) and wild-type (WT) mice for interleukin (IL)-1alpha-induced glycosaminoglycan (GAG) release from the articular cartilage.	Glycosaminoglycans	125-142	interleukin 1 alpha	Mus musculus	93-116
21372110-5	2011	Using surface plasmon resonance and cell-binding assays, we report that the IFNalpha/betaBP from vaccinia virus, the smallpox vaccine, interacts with cell surface glycosaminoglycans (GAGs).	Glycosaminoglycans	163-181	interferon alpha 1	Homo sapiens	76-84
21624346-4	2011	We examined, in culture, the difference between GlcNAc6ST-1(-/-) and wild-type (WT) mice for interleukin (IL)-1alpha-induced glycosaminoglycan (GAG) release from the articular cartilage.	Glycosaminoglycans	144-147	carbohydrate sulfotransferase 2	Mus musculus	48-59
21624346-4	2011	We examined, in culture, the difference between GlcNAc6ST-1(-/-) and wild-type (WT) mice for interleukin (IL)-1alpha-induced glycosaminoglycan (GAG) release from the articular cartilage.	Glycosaminoglycans	144-147	interleukin 1 alpha	Mus musculus	93-116
21624346-8	2011	GAG release induced by IL-1alpha in the explants, and severity of arthritis were greater in GlcNAc6ST-1(-/-) mice than their WT littermates.	Glycosaminoglycans	0-3	interleukin 1 alpha	Mus musculus	23-32
21330456-2	2011	IL-8 is protected from proteolytic degradation in the airways by binding to glycosaminoglycans, while remaining active.	Glycosaminoglycans	76-94	C-X-C motif chemokine ligand 8	Homo sapiens	0-4
21330456-10	2011	CONCLUSIONS: Glycosaminoglycans possess the ability to influence the chemokine profile of the CF lung by binding and stabilizing IL-8, which promotes neutrophil chemotaxis and activation.	Glycosaminoglycans	13-31	C-X-C motif chemokine ligand 8	Homo sapiens	129-133
21672195-9	2011	HD5 and HD6 blocked anti-HIV activities of soluble glycosaminoglycans including heparin, chondroitin sulfate, and dextran sulfate.	Glycosaminoglycans	51-69	defensin alpha 5	Homo sapiens	0-3
21672195-9	2011	HD5 and HD6 blocked anti-HIV activities of soluble glycosaminoglycans including heparin, chondroitin sulfate, and dextran sulfate.	Glycosaminoglycans	51-69	defensin alpha 6	Homo sapiens	8-11
21372110-8	2011	Functional conservation of GAG-binding sites is demonstrated for the IFNalpha/betaBP from variola and monkeypox viruses, extending our understanding of immune modulation by the most virulent human poxviruses.	Glycosaminoglycans	27-30	interferon alpha 1	Homo sapiens	69-77
21365186-6	2011	Additionally, glycosaminoglycan levels in culture medium of murine cartilage explants stimulated with interleukin-1-alpha plus retinoic acid are reduced by the presence of the flavonoid.	Glycosaminoglycans	14-31	interleukin 1 alpha	Mus musculus	102-121
21327479-2	2011	The efficacy of ERT was established based primarily on reduction in urine glycosaminoglycans:creatinine (GAG:Cr) ratio and improvement in a composite score of predicted forced vital capacity (FVC% predicted) and 6-min walk-test distance (6MWT).	Glycosaminoglycans	74-92	E74 like ETS transcription factor 3	Homo sapiens	16-19
21327479-2	2011	The efficacy of ERT was established based primarily on reduction in urine glycosaminoglycans:creatinine (GAG:Cr) ratio and improvement in a composite score of predicted forced vital capacity (FVC% predicted) and 6-min walk-test distance (6MWT).	Glycosaminoglycans	105-108	E74 like ETS transcription factor 3	Homo sapiens	16-19
21391299-7	2011	We actually transplanted the poly-L-lactide porous scaffolds carrying the chondrocytes and the atelocollagen mixed with or without insulin, into the nude mice, showing that glycosaminoglycan accumulation was evident in the group with insulin although less without insulin.	Glycosaminoglycans	173-190	insulin	Homo sapiens	131-138
21994749-6	2011	Coding sequences for gag, pro and pol were present in three different reading-frames, as common for beta-retroviruses, and the reading frames were completely open, except that the env gene was interrupted by a single stopcodon.	Glycosaminoglycans	21-24	gPr73	Mouse mammary tumor virus	180-183
21256835-6	2011	RESULTS: Glycosaminoglycans extracted from aneurysms have a more potent anticoagulant activity than those from normal arteries of young adults, mostly due to a relative enrichment of dermatan sulfate, which potentiates heparin cofactor II inhibition of thrombin.	Glycosaminoglycans	9-27	coagulation factor II, thrombin	Homo sapiens	253-261
21108488-7	2011	In IL-1beta-induced rat articular chondrocytes, berberine decreased IL-1beta-induced GAG release and NO production.	Glycosaminoglycans	85-88	interleukin 1 beta	Rattus norvegicus	68-76
21805439-6	2011	In particular, HCII binds many glycosaminoglycans (GAGs) such as heparin and heparin sulfate as well as several different polyanions to enhance its inhibition of thrombin.	Glycosaminoglycans	31-49	serpin family D member 1	Homo sapiens	15-19
21627827-13	2011	Matricellular proteins, such as clusterin and tenascin, are likely to be important to optimize differentiation of MSCs for maximum GAG production and reduced collagen fiber expression.	Glycosaminoglycans	131-134	tenascin C	Homo sapiens	46-54
21605424-3	2011	We report the IDS mutation and polymorphisms causing the Hunter syndrome in patients from one family in Tunisia PATIENTS AND METHODS: A preliminary diagnosis was made by qualitative detection of urinary glycosaminoglycans of the suspected MPS II probands.	Glycosaminoglycans	203-221	iduronate 2-sulfatase	Homo sapiens	14-17
21306436-4	2011	Formation of this complex was blocked by a mutation of the glycosaminoglycan-binding basic cluster (Lys(23) -Lys(29) ) in RP S19.	Glycosaminoglycans	59-76	ribosomal protein S19	Homo sapiens	122-128
21354134-6	2011	The rate of proteoglycan synthesis was estimated by the incorporation of (3)(5)c in cetylpyridinium chloride-precipitable glycosaminoglycans by isolated sclera of control and treated eyes.	Glycosaminoglycans	122-140	versican	Gallus gallus	12-24
21518320-0	2011	Inhibition of P-glycoprotein facilitated glycosaminoglycan accumulation during chondrogenesis of human bone marrow mesenchymal stem cells.	Glycosaminoglycans	41-58	ATP binding cassette subfamily B member 1	Homo sapiens	14-28
21518320-9	2011	CONCLUSION: Inhibition of P-gp facilitated GAG accumulation via HA export inhibition during chondrogenic differentiation of human BM-MSCs.	Glycosaminoglycans	43-46	ATP binding cassette subfamily B member 1	Homo sapiens	26-30
21391299-7	2011	We actually transplanted the poly-L-lactide porous scaffolds carrying the chondrocytes and the atelocollagen mixed with or without insulin, into the nude mice, showing that glycosaminoglycan accumulation was evident in the group with insulin although less without insulin.	Glycosaminoglycans	173-190	insulin	Homo sapiens	234-241
21391299-7	2011	We actually transplanted the poly-L-lactide porous scaffolds carrying the chondrocytes and the atelocollagen mixed with or without insulin, into the nude mice, showing that glycosaminoglycan accumulation was evident in the group with insulin although less without insulin.	Glycosaminoglycans	173-190	insulin	Homo sapiens	234-241
21467219-5	2011	DEC-HIV Gag p24 showed better cross-priming for CD8(+) T cells, whereas the avidity of anti-Gag antibodies was ~10-fold higher with nontargeted Gag 24 protein.	Glycosaminoglycans	8-11	transmembrane p24 trafficking protein 2	Homo sapiens	12-15
21383673-1	2011	Mucopolysaccharidosis-I (MPS-I) is an inherited deficiency of alpha-L-iduronidase (IdU) that causes lysosomal accumulation of glycosaminoglycans (GAG) in a variety of parenchymal cell types and connective tissues.	Glycosaminoglycans	126-144	alpha-L-iduronidase	Canis lupus familiaris	62-81
21383673-1	2011	Mucopolysaccharidosis-I (MPS-I) is an inherited deficiency of alpha-L-iduronidase (IdU) that causes lysosomal accumulation of glycosaminoglycans (GAG) in a variety of parenchymal cell types and connective tissues.	Glycosaminoglycans	126-144	alpha-L-iduronidase	Canis lupus familiaris	83-86
21383673-1	2011	Mucopolysaccharidosis-I (MPS-I) is an inherited deficiency of alpha-L-iduronidase (IdU) that causes lysosomal accumulation of glycosaminoglycans (GAG) in a variety of parenchymal cell types and connective tissues.	Glycosaminoglycans	146-149	alpha-L-iduronidase	Canis lupus familiaris	62-81
21383673-1	2011	Mucopolysaccharidosis-I (MPS-I) is an inherited deficiency of alpha-L-iduronidase (IdU) that causes lysosomal accumulation of glycosaminoglycans (GAG) in a variety of parenchymal cell types and connective tissues.	Glycosaminoglycans	146-149	alpha-L-iduronidase	Canis lupus familiaris	83-86
21790014-1	2011	The amino acid sequence of the drosophila retrovirus MDG4 (gypsy) structural protein Gag does not contain a canonical motif known for the majority of vertebrate retroviruses.	Glycosaminoglycans	85-88	modifier of mdg4	Drosophila melanogaster	53-57
21467219-5	2011	DEC-HIV Gag p24 showed better cross-priming for CD8(+) T cells, whereas the avidity of anti-Gag antibodies was ~10-fold higher with nontargeted Gag 24 protein.	Glycosaminoglycans	8-11	CD8a molecule	Homo sapiens	48-51
21467219-8	2011	Gag-specific CD4(+) and CD8(+) T-cell responses increased markedly after priming with both protein vaccines and poly ICLC.	Glycosaminoglycans	0-3	CD4 molecule	Homo sapiens	13-16
21533229-5	2011	The overall profiles of cytokine responses to Gag and Ad5 had similar combinations of induced Th1- and Th2-type cytokines, including IFN-gamma, IL-2, TNF-alpha, IP-10, IL-13, and IL-10, although the Ad5-specific responses were uniformly higher than the Gag-specific responses (p&lt;0.0001 for 9 out of 11 significantly expressed analytes).	Glycosaminoglycans	46-49	negative elongation factor complex member C/D	Homo sapiens	94-97
21544209-7	2011	This is associated with preserved selection pressure at specific viral amino acids (e.g., the T242N polymorphism within the HLA-B*57/5801 restricted TW10 epitope), but with reversion at other sites (e.g., the T186S polymorphism within the HLA-B*8101 restricted TL9 epitope), most notably in Gag and suggestive of "immune relaxation".	Glycosaminoglycans	291-294	major histocompatibility complex, class I, B	Homo sapiens	124-129
21533229-6	2011	At the peak response time point, PBMC from Ad5-seronegative vaccinees secreted significantly more IP-10 in response to Gag (p = 0.008), and significantly more IP-10 (p = 0.0009), IL-2 (p = 0.006) and IL-10 (p = 0.05) in response to Ad5 empty vector than PBMC from Ad5-seropositive vaccinees.	Glycosaminoglycans	119-122	Alzheimer disease, familial, type 5	Homo sapiens	43-46
21533229-5	2011	The overall profiles of cytokine responses to Gag and Ad5 had similar combinations of induced Th1- and Th2-type cytokines, including IFN-gamma, IL-2, TNF-alpha, IP-10, IL-13, and IL-10, although the Ad5-specific responses were uniformly higher than the Gag-specific responses (p&lt;0.0001 for 9 out of 11 significantly expressed analytes).	Glycosaminoglycans	46-49	interferon gamma	Homo sapiens	133-142
21533229-6	2011	At the peak response time point, PBMC from Ad5-seronegative vaccinees secreted significantly more IP-10 in response to Gag (p = 0.008), and significantly more IP-10 (p = 0.0009), IL-2 (p = 0.006) and IL-10 (p = 0.05) in response to Ad5 empty vector than PBMC from Ad5-seropositive vaccinees.	Glycosaminoglycans	119-122	C-X-C motif chemokine ligand 10	Homo sapiens	98-103
21533229-5	2011	The overall profiles of cytokine responses to Gag and Ad5 had similar combinations of induced Th1- and Th2-type cytokines, including IFN-gamma, IL-2, TNF-alpha, IP-10, IL-13, and IL-10, although the Ad5-specific responses were uniformly higher than the Gag-specific responses (p&lt;0.0001 for 9 out of 11 significantly expressed analytes).	Glycosaminoglycans	46-49	interleukin 2	Homo sapiens	144-148
21533229-8	2011	The cytokine response profile of Gag-specific T cells mirrored the Ad5-specific response present in all subjects before vaccination, and included a number of Th1- and Th2-associated cytokines not routinely assessed in current vaccine trials, such as IP-10, IL-10, IL-13, and GM-CSF.	Glycosaminoglycans	33-36	Alzheimer disease, familial, type 5	Homo sapiens	67-70
21533229-8	2011	The cytokine response profile of Gag-specific T cells mirrored the Ad5-specific response present in all subjects before vaccination, and included a number of Th1- and Th2-associated cytokines not routinely assessed in current vaccine trials, such as IP-10, IL-10, IL-13, and GM-CSF.	Glycosaminoglycans	33-36	C-X-C motif chemokine ligand 10	Homo sapiens	250-255
21533229-5	2011	The overall profiles of cytokine responses to Gag and Ad5 had similar combinations of induced Th1- and Th2-type cytokines, including IFN-gamma, IL-2, TNF-alpha, IP-10, IL-13, and IL-10, although the Ad5-specific responses were uniformly higher than the Gag-specific responses (p&lt;0.0001 for 9 out of 11 significantly expressed analytes).	Glycosaminoglycans	46-49	interleukin 13	Homo sapiens	168-173
21533229-8	2011	The cytokine response profile of Gag-specific T cells mirrored the Ad5-specific response present in all subjects before vaccination, and included a number of Th1- and Th2-associated cytokines not routinely assessed in current vaccine trials, such as IP-10, IL-10, IL-13, and GM-CSF.	Glycosaminoglycans	33-36	interleukin 10	Homo sapiens	257-262
21533229-5	2011	The overall profiles of cytokine responses to Gag and Ad5 had similar combinations of induced Th1- and Th2-type cytokines, including IFN-gamma, IL-2, TNF-alpha, IP-10, IL-13, and IL-10, although the Ad5-specific responses were uniformly higher than the Gag-specific responses (p&lt;0.0001 for 9 out of 11 significantly expressed analytes).	Glycosaminoglycans	46-49	interleukin 10	Homo sapiens	179-184
21533229-8	2011	The cytokine response profile of Gag-specific T cells mirrored the Ad5-specific response present in all subjects before vaccination, and included a number of Th1- and Th2-associated cytokines not routinely assessed in current vaccine trials, such as IP-10, IL-10, IL-13, and GM-CSF.	Glycosaminoglycans	33-36	interleukin 13	Homo sapiens	264-269
21533229-5	2011	The overall profiles of cytokine responses to Gag and Ad5 had similar combinations of induced Th1- and Th2-type cytokines, including IFN-gamma, IL-2, TNF-alpha, IP-10, IL-13, and IL-10, although the Ad5-specific responses were uniformly higher than the Gag-specific responses (p&lt;0.0001 for 9 out of 11 significantly expressed analytes).	Glycosaminoglycans	46-49	Alzheimer disease, familial, type 5	Homo sapiens	199-202
21533229-8	2011	The cytokine response profile of Gag-specific T cells mirrored the Ad5-specific response present in all subjects before vaccination, and included a number of Th1- and Th2-associated cytokines not routinely assessed in current vaccine trials, such as IP-10, IL-10, IL-13, and GM-CSF.	Glycosaminoglycans	33-36	colony stimulating factor 2	Homo sapiens	275-281
21348501-8	2011	Because GAG overexpression, which is common in amyloidosis, may represent a strategy for minimizing cross-beta-sheet oligomer toxicity by transforming them into amyloid fibrils, the mechanism described herein for GAG-mediated acceleration of 8 kDa gelsolin amyloidogenesis provides a starting point for therapeutic strategy development.	Glycosaminoglycans	8-11	gelsolin	Homo sapiens	248-256
21348501-8	2011	Because GAG overexpression, which is common in amyloidosis, may represent a strategy for minimizing cross-beta-sheet oligomer toxicity by transforming them into amyloid fibrils, the mechanism described herein for GAG-mediated acceleration of 8 kDa gelsolin amyloidogenesis provides a starting point for therapeutic strategy development.	Glycosaminoglycans	213-216	gelsolin	Homo sapiens	248-256
21334454-1	2011	Mucopolysaccharidosis type II (MPS II) is an X-linked recessive disease caused by deficiency of the lysosomal enzyme iduronate-2-sulfatase, leading to progressive accumulation of glycosaminoglycans in nearly all cell types, tissues and organs.	Glycosaminoglycans	179-197	iduronate 2-sulfatase	Homo sapiens	117-138
21483689-9	2011	Lymph nodes contained increased numbers of Tregs as compared to peripheral blood, which positively correlated with gp120 levels; T regulatory cell depletion restored CD8 T cell responses to Gag but not to gp120.	Glycosaminoglycans	190-193	CD8a molecule	Homo sapiens	166-169
21216815-11	2011	Ex vivo treatment of normal human cartilage with recombinant MMP17 protein increased NITEGE generation in the cartilage and GAG loss into the media.	Glycosaminoglycans	124-127	matrix metallopeptidase 17	Homo sapiens	61-66
21216815-13	2011	IAI of IL-1beta into C57BL6/Jax mice resulted in increased MMP17 expression in articular cartilage and increased GAG content in the synovial fluid.	Glycosaminoglycans	113-116	interleukin 1 beta	Mus musculus	7-15
21062785-1	2011	The proteoglycan serglycin (SG) fused to green fluorescent protein (GFP) is secreted predominantly from the apical surface of polarized epithelial Madin-Darby canine kidney (MDCK) cell monolayers, but the minor fraction secreted basolaterally carries more intensely sulfated glycosaminoglycan (GAG) chains (Tveit H, Dick G, Skibeli V, Prydz K. 2005.	Glycosaminoglycans	275-292	serglycin	Canis lupus familiaris	17-26
21360441-6	2011	Extracellular decorin recognition in culture supernatant was only possible after chondroitin lyase digestion suggesting that the core protein of secreted proteoglycan is more encrypted by glycosaminoglycans than the intracellular one.	Glycosaminoglycans	188-206	decorin	Mus musculus	14-21
21062785-1	2011	The proteoglycan serglycin (SG) fused to green fluorescent protein (GFP) is secreted predominantly from the apical surface of polarized epithelial Madin-Darby canine kidney (MDCK) cell monolayers, but the minor fraction secreted basolaterally carries more intensely sulfated glycosaminoglycan (GAG) chains (Tveit H, Dick G, Skibeli V, Prydz K. 2005.	Glycosaminoglycans	275-292	serglycin	Canis lupus familiaris	28-30
21062785-1	2011	The proteoglycan serglycin (SG) fused to green fluorescent protein (GFP) is secreted predominantly from the apical surface of polarized epithelial Madin-Darby canine kidney (MDCK) cell monolayers, but the minor fraction secreted basolaterally carries more intensely sulfated glycosaminoglycan (GAG) chains (Tveit H, Dick G, Skibeli V, Prydz K. 2005.	Glycosaminoglycans	294-297	serglycin	Canis lupus familiaris	17-26
21062785-1	2011	The proteoglycan serglycin (SG) fused to green fluorescent protein (GFP) is secreted predominantly from the apical surface of polarized epithelial Madin-Darby canine kidney (MDCK) cell monolayers, but the minor fraction secreted basolaterally carries more intensely sulfated glycosaminoglycan (GAG) chains (Tveit H, Dick G, Skibeli V, Prydz K. 2005.	Glycosaminoglycans	294-297	serglycin	Canis lupus familiaris	28-30
21062785-6	2011	Transfer of the GAG attachment domain from SG to the new rGH context abolished the differences in sulfation intensity and positions observed for SG in the apical and basolateral secretory routes.	Glycosaminoglycans	16-19	serglycin	Canis lupus familiaris	43-45
21062785-6	2011	Transfer of the GAG attachment domain from SG to the new rGH context abolished the differences in sulfation intensity and positions observed for SG in the apical and basolateral secretory routes.	Glycosaminoglycans	16-19	serglycin	Canis lupus familiaris	145-147
21394083-5	2011	In contrast, ESCRT-III and Vps4A were transiently recruited only when the accumulation of Gag was complete.	Glycosaminoglycans	90-93	vacuolar protein sorting 4 homolog A	Homo sapiens	27-32
21193412-8	2011	We show that removal of cell surface glycosaminoglycans (GAGs) by enzymatic or chemical treatment of cells or competition with heparin completely inhibited binding of PSG1.	Glycosaminoglycans	37-55	pregnancy specific beta-1-glycoprotein 1	Homo sapiens	167-171
21317894-3	2011	We used NMR and X-ray crystallography to study the C3d-FH19-20 complex in atomic detail and identify glycosaminoglycan-binding residues in factor H module 20 of the C3d-FH19-20 complex.	Glycosaminoglycans	101-118	complement factor H	Homo sapiens	139-147
21317894-3	2011	We used NMR and X-ray crystallography to study the C3d-FH19-20 complex in atomic detail and identify glycosaminoglycan-binding residues in factor H module 20 of the C3d-FH19-20 complex.	Glycosaminoglycans	101-118	endogenous retrovirus group K member 13	Homo sapiens	165-168
21091327-8	2011	In micromass pellet cultures, bFGF-treated SDSCs showed augmented sizes, weights, and glycosaminoglycan accumulation of pellets by bFGF supplementation.	Glycosaminoglycans	86-103	fibroblast growth factor 2	Homo sapiens	30-34
21490953-9	2011	Mutation of lysines at a potential site of SUMOylation in the CA region of the Gag gene reduced the SUMO-1 block and the TRIM5alpha restriction of N-MLV.	Glycosaminoglycans	79-82	small ubiquitin like modifier 1	Homo sapiens	100-106
21490953-9	2011	Mutation of lysines at a potential site of SUMOylation in the CA region of the Gag gene reduced the SUMO-1 block and the TRIM5alpha restriction of N-MLV.	Glycosaminoglycans	79-82	tripartite motif containing 5	Homo sapiens	121-131
21624210-3	2011	The deficiency of IDUA leads to widespread accumulation of partially degraded mucopolysaccharides inside lysosomes, resulting in progressive cellular and multiorgan dysfunction.	Glycosaminoglycans	78-97	alpha-L-iduronidase	Homo sapiens	18-22
21479250-2	2011	It is caused by a trinucleotide deletion of a GAG (DeltaGAG) in the DYT1 (TOR1A) gene encoding torsinA; the mouse homolog of this gene is Dyt1 (Tor1a).	Glycosaminoglycans	46-49	torsin family 1, member A (torsin A)	Mus musculus	68-72
21479250-2	2011	It is caused by a trinucleotide deletion of a GAG (DeltaGAG) in the DYT1 (TOR1A) gene encoding torsinA; the mouse homolog of this gene is Dyt1 (Tor1a).	Glycosaminoglycans	46-49	torsin family 1, member A (torsin A)	Mus musculus	74-79
21479250-2	2011	It is caused by a trinucleotide deletion of a GAG (DeltaGAG) in the DYT1 (TOR1A) gene encoding torsinA; the mouse homolog of this gene is Dyt1 (Tor1a).	Glycosaminoglycans	46-49	torsin family 1, member A (torsin A)	Mus musculus	95-102
21479250-2	2011	It is caused by a trinucleotide deletion of a GAG (DeltaGAG) in the DYT1 (TOR1A) gene encoding torsinA; the mouse homolog of this gene is Dyt1 (Tor1a).	Glycosaminoglycans	46-49	torsin family 1, member A (torsin A)	Mus musculus	138-142
21479250-2	2011	It is caused by a trinucleotide deletion of a GAG (DeltaGAG) in the DYT1 (TOR1A) gene encoding torsinA; the mouse homolog of this gene is Dyt1 (Tor1a).	Glycosaminoglycans	46-49	torsin family 1, member A (torsin A)	Mus musculus	144-149
21241782-1	2011	DYT1 dystonia is caused by a GAG deletion in TOR1A, the gene which encodes torsinA.	Glycosaminoglycans	29-32	torsin family 1, member A (torsin A)	Mus musculus	0-4
21241782-1	2011	DYT1 dystonia is caused by a GAG deletion in TOR1A, the gene which encodes torsinA.	Glycosaminoglycans	29-32	torsin family 1, member A (torsin A)	Mus musculus	45-50
21193412-11	2011	This finding indicates that the PSG1-GAG interaction mediates at least some of the PSG1 proposed functions.	Glycosaminoglycans	37-40	pregnancy specific beta-1-glycoprotein 1	Homo sapiens	32-36
21193412-11	2011	This finding indicates that the PSG1-GAG interaction mediates at least some of the PSG1 proposed functions.	Glycosaminoglycans	37-40	pregnancy specific beta-1-glycoprotein 1	Homo sapiens	83-87
20825472-6	2011	RESULTS: Three subjects were found to have the GAG deletion in the TOR1A gene, and two patients were detected with THAP1 gene mutations/variations (c.224A>T, c.449A>C).	Glycosaminoglycans	47-50	torsin family 1 member A	Homo sapiens	67-72
21205989-4	2011	Ox-LDL increased mRNA abundance of both xylosyltransferase (XT)-I, the key enzyme responsible for GAG chain biosynthesis and Msx2, a marker of osteogenic differentiation.	Glycosaminoglycans	98-101	xylosyltransferase 1	Homo sapiens	40-65
20882590-9	2011	GAG production was increased by BMP-2.	Glycosaminoglycans	0-3	bone morphogenetic protein 2	Homo sapiens	32-37
21156206-8	2011	This observation was confirmed in primary fibroblast cells, in which the combination of GAG TNR 7/7 and -129C/T genotypes decreased the GCLC protein level.	Glycosaminoglycans	88-91	glutamate-cysteine ligase catalytic subunit	Homo sapiens	136-140
20681952-5	2011	Both PrP(C) and PrP(Sc) co-immunoprecipitated with glypican-1 and the interaction was dependent on the glycosaminoglycan side chains of glypican-1.	Glycosaminoglycans	103-120	proline rich protein HaeIII subfamily 1	Mus musculus	5-8
20681952-5	2011	Both PrP(C) and PrP(Sc) co-immunoprecipitated with glypican-1 and the interaction was dependent on the glycosaminoglycan side chains of glypican-1.	Glycosaminoglycans	103-120	proline rich protein HaeIII subfamily 1	Mus musculus	16-19
20681952-5	2011	Both PrP(C) and PrP(Sc) co-immunoprecipitated with glypican-1 and the interaction was dependent on the glycosaminoglycan side chains of glypican-1.	Glycosaminoglycans	103-120	glypican 1	Mus musculus	51-61
20681952-5	2011	Both PrP(C) and PrP(Sc) co-immunoprecipitated with glypican-1 and the interaction was dependent on the glycosaminoglycan side chains of glypican-1.	Glycosaminoglycans	103-120	glypican 1	Mus musculus	136-146
21378286-1	2011	The enzyme arylsulfatase B (N-acetylgalactosamine-4-sulfatase; ARSB; ASB) removes 4-sulfate groups from the sulfated glycosaminoglycans (sGAG) chondroitin-4-sulfate (C4S) and dermatan sulfate (DS).	Glycosaminoglycans	117-135	arylsulfatase B	Homo sapiens	28-61
21378286-1	2011	The enzyme arylsulfatase B (N-acetylgalactosamine-4-sulfatase; ARSB; ASB) removes 4-sulfate groups from the sulfated glycosaminoglycans (sGAG) chondroitin-4-sulfate (C4S) and dermatan sulfate (DS).	Glycosaminoglycans	117-135	arylsulfatase B	Homo sapiens	63-67
21378286-1	2011	The enzyme arylsulfatase B (N-acetylgalactosamine-4-sulfatase; ARSB; ASB) removes 4-sulfate groups from the sulfated glycosaminoglycans (sGAG) chondroitin-4-sulfate (C4S) and dermatan sulfate (DS).	Glycosaminoglycans	117-135	arylsulfatase B	Homo sapiens	69-72
21119624-1	2011	Mucopolysaccharidosis VI (MPS VI) is caused by deficient arylsulfatase B (ARSB) activity resulting in lysosomal storage of glycosaminoglycans (GAGs).	Glycosaminoglycans	123-141	arylsulfatase B	Felis catus	74-78
20653042-13	2011	rGDF-5 led to an increase in total DNA, glycosaminoglycan (GAG) and hydroxyproline (OHP).	Glycosaminoglycans	40-57	growth differentiation factor 5	Rattus norvegicus	0-6
20653042-13	2011	rGDF-5 led to an increase in total DNA, glycosaminoglycan (GAG) and hydroxyproline (OHP).	Glycosaminoglycans	59-62	growth differentiation factor 5	Rattus norvegicus	0-6
21159859-6	2011	Our data also reveal a direct relationship of gag and tat transcripts with CD4 and CD8 T cell activation, respectively.	Glycosaminoglycans	46-49	CD4 molecule	Homo sapiens	75-78
21159859-6	2011	Our data also reveal a direct relationship of gag and tat transcripts with CD4 and CD8 T cell activation, respectively.	Glycosaminoglycans	46-49	CD8a molecule	Homo sapiens	83-86
21081900-1	2011	The loss of IDUA protein results in the progressive accumulation of glycosaminoglycans within the lysosomes resulting in severe, multi-organ system pathology.	Glycosaminoglycans	68-86	iduronidase, alpha-L	Mus musculus	12-16
21119624-6	2011	In MPS VI cats showing high serum ARSB levels, independent of the age at treatment, we observed: (i) clearance of GAG storage, (ii) improvement of long bone length, (iii) reduction of heart valve thickness, and (iv) improvement in spontaneous mobility.	Glycosaminoglycans	114-117	arylsulfatase B	Felis catus	34-38
21264442-2	2011	The F12 of this proband had a 9775G to C mutation in exon 10 and an 11276G to A mutation in exon 13 that resulted in two amino acid substitutions of Ala324Pro (GCG CCG) in the proline-rich connecting region and Gly531Glu (GGG GAG) near the active Ser544 in the catalytic domain.	Glycosaminoglycans	226-229	coagulation factor XII	Homo sapiens	4-7
20929284-6	2011	FGF-2 pretreatment led to the highest glycosaminoglycans and DNA content; intriguingly, it also contributed to the highest expression level of hypertrophic marker genes.	Glycosaminoglycans	38-56	fibroblast growth factor 2	Homo sapiens	0-5
21339334-7	2011	We also show that GPC5 binds to both Hh and Ptc1 through its glycosaminoglycan chains and that, unlike GPC3, GPC5 localizes to the primary cilia.	Glycosaminoglycans	61-78	glypican 5	Homo sapiens	18-22
21319344-10	2011	A higher dose of IdS infusion in MPS II mice led to disappearance of lysosomal GAG and restoration of glycogen to the cytoplasm of hepatocytes.	Glycosaminoglycans	79-82	iduronate 2-sulfatase	Mus musculus	17-20
21177248-2	2011	LPL also plays a role in the binding of lipoprotein particles to cell-surface molecules, including sulfated glycosaminoglycans (GAGs).	Glycosaminoglycans	128-132	lipoprotein lipase	Mus musculus	0-3
21177248-7	2011	We also found that sulfated GAGs were involved in the LPL-mediated cellular uptake of Abeta.	Glycosaminoglycans	28-32	lipoprotein lipase	Mus musculus	54-57
21177248-7	2011	We also found that sulfated GAGs were involved in the LPL-mediated cellular uptake of Abeta.	Glycosaminoglycans	28-32	amyloid beta (A4) precursor protein	Mus musculus	86-91
21339334-7	2011	We also show that GPC5 binds to both Hh and Ptc1 through its glycosaminoglycan chains and that, unlike GPC3, GPC5 localizes to the primary cilia.	Glycosaminoglycans	61-78	patched 1	Homo sapiens	44-48
21638930-9	2011	CONCLUSION: bFGF increase GAG and type II collagen mRNA expression, increased extracellular matrix type II collagen and GAG expression in short-term.	Glycosaminoglycans	26-29	fibroblast growth factor 2	Homo sapiens	12-16
21638930-9	2011	CONCLUSION: bFGF increase GAG and type II collagen mRNA expression, increased extracellular matrix type II collagen and GAG expression in short-term.	Glycosaminoglycans	120-123	fibroblast growth factor 2	Homo sapiens	12-16
21177248-0	2011	Lipoprotein lipase is a novel amyloid beta (Abeta)-binding protein that promotes glycosaminoglycan-dependent cellular uptake of Abeta in astrocytes.	Glycosaminoglycans	81-98	amyloid beta (A4) precursor protein	Mus musculus	44-49
21177248-0	2011	Lipoprotein lipase is a novel amyloid beta (Abeta)-binding protein that promotes glycosaminoglycan-dependent cellular uptake of Abeta in astrocytes.	Glycosaminoglycans	81-98	amyloid beta (A4) precursor protein	Mus musculus	128-133
21291557-12	2011	Porcine Dsp GAG attachments were found at Ser238 and Ser250 and were comprised of chondroitin 6-sulfate and chondroitin 4-sulfate in a ratio of 7 to 3, respectively.	Glycosaminoglycans	12-15	dentin sialophosphoprotein	Homo sapiens	8-11
21135108-5	2011	However, in contrast, the prodomain of GDF-8 (myostatin) interacts with the glycosaminoglycan side chains of perlecan.	Glycosaminoglycans	76-93	myostatin	Homo sapiens	39-44
21285368-2	2011	It is unresolved how host and nonhost surfaces are distinguished at the molecular level, but key components are domains 19-20 of the complement regulator factor H (FH), which interact with host (i.e., nonactivator surface glycosaminoglycans or sialic acids) and the C3d part of C3b.	Glycosaminoglycans	222-240	complement factor H	Homo sapiens	154-162
21285368-2	2011	It is unresolved how host and nonhost surfaces are distinguished at the molecular level, but key components are domains 19-20 of the complement regulator factor H (FH), which interact with host (i.e., nonactivator surface glycosaminoglycans or sialic acids) and the C3d part of C3b.	Glycosaminoglycans	222-240	complement factor H	Homo sapiens	164-166
21285368-4	2011	We show simultaneous binding of FH19 to C3b and FH20 to nonactivator surface glycosaminoglycans, and we show that both of these interactions are necessary for full binding of FH to C3b on nonactivator surfaces (i.e., for target discrimination).	Glycosaminoglycans	77-95	complement factor H	Homo sapiens	32-34
21285368-5	2011	We also show that C3d could replace glycosaminoglycan binding to FH20, thus providing a feedback control for preventing excess C3b deposition and complement amplification.	Glycosaminoglycans	36-53	endogenous retrovirus group K member 13	Homo sapiens	18-21
21285368-5	2011	We also show that C3d could replace glycosaminoglycan binding to FH20, thus providing a feedback control for preventing excess C3b deposition and complement amplification.	Glycosaminoglycans	36-53	complement C3	Homo sapiens	127-130
21262813-5	2011	When the mAb heavy chains were engineered to express gag-p24, the alpha-Langerin, alpha-DEC205, and alpha-Clec9A fusion mAbs given along with a maturation stimulus induced comparable levels of gag-specific T helper 1 (Th1) and CD8(+) T cells in BALB/c x C57BL/6 F1 mice.	Glycosaminoglycans	53-56	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	57-60
21262813-7	2011	In an in vivo assay in which gag-primed T cells were used to report the early stages of T-cell responses, alpha-Langerin, alpha-DEC205, and alpha-Clec9A also mediated cross-presentation to primed CD8(+) T cells if, in parallel to antigen uptake, the DCs were stimulated with alpha-CD40.	Glycosaminoglycans	29-32	CD207 antigen	Mus musculus	112-120
21262813-7	2011	In an in vivo assay in which gag-primed T cells were used to report the early stages of T-cell responses, alpha-Langerin, alpha-DEC205, and alpha-Clec9A also mediated cross-presentation to primed CD8(+) T cells if, in parallel to antigen uptake, the DCs were stimulated with alpha-CD40.	Glycosaminoglycans	29-32	lymphocyte antigen 75	Mus musculus	128-134
21262813-7	2011	In an in vivo assay in which gag-primed T cells were used to report the early stages of T-cell responses, alpha-Langerin, alpha-DEC205, and alpha-Clec9A also mediated cross-presentation to primed CD8(+) T cells if, in parallel to antigen uptake, the DCs were stimulated with alpha-CD40.	Glycosaminoglycans	29-32	C-type lectin domain family 9, member a	Mus musculus	146-152
21219861-2	2011	In this study we investigated the role of glycosaminoglycans (GAGs) of BGN in this function using in vitro and in vivo models.	Glycosaminoglycans	42-60	biglycan	Rattus norvegicus	71-74
21219861-2	2011	In this study we investigated the role of glycosaminoglycans (GAGs) of BGN in this function using in vitro and in vivo models.	Glycosaminoglycans	62-66	biglycan	Rattus norvegicus	71-74
21219861-8	2011	The data indicate that the GAG component of BGN functions as a suppressor for the BGN-assisted BMP function.	Glycosaminoglycans	27-30	biglycan	Rattus norvegicus	44-47
21219861-8	2011	The data indicate that the GAG component of BGN functions as a suppressor for the BGN-assisted BMP function.	Glycosaminoglycans	27-30	biglycan	Rattus norvegicus	82-85
21291557-13	2011	CONCLUSIONS: The distribution of porcine Dsp posttranslational modifications indicate that porcine Dsp has an N-terminal domain with at least six N-glycosylations and a C-terminal domain with two GAG attachments and at least two O-glycosylations.	Glycosaminoglycans	196-199	dentin sialophosphoprotein	Homo sapiens	99-102
21078848-2	2011	Previous studies in a Drosophila melanogaster model showed that binding of ACP to the sulfated polysaccharide chains (glycosaminoglycans) of HSPGs promotes host death and is associated with higher bacterial burdens.	Glycosaminoglycans	118-136	Accessory gland protein 26Ab	Drosophila melanogaster	75-78
21056957-8	2011	TGF-beta(1) upregulated GlcAT-I and versican expression in lung fibroblasts, and signaling through TGF-beta type I receptor/p38 MAPK was required for TGF-beta(1)-mediated GlcAT-I and CS-GAG expression in fibroblasts.	Glycosaminoglycans	186-189	transforming growth factor, beta 1	Rattus norvegicus	0-11
21056957-8	2011	TGF-beta(1) upregulated GlcAT-I and versican expression in lung fibroblasts, and signaling through TGF-beta type I receptor/p38 MAPK was required for TGF-beta(1)-mediated GlcAT-I and CS-GAG expression in fibroblasts.	Glycosaminoglycans	186-189	transforming growth factor, beta receptor 1	Rattus norvegicus	99-123
21056957-8	2011	TGF-beta(1) upregulated GlcAT-I and versican expression in lung fibroblasts, and signaling through TGF-beta type I receptor/p38 MAPK was required for TGF-beta(1)-mediated GlcAT-I and CS-GAG expression in fibroblasts.	Glycosaminoglycans	186-189	transforming growth factor, beta 1	Rattus norvegicus	150-161
21111666-5	2011	Both glycosaminoglycans (GAG) and CXCR3 are implicated in the activities of the PF-4 variants.	Glycosaminoglycans	5-23	platelet factor 4	Homo sapiens	80-84
21111666-5	2011	Both glycosaminoglycans (GAG) and CXCR3 are implicated in the activities of the PF-4 variants.	Glycosaminoglycans	25-28	platelet factor 4	Homo sapiens	80-84
21268013-5	2011	C1q-binding is mediated through the glycosaminoglycan moieties of SG, whereas MBL binds additionally to SG protein core.	Glycosaminoglycans	36-53	complement C1q A chain	Homo sapiens	0-3
21268013-5	2011	C1q-binding is mediated through the glycosaminoglycan moieties of SG, whereas MBL binds additionally to SG protein core.	Glycosaminoglycans	36-53	serglycin	Homo sapiens	66-68
21115724-9	2011	Two of these genes, heparan sulfate d-glucosaminyl 3-O-sulfotransferase 3A1 and hyaluronan synthase 2, are also potentially important mediators of wound repair via the production of glycosaminoglycan components.	Glycosaminoglycans	182-199	hyaluronan synthase 2	Canis lupus familiaris	80-101
21078848-5	2011	Strikingly, host survival after infection with wild-type streptococci was enhanced among flies overexpressing the endogenous glycosaminoglycan/HSPG-binding morphogen Decapentaplegic-a transforming growth factor beta-like Drosophila homolog of mammalian bone morphogenetic proteins-but not by flies overexpressing a mutant, non-glycosaminoglycan-binding Decapentaplegic, or the other endogenous glycosaminoglycan/HSPG-binding morphogens, Hedgehog and Wingless.	Glycosaminoglycans	125-142	syndecan 2	Homo sapiens	143-147
21078848-5	2011	Strikingly, host survival after infection with wild-type streptococci was enhanced among flies overexpressing the endogenous glycosaminoglycan/HSPG-binding morphogen Decapentaplegic-a transforming growth factor beta-like Drosophila homolog of mammalian bone morphogenetic proteins-but not by flies overexpressing a mutant, non-glycosaminoglycan-binding Decapentaplegic, or the other endogenous glycosaminoglycan/HSPG-binding morphogens, Hedgehog and Wingless.	Glycosaminoglycans	125-142	syndecan 2	Homo sapiens	412-416
21078848-8	2011	These data suggest that, in addition to promoting bacterial entry into host cells, ACP competes with Decapentaplegic for binding to glycosaminoglycans/HSPGs during infection and that these bacterial and endogenous glycosaminoglycan-binding structures determine host survival and regulate antimicrobial peptide transcription.	Glycosaminoglycans	132-150	Accessory gland protein 26Ab	Drosophila melanogaster	83-86
21075170-8	2011	Dynamic trafficking to aggresomes contributes to the dominant negative activity of v-ErbA and may be enhanced by the viral Gag sequence.	Glycosaminoglycans	123-126	thyroid hormone receptor alpha	Homo sapiens	85-89
21123385-7	2011	However, these zip mutants neither cleave Gag nor incorporate Pol into virions.	Glycosaminoglycans	42-45	death associated protein kinase 3	Homo sapiens	15-18
21283635-6	2011	Myoc-OLF is stable in the presence of glycosaminoglycans, as well as in a wide pH range in buffers with functional groups reminiscent of such glycosaminoglycans.	Glycosaminoglycans	38-56	myocilin	Homo sapiens	0-4
21098039-7	2011	Another surface protein of GGS, FOG, was found to mediate adherence of the bacteria to pharyngeal epithelial cells through interaction with glycosaminoglycans.	Glycosaminoglycans	140-158	zinc finger protein, FOG family member 1	Homo sapiens	32-35
21283635-6	2011	Myoc-OLF is stable in the presence of glycosaminoglycans, as well as in a wide pH range in buffers with functional groups reminiscent of such glycosaminoglycans.	Glycosaminoglycans	142-160	myocilin	Homo sapiens	0-4
21888631-10	2011	The combination of mechanical injury, TNFalpha and IL-6/sIL-6R caused the most severe GAG loss; dexamethasone reduced this GAG loss to control levels in bovine and human cartilage.	Glycosaminoglycans	86-89	tumor necrosis factor	Bos taurus	38-46
21037085-1	2011	Mucopolysaccharidosis type I (MPS IH; Hurler syndrome) is a congenital deficiency of alpha-L-iduronidase, leading to lysosomal storage of glycosaminoglycans that is ultimately fatal following an insidious onset after birth.	Glycosaminoglycans	138-156	alpha-L-iduronidase	Homo sapiens	85-104
21142149-1	2011	The conversion of cellular prion protein (PrP(C)) into the pathological conformer PrP(Sc) requires contact between both isoforms and probably also requires a cellular factor, such as a nucleic acid or a glycosaminoglycan (GAG).	Glycosaminoglycans	203-220	prion protein	Mus musculus	42-45
21142149-1	2011	The conversion of cellular prion protein (PrP(C)) into the pathological conformer PrP(Sc) requires contact between both isoforms and probably also requires a cellular factor, such as a nucleic acid or a glycosaminoglycan (GAG).	Glycosaminoglycans	203-220	prion protein	Mus musculus	82-85
21142149-1	2011	The conversion of cellular prion protein (PrP(C)) into the pathological conformer PrP(Sc) requires contact between both isoforms and probably also requires a cellular factor, such as a nucleic acid or a glycosaminoglycan (GAG).	Glycosaminoglycans	222-225	prion protein	Mus musculus	42-45
21142149-1	2011	The conversion of cellular prion protein (PrP(C)) into the pathological conformer PrP(Sc) requires contact between both isoforms and probably also requires a cellular factor, such as a nucleic acid or a glycosaminoglycan (GAG).	Glycosaminoglycans	222-225	prion protein	Mus musculus	82-85
21142149-2	2011	Little is known about the structural features implicit in the GAG-PrP interaction.	Glycosaminoglycans	62-65	prion protein	Mus musculus	66-69
21142149-11	2011	Depending on the cellular milieu, the PrP may expose different regions that can bind GAG.	Glycosaminoglycans	85-88	prion protein	Mus musculus	38-41
21078678-6	2011	Furthermore, CD44-dependent hyaluronan internalization was blocked by V3 expression and CD44 silencing, leading to an accumulation of this glycosaminoglycan in the pericellular matrix and to changes in cell migration on hyaluronan.	Glycosaminoglycans	139-156	CD44 molecule (Indian blood group)	Homo sapiens	13-17
21078678-6	2011	Furthermore, CD44-dependent hyaluronan internalization was blocked by V3 expression and CD44 silencing, leading to an accumulation of this glycosaminoglycan in the pericellular matrix and to changes in cell migration on hyaluronan.	Glycosaminoglycans	139-156	CD44 molecule (Indian blood group)	Homo sapiens	88-92
21211021-10	2011	However, antibody reactivity to gag antigens varied among the women, being 100%, 90%, 70% and 63% for p24, p17, p39 and p55, respectively.	Glycosaminoglycans	32-35	transmembrane p24 trafficking protein 2	Homo sapiens	102-105
21211021-10	2011	However, antibody reactivity to gag antigens varied among the women, being 100%, 90%, 70% and 63% for p24, p17, p39 and p55, respectively.	Glycosaminoglycans	32-35	family with sequence similarity 72 member B	Homo sapiens	107-110
21211021-10	2011	However, antibody reactivity to gag antigens varied among the women, being 100%, 90%, 70% and 63% for p24, p17, p39 and p55, respectively.	Glycosaminoglycans	32-35	cyclin dependent kinase 5 regulatory subunit 2	Homo sapiens	112-115
21211021-10	2011	However, antibody reactivity to gag antigens varied among the women, being 100%, 90%, 70% and 63% for p24, p17, p39 and p55, respectively.	Glycosaminoglycans	32-35	H3 histone pseudogene 44	Homo sapiens	120-123
21110947-2	2011	ZG16p interacts with glycosaminoglycans and the binding is considered to be important for condensation-sorting of pancreatic enzymes.	Glycosaminoglycans	21-39	zymogen granule protein 16	Homo sapiens	0-5
21110947-9	2011	A positively charged patch, which may bind sulfated groups of the glycosaminoglycans, is located around the putative sugar-binding site of ZG16p and ZG16b.	Glycosaminoglycans	66-84	zymogen granule protein 16	Homo sapiens	139-144
21110947-9	2011	A positively charged patch, which may bind sulfated groups of the glycosaminoglycans, is located around the putative sugar-binding site of ZG16p and ZG16b.	Glycosaminoglycans	66-84	zymogen granule protein 16B	Homo sapiens	149-154
21888631-10	2011	The combination of mechanical injury, TNFalpha and IL-6/sIL-6R caused the most severe GAG loss; dexamethasone reduced this GAG loss to control levels in bovine and human cartilage.	Glycosaminoglycans	86-89	interleukin 6	Bos taurus	51-55
21888631-15	2011	RVKR-CMK significantly reduced GAG loss caused by TNFalpha + IL-6 + injury.	Glycosaminoglycans	31-34	tumor necrosis factor	Bos taurus	50-58
21888631-15	2011	RVKR-CMK significantly reduced GAG loss caused by TNFalpha + IL-6 + injury.	Glycosaminoglycans	31-34	interleukin 6	Bos taurus	61-65
21250863-4	2011	Temporal and concentration analysis revealed that GDF-5 increases total DNA, glycosaminoglycan (GAG), and hydroxyproline (HYP) content.	Glycosaminoglycans	77-94	growth differentiation factor 5	Rattus norvegicus	50-55
21250863-4	2011	Temporal and concentration analysis revealed that GDF-5 increases total DNA, glycosaminoglycan (GAG), and hydroxyproline (HYP) content.	Glycosaminoglycans	96-99	growth differentiation factor 5	Rattus norvegicus	50-55
21261615-1	2011	Syndecan-4 is a cell membrane heparan sulfate proteoglycan that is composed of a core protein and covalently attached glycosaminoglycans (GAG) and N-linked glycosylated (N-glycosylated) chains.	Glycosaminoglycans	118-136	syndecan-4	Meleagris gallopavo	0-10
21261615-1	2011	Syndecan-4 is a cell membrane heparan sulfate proteoglycan that is composed of a core protein and covalently attached glycosaminoglycans (GAG) and N-linked glycosylated (N-glycosylated) chains.	Glycosaminoglycans	138-141	syndecan-4	Meleagris gallopavo	0-10
21261615-8	2011	The overexpression of syndecan-4 N-glycosylated mutants with or without GAG chains did not change cell proliferation, differentiation, and responsiveness to FGF2 compared to the wild type syndecan-4 except that the overexpression of syndecan-4 N-glycosylated mutants without GAG chains increased cell proliferation at 48 and 72 h post-transfection.	Glycosaminoglycans	275-278	syndecan-4	Meleagris gallopavo	22-32
21786328-1	2011	BACKGROUND: Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of the alpha-L-iduronidase (IDUA), which leads to the accumulation of glycosaminoglycans in lysosomes.	Glycosaminoglycans	145-163	alpha-L-iduronidase	Homo sapiens	82-101
21261615-9	2011	These data suggest that syndecan-4 functions in an FGF2-independent manner, and the N-glycosylated and GAG chains are required for syndecan-4 to regulate turkey myogenic satellite cell proliferation, but not differentiation.	Glycosaminoglycans	103-106	syndecan-4	Meleagris gallopavo	131-141
21786328-1	2011	BACKGROUND: Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of the alpha-L-iduronidase (IDUA), which leads to the accumulation of glycosaminoglycans in lysosomes.	Glycosaminoglycans	145-163	alpha-L-iduronidase	Homo sapiens	103-107
20213669-0	2011	Eosinophil cationic protein (ECP) can bind heparin and other glycosaminoglycans through its RNase active site.	Glycosaminoglycans	61-79	ribonuclease A family member 3	Homo sapiens	0-27
20213669-0	2011	Eosinophil cationic protein (ECP) can bind heparin and other glycosaminoglycans through its RNase active site.	Glycosaminoglycans	61-79	ribonuclease A family member 3	Homo sapiens	29-32
20213669-8	2011	ECP affinity for heparin and other negatively charged glycosaminoglycans (GAGs) can explain not only its binding to the eukaryote cells glycocalix but also the reported high affinity for the specific carbohydrates at bacteria cell wall, promoting its antimicrobial action.	Glycosaminoglycans	54-72	ribonuclease A family member 3	Homo sapiens	0-3
21068242-5	2011	This seemed to reflect an interaction of gp180 with glycosaminoglycans (GAGs), since compared to the wild-type virus, the Bo10 mutant virus was both less infectious for GAG-positive (GAG(+)) cells and more infectious for GAG-negative (GAG(-)) cells.	Glycosaminoglycans	169-172	protein tyrosine phosphatase receptor type C	Homo sapiens	41-46
22200993-10	2011	These results suggested that the versican splice variant V1 implicates both the control of the mineralization and the activities of the predentin metalloproteinases, because it has 13 GAG chains that bind a large amount of calcium.	Glycosaminoglycans	184-187	versican	Sus scrofa	33-41
21068242-5	2011	This seemed to reflect an interaction of gp180 with glycosaminoglycans (GAGs), since compared to the wild-type virus, the Bo10 mutant virus was both less infectious for GAG-positive (GAG(+)) cells and more infectious for GAG-negative (GAG(-)) cells.	Glycosaminoglycans	169-172	protein tyrosine phosphatase receptor type C	Homo sapiens	41-46
21068242-5	2011	This seemed to reflect an interaction of gp180 with glycosaminoglycans (GAGs), since compared to the wild-type virus, the Bo10 mutant virus was both less infectious for GAG-positive (GAG(+)) cells and more infectious for GAG-negative (GAG(-)) cells.	Glycosaminoglycans	169-172	protein tyrosine phosphatase receptor type C	Homo sapiens	41-46
22114714-8	2011	CONCLUSIONS: This study demonstrates that a stimulation regimen of simultaneous tension and compression mechanical stimulation, C-ABC, and TGF-beta1 is able to create anatomic meniscus constructs replicating the compressive mechanical properties, and collagen and GAG content of native tissue.	Glycosaminoglycans	264-267	transforming growth factor beta 1	Homo sapiens	139-148
22028895-7	2011	In the CF lung, polyanionic molecules such as glycosaminoglycans (GAGs) and DNA bind LL-37 and impact negatively on its antibacterial activity.	Glycosaminoglycans	46-64	cathelicidin antimicrobial peptide	Homo sapiens	85-90
21857901-8	2011	T-cell responses, detected by interferon-gamma (IFN-gamma) ELISpot to global potential T-cell epitopes (PTEs) were observed in 70.8% (136/192) of vaccine recipients overall, most frequently to Gag (54.7%) and to Env (54.2%).	Glycosaminoglycans	193-196	interferon gamma	Homo sapiens	48-57
21957484-7	2011	Using a mutant CHO-K1 cell line that lacks all glycosaminoglycans (GAGs) on its surface (CHO-745) we demonstrate that the core protein of syndecan-1 possesses the ability to modulate membrane fusion and viral spread.	Glycosaminoglycans	47-65	syndecan 1	Homo sapiens	138-148
20929444-4	2010	Our results demonstrate that an intramolecular interaction between Patch 2 in the Bro1 domain and the TSG101 (tumour susceptibility gene 101 protein)-docking site in the proline-rich domain locks ALIX into a closed conformation that renders ALIX unable to interact with CHMP4 and retroviral Gag proteins.	Glycosaminoglycans	291-294	tumor susceptibility 101	Homo sapiens	102-108
21747937-2	2011	Chondroitin 6-sulphotransferase-1 (C6ST-1) is upregulated after injury leading to an increase in 6-sulphated GAG.	Glycosaminoglycans	109-112	carbohydrate sulfotransferase 3	Mus musculus	35-41
21818255-10	2011	The differentiation profiles and multifunctionality of Gag-specific CD8+ T cells, regardless of immunodominance, also failed to demonstrate meaningful differences between the two groups.	Glycosaminoglycans	55-58	CD8a molecule	Homo sapiens	68-71
21062061-3	2010	Analyses in vitro and in cellulo revealed that RNase A interacts tightly with abundant cell-surface proteoglycans containing glycosaminoglycans, such as heparan sulfate and chondroitin sulfate, as well as with sialic acid-containing glycoproteins.	Glycosaminoglycans	125-143	ribonuclease A family member 1, pancreatic	Homo sapiens	47-54
20929444-4	2010	Our results demonstrate that an intramolecular interaction between Patch 2 in the Bro1 domain and the TSG101 (tumour susceptibility gene 101 protein)-docking site in the proline-rich domain locks ALIX into a closed conformation that renders ALIX unable to interact with CHMP4 and retroviral Gag proteins.	Glycosaminoglycans	291-294	tumor susceptibility 101	Homo sapiens	110-148
20929444-4	2010	Our results demonstrate that an intramolecular interaction between Patch 2 in the Bro1 domain and the TSG101 (tumour susceptibility gene 101 protein)-docking site in the proline-rich domain locks ALIX into a closed conformation that renders ALIX unable to interact with CHMP4 and retroviral Gag proteins.	Glycosaminoglycans	291-294	programmed cell death 6 interacting protein	Homo sapiens	196-200
20929444-4	2010	Our results demonstrate that an intramolecular interaction between Patch 2 in the Bro1 domain and the TSG101 (tumour susceptibility gene 101 protein)-docking site in the proline-rich domain locks ALIX into a closed conformation that renders ALIX unable to interact with CHMP4 and retroviral Gag proteins.	Glycosaminoglycans	291-294	programmed cell death 6 interacting protein	Homo sapiens	241-245
20929444-4	2010	Our results demonstrate that an intramolecular interaction between Patch 2 in the Bro1 domain and the TSG101 (tumour susceptibility gene 101 protein)-docking site in the proline-rich domain locks ALIX into a closed conformation that renders ALIX unable to interact with CHMP4 and retroviral Gag proteins.	Glycosaminoglycans	291-294	charged multivesicular body protein 4A	Homo sapiens	270-275
21058683-5	2010	Here, ab initio computational methods, together with our recent high-resolution 3-D structure of human LysRS, produced an energy-minimized model where Gag, tRNA(Lys), and LysRS form a ternary complex.	Glycosaminoglycans	151-154	lysyl-tRNA synthetase 1	Homo sapiens	103-108
21058683-5	2010	Here, ab initio computational methods, together with our recent high-resolution 3-D structure of human LysRS, produced an energy-minimized model where Gag, tRNA(Lys), and LysRS form a ternary complex.	Glycosaminoglycans	151-154	lysyl-tRNA synthetase 1	Homo sapiens	171-176
21058683-6	2010	Interestingly, the model requires normally homodimeric LysRS to dissociate into a monomer that bridges between Gag and tRNA(Lys3).	Glycosaminoglycans	111-114	lysyl-tRNA synthetase 1	Homo sapiens	55-60
21062008-0	2010	Interaction of human beta-defensin 2 (HBD2) with glycosaminoglycans.	Glycosaminoglycans	49-67	defensin beta 4A	Homo sapiens	21-36
20939056-3	2010	To overcome this problem, glycosaminoglycans were coblended with tropoelastin during the formation of synthetic elastin hydrogels.	Glycosaminoglycans	26-44	elastin	Homo sapiens	70-77
22473175-6	2010	On positively charged APS mica the GAG chains of the aggrecan molecules are distinguishable, and their average dimensions are practically unaffected by the presence of salt ions.	Glycosaminoglycans	35-38	MHC class I polypeptide-related sequence A	Homo sapiens	26-30
21062008-5	2010	We used NMR spectroscopy of (15)N-labeled HBD2 to map the binding sites for two GAG model compounds, a heparin/HS pentasaccharide (fondaparinux sodium; FX) and enzymatically prepared DS hexasaccharide (DSdp6).	Glycosaminoglycans	80-83	defensin beta 4A	Homo sapiens	42-46
21062008-0	2010	Interaction of human beta-defensin 2 (HBD2) with glycosaminoglycans.	Glycosaminoglycans	49-67	defensin beta 4A	Homo sapiens	38-42
20800524-1	2010	BACKGROUND: Maroteaux-Lamy syndrome, or mucopolysaccharidosis (MPS) type VI, is the autosomal recessive lysosomal disorder resulting from deficient N-acetylgalactosamine 4-sulfatase (ARSB) and the consequent accumulation of glycosaminoglycan (GAG).	Glycosaminoglycans	224-241	arylsulfatase B	Homo sapiens	148-181
21108465-0	2010	Robust genital gag-specific CD8+ T-cell responses in mice upon intramuscular immunization with simian adenoviral vectors expressing HIV-1-gag.	Glycosaminoglycans	15-18	CD8a molecule	Homo sapiens	28-31
20847202-1	2010	Type I mucopolysaccharidosis (MPS I) is a lysosomal storage disorder caused by the deficiency of alpha-L-iduronidase, which results in glycosaminoglycan accumulation in tissues.	Glycosaminoglycans	135-152	iduronidase, alpha-L	Mus musculus	97-116
20864536-6	2010	In both wild type and serglycin-deficient mice, parasite infection resulted in highly increased extracellular levels of glycosaminoglycans, including hyaluronan and chondroitin sulfate A, suggesting a role of these substances in the general defense mechanism.	Glycosaminoglycans	120-138	serglycin	Mus musculus	22-31
20926562-3	2010	Here, we demonstrate that 7SL RNA is an integral component of the viral ribonucleoprotein (RNP) complex containing Gag, viral genomic RNA, and tRNA(3)(Lys).	Glycosaminoglycans	115-118	RNA component of signal recognition particle 7SL1	Homo sapiens	26-29
20926562-3	2010	Here, we demonstrate that 7SL RNA is an integral component of the viral ribonucleoprotein (RNP) complex containing Gag, viral genomic RNA, and tRNA(3)(Lys).	Glycosaminoglycans	115-118	RNA binding region (RNP1, RRM) containing 3	Homo sapiens	72-89
20926562-3	2010	Here, we demonstrate that 7SL RNA is an integral component of the viral ribonucleoprotein (RNP) complex containing Gag, viral genomic RNA, and tRNA(3)(Lys).	Glycosaminoglycans	115-118	RNA binding region (RNP1, RRM) containing 3	Homo sapiens	91-94
20800524-1	2010	BACKGROUND: Maroteaux-Lamy syndrome, or mucopolysaccharidosis (MPS) type VI, is the autosomal recessive lysosomal disorder resulting from deficient N-acetylgalactosamine 4-sulfatase (ARSB) and the consequent accumulation of glycosaminoglycan (GAG).	Glycosaminoglycans	224-241	arylsulfatase B	Homo sapiens	183-187
20800524-1	2010	BACKGROUND: Maroteaux-Lamy syndrome, or mucopolysaccharidosis (MPS) type VI, is the autosomal recessive lysosomal disorder resulting from deficient N-acetylgalactosamine 4-sulfatase (ARSB) and the consequent accumulation of glycosaminoglycan (GAG).	Glycosaminoglycans	243-246	arylsulfatase B	Homo sapiens	148-181
20800524-1	2010	BACKGROUND: Maroteaux-Lamy syndrome, or mucopolysaccharidosis (MPS) type VI, is the autosomal recessive lysosomal disorder resulting from deficient N-acetylgalactosamine 4-sulfatase (ARSB) and the consequent accumulation of glycosaminoglycan (GAG).	Glycosaminoglycans	243-246	arylsulfatase B	Homo sapiens	183-187
21123810-0	2010	Replacing the enzyme alpha-L-iduronidase at birth ameliorates symptoms in the brain and periphery of dogs with mucopolysaccharidosis type I. Mucopolysaccharidosis type I (MPS I) is a lysosomal storage disease caused by loss of activity of alpha-l-iduronidase and attendant accumulation of the glycosaminoglycans dermatan sulfate and heparan sulfate.	Glycosaminoglycans	293-311	alpha-L-iduronidase	Canis lupus familiaris	21-40
21714469-8	2010	Sequencing of TSHR gene revealed a homozygous mutation (CGC --&gt; CAC, Arg450His) and a polymorphism (GAC --&gt; GAG, Asp727Glu).	Glycosaminoglycans	114-117	thyroid stimulating hormone receptor	Homo sapiens	14-18
21151640-9	2010	Initiation of disassembly of the immature Gag lattice requires cleavage to occur on both sides of CA-SP1, while assembly of the mature core also requires cleavage of SP1 from CA.	Glycosaminoglycans	42-45	caspase 1	Homo sapiens	98-104
20688960-2	2010	Because interactions with glycosaminoglycans play a crucial role in chemokines activity, we determined the binding parameters of CXCL4 and CXCL4L1 for heparin, heparan sulfate, and chondroitin sulfate B.	Glycosaminoglycans	26-44	platelet factor 4	Homo sapiens	129-134
20688960-2	2010	Because interactions with glycosaminoglycans play a crucial role in chemokines activity, we determined the binding parameters of CXCL4 and CXCL4L1 for heparin, heparan sulfate, and chondroitin sulfate B.	Glycosaminoglycans	26-44	platelet factor 4 variant 1	Homo sapiens	139-146
21087715-1	2010	OBJECTIVES: A nonagonist monocyte chemotactic protein-1 (MCP-1/CCL2) mutant (PA508) with increased affinity for glycosaminoglycans and thus competing with CCL2 was evaluated as a candidate for preventing neointima formation or myocardial ischemia/reperfusion injury.	Glycosaminoglycans	112-130	chemokine (C-C motif) ligand 2	Mus musculus	25-55
21087715-1	2010	OBJECTIVES: A nonagonist monocyte chemotactic protein-1 (MCP-1/CCL2) mutant (PA508) with increased affinity for glycosaminoglycans and thus competing with CCL2 was evaluated as a candidate for preventing neointima formation or myocardial ischemia/reperfusion injury.	Glycosaminoglycans	112-130	chemokine (C-C motif) ligand 2	Mus musculus	57-62
21087715-1	2010	OBJECTIVES: A nonagonist monocyte chemotactic protein-1 (MCP-1/CCL2) mutant (PA508) with increased affinity for glycosaminoglycans and thus competing with CCL2 was evaluated as a candidate for preventing neointima formation or myocardial ischemia/reperfusion injury.	Glycosaminoglycans	112-130	chemokine (C-C motif) ligand 2	Mus musculus	63-67
20843813-0	2010	Identification of key functional residues in the active site of human {beta}1,4-galactosyltransferase 7: a major enzyme in the glycosaminoglycan synthesis pathway.	Glycosaminoglycans	127-144	beta-1,4-galactosyltransferase 7	Homo sapiens	71-103
20843813-1	2010	Glycosaminoglycans (GAGs) play a central role in many pathophysiological events, and exogenous xyloside substrates of beta1,4-galactosyltransferase 7 (beta4GalT7), a major enzyme of GAG biosynthesis, have interesting biomedical applications.	Glycosaminoglycans	0-18	beta-1,4-galactosyltransferase 7	Homo sapiens	151-161
20843813-1	2010	Glycosaminoglycans (GAGs) play a central role in many pathophysiological events, and exogenous xyloside substrates of beta1,4-galactosyltransferase 7 (beta4GalT7), a major enzyme of GAG biosynthesis, have interesting biomedical applications.	Glycosaminoglycans	20-23	beta-1,4-galactosyltransferase 7	Homo sapiens	151-161
20843813-10	2010	Altogether, this study provides novel insight into human beta4GalT7 active site functional domains, allowing manipulation of this enzyme critical for the regulation of GAG synthesis.	Glycosaminoglycans	168-171	beta-1,4-galactosyltransferase 7	Homo sapiens	57-67
20723588-7	2010	RESULTS: IL-1beta treatment increased the level of GAG released into the culture media, and induced the gene expression of MMP-3 and inhibited the gene expression of TIMP-1 in cartilage explants.	Glycosaminoglycans	51-54	interleukin-1 beta	Oryctolagus cuniculus	9-17
20670608-1	2010	Irreversible inactivation of alpha-thrombin (T) by the serpin, heparin cofactor II (HCII), is accelerated by ternary complex formation with the glycosaminoglycans (GAGs) heparin and dermatan sulfate (DS).	Glycosaminoglycans	144-162	coagulation factor II, thrombin	Homo sapiens	35-43
20670608-1	2010	Irreversible inactivation of alpha-thrombin (T) by the serpin, heparin cofactor II (HCII), is accelerated by ternary complex formation with the glycosaminoglycans (GAGs) heparin and dermatan sulfate (DS).	Glycosaminoglycans	144-162	serpin family D member 1	Homo sapiens	63-82
20670608-1	2010	Irreversible inactivation of alpha-thrombin (T) by the serpin, heparin cofactor II (HCII), is accelerated by ternary complex formation with the glycosaminoglycans (GAGs) heparin and dermatan sulfate (DS).	Glycosaminoglycans	144-162	serpin family D member 1	Homo sapiens	84-88
20670608-7	2010	Second-order rate constants for thrombin inactivation by recombinant and deglycosylated HCII were comparable, at optimal GAG concentrations that were lower than those for plasma HCII, consistent with its weaker GAG binding.	Glycosaminoglycans	121-124	coagulation factor II, thrombin	Homo sapiens	32-40
20670608-7	2010	Second-order rate constants for thrombin inactivation by recombinant and deglycosylated HCII were comparable, at optimal GAG concentrations that were lower than those for plasma HCII, consistent with its weaker GAG binding.	Glycosaminoglycans	121-124	serpin family D member 1	Homo sapiens	88-92
20670608-7	2010	Second-order rate constants for thrombin inactivation by recombinant and deglycosylated HCII were comparable, at optimal GAG concentrations that were lower than those for plasma HCII, consistent with its weaker GAG binding.	Glycosaminoglycans	211-214	coagulation factor II, thrombin	Homo sapiens	32-40
20670608-7	2010	Second-order rate constants for thrombin inactivation by recombinant and deglycosylated HCII were comparable, at optimal GAG concentrations that were lower than those for plasma HCII, consistent with its weaker GAG binding.	Glycosaminoglycans	211-214	serpin family D member 1	Homo sapiens	88-92
20691680-1	2010	UDP-glucose dehydrogenase (UGDH) catalyzes oxidation of UDP-glucose to yield UDP-glucuronic acid, a precursor of hyaluronic acid (HA) and other glycosaminoglycans (GAGs) in extracellular matrix.	Glycosaminoglycans	144-162	UDP-glucose 6-dehydrogenase	Homo sapiens	0-25
20581009-3	2010	In this work, we characterized the glycosaminoglycan (GAG) chain of Endocan, purified either from the naturally producing human umbilical vein endothelial cells (HUVEC) or from a recombinant over-expression system in human embryonic kidney cells (HEK).	Glycosaminoglycans	35-52	endothelial cell specific molecule 1	Homo sapiens	68-75
20581009-3	2010	In this work, we characterized the glycosaminoglycan (GAG) chain of Endocan, purified either from the naturally producing human umbilical vein endothelial cells (HUVEC) or from a recombinant over-expression system in human embryonic kidney cells (HEK).	Glycosaminoglycans	54-57	endothelial cell specific molecule 1	Homo sapiens	68-75
21176682-9	2010	Genetic distance analysis on gag genes showed that the diversity of sub-clusters Homo-Max and Homo-Min was obviously less than that of the sub-cluster Hetero or Mix.	Glycosaminoglycans	29-32	Mix paired-like homeobox	Homo sapiens	161-164
20668893-2	2010	It could enhance HIV-1 Gag expression via both rev-dependent and CTE (constitutive transport element)-dependent pathways.	Glycosaminoglycans	23-26	Rev	Human immunodeficiency virus 1	47-50
20668893-4	2010	We show here that ASF/SF2 bound to this sequence in an electrophoretic mobility shift assay and that the putative ASF/SF2-binding sequence was required for the enhancement of Gag expression by CES and might play a role in HIV-1 posttranscriptional regulation.	Glycosaminoglycans	175-178	serine and arginine rich splicing factor 1	Homo sapiens	18-25
20668893-4	2010	We show here that ASF/SF2 bound to this sequence in an electrophoretic mobility shift assay and that the putative ASF/SF2-binding sequence was required for the enhancement of Gag expression by CES and might play a role in HIV-1 posttranscriptional regulation.	Glycosaminoglycans	175-178	serine and arginine rich splicing factor 1	Homo sapiens	114-121
20739527-6	2010	These results illustrate that HLA-C-restricted CTL responses are capable of driving viral immune escape within Gag, but in contrast to what was previously described for HLA-B-restricted Gag escape mutants, the common Cw*03-Gag-303V variant selected resulted in no detectable benefit to the host.	Glycosaminoglycans	111-114	major histocompatibility complex, class I, C	Homo sapiens	30-35
20727121-5	2010	Our results show that clustering of CD9 correlates with multimerization of the major viral structural component, Gag, at the plasma membrane.	Glycosaminoglycans	113-116	CD9 molecule	Homo sapiens	36-39
20727121-6	2010	CD9 exhibited confined behavior and reduced lateral mobility at viral assembly sites, suggesting that Gag locally traps tetraspanins.	Glycosaminoglycans	102-105	CD9 molecule	Homo sapiens	0-3
20955553-10	2010	CONCLUSIONS: These results present in vitro and in vivo evidence implicating the interaction between Gag residues 205 in CA NTD and 340 in CA CTD in SIV replication.	Glycosaminoglycans	101-104	CTD	Homo sapiens	142-145
20691680-0	2010	Down-regulation of UDP-glucose dehydrogenase affects glycosaminoglycans synthesis and motility in HCT-8 colorectal carcinoma cells.	Glycosaminoglycans	53-71	UDP-glucose 6-dehydrogenase	Homo sapiens	19-44
20691680-1	2010	UDP-glucose dehydrogenase (UGDH) catalyzes oxidation of UDP-glucose to yield UDP-glucuronic acid, a precursor of hyaluronic acid (HA) and other glycosaminoglycans (GAGs) in extracellular matrix.	Glycosaminoglycans	144-162	UDP-glucose 6-dehydrogenase	Homo sapiens	27-31
20691680-6	2010	These results indicate that UGDH can regulate cell motility through the production of GAG.	Glycosaminoglycans	86-89	UDP-glucose 6-dehydrogenase	Homo sapiens	28-32
20919899-6	2010	RESULTS: The GAG concentrations of cartilage expiants cultured in IL-1beta (100 ng/mL) with 2 concentrations of PGJ2 were significantly higher than those in all other groups, whereas media GAG concentrations were significantly lower in the high-concentration PGJ2-treated groups, compared with all other groups.	Glycosaminoglycans	13-16	interleukin 1 beta	Canis lupus familiaris	66-74
20863317-1	2010	Biosynthesis of the glycosaminoglycan precursor UDP-alpha-D-glucuronic acid occurs through a 2-fold oxidation of UDP-alpha-D-glucose that is catalysed by UGDH (UDP-alpha-D-glucose 6-dehydrogenase).	Glycosaminoglycans	20-37	UDP-glucose 6-dehydrogenase	Homo sapiens	154-158
20863317-1	2010	Biosynthesis of the glycosaminoglycan precursor UDP-alpha-D-glucuronic acid occurs through a 2-fold oxidation of UDP-alpha-D-glucose that is catalysed by UGDH (UDP-alpha-D-glucose 6-dehydrogenase).	Glycosaminoglycans	20-37	UDP-glucose 6-dehydrogenase	Homo sapiens	160-195
20524207-8	2010	This was confirmed by surface plasmon resonance binding studies using sugar chips immobilized with defined oligosaccharide structures, which showed that VEGF-A(165) binds to a relatively broad range of sulfated glycosaminoglycan structures.	Glycosaminoglycans	211-228	vascular endothelial growth factor A	Homo sapiens	153-159
20506225-6	2010	Relative to cultures without added growth factors, treatment of the stem cells with TGF-beta1 and insulin resulted in a 59% increase in GAG synthesis, but there was no significant change in collagen production even though collagen type II gene expression was upregulated 530-fold.	Glycosaminoglycans	136-139	transforming growth factor beta 1	Homo sapiens	84-93
20506225-6	2010	Relative to cultures without added growth factors, treatment of the stem cells with TGF-beta1 and insulin resulted in a 59% increase in GAG synthesis, but there was no significant change in collagen production even though collagen type II gene expression was upregulated 530-fold.	Glycosaminoglycans	136-139	insulin	Homo sapiens	98-105
20721606-6	2010	In pellet cultures of MSCs TGF-beta1 successfully induced chondrogenic differentiation and GAG synthesis.	Glycosaminoglycans	91-94	transforming growth factor beta 1	Homo sapiens	27-36
20721606-8	2010	Similar cultures induced with TGF-beta1 and treated with different doses of CNP showed that CNP supplementation at 10(-8) and 10(-7) M concentrations significantly increased GAG synthesis in a dose dependent manner, whereas at 10(-6) M concentration this stimulatory effect was diminished.	Glycosaminoglycans	174-177	natriuretic peptide C	Homo sapiens	92-95
20721606-9	2010	In conclusion, CNP/NPR-B signaling pathway is activated during TGF-beta1 induced chondrogenic differentiation of human trabecular bone-derived MSCs and may strongly be involved in GAG synthesis during this process.	Glycosaminoglycans	180-183	natriuretic peptide C	Homo sapiens	15-18
20721606-9	2010	In conclusion, CNP/NPR-B signaling pathway is activated during TGF-beta1 induced chondrogenic differentiation of human trabecular bone-derived MSCs and may strongly be involved in GAG synthesis during this process.	Glycosaminoglycans	180-183	natriuretic peptide receptor 2	Homo sapiens	19-24
20721606-9	2010	In conclusion, CNP/NPR-B signaling pathway is activated during TGF-beta1 induced chondrogenic differentiation of human trabecular bone-derived MSCs and may strongly be involved in GAG synthesis during this process.	Glycosaminoglycans	180-183	transforming growth factor beta 1	Homo sapiens	63-72
20668079-10	2010	Taken together, these findings demonstrate that (i) Gag-specific responses dominate in mucosal tissues of HIV controllers; (ii) there is extensive overlap between CD8(+) T cells in blood and mucosal tissues, with responses to immunodominant epitopes generally shared by both sites; and (iii) mucosal T-cell response breadth alone cannot account for immune control.	Glycosaminoglycans	52-55	CD8a molecule	Homo sapiens	163-166
20702647-0	2010	The glycosylated Gag protein of a murine leukemia virus inhibits the antiretroviral function of APOBEC3.	Glycosaminoglycans	17-20	apolipoprotein B mRNA editing enzyme, catalytic polypeptide 3	Mus musculus	96-103
20631122-3	2010	The cellular protein annexin 2 (Anx2) is incorporated into HIV-1 particles, and knockdown of Anx2 has been reported to cause defects in Gag processing and infectivity of HIV-1 particles in macrophages.	Glycosaminoglycans	136-139	annexin A2	Homo sapiens	32-36
20631122-3	2010	The cellular protein annexin 2 (Anx2) is incorporated into HIV-1 particles, and knockdown of Anx2 has been reported to cause defects in Gag processing and infectivity of HIV-1 particles in macrophages.	Glycosaminoglycans	136-139	annexin A2	Homo sapiens	93-97
20631129-4	2010	The TLR3 ligand poly(I:C) suppressed Gag-specific cellular immune responses, whereas the TLR4 ligands lipopolysaccharide and monophosphoryl lipid A substantially augmented the magnitude and functionality of these responses by a MyD88- and TRIF-dependent mechanism.	Glycosaminoglycans	37-40	toll like receptor 3	Homo sapiens	4-8
20178406-11	2010	RESULTS: In part I, GAG accumulation was highest for growth factor combinations including both IGF-1 and GDF-5.	Glycosaminoglycans	20-23	insulin like growth factor 1	Homo sapiens	95-100
20170425-7	2010	It was also found that the amount of two representative bioactive factors, platelet-derived growth factor BB and vascular endothelial growth factor, was positively correlated with the sulfated GAG content in the porcine BAM, implying that the amount of sulfated GAG might be a determinant for preservation of bioactive factors in the decellularized tissues.	Glycosaminoglycans	193-196	vascular endothelial growth factor A	Homo sapiens	113-147
20170425-7	2010	It was also found that the amount of two representative bioactive factors, platelet-derived growth factor BB and vascular endothelial growth factor, was positively correlated with the sulfated GAG content in the porcine BAM, implying that the amount of sulfated GAG might be a determinant for preservation of bioactive factors in the decellularized tissues.	Glycosaminoglycans	262-265	vascular endothelial growth factor A	Homo sapiens	113-147
20178406-11	2010	RESULTS: In part I, GAG accumulation was highest for growth factor combinations including both IGF-1 and GDF-5.	Glycosaminoglycans	20-23	growth differentiation factor 5	Homo sapiens	105-110
20178406-13	2010	GAG and type II collagen accumulation was significantly higher with IGF-1 and GDF-5.	Glycosaminoglycans	0-3	insulin like growth factor 1	Homo sapiens	68-73
20178406-13	2010	GAG and type II collagen accumulation was significantly higher with IGF-1 and GDF-5.	Glycosaminoglycans	0-3	growth differentiation factor 5	Homo sapiens	78-83
20178406-15	2010	CONCLUSION: Supplementation of medium with IGF-1 and GDF-5 during creation of neocartilage constructs results in increased accumulation of GAG and type II collagen and improved biomechanical properties compared with constructs created without the growth factors.	Glycosaminoglycans	139-142	insulin like growth factor 1	Homo sapiens	43-48
20178406-15	2010	CONCLUSION: Supplementation of medium with IGF-1 and GDF-5 during creation of neocartilage constructs results in increased accumulation of GAG and type II collagen and improved biomechanical properties compared with constructs created without the growth factors.	Glycosaminoglycans	139-142	growth differentiation factor 5	Homo sapiens	53-58
20712376-0	2010	Characterization of the interactions of vMIP-II, and a dimeric variant of vMIP-II, with glycosaminoglycans.	Glycosaminoglycans	88-106	K4	Human gammaherpesvirus 8	40-47
20671542-2	2010	Escape mutations in HLA-B*57-restricted Gag epitopes were present at study entry in all patients, but were not associated with significant increases in viremia.	Glycosaminoglycans	40-43	major histocompatibility complex, class I, B	Homo sapiens	20-25
20561662-3	2010	By phylogenetic analyses of env, nef, vif, and gag sequences obtained at different time points, we suggest here that this patient was initially infected by a putatively attenuated nef-defective variant and that loss of control was due to superinfection with a fully competent virus belonging to the same clade B.	Glycosaminoglycans	47-50	S100 calcium binding protein B	Homo sapiens	180-183
20561662-4	2010	At the time of superinfection, its plasma was unable to efficiently neutralize the superinfecting virus and moderate Gag-specific CD8(+) T-cell responses were observed.	Glycosaminoglycans	117-120	CD8a molecule	Homo sapiens	130-133
20610572-10	2010	Inhibition of PDGFRbeta tyrosine kinase activity leads to inhibition of GAG synthesis on vascular PGs and aortic lipid area in vivo.	Glycosaminoglycans	72-75	platelet derived growth factor receptor beta	Homo sapiens	14-23
20637812-4	2010	The fixation of positively charged residues at position 110-112 in the beta F-beta G loop of VP1 of SAT1 isolates is thought to correlate with the acquisition of the ability to utilise alternative glycosaminoglycan (GAG) molecules for cell entry.	Glycosaminoglycans	197-214	diamine acetyltransferase 1	Mesocricetus auratus	100-104
20637812-4	2010	The fixation of positively charged residues at position 110-112 in the beta F-beta G loop of VP1 of SAT1 isolates is thought to correlate with the acquisition of the ability to utilise alternative glycosaminoglycan (GAG) molecules for cell entry.	Glycosaminoglycans	216-219	diamine acetyltransferase 1	Mesocricetus auratus	100-104
20691685-4	2010	We showed that R270C substitution strongly reduced beta4GalT7 affinity towards xyloside acceptor, thus affecting GAG chains formation.	Glycosaminoglycans	113-116	beta-1,4-galactosyltransferase 7	Homo sapiens	51-61
20691685-5	2010	This study establishes the molecular basis for beta4GalT7 defects associated with altered GAG synthesis in EDS.	Glycosaminoglycans	90-93	beta-1,4-galactosyltransferase 7	Homo sapiens	47-57
20570267-5	2010	Culture with IGF-1 resulted in softening in CC and UCC, increased Poisson"s ratios, substantially increased tissue volume, and accumulation of glycosaminoglycan (GAG) and collagen (COL).	Glycosaminoglycans	143-160	insulin like growth factor 1	Bos taurus	13-18
20570267-5	2010	Culture with IGF-1 resulted in softening in CC and UCC, increased Poisson"s ratios, substantially increased tissue volume, and accumulation of glycosaminoglycan (GAG) and collagen (COL).	Glycosaminoglycans	162-165	insulin like growth factor 1	Bos taurus	13-18
20570267-6	2010	Culture with TGF-beta1 promoted maturational changes in the S layer, including stiffening in CC and UCC and increased concentrations of GAG, COL, and pyridinoline crosslinks (PYR), but little growth.	Glycosaminoglycans	136-139	transforming growth factor beta 1	Bos taurus	13-22
21171714-7	2010	With poly-L-lysine as the underlying layer, biologically significant differences (greater than twofold) in the expression of VWF, VEGFR, VEGFA, endoglin, and ICAM1 were observed among the three glycosaminoglycans.	Glycosaminoglycans	194-212	von Willebrand factor	Homo sapiens	125-128
21171714-7	2010	With poly-L-lysine as the underlying layer, biologically significant differences (greater than twofold) in the expression of VWF, VEGFR, VEGFA, endoglin, and ICAM1 were observed among the three glycosaminoglycans.	Glycosaminoglycans	194-212	kinase insert domain receptor	Homo sapiens	130-135
21171714-7	2010	With poly-L-lysine as the underlying layer, biologically significant differences (greater than twofold) in the expression of VWF, VEGFR, VEGFA, endoglin, and ICAM1 were observed among the three glycosaminoglycans.	Glycosaminoglycans	194-212	vascular endothelial growth factor A	Homo sapiens	137-142
21171714-7	2010	With poly-L-lysine as the underlying layer, biologically significant differences (greater than twofold) in the expression of VWF, VEGFR, VEGFA, endoglin, and ICAM1 were observed among the three glycosaminoglycans.	Glycosaminoglycans	194-212	endoglin	Homo sapiens	144-152
21171714-7	2010	With poly-L-lysine as the underlying layer, biologically significant differences (greater than twofold) in the expression of VWF, VEGFR, VEGFA, endoglin, and ICAM1 were observed among the three glycosaminoglycans.	Glycosaminoglycans	194-212	intercellular adhesion molecule 1	Homo sapiens	158-163
21171714-8	2010	With chitosan as the underlying layer, all three glycosaminoglycans displayed biologically significant differences in the expression of VWF and VEGFR compared to the chitosan control.	Glycosaminoglycans	49-67	von Willebrand factor	Homo sapiens	136-139
21171714-8	2010	With chitosan as the underlying layer, all three glycosaminoglycans displayed biologically significant differences in the expression of VWF and VEGFR compared to the chitosan control.	Glycosaminoglycans	49-67	kinase insert domain receptor	Homo sapiens	144-149
20712376-0	2010	Characterization of the interactions of vMIP-II, and a dimeric variant of vMIP-II, with glycosaminoglycans.	Glycosaminoglycans	88-106	K4	Human gammaherpesvirus 8	74-81
20712376-4	2010	The goal of this work was to determine the mechanism of binding of GAG by vMIP-II.	Glycosaminoglycans	67-70	K4	Human gammaherpesvirus 8	74-81
20712376-6	2010	Important binding sites were further analyzed by mutagenesis studies, in which corresponding vMIP-II mutants were tested for GAG binding ability using heparin chromatography and NMR.	Glycosaminoglycans	125-128	K4	Human gammaherpesvirus 8	93-100
20712376-11	2010	Structural differences between monomeric and dimeric vMIP-II upon GAG binding were characterized by NMR and molecular docking.	Glycosaminoglycans	66-69	K4	Human gammaherpesvirus 8	53-60
20573963-4	2010	These currents are produced by relatively non-selective, cation-permeable channels or pores in the cell membrane and can be silenced by overexpression of wild-type PrP, as well as by treatment with a sulfated glycosaminoglycan.	Glycosaminoglycans	209-226	prion protein	Homo sapiens	164-167
20808809-6	2010	Modification of the negative charge afforded by the sulphation of glycosaminoglycans increased the ability of a familial PrP mutant to act as a substrate for PrP(res) formation, while having no effect on PrP(res) formed by wildtype PrP.	Glycosaminoglycans	66-84	prion protein	Mus musculus	121-124
20808809-6	2010	Modification of the negative charge afforded by the sulphation of glycosaminoglycans increased the ability of a familial PrP mutant to act as a substrate for PrP(res) formation, while having no effect on PrP(res) formed by wildtype PrP.	Glycosaminoglycans	66-84	prion protein	Mus musculus	158-161
20808809-6	2010	Modification of the negative charge afforded by the sulphation of glycosaminoglycans increased the ability of a familial PrP mutant to act as a substrate for PrP(res) formation, while having no effect on PrP(res) formed by wildtype PrP.	Glycosaminoglycans	66-84	prion protein	Mus musculus	158-161
20808809-6	2010	Modification of the negative charge afforded by the sulphation of glycosaminoglycans increased the ability of a familial PrP mutant to act as a substrate for PrP(res) formation, while having no effect on PrP(res) formed by wildtype PrP.	Glycosaminoglycans	66-84	prion protein	Mus musculus	158-161
20808809-7	2010	This difference may be due to the observed differences in the binding of wild type and mutant PrP for glycosaminoglycans.	Glycosaminoglycans	102-120	prion protein	Mus musculus	94-97
20408770-5	2010	Biochemical GAG measurement showed that production was significantly greater in TGF-beta3-treated AD-MSC in 3D culture versus untreated controls (p &lt; 0.05).	Glycosaminoglycans	12-15	transforming growth factor beta 3	Homo sapiens	80-89
20471881-5	2010	The combination of IL-1beta and OSM, both at 20 ng/ml, was able to promote GAG release to the greatest extent at 14 days.	Glycosaminoglycans	75-78	interleukin 1 beta	Felis catus	19-27
20533528-6	2010	CHST14 mutations altered the glycosaminoglycan (GAG) components in patients" fibroblasts.	Glycosaminoglycans	29-46	carbohydrate sulfotransferase 14	Homo sapiens	0-6
20533528-6	2010	CHST14 mutations altered the glycosaminoglycan (GAG) components in patients" fibroblasts.	Glycosaminoglycans	48-51	carbohydrate sulfotransferase 14	Homo sapiens	0-6
20043808-3	2010	Other experimental evidence, though, indicates that certain polymeric carbohydrates like the glycosaminoglycan (GAG) chains found in proteoglycan molecules attenuate the neurotoxic effect of Abeta in primary neuronal cultures.	Glycosaminoglycans	93-110	amyloid beta precursor protein	Homo sapiens	191-196
20043808-3	2010	Other experimental evidence, though, indicates that certain polymeric carbohydrates like the glycosaminoglycan (GAG) chains found in proteoglycan molecules attenuate the neurotoxic effect of Abeta in primary neuronal cultures.	Glycosaminoglycans	112-115	amyloid beta precursor protein	Homo sapiens	191-196
20043808-4	2010	Pretreatment of the 42-residue Abeta fragment (Abeta1-42) with the ubiquitous brain carbohydrates, glucose, fructose, and the GAG chondroitin sulfate B (CSB) inhibits Abeta1-42-induced apoptosis and reduces the peptide neurotoxicity on neuroblastoma cells, a cytoprotective effect that is partially reverted by AGE inhibitors such as pyridoxamine and L-carnosine.	Glycosaminoglycans	126-129	amyloid beta precursor protein	Homo sapiens	31-36
20400719-5	2010	Disaccharide analysis showed that rat HMW-DSP contains glycosaminoglycan chains made of chondroitin-4-sulfate and has an average of 31-32 disaccharides/mol.	Glycosaminoglycans	55-72	dentin sialophosphoprotein	Rattus norvegicus	42-45
20519396-9	2010	Surprisingly, virion incorporation experiments using Gag deletion mutants demonstrated that A3H haplotypes interacted with different Gag regions.	Glycosaminoglycans	53-56	apolipoprotein B mRNA editing enzyme catalytic subunit 3H	Homo sapiens	92-95
20463016-0	2010	The TSG-6/HC2-mediated transfer is a dynamic process shuffling heavy chains between glycosaminoglycans.	Glycosaminoglycans	84-102	TNF alpha induced protein 6	Homo sapiens	4-9
20463016-0	2010	The TSG-6/HC2-mediated transfer is a dynamic process shuffling heavy chains between glycosaminoglycans.	Glycosaminoglycans	84-102	CYCS pseudogene 38	Homo sapiens	10-13
20575564-5	2010	The extended VEGF retention was likely due to equilibrium binding of VEGF to DS and to endogenous glycosaminoglycans.	Glycosaminoglycans	98-116	vascular endothelial growth factor A	Rattus norvegicus	13-17
20450492-8	2010	All glycosaminoglycans stimulate the elastinolytic activity of cathepsin K at physiological plasma pH, but only heparin also increases the collagenolytic activity of the enzyme under these conditions.	Glycosaminoglycans	4-22	cathepsin K	Homo sapiens	63-74
20450492-5	2010	We identify and characterize sulfated glycosaminoglycans as natural allosteric modifiers of cathepsin K that exploit the conformational flexibility of the enzyme to regulate its activity and stability against autoproteolysis.	Glycosaminoglycans	38-56	cathepsin K	Homo sapiens	92-103
20439606-7	2010	Baseline cleavage site substitutions in the product of the gag open reading frame at positions 128 (p17/p24) (P = 0.04) and 449 (p1/p6(gag)) (P = 0.01) were significantly more frequent in those patients not achieving virological response.	Glycosaminoglycans	59-62	family with sequence similarity 72 member B	Homo sapiens	100-103
20439606-7	2010	Baseline cleavage site substitutions in the product of the gag open reading frame at positions 128 (p17/p24) (P = 0.04) and 449 (p1/p6(gag)) (P = 0.01) were significantly more frequent in those patients not achieving virological response.	Glycosaminoglycans	59-62	transmembrane p24 trafficking protein 2	Homo sapiens	104-107
20531016-3	2010	Gag-Env pseudovirions recapitulate the native trimer and could serve as an effective epitope presentation platform for study of the neutralizing antibody response in HIV-infected individuals.	Glycosaminoglycans	0-3	endogenous retrovirus group K member 20	Homo sapiens	4-7
20531016-5	2010	By blue native gel shift assays, Gag-Env pseudovirions were shown to contain native trimers that were competent for binding to neutralizing monoclonal antibodies.	Glycosaminoglycans	33-36	endogenous retrovirus group K member 20	Homo sapiens	37-40
20531016-12	2010	These data demonstrate that Gag-Env pseudovirions recapitulate CD4 and coreceptor binding pocket antigenic structures and can facilitate identification of B-cell clones that secrete neutralizing antibodies.	Glycosaminoglycans	28-31	endogenous retrovirus group K member 20	Homo sapiens	32-35
20531016-12	2010	These data demonstrate that Gag-Env pseudovirions recapitulate CD4 and coreceptor binding pocket antigenic structures and can facilitate identification of B-cell clones that secrete neutralizing antibodies.	Glycosaminoglycans	28-31	CD4 molecule	Homo sapiens	63-66
20346402-11	2010	GRIP1 siRNA repressed col2a1 expression and GAG production in ATDC5 cells.	Glycosaminoglycans	44-47	nuclear receptor coactivator 2	Mus musculus	0-5
20652491-1	2010	Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked inherited disorder caused by a deficiency of the enzyme iduronate-2-sulfatase (IDS), which results in the lysosomal accumulation of glycosaminoglycans (GAG) such as dermatan and heparan sulfate.	Glycosaminoglycans	203-221	iduronate 2-sulfatase	Homo sapiens	127-148
20652491-1	2010	Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked inherited disorder caused by a deficiency of the enzyme iduronate-2-sulfatase (IDS), which results in the lysosomal accumulation of glycosaminoglycans (GAG) such as dermatan and heparan sulfate.	Glycosaminoglycans	203-221	iduronate 2-sulfatase	Homo sapiens	150-153
20652491-1	2010	Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked inherited disorder caused by a deficiency of the enzyme iduronate-2-sulfatase (IDS), which results in the lysosomal accumulation of glycosaminoglycans (GAG) such as dermatan and heparan sulfate.	Glycosaminoglycans	223-226	iduronate 2-sulfatase	Homo sapiens	127-148
20652491-1	2010	Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked inherited disorder caused by a deficiency of the enzyme iduronate-2-sulfatase (IDS), which results in the lysosomal accumulation of glycosaminoglycans (GAG) such as dermatan and heparan sulfate.	Glycosaminoglycans	223-226	iduronate 2-sulfatase	Homo sapiens	150-153
20585587-10	2010	CONCLUSIONS/SIGNIFICANCE: This study demonstrates that CIITA enhances HIV Gag processing, and provides the first evidence of a novel, post-transcriptional, cytoplasmic function for a well-known transactivator.	Glycosaminoglycans	74-77	class II major histocompatibility complex transactivator	Homo sapiens	55-60
19737074-5	2010	For early chondrogenesis, both DKK-1 and sFRP-1 increased glycosaminoglycan synthesis as well as the gene and protein expressions of SOX-9 and type II collagen, more prominently by sFRP-1 than by DKK-1.	Glycosaminoglycans	58-75	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	31-36
19737074-5	2010	For early chondrogenesis, both DKK-1 and sFRP-1 increased glycosaminoglycan synthesis as well as the gene and protein expressions of SOX-9 and type II collagen, more prominently by sFRP-1 than by DKK-1.	Glycosaminoglycans	58-75	secreted frizzled related protein 1	Homo sapiens	41-47
20418372-8	2010	Consistent with the eRF1 role in modulating HIV PRF, depleting eRF1 increased the Gag-Pol to Gag ratio in cells infected with replication-competent virus.	Glycosaminoglycans	82-85	eukaryotic translation termination factor 1	Homo sapiens	63-67
20565707-10	2010	RESULTS: Significantly higher glycosaminoglycan accumulation was seen in NCCM treated pellets than in CM or TGFbeta groups.	Glycosaminoglycans	30-47	transforming growth factor beta 1	Homo sapiens	108-115
20585562-7	2010	Tetherin accumulates with Gag at the contact zone between infected and target cells, but does not prevent the formation of virological synapses.	Glycosaminoglycans	26-29	bone marrow stromal cell antigen 2	Homo sapiens	0-8
20501592-2	2010	Hh signaling is regulated by two conserved cell-surface proteins: Ig/fibronectin superfamily member Interference hedgehog (Ihog) and Dally-like (Dlp), a glypican that comprises a core protein and heparan sulfate glycosaminoglycan (GAG) chains.	Glycosaminoglycans	231-234	hedgehog	Drosophila melanogaster	113-121
19876951-6	2010	Results demonstrated a gradual, sustained release of HGF for at least 7 days in vitro, consistent with the detection of glycosaminoglycans inherent of the scaffold.	Glycosaminoglycans	120-138	hepatocyte growth factor	Rattus norvegicus	53-56
20371359-0	2010	Substrate specificity and inhibition of human kallikrein-related peptidase 3 (KLK3 or PSA) activated with sodium citrate and glycosaminoglycans.	Glycosaminoglycans	125-143	kallikrein related peptidase 3	Homo sapiens	46-76
20371359-0	2010	Substrate specificity and inhibition of human kallikrein-related peptidase 3 (KLK3 or PSA) activated with sodium citrate and glycosaminoglycans.	Glycosaminoglycans	125-143	kallikrein related peptidase 3	Homo sapiens	78-82
20371359-0	2010	Substrate specificity and inhibition of human kallikrein-related peptidase 3 (KLK3 or PSA) activated with sodium citrate and glycosaminoglycans.	Glycosaminoglycans	125-143	kallikrein related peptidase 3	Homo sapiens	86-89
20371359-1	2010	We report the enzymatic properties and substrate specificity of human recombinant KLK3 in the presence of glycosaminoglycans (GAGs) and sodium citrate.	Glycosaminoglycans	106-124	kallikrein related peptidase 3	Homo sapiens	82-86
20501592-2	2010	Hh signaling is regulated by two conserved cell-surface proteins: Ig/fibronectin superfamily member Interference hedgehog (Ihog) and Dally-like (Dlp), a glypican that comprises a core protein and heparan sulfate glycosaminoglycan (GAG) chains.	Glycosaminoglycans	231-234	interference hedgehog	Drosophila melanogaster	123-127
20501592-2	2010	Hh signaling is regulated by two conserved cell-surface proteins: Ig/fibronectin superfamily member Interference hedgehog (Ihog) and Dally-like (Dlp), a glypican that comprises a core protein and heparan sulfate glycosaminoglycan (GAG) chains.	Glycosaminoglycans	231-234	dally-like	Drosophila melanogaster	133-143
20501592-2	2010	Hh signaling is regulated by two conserved cell-surface proteins: Ig/fibronectin superfamily member Interference hedgehog (Ihog) and Dally-like (Dlp), a glypican that comprises a core protein and heparan sulfate glycosaminoglycan (GAG) chains.	Glycosaminoglycans	231-234	dally-like	Drosophila melanogaster	145-148
20553487-2	2010	Glycosaminoglycans bound to the matrix or released after proteolytic processing of the core proteins of proteoglycans are potential ligands of elastase-2.	Glycosaminoglycans	0-18	elastase, neutrophil expressed	Homo sapiens	143-153
20067399-9	2010	The combination of SOX9 and mechanical load boosted GAG synthesis as shown by (35)S incorporation.	Glycosaminoglycans	52-55	SRY-box transcription factor 9	Homo sapiens	19-23
20202487-10	2010	RESULTS: IL-1 increased MMP activity, S-GAG release, and NO production, while decreasing the shear strength and tissue repair in the interface.	Glycosaminoglycans	40-43	interleukin 1 alpha	Homo sapiens	9-13
23675183-8	2010	Both GAG and proMMP-3 concentrations in the culture media were significantly increased after IL-1beta stimulation.	Glycosaminoglycans	5-8	interleukin-1 beta	Oryctolagus cuniculus	93-101
20067399-10	2010	GAG production rate corresponded well with the amount of (endogenous) transforming growth factor-beta1.	Glycosaminoglycans	0-3	transforming growth factor beta 1	Homo sapiens	70-102
20463901-5	2010	Inflammatory cell invasion and neointimal hyperplasia were significantly reduced in N-deacetylase-N-sulfotransferase-1 (Ndst1(f/f)TekCre(+)) heparan sulfate (GAG)-deficient (Ndst1(-/-), p&lt;0.044) and CCR2-deficient (Ccr2(-/-), p&lt;0.04) donor transplants.	Glycosaminoglycans	158-161	N-deacetylase and N-sulfotransferase 1	Homo sapiens	84-118
20226781-3	2010	Uxs1 synthesizes UDP-xylose, which initiates glycosaminoglycan attachment to a protein core during proteoglycan formation.	Glycosaminoglycans	45-62	UDP-glucuronate decarboxylase 1	Homo sapiens	0-4
20394361-3	2010	Under identical conditions and using (15)N-labeled protein, we then cross-linked tetrasaccharide to CFH approximately 7 and confirmed the 1:1 stoichiometry by FT-ICR-MS. We subsequently characterized this covalent protein-GAG conjugate by NMR and further MS techniques.	Glycosaminoglycans	222-225	complement factor H	Homo sapiens	100-103
20176392-6	2010	We conclude that in HaCaT cells and in cell systems showing restricted expression of glycosaminoglycans, human and some monoclonal anti-gC1 antibodies can target the cell-binding domain of this protein and neutralize viral infectivity.	Glycosaminoglycans	85-103	solute carrier family 25 member 22	Homo sapiens	136-139
20153043-5	2010	Bone morphogenetic protein-6 (BMP-6) in the presence of TGF-beta1 was effective in improving GAG and total collagen production when the cells were pre-treated with fibroblast growth factor-2 (FGF-2) prior to scaffold seeding.	Glycosaminoglycans	93-96	bone morphogenetic protein 6	Homo sapiens	0-28
20152898-5	2010	Silencing or overexpression of ASB in normal rat kidney epithelial cells in tissue culture modified the content of total sulfated glycosaminoglycans (sGAGs), C4S, kininogen, and bradykinin in spent media and cell lysates.	Glycosaminoglycans	130-148	arylsulfatase B	Rattus norvegicus	31-34
20153043-5	2010	Bone morphogenetic protein-6 (BMP-6) in the presence of TGF-beta1 was effective in improving GAG and total collagen production when the cells were pre-treated with fibroblast growth factor-2 (FGF-2) prior to scaffold seeding.	Glycosaminoglycans	93-96	bone morphogenetic protein 6	Homo sapiens	30-35
20153043-4	2010	Although gene expression levels for both aggrecan and collagen type II were up-regulated significantly in PGA cultures treated with transforming growth factor beta1 (TGF-beta1), synthesis of GAG but not collagen type II was enhanced in tissue constructs when TGF-beta1 was added to the medium.	Glycosaminoglycans	191-194	transforming growth factor beta 1	Homo sapiens	132-164
20153043-5	2010	Bone morphogenetic protein-6 (BMP-6) in the presence of TGF-beta1 was effective in improving GAG and total collagen production when the cells were pre-treated with fibroblast growth factor-2 (FGF-2) prior to scaffold seeding.	Glycosaminoglycans	93-96	transforming growth factor beta 1	Homo sapiens	56-65
20153043-5	2010	Bone morphogenetic protein-6 (BMP-6) in the presence of TGF-beta1 was effective in improving GAG and total collagen production when the cells were pre-treated with fibroblast growth factor-2 (FGF-2) prior to scaffold seeding.	Glycosaminoglycans	93-96	fibroblast growth factor 2	Homo sapiens	164-190
19961337-8	2010	Treatment with MAPK inhibitors blocked BMP-2- and TGF-beta-induced AP1 reporter function, GlcAT-1 expression, and GAG accumulation.	Glycosaminoglycans	114-117	bone morphogenetic protein 2	Homo sapiens	39-44
20572342-5	2010	Both Gag single-gene expression plasmid and Gag-RTN double-gene expression plasmid separately inoculating induced stronger antibody response against Gag than Gag-Gp160 double-gene expression plasmid and Gagpol-Gp160-RTN multi-gene expression plasmid or combined inoculation of Gag and Gp160 single-gene expression plasmids did.	Glycosaminoglycans	5-8	glutamyl aminopeptidase	Homo sapiens	162-167
20572342-5	2010	Both Gag single-gene expression plasmid and Gag-RTN double-gene expression plasmid separately inoculating induced stronger antibody response against Gag than Gag-Gp160 double-gene expression plasmid and Gagpol-Gp160-RTN multi-gene expression plasmid or combined inoculation of Gag and Gp160 single-gene expression plasmids did.	Glycosaminoglycans	5-8	glutamyl aminopeptidase	Homo sapiens	210-215
20572342-5	2010	Both Gag single-gene expression plasmid and Gag-RTN double-gene expression plasmid separately inoculating induced stronger antibody response against Gag than Gag-Gp160 double-gene expression plasmid and Gagpol-Gp160-RTN multi-gene expression plasmid or combined inoculation of Gag and Gp160 single-gene expression plasmids did.	Glycosaminoglycans	5-8	glutamyl aminopeptidase	Homo sapiens	210-215
20572342-5	2010	Both Gag single-gene expression plasmid and Gag-RTN double-gene expression plasmid separately inoculating induced stronger antibody response against Gag than Gag-Gp160 double-gene expression plasmid and Gagpol-Gp160-RTN multi-gene expression plasmid or combined inoculation of Gag and Gp160 single-gene expression plasmids did.	Glycosaminoglycans	44-47	glutamyl aminopeptidase	Homo sapiens	162-167
20572342-5	2010	Both Gag single-gene expression plasmid and Gag-RTN double-gene expression plasmid separately inoculating induced stronger antibody response against Gag than Gag-Gp160 double-gene expression plasmid and Gagpol-Gp160-RTN multi-gene expression plasmid or combined inoculation of Gag and Gp160 single-gene expression plasmids did.	Glycosaminoglycans	44-47	glutamyl aminopeptidase	Homo sapiens	210-215
20572342-5	2010	Both Gag single-gene expression plasmid and Gag-RTN double-gene expression plasmid separately inoculating induced stronger antibody response against Gag than Gag-Gp160 double-gene expression plasmid and Gagpol-Gp160-RTN multi-gene expression plasmid or combined inoculation of Gag and Gp160 single-gene expression plasmids did.	Glycosaminoglycans	44-47	glutamyl aminopeptidase	Homo sapiens	210-215
20572342-5	2010	Both Gag single-gene expression plasmid and Gag-RTN double-gene expression plasmid separately inoculating induced stronger antibody response against Gag than Gag-Gp160 double-gene expression plasmid and Gagpol-Gp160-RTN multi-gene expression plasmid or combined inoculation of Gag and Gp160 single-gene expression plasmids did.	Glycosaminoglycans	44-47	glutamyl aminopeptidase	Homo sapiens	162-167
20572342-5	2010	Both Gag single-gene expression plasmid and Gag-RTN double-gene expression plasmid separately inoculating induced stronger antibody response against Gag than Gag-Gp160 double-gene expression plasmid and Gagpol-Gp160-RTN multi-gene expression plasmid or combined inoculation of Gag and Gp160 single-gene expression plasmids did.	Glycosaminoglycans	44-47	glutamyl aminopeptidase	Homo sapiens	210-215
20572342-5	2010	Both Gag single-gene expression plasmid and Gag-RTN double-gene expression plasmid separately inoculating induced stronger antibody response against Gag than Gag-Gp160 double-gene expression plasmid and Gagpol-Gp160-RTN multi-gene expression plasmid or combined inoculation of Gag and Gp160 single-gene expression plasmids did.	Glycosaminoglycans	44-47	glutamyl aminopeptidase	Homo sapiens	210-215
20572342-5	2010	Both Gag single-gene expression plasmid and Gag-RTN double-gene expression plasmid separately inoculating induced stronger antibody response against Gag than Gag-Gp160 double-gene expression plasmid and Gagpol-Gp160-RTN multi-gene expression plasmid or combined inoculation of Gag and Gp160 single-gene expression plasmids did.	Glycosaminoglycans	44-47	glutamyl aminopeptidase	Homo sapiens	162-167
20572342-5	2010	Both Gag single-gene expression plasmid and Gag-RTN double-gene expression plasmid separately inoculating induced stronger antibody response against Gag than Gag-Gp160 double-gene expression plasmid and Gagpol-Gp160-RTN multi-gene expression plasmid or combined inoculation of Gag and Gp160 single-gene expression plasmids did.	Glycosaminoglycans	44-47	glutamyl aminopeptidase	Homo sapiens	210-215
20572342-5	2010	Both Gag single-gene expression plasmid and Gag-RTN double-gene expression plasmid separately inoculating induced stronger antibody response against Gag than Gag-Gp160 double-gene expression plasmid and Gagpol-Gp160-RTN multi-gene expression plasmid or combined inoculation of Gag and Gp160 single-gene expression plasmids did.	Glycosaminoglycans	44-47	glutamyl aminopeptidase	Homo sapiens	210-215
19961337-8	2010	Treatment with MAPK inhibitors blocked BMP-2- and TGF-beta-induced AP1 reporter function, GlcAT-1 expression, and GAG accumulation.	Glycosaminoglycans	114-117	transforming growth factor beta 1	Homo sapiens	50-58
20219921-5	2010	Human APOBEC3G, a potent Ty1 restriction factor that is packaged into Ty1 VLPs via an interaction with Gag, also localizes to P bodies.	Glycosaminoglycans	103-106	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	6-14
20053375-1	2010	DYT1 dystonia is an autosomal-dominantly inherited movement disorder, which is usually caused by a GAG deletion in the TOR1A gene.	Glycosaminoglycans	99-102	torsin family 1 member A	Homo sapiens	0-4
20053375-1	2010	DYT1 dystonia is an autosomal-dominantly inherited movement disorder, which is usually caused by a GAG deletion in the TOR1A gene.	Glycosaminoglycans	99-102	torsin family 1 member A	Homo sapiens	119-124
20455661-1	2010	In mucopolysaccharidosis type I (MPS I; alpha-L-iduronidase deficiency), glycosaminoglycans (GAGs) accumulate in different cell types, causing characteristic vacuolization.	Glycosaminoglycans	73-91	alpha-L-iduronidase	Homo sapiens	40-59
20455661-1	2010	In mucopolysaccharidosis type I (MPS I; alpha-L-iduronidase deficiency), glycosaminoglycans (GAGs) accumulate in different cell types, causing characteristic vacuolization.	Glycosaminoglycans	93-97	alpha-L-iduronidase	Homo sapiens	40-59
20357254-9	2010	EM CD4+ T cells lack any known PECAM-1 counter receptor, but heterophilic engagement of PECAM-1 can involve glycosaminoglycans.	Glycosaminoglycans	108-126	platelet and endothelial cell adhesion molecule 1	Homo sapiens	88-95
20028218-10	2010	Further, the clusters formed in the presence of Nell-1 contained more type II collagen and glycosaminoglycans than clusters formed within Nell-free control gels.	Glycosaminoglycans	91-109	neural EGFL like 1	Homo sapiens	48-54
20179574-0	2010	Cytotoxic granule release dominates gag-specific CD4+ T-cell response in different phases of HIV infection.	Glycosaminoglycans	36-39	CD4 molecule	Homo sapiens	49-52
20179574-9	2010	CONCLUSION: In all the aforementioned phases of HIV infection, the large majority of gag-specific CD4 T lymphocytes cannot be identified by the sole expression of interleukin-2 and interferon-gamma, which is early impaired.	Glycosaminoglycans	85-88	CD4 molecule	Homo sapiens	98-101
20179574-9	2010	CONCLUSION: In all the aforementioned phases of HIV infection, the large majority of gag-specific CD4 T lymphocytes cannot be identified by the sole expression of interleukin-2 and interferon-gamma, which is early impaired.	Glycosaminoglycans	85-88	interferon gamma	Homo sapiens	181-197
20100602-2	2010	Tumor necrosis factor stimulated gene-6 protein (TSG-6)/heavy chain 2 (HC2) cleaves this unique cross-link and transfers the HCs to hyaluronan and other glycosaminoglycans via a covalent HC*TSG-6 intermediate.	Glycosaminoglycans	153-171	TNF alpha induced protein 6	Homo sapiens	0-47
20164174-0	2010	Impairment of embryonic cell division and glycosaminoglycan biosynthesis in glucuronyltransferase-I-deficient mice.	Glycosaminoglycans	42-59	beta-1,3-glucuronyltransferase 3 (glucuronosyltransferase I)	Mus musculus	76-99
20100602-2	2010	Tumor necrosis factor stimulated gene-6 protein (TSG-6)/heavy chain 2 (HC2) cleaves this unique cross-link and transfers the HCs to hyaluronan and other glycosaminoglycans via a covalent HC*TSG-6 intermediate.	Glycosaminoglycans	153-171	TNF alpha induced protein 6	Homo sapiens	49-54
20100602-2	2010	Tumor necrosis factor stimulated gene-6 protein (TSG-6)/heavy chain 2 (HC2) cleaves this unique cross-link and transfers the HCs to hyaluronan and other glycosaminoglycans via a covalent HC*TSG-6 intermediate.	Glycosaminoglycans	153-171	proteasome 20S subunit alpha 1	Homo sapiens	71-74
20100602-2	2010	Tumor necrosis factor stimulated gene-6 protein (TSG-6)/heavy chain 2 (HC2) cleaves this unique cross-link and transfers the HCs to hyaluronan and other glycosaminoglycans via a covalent HC*TSG-6 intermediate.	Glycosaminoglycans	153-171	TNF alpha induced protein 6	Homo sapiens	190-195
19903083-5	2010	The Gag protein lacking the DC-LAMP-derived sequence altogether elicited only weak T cell responses.	Glycosaminoglycans	4-7	lysosomal associated membrane protein 3	Homo sapiens	28-35
20217136-0	2010	Interleukin-1alpha treatment of meniscal explants stimulates the production and release of aggrecanase-generated, GAG-substituted aggrecan products and also the release of pre-formed, aggrecanase-generated G1 and m-calpain-generated G1-G2.	Glycosaminoglycans	114-117	interleukin 1 alpha	Bos taurus	0-18
20217136-9	2010	TIMP-3 (but not TIMP-1 and -2 or a broad spectrum MMP inhibitor) inhibited IL-1-dependent GAG loss.	Glycosaminoglycans	90-93	TIMP metallopeptidase inhibitor 3	Bos taurus	0-6
20299390-4	2010	It is possible that the antibodies could be elicited by PF4 associated with endogenous, heparin-like glycosaminoglycans (GAGs).	Glycosaminoglycans	101-119	platelet factor 4	Homo sapiens	56-59
20198421-2	2010	This initial and rate-limiting step in glycosaminoglycan biosynthesis is catalyzed by human xylosyltransferase I (XT-I).	Glycosaminoglycans	39-56	xylosyltransferase 1	Homo sapiens	92-112
20198421-2	2010	This initial and rate-limiting step in glycosaminoglycan biosynthesis is catalyzed by human xylosyltransferase I (XT-I).	Glycosaminoglycans	39-56	xylosyltransferase 1	Homo sapiens	114-118
19903083-6	2010	DCs electroporated with Gag or TaReNef linked to DC-LAMP were able to elicit similar levels of antigen-specific CD4(+) and CD8(+) T cell responses for both Gag and TaReNef, irrespective of the addition of the DC-LAMP lumenal domain.	Glycosaminoglycans	24-27	lysosomal associated membrane protein 3	Homo sapiens	49-56
19903083-6	2010	DCs electroporated with Gag or TaReNef linked to DC-LAMP were able to elicit similar levels of antigen-specific CD4(+) and CD8(+) T cell responses for both Gag and TaReNef, irrespective of the addition of the DC-LAMP lumenal domain.	Glycosaminoglycans	24-27	lysosomal associated membrane protein 3	Homo sapiens	209-216
19903083-6	2010	DCs electroporated with Gag or TaReNef linked to DC-LAMP were able to elicit similar levels of antigen-specific CD4(+) and CD8(+) T cell responses for both Gag and TaReNef, irrespective of the addition of the DC-LAMP lumenal domain.	Glycosaminoglycans	156-159	lysosomal associated membrane protein 3	Homo sapiens	49-56
20036175-1	2010	In mucopolysaccharidosis VI, or Maroteaux-Lamy syndrome, deficiency of N-acetylgalactosamine 4-sulfatase leads to storage of glycosaminoglycans (GAGs) and MPS VI patients often develop spinal cord compression during the course of the disease due to GAG storage within the cervical meninges, requiring neurosurgical intervention, as intravenous (IV) enzyme replacement therapy (ERT) is not expected to cross the blood-brain barrier.	Glycosaminoglycans	125-143	arylsulfatase B	Homo sapiens	71-104
20036175-1	2010	In mucopolysaccharidosis VI, or Maroteaux-Lamy syndrome, deficiency of N-acetylgalactosamine 4-sulfatase leads to storage of glycosaminoglycans (GAGs) and MPS VI patients often develop spinal cord compression during the course of the disease due to GAG storage within the cervical meninges, requiring neurosurgical intervention, as intravenous (IV) enzyme replacement therapy (ERT) is not expected to cross the blood-brain barrier.	Glycosaminoglycans	145-148	arylsulfatase B	Homo sapiens	71-104
20067575-0	2010	Glycosaminoglycan-induced activation of the beta-secretase (BACE1) of Alzheimer"s disease.	Glycosaminoglycans	0-17	beta-secretase 1	Homo sapiens	60-65
20042606-5	2010	Interestingly, blocking protein synthesis in the presence of cycloheximide abolished the PDGF effect, but not in the presence of xyloside, indicating that GAG synthesis that results from PKC activation is independent from de novo protein synthesis.	Glycosaminoglycans	155-158	proline rich transmembrane protein 2	Homo sapiens	187-190
20042606-6	2010	PDGF also stimulated an increase in the chondroitin-6-sulfate to chondroitin-4-sulfate ratio of GAG chains on versican, and this effect was blocked by PKC inhibitors.	Glycosaminoglycans	96-99	proline rich transmembrane protein 2	Homo sapiens	151-154
20042606-7	2010	These data show that PKC activation is sufficient to cause GAG chain elongation, but both PKC and ERK activation are required for versican mRNA core protein expression.	Glycosaminoglycans	59-62	proline rich transmembrane protein 2	Homo sapiens	21-24
20187128-8	2010	Expression of ULK1, Beclin1, and LC3 decreased together with GAG loss, while PARP p85 expression was increased.	Glycosaminoglycans	61-64	unc-51 like autophagy activating kinase 1	Homo sapiens	14-18
20187128-8	2010	Expression of ULK1, Beclin1, and LC3 decreased together with GAG loss, while PARP p85 expression was increased.	Glycosaminoglycans	61-64	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	33-36
20044292-1	2010	Mucopolysaccharidosis I (MPS I) and MPS VII are due to loss-of-function mutations within the genes that encode the lysosomal enzymes alpha-l-iduronidase and beta-glucuronidase, respectively, and result in accumulation of glycosaminoglycans and multisystemic disease.	Glycosaminoglycans	221-239	alpha-L-iduronidase	Canis lupus familiaris	133-152
20044292-1	2010	Mucopolysaccharidosis I (MPS I) and MPS VII are due to loss-of-function mutations within the genes that encode the lysosomal enzymes alpha-l-iduronidase and beta-glucuronidase, respectively, and result in accumulation of glycosaminoglycans and multisystemic disease.	Glycosaminoglycans	221-239	glucuronidase beta	Canis lupus familiaris	157-175
20097750-4	2010	We have therefore generated novel MCP-1/CCL2 mutants with increased GAG binding affinity and knocked out CCR2 activity, which were designed to interrupt the MCP-1/CCL2-related signaling cascade.	Glycosaminoglycans	68-71	C-C motif chemokine ligand 2	Homo sapiens	34-39
20097750-4	2010	We have therefore generated novel MCP-1/CCL2 mutants with increased GAG binding affinity and knocked out CCR2 activity, which were designed to interrupt the MCP-1/CCL2-related signaling cascade.	Glycosaminoglycans	68-71	C-C motif chemokine ligand 2	Homo sapiens	40-44
20097750-4	2010	We have therefore generated novel MCP-1/CCL2 mutants with increased GAG binding affinity and knocked out CCR2 activity, which were designed to interrupt the MCP-1/CCL2-related signaling cascade.	Glycosaminoglycans	68-71	C-C motif chemokine ligand 2	Homo sapiens	157-162
20097750-4	2010	We have therefore generated novel MCP-1/CCL2 mutants with increased GAG binding affinity and knocked out CCR2 activity, which were designed to interrupt the MCP-1/CCL2-related signaling cascade.	Glycosaminoglycans	68-71	C-C motif chemokine ligand 2	Homo sapiens	163-167
20002544-9	2010	Certain glycosaminoglycans, including heparin, only partially competed with polyphosphate for binding to thrombin, and polyphosphate did not reduce heparin-catalyzed inactivation of thrombin by antithrombin.	Glycosaminoglycans	8-26	coagulation factor II, thrombin	Homo sapiens	105-113
19951947-3	2010	Efficient encapsidation of TRIM5alpharh, but not human TRIM5alpha (TRIM5alphahu), in HIV-1 virus-like particles suggests the interaction between Gag and TRIM5alpharh during viral assembly.	Glycosaminoglycans	145-148	tripartite motif containing 5	Homo sapiens	27-32
19895887-8	2010	This biochemistry models glycosaminoglycan interactions on the cell surface during elastogenesis which is characterized by the clustering of nascent tropoelastin aggregates to form micron-sized spherules.	Glycosaminoglycans	25-42	elastin	Homo sapiens	149-161
19840848-7	2010	The proliferation of porcine articular chondrocytes and GAG secretion in SW1353 cells were synergistically increased by co-stimulation with type II collagen and TGF-beta1.	Glycosaminoglycans	56-59	transforming growth factor beta 1	Homo sapiens	161-170
19840848-9	2010	Therefore, we suggest that FAK-SMAD 2/3 mediates signal crosstalk between type II collagen and TGF-beta1 and regulates GAG secretion in chondrocytic cells.	Glycosaminoglycans	119-122	protein tyrosine kinase 2	Homo sapiens	27-30
19840848-9	2010	Therefore, we suggest that FAK-SMAD 2/3 mediates signal crosstalk between type II collagen and TGF-beta1 and regulates GAG secretion in chondrocytic cells.	Glycosaminoglycans	119-122	SMAD family member 2	Homo sapiens	31-39
19951947-3	2010	Efficient encapsidation of TRIM5alpharh, but not human TRIM5alpha (TRIM5alphahu), in HIV-1 virus-like particles suggests the interaction between Gag and TRIM5alpharh during viral assembly.	Glycosaminoglycans	145-148	tripartite motif containing 5	Homo sapiens	27-37
19942287-2	2010	In vivo, fibroblast growth factor 2 (FGF-2) binds to the sulfated glycosaminoglycan heparan sulfate, which is a major component of the ECM.	Glycosaminoglycans	66-83	fibroblast growth factor 2	Homo sapiens	9-35
20113225-6	2010	RESULTS: IL-1 beta increased GAG release and aggrecanase activity (11-fold).	Glycosaminoglycans	29-32	interleukin-1 beta	Equus caballus	9-18
19942287-2	2010	In vivo, fibroblast growth factor 2 (FGF-2) binds to the sulfated glycosaminoglycan heparan sulfate, which is a major component of the ECM.	Glycosaminoglycans	66-83	fibroblast growth factor 2	Homo sapiens	37-42
19886734-0	2010	Differences in the expression of glycosaminoglycans in human fibroblasts derived from gingival overgrowths is related to TGF-beta up-regulation.	Glycosaminoglycans	33-51	transforming growth factor beta 1	Homo sapiens	121-129
19895604-6	2010	Histological analyses of tumors revealed increased (by approximately 2.4-fold) vessel content, as well as markedly reduced collagen and immunoreactivity against glycosaminoglycan structural epitopes in the tumors from Nas1(-/-) mice.	Glycosaminoglycans	161-178	solute carrier family 13 (sodium/sulfate symporters), member 1	Mus musculus	218-222
19845689-8	2010	CONCLUSIONS: This study demonstrates that an extracellular glycosaminoglycan, heparin, finely modulates expression of genes crucial to cell cycle regulation through specific activation of p38 MAP kinase to stimulate colon cancer cell growth.	Glycosaminoglycans	59-76	mitogen-activated protein kinase 14	Homo sapiens	188-191
19690583-5	2010	The three EXTL2-specific shRNA constructs reduced endogenous target gene expression by 68, 32 and 65%, and decreased gag synthesis by 46, 50 and 27%.	Glycosaminoglycans	117-120	exostosin-like glycosyltransferase 2	Mus musculus	10-15
19690583-6	2010	One EXTL3-specific shRNA construct reduced endogenous target gene expression by 14% and gag synthesis by 39%.	Glycosaminoglycans	88-91	exostosin-like glycosyltransferase 3	Mus musculus	4-9
19690583-7	2010	Lysosomal gag levels in MPS IIIA and MPS I fibroblasts were also reduced by EXTL2 and EXTL3-specific shRNA.	Glycosaminoglycans	10-13	exostosin-like glycosyltransferase 2	Mus musculus	76-81
19690583-7	2010	Lysosomal gag levels in MPS IIIA and MPS I fibroblasts were also reduced by EXTL2 and EXTL3-specific shRNA.	Glycosaminoglycans	10-13	exostosin-like glycosyltransferase 3	Mus musculus	86-91
19690583-8	2010	Incorporation of shRNAs into a lentiviral expression system reduced gene expression, and one EXTL2-specific shRNA reduced gag synthesis.	Glycosaminoglycans	122-125	exostosin-like glycosyltransferase 2	Mus musculus	93-98
19690584-7	2010	In this report we show that, in MPS IIIA fibroblasts, we were able to reduce mRNA levels of four genes, XYLT1, XYLT2, GALTI and GALTII, whose products are involved in GAG synthesis.	Glycosaminoglycans	167-170	xylosyltransferase 1	Homo sapiens	104-109
19690584-7	2010	In this report we show that, in MPS IIIA fibroblasts, we were able to reduce mRNA levels of four genes, XYLT1, XYLT2, GALTI and GALTII, whose products are involved in GAG synthesis.	Glycosaminoglycans	167-170	xylosyltransferase 2	Homo sapiens	111-116
19844196-1	2010	Mucopolysaccharidosis I (MPS I) is a lysosomal storage disease due to deficiency in alpha-L-iduronidase (IDUA) that results in accumulation of glycosaminoglycans (GAGs) throughout the body, causing numerous clinical defects.	Glycosaminoglycans	143-161	alpha-L-iduronidase	Canis lupus familiaris	105-109
20026745-2	2010	Inflammation is mediated by inflammatory cytokines, including IL-8, which illustrates an increase in biological half-life and proinflammatory activity when bound to glycosaminoglycans (GAGs).	Glycosaminoglycans	165-183	C-X-C motif chemokine ligand 8	Homo sapiens	62-66
19951286-2	2010	A non-GAG-binding mutant CCL7 (mtCCL7) was developed that retained its affinity for chemokine receptors.	Glycosaminoglycans	6-9	C-C motif chemokine ligand 7	Homo sapiens	25-29
20004976-4	2010	The agent displayed enhanced binding to GAG structures in vitro and could antagonize CXCL8-induced firm adhesion of monocytes as well as neutrophils to activated microvascular endothelium in physiologic flow assays.	Glycosaminoglycans	40-43	C-X-C motif chemokine ligand 8	Homo sapiens	85-90
19903485-4	2010	In this study we used a new approach to identify and characterize potential epitopes in the gag region containing PS mutations that significantly correlated with HLA-A*0301.	Glycosaminoglycans	92-95	major histocompatibility complex, class I, A	Homo sapiens	162-167
19903485-7	2010	Using this approach we identified/confirmed the predicted HLA-A*0301 epitopes in two regions of gag containing PS mutations V7I and K403R, one previously reported and the other novel.	Glycosaminoglycans	96-99	major histocompatibility complex, class I, A	Homo sapiens	58-63
20085648-12	2010	CD4+ and CD8+ T cells in viremic cats were more likely to produce cytokines in response to Gag stimulation, whereas aviremic cats T cells tended to produce cytokines in response to Env stimulation.	Glycosaminoglycans	91-94	CD4 molecule	Felis catus	0-3
19676054-1	2010	Uridine diphosphate (UDP)-glucose dehydrogenase (UGDH) catalyzes the oxidation of UDP-glucose to yield UDP-glucuronic acid, a precursor for synthesis of glycosaminoglycans and proteoglycans that promote aggressive prostate cancer (PC) progression.	Glycosaminoglycans	153-171	UDP-glucose 6-dehydrogenase	Homo sapiens	49-53
19944077-1	2010	The xylosyltransferase (XT) isoforms XT-I and XT-II initiate the posttranslational glycosaminoglycan (GAG) synthesis.	Glycosaminoglycans	83-100	xylosyltransferase 1	Homo sapiens	37-41
20307272-5	2010	IFN-gamma did not affect IL-1beta induced tissue inhibitor of metalloproteinase-1 (TIMP-1) production by RA FLS but skewed the MMP/TIMP-1 balance sufficiently to attenuate glycosaminoglycan-depletion in our BACE model.	Glycosaminoglycans	172-189	interferon gamma	Bos taurus	0-9
19701788-9	2010	Of note, the molecular weight of biglycan GAG chains was even further increased by NO donors compared to control and PDGF-BB stimulation.	Glycosaminoglycans	42-45	biglycan	Mus musculus	33-41
19944077-1	2010	The xylosyltransferase (XT) isoforms XT-I and XT-II initiate the posttranslational glycosaminoglycan (GAG) synthesis.	Glycosaminoglycans	83-100	xylosyltransferase 2	Homo sapiens	46-51
19944077-1	2010	The xylosyltransferase (XT) isoforms XT-I and XT-II initiate the posttranslational glycosaminoglycan (GAG) synthesis.	Glycosaminoglycans	102-105	xylosyltransferase 1	Homo sapiens	37-41
19944077-1	2010	The xylosyltransferase (XT) isoforms XT-I and XT-II initiate the posttranslational glycosaminoglycan (GAG) synthesis.	Glycosaminoglycans	102-105	xylosyltransferase 2	Homo sapiens	46-51
20939824-0	2010	Glycosaminoglycans as key molecules in atherosclerosis: the role of versican and hyaluronan.	Glycosaminoglycans	0-18	versican	Homo sapiens	68-76
19748976-5	2010	Using precursors to GAG biosynthesis combined with immunoabsorption with a versican antibody an increased versican synthesis was detected at hypoxia.	Glycosaminoglycans	20-23	versican	Homo sapiens	106-114
20224283-2	2010	BACE1 binds strongly to heparin and other glycosaminoglycans, and there is evidence that the enzyme may interact with proteoglycans in vivo.	Glycosaminoglycans	42-60	beta-site APP cleaving enzyme 1	Mus musculus	0-5
19889767-7	2010	Our results demonstrate that a single amino acid substitution at HIV-1 RT can radically affect virus assembly by enhancing Gag cleavage efficiency, suggesting that in addition to contributing to RT biological function during the early stages of virus replication, the HIV-1 RT tryptophan repeat motif in a Gag-Pol context may play an important role in suppressing the premature activation of PR during late-stage virus replication.	Glycosaminoglycans	123-126	Gag-Pol	Human immunodeficiency virus 1	306-313
20008810-9	2010	Cells overexpressing glypican-1 N-glycosylated mutants with or without GAG chains increased cell responsiveness to FGF2 compared with wild-type glypican-1.	Glycosaminoglycans	71-74	glypican-1	Meleagris gallopavo	21-31
20008810-9	2010	Cells overexpressing glypican-1 N-glycosylated mutants with or without GAG chains increased cell responsiveness to FGF2 compared with wild-type glypican-1.	Glycosaminoglycans	71-74	fibroblast growth factor 2	Meleagris gallopavo	115-119
20008810-10	2010	These data suggest that glypican-1 N-glycosylated chains and GAG chains are critical in regulating turkey myogenic satellite cell proliferation, differentiation, and responsivness to FGF2.	Glycosaminoglycans	61-64	fibroblast growth factor 2	Meleagris gallopavo	183-187
19910798-2	2010	In the 2 subjects who exhibited the best viral control, we detected CD8(+) T-cell responses against 1-2 Gag epitopes during the early weeks of TI and a subsequent increase in the number of epitopes recognized by the later time points.	Glycosaminoglycans	104-107	CD8a molecule	Homo sapiens	68-71
19615011-9	2010	Mucin proved to be a dermal-type mucin, composed of both hyaluronic acid and sulfated glycosaminoglycans.	Glycosaminoglycans	86-104	LOC100508689	Homo sapiens	0-5
19615011-9	2010	Mucin proved to be a dermal-type mucin, composed of both hyaluronic acid and sulfated glycosaminoglycans.	Glycosaminoglycans	86-104	LOC100508689	Homo sapiens	33-38
19896517-3	2010	The efficacy of SHP-1 was determined on cartilage protective effects such as inhibition of collagen and GAG release.	Glycosaminoglycans	104-107	nuclear receptor subfamily 0 group B member 2	Homo sapiens	16-21
20008810-1	2010	Glypican-1 is a cell membrane heparan sulfate proteoglycan that is composed of a core protein and covalently attached glycosaminoglycan (GAG) chains and N-linked glycosylated (N-glycosylated) chains.	Glycosaminoglycans	118-135	glypican-1	Meleagris gallopavo	0-10
20008810-1	2010	Glypican-1 is a cell membrane heparan sulfate proteoglycan that is composed of a core protein and covalently attached glycosaminoglycan (GAG) chains and N-linked glycosylated (N-glycosylated) chains.	Glycosaminoglycans	137-140	glypican-1	Meleagris gallopavo	0-10
20008810-2	2010	The glypican-1 GAG chains are required for cell differentiation and responsiveness to fibroblast growth factor 2 (FGF2).	Glycosaminoglycans	15-18	glypican-1	Meleagris gallopavo	4-14
20008810-2	2010	The glypican-1 GAG chains are required for cell differentiation and responsiveness to fibroblast growth factor 2 (FGF2).	Glycosaminoglycans	15-18	fibroblast growth factor 2	Meleagris gallopavo	86-112
20008810-2	2010	The glypican-1 GAG chains are required for cell differentiation and responsiveness to fibroblast growth factor 2 (FGF2).	Glycosaminoglycans	15-18	fibroblast growth factor 2	Meleagris gallopavo	114-118
20008810-5	2010	The wild-type turkey glypican-1 and turkey glypican-1 with mutated GAG chain attachment sites were cloned into the pCMS-EGFP mammalian expression vector and were used as templates to generate glypican-1 N-glycosylated 1-chain and no-chain mutants with or without GAG chains by site-directed mutagenesis.	Glycosaminoglycans	67-70	glypican-1	Meleagris gallopavo	43-53
20008810-5	2010	The wild-type turkey glypican-1 and turkey glypican-1 with mutated GAG chain attachment sites were cloned into the pCMS-EGFP mammalian expression vector and were used as templates to generate glypican-1 N-glycosylated 1-chain and no-chain mutants with or without GAG chains by site-directed mutagenesis.	Glycosaminoglycans	67-70	glypican-1	Meleagris gallopavo	43-53
20008810-8	2010	The overexpression of glypican-1 N-glycosylated 1-chain and no-chain mutants without GAG chains increased cell proliferation and differentiation compared with the wild-type glypican-1 but not the glypican-1 N-glycosylated mutants with GAG chains attached.	Glycosaminoglycans	85-88	glypican-1	Meleagris gallopavo	22-32
20008810-8	2010	The overexpression of glypican-1 N-glycosylated 1-chain and no-chain mutants without GAG chains increased cell proliferation and differentiation compared with the wild-type glypican-1 but not the glypican-1 N-glycosylated mutants with GAG chains attached.	Glycosaminoglycans	235-238	glypican-1	Meleagris gallopavo	22-32
19682969-2	2009	The enzyme ASB is a lysosomal exohydrolase, cleaving sulfate from the N-acetylgalactosamine-4-sulfate (GalNAc-4S) residue at the nonreducing terminal of GAG structures.	Glycosaminoglycans	153-156	arylsulfatase B	Homo sapiens	11-14
20807657-5	2010	It is established that chemically oversulfated glycosaminoglycans (GAGs) induce thrombin generation through contact system activation in human plasma.	Glycosaminoglycans	47-65	coagulation factor II, thrombin	Homo sapiens	80-88
19682969-1	2009	A functional bioassay has been developed for measuring the intracellular activity of recombinant human arylsulfatase B (rhASB) on its natural glycosaminoglycan (GAG) substrates, dermatan sulfate (DS), and chondroitin sulfate (CS) when the enzyme is taken up into cultured ASB-deficient human fibroblasts (GM00519).	Glycosaminoglycans	142-159	arylsulfatase B	Homo sapiens	103-118
19682969-1	2009	A functional bioassay has been developed for measuring the intracellular activity of recombinant human arylsulfatase B (rhASB) on its natural glycosaminoglycan (GAG) substrates, dermatan sulfate (DS), and chondroitin sulfate (CS) when the enzyme is taken up into cultured ASB-deficient human fibroblasts (GM00519).	Glycosaminoglycans	142-159	arylsulfatase B	Homo sapiens	122-125
20807639-6	2010	Here, we summarize the recent knowledge on the roles of GlcAT-I in mammalian GAG biosynthesis and embryonic cell division using GlcAT-I knock-out mice.	Glycosaminoglycans	77-80	beta-1,3-glucuronyltransferase 3	Homo sapiens	56-63
19682969-1	2009	A functional bioassay has been developed for measuring the intracellular activity of recombinant human arylsulfatase B (rhASB) on its natural glycosaminoglycan (GAG) substrates, dermatan sulfate (DS), and chondroitin sulfate (CS) when the enzyme is taken up into cultured ASB-deficient human fibroblasts (GM00519).	Glycosaminoglycans	161-164	arylsulfatase B	Homo sapiens	103-118
19717493-0	2009	Glycosaminoglycan mimetics inhibit SDF-1/CXCL12-mediated migration and invasion of human hepatoma cells.	Glycosaminoglycans	0-17	C-X-C motif chemokine ligand 12	Homo sapiens	35-40
19682969-1	2009	A functional bioassay has been developed for measuring the intracellular activity of recombinant human arylsulfatase B (rhASB) on its natural glycosaminoglycan (GAG) substrates, dermatan sulfate (DS), and chondroitin sulfate (CS) when the enzyme is taken up into cultured ASB-deficient human fibroblasts (GM00519).	Glycosaminoglycans	161-164	arylsulfatase B	Homo sapiens	122-125
19695308-2	2009	The CXC-chemokine stromal cell-derived factor-1 (SDF-1)/CXCL12 mediates its biological activities through activation of G protein-coupled receptor CXCR4 and binds to glycosaminoglycans (GAGs).	Glycosaminoglycans	166-184	C-X-C motif chemokine ligand 12	Homo sapiens	49-54
19695308-2	2009	The CXC-chemokine stromal cell-derived factor-1 (SDF-1)/CXCL12 mediates its biological activities through activation of G protein-coupled receptor CXCR4 and binds to glycosaminoglycans (GAGs).	Glycosaminoglycans	166-184	C-X-C motif chemokine ligand 12	Homo sapiens	56-62
19620133-12	2009	Western blotting for HS showed significant reduction in expression of HS, one of the main glycosaminoglycans in the glycocalyx, with C-reactive protein treatment.	Glycosaminoglycans	90-108	C-reactive protein	Homo sapiens	133-151
20004762-4	2009	Mass spectrometry of glycosaminoglycans from a patient"s fibroblasts revealed absence of dermatan sulfate and excess of chondroitin sulfate, showing that 4-O sulfation by CHST14 is essential for dermatan sulfate formation in vivo.	Glycosaminoglycans	21-39	carbohydrate sulfotransferase 14	Homo sapiens	171-177
19717493-0	2009	Glycosaminoglycan mimetics inhibit SDF-1/CXCL12-mediated migration and invasion of human hepatoma cells.	Glycosaminoglycans	0-17	C-X-C motif chemokine ligand 12	Homo sapiens	41-47
19717493-1	2009	We have recently reported that the CXC-chemokine stromal cell-derived factor-1 (SDF-1)/CXCL12 induces proliferation, migration, and invasion of the Huh7 human hepatoma cells through its G-protein-coupled receptor CXCR4 and that glycosaminoglycans (GAGs) are involved in these events.	Glycosaminoglycans	228-246	C-X-C motif chemokine ligand 12	Homo sapiens	80-85
19717493-1	2009	We have recently reported that the CXC-chemokine stromal cell-derived factor-1 (SDF-1)/CXCL12 induces proliferation, migration, and invasion of the Huh7 human hepatoma cells through its G-protein-coupled receptor CXCR4 and that glycosaminoglycans (GAGs) are involved in these events.	Glycosaminoglycans	228-246	C-X-C motif chemokine ligand 12	Homo sapiens	87-93
19717493-1	2009	We have recently reported that the CXC-chemokine stromal cell-derived factor-1 (SDF-1)/CXCL12 induces proliferation, migration, and invasion of the Huh7 human hepatoma cells through its G-protein-coupled receptor CXCR4 and that glycosaminoglycans (GAGs) are involved in these events.	Glycosaminoglycans	228-246	C-X-C motif chemokine receptor 4	Homo sapiens	213-218
19717493-4	2009	The binding of GAG mimetics to the chemokine and their effects in modulating the SDF-1/CXCL12 biological activities are mainly related to the presence of sulfate groups.	Glycosaminoglycans	15-18	C-X-C motif chemokine ligand 12	Homo sapiens	81-86
19717493-4	2009	The binding of GAG mimetics to the chemokine and their effects in modulating the SDF-1/CXCL12 biological activities are mainly related to the presence of sulfate groups.	Glycosaminoglycans	15-18	C-X-C motif chemokine ligand 12	Homo sapiens	87-93
19717493-8	2009	Altogether, these data suggest that GAG mimetics may compete with cellular heparan sulfate chains for the binding to SDF-1/CXCL12 and may affect heparanase expression, leading to reduced SDF-1/CXCL12 mediated in vitro chemotaxis and growth of hepatoma cells.	Glycosaminoglycans	36-39	C-X-C motif chemokine ligand 12	Homo sapiens	117-122
19717493-8	2009	Altogether, these data suggest that GAG mimetics may compete with cellular heparan sulfate chains for the binding to SDF-1/CXCL12 and may affect heparanase expression, leading to reduced SDF-1/CXCL12 mediated in vitro chemotaxis and growth of hepatoma cells.	Glycosaminoglycans	36-39	C-X-C motif chemokine ligand 12	Homo sapiens	123-129
19717493-8	2009	Altogether, these data suggest that GAG mimetics may compete with cellular heparan sulfate chains for the binding to SDF-1/CXCL12 and may affect heparanase expression, leading to reduced SDF-1/CXCL12 mediated in vitro chemotaxis and growth of hepatoma cells.	Glycosaminoglycans	36-39	C-X-C motif chemokine ligand 12	Homo sapiens	187-192
19717493-8	2009	Altogether, these data suggest that GAG mimetics may compete with cellular heparan sulfate chains for the binding to SDF-1/CXCL12 and may affect heparanase expression, leading to reduced SDF-1/CXCL12 mediated in vitro chemotaxis and growth of hepatoma cells.	Glycosaminoglycans	36-39	C-X-C motif chemokine ligand 12	Homo sapiens	193-199
19915053-8	2009	In contrast, NDST-2 was down-regulated after MC activation, suggesting that MC activation modulates the nature of the glycosaminoglycan chains attached to the SG core protein.	Glycosaminoglycans	118-135	N-deacetylase and N-sulfotransferase 2	Homo sapiens	13-19
19643812-3	2009	In the case of beta(2)-microglobulin-related amyloidosis, an extracellular protein misfolding disease, many kinds of biological molecules including glycosaminoglycans, proteoglycans and lipids partially unfold beta(2)-microglobulin and catalyse its subsequent nucleus formation.	Glycosaminoglycans	148-166	beta-2-microglobulin	Homo sapiens	15-36
19643812-3	2009	In the case of beta(2)-microglobulin-related amyloidosis, an extracellular protein misfolding disease, many kinds of biological molecules including glycosaminoglycans, proteoglycans and lipids partially unfold beta(2)-microglobulin and catalyse its subsequent nucleus formation.	Glycosaminoglycans	148-166	beta-2-microglobulin	Homo sapiens	210-231
19951916-0	2009	The glycosaminoglycan-binding domain of PRELP acts as a cell type-specific NF-kappaB inhibitor that impairs osteoclastogenesis.	Glycosaminoglycans	4-21	proline arginine-rich end leucine-rich repeat	Mus musculus	40-45
19492402-5	2009	Among males, GDF6-/- tail tendon fascicles had significantly less collagen and glycosaminoglycan content, and these compositional differences were associated with compromised material properties.	Glycosaminoglycans	79-96	growth differentiation factor 6	Mus musculus	13-17
19951916-0	2009	The glycosaminoglycan-binding domain of PRELP acts as a cell type-specific NF-kappaB inhibitor that impairs osteoclastogenesis.	Glycosaminoglycans	4-21	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	75-84
19951916-1	2009	Proline/arginine-rich end leucine-rich repeat protein (PRELP) is a glycosaminoglycan (GAG)- and collagen-binding anchor protein highly expressed in cartilage, basement membranes, and developing bone.	Glycosaminoglycans	67-84	proline arginine-rich end leucine-rich repeat	Mus musculus	0-53
19951916-1	2009	Proline/arginine-rich end leucine-rich repeat protein (PRELP) is a glycosaminoglycan (GAG)- and collagen-binding anchor protein highly expressed in cartilage, basement membranes, and developing bone.	Glycosaminoglycans	67-84	proline arginine-rich end leucine-rich repeat	Mus musculus	55-60
19762916-1	2009	Human xylosyltransferase I catalyzes the initial and rate-limiting step in the biosynthesis of glycosaminoglycans and proteoglycans.	Glycosaminoglycans	95-113	xylosyltransferase 1	Homo sapiens	6-26
19951916-1	2009	Proline/arginine-rich end leucine-rich repeat protein (PRELP) is a glycosaminoglycan (GAG)- and collagen-binding anchor protein highly expressed in cartilage, basement membranes, and developing bone.	Glycosaminoglycans	86-89	proline arginine-rich end leucine-rich repeat	Mus musculus	0-53
19951916-1	2009	Proline/arginine-rich end leucine-rich repeat protein (PRELP) is a glycosaminoglycan (GAG)- and collagen-binding anchor protein highly expressed in cartilage, basement membranes, and developing bone.	Glycosaminoglycans	86-89	proline arginine-rich end leucine-rich repeat	Mus musculus	55-60
19951916-2	2009	We observed that PRELP inhibited in vitro and in vivo mouse osteoclastogenesis through its GAG-binding domain ((hbd)PRELP), involving (a) cell internalization through a chondroitin sulfate- and annexin II-dependent mechanism, (b) nuclear translocation, (c) interaction with p65 nuclear factor kappaB (NF-kappaB) and inhibition of its DNA binding, and (d) impairment of NF-kappaB transcriptional activity and reduction of osteoclast-specific gene expression.	Glycosaminoglycans	91-94	proline arginine-rich end leucine-rich repeat	Mus musculus	17-22
19951916-2	2009	We observed that PRELP inhibited in vitro and in vivo mouse osteoclastogenesis through its GAG-binding domain ((hbd)PRELP), involving (a) cell internalization through a chondroitin sulfate- and annexin II-dependent mechanism, (b) nuclear translocation, (c) interaction with p65 nuclear factor kappaB (NF-kappaB) and inhibition of its DNA binding, and (d) impairment of NF-kappaB transcriptional activity and reduction of osteoclast-specific gene expression.	Glycosaminoglycans	91-94	exocyst complex component 6	Mus musculus	112-115
19951916-2	2009	We observed that PRELP inhibited in vitro and in vivo mouse osteoclastogenesis through its GAG-binding domain ((hbd)PRELP), involving (a) cell internalization through a chondroitin sulfate- and annexin II-dependent mechanism, (b) nuclear translocation, (c) interaction with p65 nuclear factor kappaB (NF-kappaB) and inhibition of its DNA binding, and (d) impairment of NF-kappaB transcriptional activity and reduction of osteoclast-specific gene expression.	Glycosaminoglycans	91-94	proline arginine-rich end leucine-rich repeat	Mus musculus	116-121
19700613-11	2009	Neutralizing TGF-beta3 antibody decreased the expression of the GAG-rich versican variants 2 to 8 fold in leiomyoma cells.	Glycosaminoglycans	64-67	transforming growth factor beta 3	Homo sapiens	13-22
19758826-4	2009	We propose that this newly discovered unstable M-hemoglobin (M-Hb) variant, named Hb Dothan [GGT/GAG-->GAG//Gly/Glu-->Glu], is caused by a shift in the amino acid sequence and altered packing of the B and E helices during beta globin synthesis, and also changes the orientation of the critical proximal and distal histidine in the F and E helices respectively.	Glycosaminoglycans	97-100	hemoglobin subunit beta	Homo sapiens	222-233
19937589-1	2009	Chondroitin-4-sulfotransferase-1(C4ST-1)/carbohydrate sulfotransferase 11 (CHST11) is a Golgi-bound enzyme involved in the biosynthesis of the glycosaminoglycan chondroitin sulfate.	Glycosaminoglycans	143-160	carbohydrate sulfotransferase 11	Mus musculus	0-40
19937589-1	2009	Chondroitin-4-sulfotransferase-1(C4ST-1)/carbohydrate sulfotransferase 11 (CHST11) is a Golgi-bound enzyme involved in the biosynthesis of the glycosaminoglycan chondroitin sulfate.	Glycosaminoglycans	143-160	carbohydrate sulfotransferase 11	Mus musculus	41-73
19937589-1	2009	Chondroitin-4-sulfotransferase-1(C4ST-1)/carbohydrate sulfotransferase 11 (CHST11) is a Golgi-bound enzyme involved in the biosynthesis of the glycosaminoglycan chondroitin sulfate.	Glycosaminoglycans	143-160	carbohydrate sulfotransferase 11	Mus musculus	75-81
19800307-5	2009	Specific TLR-4 blocking antibody confirmed that TLR-4 was the target of GAG action.	Glycosaminoglycans	72-75	toll-like receptor 4	Mus musculus	48-53
19800307-0	2009	Glycosaminoglycans reduced inflammatory response by modulating toll-like receptor-4 in LPS-stimulated chondrocytes.	Glycosaminoglycans	0-18	toll-like receptor 4	Mus musculus	63-83
19800307-2	2009	As previous data reported that hyaluronan (HA) and heparan sulfate (HS) may interact with TLR-4, the aim of this study was to investigate whether glycosaminoglycans (GAGs) may modulate the TLR-4 receptor in a model of LPS-induced inflammatory cytokines in mouse chondrocytes.	Glycosaminoglycans	146-164	toll-like receptor 4	Mus musculus	189-194
19800307-5	2009	Specific TLR-4 blocking antibody confirmed that TLR-4 was the target of GAG action.	Glycosaminoglycans	72-75	toll-like receptor 4	Mus musculus	9-14
19758826-4	2009	We propose that this newly discovered unstable M-hemoglobin (M-Hb) variant, named Hb Dothan [GGT/GAG-->GAG//Gly/Glu-->Glu], is caused by a shift in the amino acid sequence and altered packing of the B and E helices during beta globin synthesis, and also changes the orientation of the critical proximal and distal histidine in the F and E helices respectively.	Glycosaminoglycans	103-106	hemoglobin subunit beta	Homo sapiens	222-233
19157930-9	2009	The unique underlying mutation is a GAG deletion in the coding region of the TOR1A gene, located at chromosome 9q34.	Glycosaminoglycans	36-39	torsin family 1 member A	Homo sapiens	77-82
19876963-6	2009	The inclusion of decorin in the coatings confirmed the importance of glycosaminoglycans in mediating the interactions between collagens and apoB-100 peptide fragments.	Glycosaminoglycans	69-87	apolipoprotein B	Homo sapiens	140-148
19780173-8	2009	Significant correlations were found between N-acetyl/Lac+Lip and GAG content in bovine discs (R = 0.77, P = 0.0007) and cadaveric discs (R = 0.83, P &lt; 0.0001).	Glycosaminoglycans	65-68	SMG1 nonsense mediated mRNA decay associated PI3K related kinase	Homo sapiens	57-60
19699504-3	2009	However, the precise role for p12 in mediating Gag-Gag interaction is still poorly understood.	Glycosaminoglycans	51-54	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	30-33
19712047-6	2009	HRG has been shown to function as an adaptor molecule to tether plasminogen to GAG (glycosaminoglycan)-bearing surfaces and to regulate plasminogen activation via various mechanisms.	Glycosaminoglycans	79-82	histidine rich glycoprotein	Homo sapiens	0-3
19712047-6	2009	HRG has been shown to function as an adaptor molecule to tether plasminogen to GAG (glycosaminoglycan)-bearing surfaces and to regulate plasminogen activation via various mechanisms.	Glycosaminoglycans	84-101	histidine rich glycoprotein	Homo sapiens	0-3
19470416-5	2009	RESULTS: For primary chondrocytes, the combination of GDF-5 and insulin led to increased proliferation and construct weight, as compared to either factor alone, however, the production of glycosaminoglycans (GAG) and collagen per cell were not affected.	Glycosaminoglycans	188-206	growth differentiation factor 5	Homo sapiens	54-59
19775117-4	2009	Recombinant glypican-1 was expressed as two glycoforms, one as proteoglycan substituted with heparan sulfate chains and one as the core protein devoid of glycosaminoglycans.	Glycosaminoglycans	154-172	glypican 1	Homo sapiens	12-22
19696445-2	2009	We demonstrate that HSPG glycosaminoglycan levels increased with increasing metastatic potential of melanoma cells.	Glycosaminoglycans	25-42	syndecan 2	Homo sapiens	20-24
20160907-7	2009	Finally, we compared the collisional activation data for the MCP-1 dimer with an MCP-1 dimer non-covalently bound to a single molecule of the semi-synthetic glycosaminoglycan (GAG) analog Arixtra ; the latter a therapeutic anti-thrombin III-activating pentasaccharide.	Glycosaminoglycans	157-174	C-C motif chemokine ligand 2	Homo sapiens	81-86
20160907-7	2009	Finally, we compared the collisional activation data for the MCP-1 dimer with an MCP-1 dimer non-covalently bound to a single molecule of the semi-synthetic glycosaminoglycan (GAG) analog Arixtra ; the latter a therapeutic anti-thrombin III-activating pentasaccharide.	Glycosaminoglycans	176-179	C-C motif chemokine ligand 2	Homo sapiens	81-86
19699504-2	2009	It was shown previously that the N-terminal part of the Gag p12 domain (wt-Np12) is required for efficient assembly.	Glycosaminoglycans	56-59	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	60-63
19803713-2	2009	Portions of gag-p24 and env-gp41 were sequenced and HIV subtype was determined for 773 subjects residing in 10 community clusters in rural Uganda.	Glycosaminoglycans	12-15	transmembrane p24 trafficking protein 2	Homo sapiens	16-19
19699504-3	2009	However, the precise role for p12 in mediating Gag-Gag interaction is still poorly understood.	Glycosaminoglycans	47-50	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	30-33
19790045-6	2009	RESULTS: In bovine cartilage samples, injury combined with TNFalpha and IL-6/sIL-6R exposure caused the most severe GAG loss.	Glycosaminoglycans	116-119	tumor necrosis factor	Bos taurus	59-67
19790045-6	2009	RESULTS: In bovine cartilage samples, injury combined with TNFalpha and IL-6/sIL-6R exposure caused the most severe GAG loss.	Glycosaminoglycans	116-119	interleukin 6	Bos taurus	72-76
19790045-6	2009	RESULTS: In bovine cartilage samples, injury combined with TNFalpha and IL-6/sIL-6R exposure caused the most severe GAG loss.	Glycosaminoglycans	116-119	STIL centriolar assembly protein	Homo sapiens	77-80
19790045-11	2009	The catabolic effects of injury plus TNFalpha appeared partly due to endogenous IL-6, since GAG loss was partially abrogated by an IL-6-blocking Fab.	Glycosaminoglycans	92-95	interleukin 6	Homo sapiens	131-135
19790045-11	2009	The catabolic effects of injury plus TNFalpha appeared partly due to endogenous IL-6, since GAG loss was partially abrogated by an IL-6-blocking Fab.	Glycosaminoglycans	92-95	FA complementation group B	Homo sapiens	145-148
24868365-3	2009	We report here a patient with the three-bp GAG deletion in the DYT1 gene (904_906delGAG) who had severe head tremor in the frame of a generalized limb dystonia.	Glycosaminoglycans	43-46	torsin family 1 member A	Homo sapiens	63-67
19800217-3	2009	In this survey, some structural aspects of the chemokine-heparan sulphate interface are described, with a focus on CXCL12; alternative splicing of which finely tunes its affinity for glycosaminoglycans, through the generation of an intrinsically disordered peptides, and on recent biochemical observations that shed light on both the fine structure and the general topology of the heparan sulphate domains that chemokines recognize.	Glycosaminoglycans	183-201	C-X-C motif chemokine ligand 12	Homo sapiens	115-121
19853561-4	2009	Dlp core protein can interact with Wg; the GAG chains enhance this interaction.	Glycosaminoglycans	43-46	dally-like	Drosophila melanogaster	0-3
19641002-3	2009	In this study, we generated dominant Gag p11C- and subdominant Env p41A-specific CD8(+) T-lymphocyte responses in Mamu-A*01(+) rhesus monkeys through vaccination with plasmid DNA and recombinant adenovirus encoding simian-human immunodeficiency virus (SHIV) proteins.	Glycosaminoglycans	37-40	major histocompatibility complex, class I, A	Macaca mulatta	114-120
19706714-5	2009	We confirm the potent effect of IFN on Gag p24 production in supernatants.	Glycosaminoglycans	39-42	transmembrane p24 trafficking protein 2	Homo sapiens	43-46
19605475-1	2009	A broad Gag-specific CD8(+) T-cell response is associated with effective control of adult human immunodeficiency virus (HIV) infection.	Glycosaminoglycans	8-11	CD8a molecule	Homo sapiens	21-24
19605475-7	2009	Slow progressors tended to make CD8(+) T-cell responses to Gag epitopes presented by the protective HLA-B alleles, in contrast to progressors expressing the same alleles (P = 0.07; Fisher"s exact test).	Glycosaminoglycans	59-62	CD8a molecule	Homo sapiens	32-35
19605475-7	2009	Slow progressors tended to make CD8(+) T-cell responses to Gag epitopes presented by the protective HLA-B alleles, in contrast to progressors expressing the same alleles (P = 0.07; Fisher"s exact test).	Glycosaminoglycans	59-62	major histocompatibility complex, class I, B	Homo sapiens	100-105
19641002-4	2009	Infection of vaccinated Mamu-A*01(+) rhesus monkeys with a SHIV Gag Deltap11C mutant virus generated a significantly increased expansion of the Env p41A-specific CD8(+) T-lymphocyte response in the absence of secondary Gag p11C-specific CD8(+) T-lymphocyte responses.	Glycosaminoglycans	64-67	major histocompatibility complex, class I, A	Macaca mulatta	24-30
19641002-4	2009	Infection of vaccinated Mamu-A*01(+) rhesus monkeys with a SHIV Gag Deltap11C mutant virus generated a significantly increased expansion of the Env p41A-specific CD8(+) T-lymphocyte response in the absence of secondary Gag p11C-specific CD8(+) T-lymphocyte responses.	Glycosaminoglycans	64-67	CD8a molecule	Homo sapiens	162-165
19641002-4	2009	Infection of vaccinated Mamu-A*01(+) rhesus monkeys with a SHIV Gag Deltap11C mutant virus generated a significantly increased expansion of the Env p41A-specific CD8(+) T-lymphocyte response in the absence of secondary Gag p11C-specific CD8(+) T-lymphocyte responses.	Glycosaminoglycans	64-67	CD8a molecule	Homo sapiens	237-240
19756298-5	2009	Based on our current knowledge of the composition of the glycome and the size of GBP binding sites, glycoproteins and glycolipids may contain approximately 3000 glycan determinants with an additional approximately 4000 theoretical pentasaccharide sequences in glycosaminoglycans.	Glycosaminoglycans	260-278	transmembrane protein 132A	Homo sapiens	81-84
19406175-1	2009	Ectopic expression of the structural protein Pr55(Gag) of HIV-1 has been limited by the presence of inhibitory sequences in the gag coding region that must normally be counteracted by HIV-1 Rev and RRE.	Glycosaminoglycans	128-131	Pr55(Gag)	Human immunodeficiency virus 1	50-53
20539743-2	2009	This study demonstrates for the first time the applicability of CA RS microscopy to the imaging of live neuronal cells in GAG hydrogels.	Glycosaminoglycans	122-125	cysteinyl-tRNA synthetase 1	Homo sapiens	64-69
19335060-9	2009	TGF-beta1-treated and TGF-beta3-treated constructs were similar at 4 weeks, but 8-week TGF-beta1 constructs had a higher aggregate modulus and GAG content compared to TGF-beta3.	Glycosaminoglycans	143-146	transforming growth factor beta 1	Sus scrofa	87-96
19344291-4	2009	C-ABC was used to deplete GAG from constructs 2 weeks after initiating culture, followed by 2 weeks culture post-treatment.	Glycosaminoglycans	26-29	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	2-5
19344291-9	2009	As GAG returned, compressive stiffness of C-ABC treated constructs recovered to be greater than 2 wk controls.	Glycosaminoglycans	3-6	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	44-47
19449355-8	2009	Experimental modulation of GAG content correlated with alterations in TAT transduction in PC12 cells and astrocyte monocultures grown in the presence of serum.	Glycosaminoglycans	27-30	tyrosine aminotransferase	Rattus norvegicus	70-73
19449355-10	2009	We conclude that culture conditions affect cellular GAG expression, which in turn dictates TAT-mediated transduction efficiency, extending previous results from cell lines to primary cells.	Glycosaminoglycans	52-55	tyrosine aminotransferase	Rattus norvegicus	91-94
19596853-7	2009	These data demonstrate that RIP will underpin emerging efforts to develop glycomics profiling strategies for HS and other glycosaminoglycans to explore their structure-function relationships in complex biological systems.	Glycosaminoglycans	122-140	regulation of phenobarbitol-inducible P450	Mus musculus	28-31
19700618-5	2009	The effects of sdc2 knockdown in the YSL can be rescued by extra-embryonic Sdc2 lacking an extracellular proteolytic cleavage (shedding) site, but not by extra-embryonic Sdc2 lacking extracellular glycosaminoglycan (GAG) addition sites, suggesting that distinct GAG chains on extra-embryonic Sdc2 regulate extracellular matrix assembly, cell migration and epithelial morphogenesis of multiple organ systems throughout the embryo.	Glycosaminoglycans	197-214	syndecan 2	Danio rerio	15-19
19700618-5	2009	The effects of sdc2 knockdown in the YSL can be rescued by extra-embryonic Sdc2 lacking an extracellular proteolytic cleavage (shedding) site, but not by extra-embryonic Sdc2 lacking extracellular glycosaminoglycan (GAG) addition sites, suggesting that distinct GAG chains on extra-embryonic Sdc2 regulate extracellular matrix assembly, cell migration and epithelial morphogenesis of multiple organ systems throughout the embryo.	Glycosaminoglycans	216-219	syndecan 2	Danio rerio	15-19
19700618-5	2009	The effects of sdc2 knockdown in the YSL can be rescued by extra-embryonic Sdc2 lacking an extracellular proteolytic cleavage (shedding) site, but not by extra-embryonic Sdc2 lacking extracellular glycosaminoglycan (GAG) addition sites, suggesting that distinct GAG chains on extra-embryonic Sdc2 regulate extracellular matrix assembly, cell migration and epithelial morphogenesis of multiple organ systems throughout the embryo.	Glycosaminoglycans	262-265	syndecan 2	Danio rerio	15-19
19539688-11	2009	In addition, GAG mimetics-induced mobilization is associated with increased levels of pro- and active MMP-9 from bone marrow cells and increased level of SDF-1 in peripheral blood.	Glycosaminoglycans	13-16	matrix metallopeptidase 9	Mus musculus	102-107
19539688-11	2009	In addition, GAG mimetics-induced mobilization is associated with increased levels of pro- and active MMP-9 from bone marrow cells and increased level of SDF-1 in peripheral blood.	Glycosaminoglycans	13-16	chemokine (C-X-C motif) ligand 12	Mus musculus	154-159
19539688-13	2009	CONCLUSION: This study demonstrates that GAG mimetics induce efficient mobilization of HSPCs, associated with an activation of pro-MMP-9 and a modification in the SDF-1 concentration gradient between bone marrow and peripheral blood.	Glycosaminoglycans	41-44	matrix metallopeptidase 9	Mus musculus	127-136
19539688-13	2009	CONCLUSION: This study demonstrates that GAG mimetics induce efficient mobilization of HSPCs, associated with an activation of pro-MMP-9 and a modification in the SDF-1 concentration gradient between bone marrow and peripheral blood.	Glycosaminoglycans	41-44	chemokine (C-X-C motif) ligand 12	Mus musculus	163-168
19616817-2	2009	In protease-negative (Pr(-)) HIV-1, the amount of tRNA(Lys3) annealed by Gag is 35% less than that annealed by mature nucleocapsid (NCp7) in protease-positive (Pr(+)) virions.	Glycosaminoglycans	73-76	mitochondrially encoded tRNA glycine	Homo sapiens	50-59
19616817-3	2009	Gag-annealed tRNA(Lys3) also has a reduced ability to initiate reverse transcription, and binds less tightly to viral RNA than NCp7-annealed tRNA(Lys3).	Glycosaminoglycans	0-3	mitochondrially encoded tRNA glycine	Homo sapiens	13-22
19653641-9	2009	We also estimated galanin receptor-mediated endocytosis of QD-AST1 at &lt;10% by blocking the cells with a galanin antagonist and transduction at &lt;30% by both removing the charge of the peptide due to arginine and suppressing the cell-surface charge due to glycosaminoglycan.	Glycosaminoglycans	260-277	glutamic-oxaloacetic transaminase 1	Homo sapiens	62-66
19542224-4	2009	New partners of endostatin include glycosaminoglycans (chondroitin and dermatan sulfate), matricellular proteins (thrombospondin-1 and SPARC), collagens (I, IV, and VI), the amyloid peptide Abeta-(1-42), and transglutaminase-2.	Glycosaminoglycans	35-53	collagen type XVIII alpha 1 chain	Homo sapiens	16-26
19401393-7	2009	Enzymatic degradation of HS GAG further increased the motility of the HMDM in hypoxia, indicating a role of reduced cell-associated HSPG in the increased HMDM motility.	Glycosaminoglycans	28-31	syndecan 2	Homo sapiens	132-136
18546186-8	2009	After 14 days in chondrogenic cultures, cells in RGDS and KLER functionalized gels produced 2.5 times as much GAG/cell as those in gels containing only RGD.	Glycosaminoglycans	110-113	ral guanine nucleotide dissociation stimulator	Homo sapiens	49-53
19723203-5	2009	Furthermore, the changes of total ceramide and glycosaminoglycan in skin were recovered significantly by JC and JCH.	Glycosaminoglycans	47-64	immunoglobulin joining chain	Mus musculus	112-115
19217622-7	2009	Endothelin-1 stimulated an increase in the 6:4 position sulfation ratio on the disaccharides of the GAG chains, an effect that was blocked by bosentan.	Glycosaminoglycans	100-103	endothelin 1	Homo sapiens	0-12
19217622-9	2009	Inhibition of protein kinase C (PKC) with GF109203X or down regulation by PMA pre-treatment attenuated the effect of endothelin-1 on GAG synthesis.	Glycosaminoglycans	133-136	endothelin 1	Homo sapiens	117-129
19217622-10	2009	CONCLUSION: These data demonstrate that endothelin-1 stimulates changes in GAG chain structure that increase binding to LDL.	Glycosaminoglycans	75-78	endothelin 1	Homo sapiens	40-52
19556463-5	2009	TFEB overexpression in cultured cells induced lysosomal biogenesis and increased the degradation of complex molecules, such as glycosaminoglycans and the pathogenic protein that causes Huntington"s disease.	Glycosaminoglycans	127-145	transcription factor EB	Homo sapiens	0-4
19458002-5	2009	Further, we document that repression of Env-induced cell-cell fusion by tetraspanins depends on the presence of viral Gag, and we demonstrate that fusion repression requires the recruitment of Env by Gag to tetraspanin-enriched microdomains (TEMs).	Glycosaminoglycans	118-121	endogenous retrovirus group K member 20	Homo sapiens	40-43
19458002-5	2009	Further, we document that repression of Env-induced cell-cell fusion by tetraspanins depends on the presence of viral Gag, and we demonstrate that fusion repression requires the recruitment of Env by Gag to tetraspanin-enriched microdomains (TEMs).	Glycosaminoglycans	200-203	endogenous retrovirus group K member 20	Homo sapiens	40-43
19458002-5	2009	Further, we document that repression of Env-induced cell-cell fusion by tetraspanins depends on the presence of viral Gag, and we demonstrate that fusion repression requires the recruitment of Env by Gag to tetraspanin-enriched microdomains (TEMs).	Glycosaminoglycans	200-203	endogenous retrovirus group K member 20	Homo sapiens	193-196
19487902-5	2009	DESIGN: A subtype B HIV-1 strain carrying a HLA-B27 CTL-escape mutation in the main Gag-p24 KK10 epitope, R264G, together with a compensatory mutation outside this epitope, E260D, was detected in four patients from Amsterdam, The Netherlands, by sequence analysis of the gag gene.	Glycosaminoglycans	84-87	major histocompatibility complex, class I, B	Homo sapiens	44-51
19487902-5	2009	DESIGN: A subtype B HIV-1 strain carrying a HLA-B27 CTL-escape mutation in the main Gag-p24 KK10 epitope, R264G, together with a compensatory mutation outside this epitope, E260D, was detected in four patients from Amsterdam, The Netherlands, by sequence analysis of the gag gene.	Glycosaminoglycans	271-274	major histocompatibility complex, class I, B	Homo sapiens	44-51
19472299-5	2009	Analysis of haplotypes consisting of four SNPs at the HERC2-OCA2 locus (rs12913832/rs7495174/rs4778241/rs4778138) showed that the most frequent haplotype in the Japanese population is A-GAG (0.568), while the frequency of this haplotype is rather low in the European population, even in the brown-eyed group (0.167).	Glycosaminoglycans	186-189	HECT and RLD domain containing E3 ubiquitin protein ligase 2	Homo sapiens	54-59
19441135-4	2009	One patient carried the GAG deletion in the DYT1 gene.	Glycosaminoglycans	24-27	torsin family 1 member A	Homo sapiens	44-48
19234354-6	2009	RESULTS: FGF-2 stimulated the highest level of proliferation and the lowest level of glycosaminoglycan synthesis and inhibited the synthesis of collagen types Iota and IotaIotaIota.	Glycosaminoglycans	85-102	fibroblast growth factor 2	Bos taurus	9-14
19582753-11	2009	Furthermore, CCL5 expression in K(d)Gag(197-205)-specific CTL was also regulated by IL-4/IL-13.	Glycosaminoglycans	36-39	chemokine (C-C motif) ligand 5	Mus musculus	13-17
19582753-11	2009	Furthermore, CCL5 expression in K(d)Gag(197-205)-specific CTL was also regulated by IL-4/IL-13.	Glycosaminoglycans	36-39	interleukin 4	Mus musculus	84-88
19582753-11	2009	Furthermore, CCL5 expression in K(d)Gag(197-205)-specific CTL was also regulated by IL-4/IL-13.	Glycosaminoglycans	36-39	interleukin 13	Mus musculus	89-94
19601881-1	2009	The cell adhesion molecule CD44 is expressed on the majority of immune cells and is responsible for mediating adhesion to the extracellular matrix glycosaminoglycan, hyaluronan.	Glycosaminoglycans	147-164	CD44 antigen	Mus musculus	27-31
19563964-3	2009	Other glycosaminoglycan analogs are known to influence MAPK signaling.	Glycosaminoglycans	6-23	mitogen activated protein kinase 3	Rattus norvegicus	55-59
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
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	N-acetyl-alpha-glucosaminidase	Homo sapiens	28-37
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
19403679-5	2009	To overcome these limitations, we created a novel NL4-3-derived provirus by displacing the original frameshift signal to the 3" end of the gag gene, thereby uncoupling the p6* gene sequence from the p1-p6(gag) reading frame.	Glycosaminoglycans	139-142	S100 calcium binding protein A12	Homo sapiens	172-175
19542465-0	2009	LL-37 complexation with glycosaminoglycans in cystic fibrosis lungs inhibits antimicrobial activity, which can be restored by hypertonic saline.	Glycosaminoglycans	24-42	cathelicidin antimicrobial peptide	Homo sapiens	0-5
19542465-7	2009	The endogenous LL-37 in CF BAL fluid is protected from this proteolysis by interactions with glycosaminoglycans, but while this protects LL-37 from proteolysis it results in inactivation of LL-37 antimicrobial activity.	Glycosaminoglycans	93-111	cathelicidin antimicrobial peptide	Homo sapiens	15-20
19542465-8	2009	By digesting glycosaminoglycans in CF BAL fluid, endogenous LL-37 is liberated and the antimicrobial properties of CF BAL fluid restored.	Glycosaminoglycans	13-31	cathelicidin antimicrobial peptide	Homo sapiens	60-65
19542465-10	2009	This is also seen in vivo in CF sputum where LL-37 is complexed to glycosaminoglycans but is liberated following nebulized hypertonic saline resulting in increased antimicrobial effect.	Glycosaminoglycans	67-85	cathelicidin antimicrobial peptide	Homo sapiens	45-50
19630810-4	2009	HIT is caused by antibodies that recognize the platelet chemokine, Platelet Factor 4 (PF4), complexed to heparin or to cellular glycosaminoglycans (GAGs).	Glycosaminoglycans	128-146	platelet factor 4	Homo sapiens	67-84
19630810-4	2009	HIT is caused by antibodies that recognize the platelet chemokine, Platelet Factor 4 (PF4), complexed to heparin or to cellular glycosaminoglycans (GAGs).	Glycosaminoglycans	128-146	platelet factor 4	Homo sapiens	86-89
19630810-6	2009	We propose that HIT antibodies recognize cell surface PF4/GAG complexes on intravascular cells, including platelets and monocytes that are dynamic and mutable.	Glycosaminoglycans	58-61	platelet factor 4	Homo sapiens	54-57
19384290-4	2009	IDUA activity was present in all examined somatic organs, as well as in the brain, and correlated with both glycosaminoglycan (GAG) reduction in these organs and level of expression in the liver, the target of transposon delivery.	Glycosaminoglycans	108-125	iduronidase, alpha-L	Mus musculus	0-4
19384290-4	2009	IDUA activity was present in all examined somatic organs, as well as in the brain, and correlated with both glycosaminoglycan (GAG) reduction in these organs and level of expression in the liver, the target of transposon delivery.	Glycosaminoglycans	127-130	iduronidase, alpha-L	Mus musculus	0-4
19478057-0	2009	Gag- and Nef-specific CD4+ T cells recognize and inhibit SIV replication in infected macrophages early after infection.	Glycosaminoglycans	0-3	CD4 molecule	Homo sapiens	22-25
19494307-11	2009	These results, on the one hand, suggest the importance of Gag responses in the antiviral potency of CD8(+) T cells from HICs and, on the other hand, propose that other host mechanisms may contribute to restraining HIV infection in HICs.	Glycosaminoglycans	58-61	CD8a molecule	Homo sapiens	100-103
19359419-3	2009	HARE is expressed in the sinusoidal endothelial cells (SECs) of liver and lymph nodes where it acts as a scavenger for uptake and degradation of glycosaminoglycans, both as free chains and proteoglycan fragments.	Glycosaminoglycans	145-163	stabilin 2	Homo sapiens	0-4
19426117-5	2009	TGF-beta3 cultured with silk elastin-like polymer scaffold carrier exhibits significantly increased glycosaminoglycan and collagen content.	Glycosaminoglycans	100-117	transforming growth factor beta 3	Homo sapiens	0-9
19457118-1	2009	A GAG deletion in the DYT1 gene is responsible for the autosomal dominant movement disorder, early onset primary torsion dystonia, which is characterised by involuntary sustained muscle contractions and abnormal posturing of the limbs.	Glycosaminoglycans	2-5	torsin family 1 member A	Homo sapiens	22-26
19160015-4	2009	These wide ranging functions have been attributed to the central glycosaminoglycan-binding region of versican, and to the N-(G1) and C-(G3) terminal globular domains which collectively interact with a large number of extracellular matrix and cell surface structural components.	Glycosaminoglycans	65-82	versican	Homo sapiens	101-109
19414521-0	2009	Engineering the glycosaminoglycan-binding affinity, kinetics and oligomerization behavior of RANTES: a tool for generating chemokine-based glycosaminoglycan antagonists.	Glycosaminoglycans	16-33	C-C motif chemokine ligand 5	Rattus norvegicus	93-99
19428572-2	2009	Development of novel and effective Gag-targeted vaccine candidates inducing CD8(+) and CD4(+) T cell responses requires large scale pre-clinical testing in a small animal model.	Glycosaminoglycans	35-38	CD8a molecule	Homo sapiens	76-79
19428572-2	2009	Development of novel and effective Gag-targeted vaccine candidates inducing CD8(+) and CD4(+) T cell responses requires large scale pre-clinical testing in a small animal model.	Glycosaminoglycans	35-38	CD4 molecule	Homo sapiens	87-90
19597321-7	2009	These findings suggest that GAG degradation-inhibitory LAB may improve colitis by inhibiting inflammatory cytokine expression via TLR-4-linked NF-kB activation and by inhibiting intestinal bacterial GAG degradation.	Glycosaminoglycans	28-31	toll-like receptor 4	Mus musculus	130-135
19414521-0	2009	Engineering the glycosaminoglycan-binding affinity, kinetics and oligomerization behavior of RANTES: a tool for generating chemokine-based glycosaminoglycan antagonists.	Glycosaminoglycans	139-156	C-C motif chemokine ligand 5	Rattus norvegicus	93-99
19414521-1	2009	Binding to glycosaminoglycans (GAGs) is a necessary prerequisite for the biological activity of the proinflammatory chemokine RANTES in vivo.	Glycosaminoglycans	11-29	C-C motif chemokine ligand 5	Rattus norvegicus	126-132
19414521-6	2009	In surface plasmon resonance experiments using immobilized heparan sulfate (HS) and physiological buffer conditions, Met-RANTES exhibited a significantly longer residual time on the GAG chip compared with the other RANTES variants.	Glycosaminoglycans	182-185	C-C motif chemokine ligand 5	Rattus norvegicus	121-127
19124046-7	2009	MSD affects the entire sulfatase family, at least seven members of which are lysosomal enzymes that are specifically involved in the degradation of sulfated glycosaminoglycans, sulfolipids or other sulfated molecules.	Glycosaminoglycans	157-175	arylsulfatase family member H	Homo sapiens	23-32
19289103-1	2009	The key enzymes in the biosynthetic pathway of glycosaminoglycan production are represented by the human xylosyltransferase I and its isoform II (XylT-I and XylT-II).	Glycosaminoglycans	47-64	xylosyltransferase 1	Homo sapiens	105-144
19289103-1	2009	The key enzymes in the biosynthetic pathway of glycosaminoglycan production are represented by the human xylosyltransferase I and its isoform II (XylT-I and XylT-II).	Glycosaminoglycans	47-64	xylosyltransferase 1	Homo sapiens	146-152
19289103-1	2009	The key enzymes in the biosynthetic pathway of glycosaminoglycan production are represented by the human xylosyltransferase I and its isoform II (XylT-I and XylT-II).	Glycosaminoglycans	47-64	xylosyltransferase 2	Homo sapiens	157-164
19435492-3	2009	To demonstrate the molecular basis for developing a better rat model for HIV-1 infection, we evaluated the effect of human CyclinT1 (hCycT1) and CRM1 (hCRM1) on Gag p24 production in rat T cells and macrophages using both established cell lines and primary cells prepared from hCycT1/hCRM1 transgenic rats.	Glycosaminoglycans	161-164	cyclin T1	Homo sapiens	123-131
19435492-3	2009	To demonstrate the molecular basis for developing a better rat model for HIV-1 infection, we evaluated the effect of human CyclinT1 (hCycT1) and CRM1 (hCRM1) on Gag p24 production in rat T cells and macrophages using both established cell lines and primary cells prepared from hCycT1/hCRM1 transgenic rats.	Glycosaminoglycans	161-164	cyclin T1	Homo sapiens	133-139
19435492-4	2009	RESULTS: Expression of hCycT1 augmented Gag production 20-50 fold in rat T cells, but had little effect in macrophages.	Glycosaminoglycans	40-43	cyclin T1	Homo sapiens	23-29
19369399-7	2009	Direct measurements of Ihh binding to defined GAG chains demonstrated that Ihh interacts with CS, particularly chondroitin-4-sulfate.	Glycosaminoglycans	46-49	Indian hedgehog	Mus musculus	23-26
19369399-7	2009	Direct measurements of Ihh binding to defined GAG chains demonstrated that Ihh interacts with CS, particularly chondroitin-4-sulfate.	Glycosaminoglycans	46-49	Indian hedgehog	Mus musculus	75-78
18690792-2	2009	We have previously noted the necessity of sulfated glycosaminoglycans for the fibroblast growth factor type 2 (FGF-2)-stimulated differentiation of osteoprogenitor cells.	Glycosaminoglycans	51-69	fibroblast growth factor 2	Rattus norvegicus	78-109
18690792-2	2009	We have previously noted the necessity of sulfated glycosaminoglycans for the fibroblast growth factor type 2 (FGF-2)-stimulated differentiation of osteoprogenitor cells.	Glycosaminoglycans	51-69	fibroblast growth factor 2	Rattus norvegicus	111-116
18826340-7	2009	We found that co-expression of IGF-1 and TGF-beta1, BMP-2, or both at low doses resulted in larger aggregates, higher levels of glycosaminoglycan synthesis, stronger staining for proteoglycans and collagen type II and X, and greater expression of cartilage-specific marker genes than with either transgene alone.	Glycosaminoglycans	128-145	insulin like growth factor 1	Homo sapiens	31-36
18826340-7	2009	We found that co-expression of IGF-1 and TGF-beta1, BMP-2, or both at low doses resulted in larger aggregates, higher levels of glycosaminoglycan synthesis, stronger staining for proteoglycans and collagen type II and X, and greater expression of cartilage-specific marker genes than with either transgene alone.	Glycosaminoglycans	128-145	transforming growth factor beta 1	Homo sapiens	41-50
18826340-7	2009	We found that co-expression of IGF-1 and TGF-beta1, BMP-2, or both at low doses resulted in larger aggregates, higher levels of glycosaminoglycan synthesis, stronger staining for proteoglycans and collagen type II and X, and greater expression of cartilage-specific marker genes than with either transgene alone.	Glycosaminoglycans	128-145	bone morphogenetic protein 2	Homo sapiens	52-57
19504438-7	2009	The novel allele had 1 nucleotide substitution of the closest matching allele HLA-DRB1*120201 at nt262(G--&gt;C) in exon 2,resulting in an amino acid change from Glu(GAG)--&gt;Gln (CAG) at codon 59.The intron 2 sequence is identical between the novel HLA-DRB1*1218 and DRB1*030101, but there are 12 nucleotides substitution in intron 1.	Glycosaminoglycans	166-169	major histocompatibility complex, class II, DR beta 1	Homo sapiens	78-86
19504438-7	2009	The novel allele had 1 nucleotide substitution of the closest matching allele HLA-DRB1*120201 at nt262(G--&gt;C) in exon 2,resulting in an amino acid change from Glu(GAG)--&gt;Gln (CAG) at codon 59.The intron 2 sequence is identical between the novel HLA-DRB1*1218 and DRB1*030101, but there are 12 nucleotides substitution in intron 1.	Glycosaminoglycans	166-169	major histocompatibility complex, class II, DR beta 1	Homo sapiens	251-259
19504438-7	2009	The novel allele had 1 nucleotide substitution of the closest matching allele HLA-DRB1*120201 at nt262(G--&gt;C) in exon 2,resulting in an amino acid change from Glu(GAG)--&gt;Gln (CAG) at codon 59.The intron 2 sequence is identical between the novel HLA-DRB1*1218 and DRB1*030101, but there are 12 nucleotides substitution in intron 1.	Glycosaminoglycans	166-169	major histocompatibility complex, class II, DR beta 1	Homo sapiens	82-86
19435492-5	2009	Expression of hCRM1 enhanced Gag production 10-15 fold in macrophages, but only marginally in T cells.	Glycosaminoglycans	29-32	exportin 1	Homo sapiens	14-19
19135418-5	2009	Of responses directed to individual HIV gene products the magnitude and breadth of only Gag p24-specific responses for the 3 functional subsets were associated with lower concurrent or set point VL.	Glycosaminoglycans	88-91	transmembrane p24 trafficking protein 2	Homo sapiens	92-95
19135418-6	2009	Therefore the early appearance of broader and more intense Gag-p24-specific responses may be a determinant of subsequent VL.	Glycosaminoglycans	59-62	transmembrane p24 trafficking protein 2	Homo sapiens	63-66
19036615-6	2009	Three single nucleotide polymorphisms (SNPs) in the SELS gene revealed four common haplotypes, one of which, GAG (frequency 3.5%) showed significant association to an anti-inflammatory (P=0.019) and acute phase related (P=0.036) component.	Glycosaminoglycans	109-112	selenoprotein S	Homo sapiens	52-56
19349605-10	2009	The GAG deletion in DYT1 was absent in all patients.	Glycosaminoglycans	4-7	torsin family 1 member A	Homo sapiens	20-24
19158248-3	2009	Cell lines derived from peripheral blood mononuclear cells stimulated in vitro with peptides representing targeted Gag epitopes consistently neutralized HIV better than Env-specific lines from the same person, although ineffective inhibition of virus replication is not a universal characteristic of Env-specific responses at the clonal level.	Glycosaminoglycans	115-118	endogenous retrovirus group K member 20	Homo sapiens	300-303
19284447-2	2009	The novel A*11 variant is identical to A*1125 in exon 2 but differs from A*1125 in exon 3 by one nucleotide substitution at position 527 causing an amino acid change at codon 152 E--&gt;V (GAG--&gt;GTG).	Glycosaminoglycans	189-192	beta-1,4-galactosyltransferase 5	Homo sapiens	183-187
19368826-5	2009	Several key enzymes required for glycosaminoglycan biosynthesis (beta3GlcNAcT-7 and GlcNAc6ST-1 for keratan sulfate; CS synthase-1 and C6ST-1 for chondroitin sulfate) were expressed at significantly higher levels in the lesion 7 days after a knife-cut injury was made to the cerebral cortex in adult mice.	Glycosaminoglycans	33-50	carbohydrate sulfotransferase 2	Mus musculus	84-95
19343217-3	2009	Here, we assess the fitness impact of escape mutations emerging in seven CTL epitopes in the gp120 Env and p24 Gag coding regions of an individual followed longitudinally from the time of acute HIV-1 infection, as well as some of these same epitopes recognized in other HIV-1-infected individuals.	Glycosaminoglycans	111-114	transmembrane p24 trafficking protein 2	Homo sapiens	107-110
19368826-5	2009	Several key enzymes required for glycosaminoglycan biosynthesis (beta3GlcNAcT-7 and GlcNAc6ST-1 for keratan sulfate; CS synthase-1 and C6ST-1 for chondroitin sulfate) were expressed at significantly higher levels in the lesion 7 days after a knife-cut injury was made to the cerebral cortex in adult mice.	Glycosaminoglycans	33-50	carbohydrate sulfotransferase 3	Mus musculus	135-141
19167466-5	2009	We suggest that versican"s glycosaminoglycan side chains present MCP-1 to a CCR2 expressing cell type in the skin that, in turn, selectively activates IB4(+)/Ret(+) nociceptors, thereby contributing to enhanced mechanical sensitivity under inflammatory conditions.	Glycosaminoglycans	27-44	chemokine (C-C motif) ligand 2	Mus musculus	65-70
19320978-8	2009	Overexpression of calnuc-GFP or cytosolic calnuc(DeltaSS)-CFP enhances ACTH secretion two-fold triggered by mastoparan or GTPgammaS but does not significantly affect glycosaminoglycan (GAG) chain secretion along the constitutive pathway or basal secretion of ACTH.	Glycosaminoglycans	185-188	nucleobindin 1	Mus musculus	18-24
19167466-5	2009	We suggest that versican"s glycosaminoglycan side chains present MCP-1 to a CCR2 expressing cell type in the skin that, in turn, selectively activates IB4(+)/Ret(+) nociceptors, thereby contributing to enhanced mechanical sensitivity under inflammatory conditions.	Glycosaminoglycans	27-44	chemokine (C-C motif) receptor 2	Mus musculus	76-80
19167466-5	2009	We suggest that versican"s glycosaminoglycan side chains present MCP-1 to a CCR2 expressing cell type in the skin that, in turn, selectively activates IB4(+)/Ret(+) nociceptors, thereby contributing to enhanced mechanical sensitivity under inflammatory conditions.	Glycosaminoglycans	27-44	ret proto-oncogene	Mus musculus	158-161
19272193-10	2009	CONCLUSION: The results presented in this report indicate that the mechanism of genistein-mediated inhibition of GAG synthesis operates through epidermal growth factor (EGF)-dependent pathway.	Glycosaminoglycans	113-116	epidermal growth factor	Homo sapiens	144-167
19272193-7	2009	RESULTS: Effects of genistein on inhibition of GAG synthesis and accumulation in fibroblasts from patients suffering from various MPS types were abolished in the presence of an excess of EGF, and were partially reversed by an increased concentration of genistein.	Glycosaminoglycans	47-50	epidermal growth factor	Homo sapiens	187-190
19272193-10	2009	CONCLUSION: The results presented in this report indicate that the mechanism of genistein-mediated inhibition of GAG synthesis operates through epidermal growth factor (EGF)-dependent pathway.	Glycosaminoglycans	113-116	epidermal growth factor	Homo sapiens	169-172
19275580-7	2009	Interestingly, Vpr is also considered as a passenger protein in the virus particles as it is incorporated into the virus particles through interaction with Gag.	Glycosaminoglycans	156-159	Vpr	Human immunodeficiency virus 1	15-18
19001053-0	2009	Modulation of xylosyltransferase I expression provides a mechanism regulating glycosaminoglycan chain synthesis during cartilage destruction and repair.	Glycosaminoglycans	78-95	xylosyltransferase 1	Rattus norvegicus	14-34
19088176-5	2009	As compared with CD16(+) NK cells and non-NK cells, enriched peripheral blood CD16(-) NK cells bound preferably to immobilized glycosaminoglycans except for keratan sulfate.	Glycosaminoglycans	127-145	Fc gamma receptor IIIa	Homo sapiens	78-82
19019854-0	2009	Interaction of the coiled-coil domain with glycosaminoglycans protects angiopoietin-like 4 from proteolysis and regulates its antiangiogenic activity.	Glycosaminoglycans	43-61	angiopoietin like 4	Homo sapiens	71-90
19100717-1	2009	Human xylosyltransferases I and II (XylT-I, XylT-II) are key enzymes in glycosaminoglycan biosynthesis.	Glycosaminoglycans	72-89	xylosyltransferase 1	Homo sapiens	6-34
18454697-8	2009	The combination of the growth factors BMP-4 + TGF-beta 3 with the fibrochondrocyte coculture led to an increase in cell proliferation and GAG production compared to either treatment alone.	Glycosaminoglycans	138-141	bone morphogenetic protein 4	Homo sapiens	38-43
18454697-8	2009	The combination of the growth factors BMP-4 + TGF-beta 3 with the fibrochondrocyte coculture led to an increase in cell proliferation and GAG production compared to either treatment alone.	Glycosaminoglycans	138-141	transforming growth factor beta 3	Homo sapiens	46-56
19459409-5	2009	Peptide A was shown to inhibit Gag precursor p55 transport from the nuclei to the plasma membrane, the site of virus assembly.	Glycosaminoglycans	31-34	H3 histone pseudogene 44	Homo sapiens	45-48
19100717-1	2009	Human xylosyltransferases I and II (XylT-I, XylT-II) are key enzymes in glycosaminoglycan biosynthesis.	Glycosaminoglycans	72-89	xylosyltransferase 1	Homo sapiens	36-42
19100717-1	2009	Human xylosyltransferases I and II (XylT-I, XylT-II) are key enzymes in glycosaminoglycan biosynthesis.	Glycosaminoglycans	72-89	xylosyltransferase 2	Homo sapiens	44-51
19040351-4	2009	When biotin-HK is incubated with rabbit aorta endothelial cells (RAECs) and CHO-K1 cells, it is internalized into acidic intracellular vesicles, whereas when incubated with CHO-745 cells, which express reduced levels of glycosaminoglycans, HK is not internalized.	Glycosaminoglycans	220-238	kininogen 1	Homo sapiens	12-14
19180510-5	2009	RESULTS: IL-1beta and OSM decreased tissue glycosaminoglycan (GAG) content by approximately 20% over 48 hours and decreased E(Y) to a similar extent (11-17%), but TGFbeta did not alter GAG content or E(Y).	Glycosaminoglycans	43-60	interleukin 1 beta	Bos taurus	9-17
19180510-5	2009	RESULTS: IL-1beta and OSM decreased tissue glycosaminoglycan (GAG) content by approximately 20% over 48 hours and decreased E(Y) to a similar extent (11-17%), but TGFbeta did not alter GAG content or E(Y).	Glycosaminoglycans	62-65	interleukin 1 beta	Bos taurus	9-17
19180510-5	2009	RESULTS: IL-1beta and OSM decreased tissue glycosaminoglycan (GAG) content by approximately 20% over 48 hours and decreased E(Y) to a similar extent (11-17%), but TGFbeta did not alter GAG content or E(Y).	Glycosaminoglycans	185-188	interleukin 1 beta	Bos taurus	9-17
18980779-5	2009	TGF-beta1 was found to increase collagen and GAG deposition in the scaffolds 15-fold and 8-fold, respectively, in Phase I.	Glycosaminoglycans	45-48	transforming growth factor beta 1	Homo sapiens	0-9
18980779-6	2009	In Phase II, the combination of TGF-beta1 and 10 MPa, 0 Hz HP resulted in 4-fold higher collagen deposition (additive increase), 3-fold higher GAG deposition and enhanced compressive properties (additive and synergistic increases), when compared to the unpressurized no growth factor culture control.	Glycosaminoglycans	143-146	transforming growth factor beta 1	Homo sapiens	32-41
18948258-4	2009	We show that glycosaminoglycans (GAGs) are the high affinity (83 nm) joint receptors for GPI.	Glycosaminoglycans	13-31	glucose-6-phosphate isomerase 1	Mus musculus	89-92
19179976-5	2009	2) Novel OA functional motifs were predicted, including N-Arg dibasic convertase cleavage site, NEC1/NEC2 cleavage site, peptide C-terminal amidation, glycosaminoglycan attachment site, and generic motif for N-glycosylation, and substrate recognition sites that interact with different cytosolic proteins, including cyclin, MAPK, Class III PDZ domains, GSK3, phosphorylase kinase, tyrosine-based sorting signal, and internalization signal.	Glycosaminoglycans	151-168	glycoprotein nmb	Rattus norvegicus	9-11
19038309-5	2009	Our results showed that the GAG deletion was identified in 7 EOPTD patients, which results in Glu302del of DYT1 gene.	Glycosaminoglycans	28-31	torsin family 1 member A	Homo sapiens	107-111
18948258-7	2009	We also identified several inhibitors that inhibit both GPI/GAG interaction and GPI enzymatic activities, which suggests that the GPI GAG-binding domain overlaps with the active site of GPI enzyme.	Glycosaminoglycans	60-63	glucose-6-phosphate isomerase 1	Mus musculus	56-59
18948258-7	2009	We also identified several inhibitors that inhibit both GPI/GAG interaction and GPI enzymatic activities, which suggests that the GPI GAG-binding domain overlaps with the active site of GPI enzyme.	Glycosaminoglycans	134-137	glucose-6-phosphate isomerase 1	Mus musculus	56-59
18948258-7	2009	We also identified several inhibitors that inhibit both GPI/GAG interaction and GPI enzymatic activities, which suggests that the GPI GAG-binding domain overlaps with the active site of GPI enzyme.	Glycosaminoglycans	134-137	glucose-6-phosphate isomerase 1	Mus musculus	80-83
18948258-7	2009	We also identified several inhibitors that inhibit both GPI/GAG interaction and GPI enzymatic activities, which suggests that the GPI GAG-binding domain overlaps with the active site of GPI enzyme.	Glycosaminoglycans	134-137	glucose-6-phosphate isomerase 1	Mus musculus	80-83
18948258-7	2009	We also identified several inhibitors that inhibit both GPI/GAG interaction and GPI enzymatic activities, which suggests that the GPI GAG-binding domain overlaps with the active site of GPI enzyme.	Glycosaminoglycans	134-137	glucose-6-phosphate isomerase 1	Mus musculus	80-83
19847325-4	2009	In RA and ReA patients, GR activity in synovial fluid correlates negatively with the concentrations of collagen and degradation products of sulfated glycosaminoglycans.	Glycosaminoglycans	149-167	glutathione-disulfide reductase	Homo sapiens	24-26
19118259-5	2009	Glycosaminoglycan production in the constructs approached that of native values under the influence of hypoxia and under the influence of insulin.	Glycosaminoglycans	0-17	insulin	Homo sapiens	138-145
19847325-5	2009	In OA patients the activity of GR was significantly lower than in RA and ReA, which positively correlated with the concentration of collagen and showed a tendency for positive correlation with the degradation products of sulfated glycosaminoglycans.	Glycosaminoglycans	230-248	glutathione-disulfide reductase	Homo sapiens	31-33
18534197-2	2009	In particular, bovine lactoferrin (bLf) has been found to prevent viral infection by binding to heparan sulphate (HS) glycosaminoglycans (GAGs) that in turn can act as cell receptors for human herpetic viruses.	Glycosaminoglycans	138-142	lactotransferrin	Bos taurus	22-33
19778432-5	2009	RESULTS: TNFalpha induced release of GAG as well as production of NO in a dose-dependent manner, while sulfate incorporation was decreased.	Glycosaminoglycans	37-40	tumor necrosis factor	Bos taurus	9-17
19778432-9	2009	Tissue inhibitor of metalloproteinases (TIMP)-3, but not TIMP-1 or -2 inhibited TNFalpha-dependent GAG release and NITEGE production, whereas inhibition of TNFalpha-dependent NO generation with the NO-synthetase inhibitor L-NMMA failed to inhibit GAG release and NITEGE production.	Glycosaminoglycans	99-102	TIMP metallopeptidase inhibitor 3	Bos taurus	0-47
19778432-9	2009	Tissue inhibitor of metalloproteinases (TIMP)-3, but not TIMP-1 or -2 inhibited TNFalpha-dependent GAG release and NITEGE production, whereas inhibition of TNFalpha-dependent NO generation with the NO-synthetase inhibitor L-NMMA failed to inhibit GAG release and NITEGE production.	Glycosaminoglycans	99-102	tumor necrosis factor	Bos taurus	80-88
19778432-9	2009	Tissue inhibitor of metalloproteinases (TIMP)-3, but not TIMP-1 or -2 inhibited TNFalpha-dependent GAG release and NITEGE production, whereas inhibition of TNFalpha-dependent NO generation with the NO-synthetase inhibitor L-NMMA failed to inhibit GAG release and NITEGE production.	Glycosaminoglycans	247-250	TIMP metallopeptidase inhibitor 3	Bos taurus	0-47
19778432-9	2009	Tissue inhibitor of metalloproteinases (TIMP)-3, but not TIMP-1 or -2 inhibited TNFalpha-dependent GAG release and NITEGE production, whereas inhibition of TNFalpha-dependent NO generation with the NO-synthetase inhibitor L-NMMA failed to inhibit GAG release and NITEGE production.	Glycosaminoglycans	247-250	tumor necrosis factor	Bos taurus	156-164
19799789-7	2009	BMP-4 and BMP-2 genes were equipotent inducers of chondrogenesis in primary MSCs as judged by lacuna formation, strong staining for proteoglycans and collagen type II, increased levels of GAG synthesis, and expression of mRNAs associated with the chondrocyte phenotype.	Glycosaminoglycans	188-191	bone morphogenetic protein 4	Homo sapiens	0-5
19799789-7	2009	BMP-4 and BMP-2 genes were equipotent inducers of chondrogenesis in primary MSCs as judged by lacuna formation, strong staining for proteoglycans and collagen type II, increased levels of GAG synthesis, and expression of mRNAs associated with the chondrocyte phenotype.	Glycosaminoglycans	188-191	bone morphogenetic protein 2	Homo sapiens	10-15
20111627-0	2009	Immunoneutralization of TGFbeta1 Improves Skeletal Muscle Regeneration: Effects on Myoblast Differentiation and Glycosaminoglycan Content.	Glycosaminoglycans	112-129	transforming growth factor, beta 1	Rattus norvegicus	24-32
19826902-4	2009	Initial deletion studies carried out on Pr55(GAG) showed that a 35-amino-acid region of the protein bridging the MA(p17)-CA(p24) junction was essential for its ability to interact with Vif.	Glycosaminoglycans	45-48	Vif	Human immunodeficiency virus 1	185-188
19319847-1	2009	Serglycin (SG), like all other proteoglycans, consists of a protein "core" to which sulfated and thereby negatively charged polysaccharide chains of glycosaminoglycan type are attached.	Glycosaminoglycans	149-166	serglycin	Mus musculus	0-9
19319847-1	2009	Serglycin (SG), like all other proteoglycans, consists of a protein "core" to which sulfated and thereby negatively charged polysaccharide chains of glycosaminoglycan type are attached.	Glycosaminoglycans	149-166	serglycin	Mus musculus	11-13
18698130-7	2009	The NH(2)-terminal fragment of DMP1 occurs as a proteoglycan form (DMP1-PG) that contains a glycosaminoglycan (GAG) chain.	Glycosaminoglycans	92-109	dentin matrix protein 1	Mus musculus	31-35
18698130-7	2009	The NH(2)-terminal fragment of DMP1 occurs as a proteoglycan form (DMP1-PG) that contains a glycosaminoglycan (GAG) chain.	Glycosaminoglycans	92-109	dentin matrix protein 1	Mus musculus	67-71
18698130-7	2009	The NH(2)-terminal fragment of DMP1 occurs as a proteoglycan form (DMP1-PG) that contains a glycosaminoglycan (GAG) chain.	Glycosaminoglycans	111-114	dentin matrix protein 1	Mus musculus	31-35
18698130-7	2009	The NH(2)-terminal fragment of DMP1 occurs as a proteoglycan form (DMP1-PG) that contains a glycosaminoglycan (GAG) chain.	Glycosaminoglycans	111-114	dentin matrix protein 1	Mus musculus	67-71
18698130-8	2009	Previously, we showed that a GAG chain is linked to Ser(74) in rat DMP1 (Ser(89) in mouse DMP1).	Glycosaminoglycans	29-32	dentin matrix acidic phosphoprotein 1	Rattus norvegicus	67-71
18698130-8	2009	Previously, we showed that a GAG chain is linked to Ser(74) in rat DMP1 (Ser(89) in mouse DMP1).	Glycosaminoglycans	29-32	dentin matrix protein 1	Mus musculus	90-94
18698130-9	2009	To confirm that mouse DMP1-PG possesses a single GAG chain attached to Ser(89), we substituted Ser(89) by Gly(89).	Glycosaminoglycans	49-52	dentin matrix protein 1	Mus musculus	22-26
18698130-10	2009	Data from transfection analysis indicated that this substitution completely prevented formation of the GAG-containing form, confirming that DMP1-PG contains a single GAG chain attached to Ser(89) in mouse DMP1.	Glycosaminoglycans	103-106	dentin matrix protein 1	Mus musculus	140-144
18698130-10	2009	Data from transfection analysis indicated that this substitution completely prevented formation of the GAG-containing form, confirming that DMP1-PG contains a single GAG chain attached to Ser(89) in mouse DMP1.	Glycosaminoglycans	103-106	dentin matrix protein 1	Mus musculus	205-209
18698130-10	2009	Data from transfection analysis indicated that this substitution completely prevented formation of the GAG-containing form, confirming that DMP1-PG contains a single GAG chain attached to Ser(89) in mouse DMP1.	Glycosaminoglycans	166-169	dentin matrix protein 1	Mus musculus	140-144
20111627-2	2009	As TGFbeta1, whose activity can be controlled by glycosaminoglycans (GAG), plays a major role in fibrosis, we hypothesized that levels of TGFbeta1 and GAG contents could account for this differential quality of regeneration.	Glycosaminoglycans	49-67	transforming growth factor, beta 1	Rattus norvegicus	3-11
20111627-2	2009	As TGFbeta1, whose activity can be controlled by glycosaminoglycans (GAG), plays a major role in fibrosis, we hypothesized that levels of TGFbeta1 and GAG contents could account for this differential quality of regeneration.	Glycosaminoglycans	69-72	transforming growth factor, beta 1	Rattus norvegicus	3-11
20111627-2	2009	As TGFbeta1, whose activity can be controlled by glycosaminoglycans (GAG), plays a major role in fibrosis, we hypothesized that levels of TGFbeta1 and GAG contents could account for this differential quality of regeneration.	Glycosaminoglycans	69-72	transforming growth factor, beta 1	Rattus norvegicus	138-146
20111627-6	2009	These results indicate that the control of TGFbeta1 activity is important to improve regeneration of injured muscle and accelerate myoblast differentiation, in part through changes in GAG composition of muscle cell environment.	Glycosaminoglycans	184-187	transforming growth factor, beta 1	Rattus norvegicus	43-51
19480914-8	2009	Our results show that the lymphotactin structural rearrangement occurs at a rate of approximately 1/s and that mutation of residues required for glycosaminoglycan binding shifts the conformational equilibrium toward the chemokine-like fold.	Glycosaminoglycans	145-162	X-C motif chemokine ligand 1	Homo sapiens	26-38
19183832-5	2009	The bile duct cancer revealed a well-differentiated adenocarcinoma without mutation of the K-ras gene and with p53 miss-sense mutation of GTG (Val) to GAG (Glu) on codon 272 in exon 8.	Glycosaminoglycans	151-154	tumor protein p53	Homo sapiens	111-114
19053244-3	2008	Here, we report the use of a bacterial reverse two-hybrid system to identify cyclic peptides that interfere with the Gag-TSG101 interaction and the finding that a five amino acid peptide discovered by this approach can disrupt the interaction and consequently inhibit HIV egress.	Glycosaminoglycans	117-120	tumor susceptibility 101	Homo sapiens	121-127
18946087-7	2009	Dlg1 knockdown is also associated with the redistribution and colocalization of Gag and Env toward CD63 and CD82 positive vesicle-like structures, including structures that seem to still be connected to the plasma membrane.	Glycosaminoglycans	80-83	discs large MAGUK scaffold protein 1	Homo sapiens	0-4
19020825-5	2009	The viral envelope (Env) glycoproteins associate with Gag during the assembly process.	Glycosaminoglycans	54-57	endogenous retrovirus group K member 20	Homo sapiens	20-23
18571441-7	2009	RESULTS: In phase I, BMP-2 and IGF-I treatment resulted in significant, &gt;1-fold increases in aggregate modulus, accompanied by increases in GAG production.	Glycosaminoglycans	143-146	bone morphogenetic protein 2	Homo sapiens	21-26
18571441-7	2009	RESULTS: In phase I, BMP-2 and IGF-I treatment resulted in significant, &gt;1-fold increases in aggregate modulus, accompanied by increases in GAG production.	Glycosaminoglycans	143-146	insulin like growth factor 1	Homo sapiens	31-36
18571441-8	2009	Additionally, TGF-beta1 treatment resulted in significant, approximately 1-fold increases in both aggregate modulus and tensile modulus, with corresponding increases in GAG and collagen content.	Glycosaminoglycans	169-172	transforming growth factor beta 1	Homo sapiens	14-23
18571441-9	2009	In phase II, combined treatment with BMP-2 and IGF-I increased aggregate modulus and GAG content further than either growth factor alone, while TGF-beta1 treatment alone remained the only treatment to also enhance tensile properties and collagen content.	Glycosaminoglycans	85-88	bone morphogenetic protein 2	Homo sapiens	37-42
18571441-9	2009	In phase II, combined treatment with BMP-2 and IGF-I increased aggregate modulus and GAG content further than either growth factor alone, while TGF-beta1 treatment alone remained the only treatment to also enhance tensile properties and collagen content.	Glycosaminoglycans	85-88	insulin like growth factor 1	Homo sapiens	47-52
19352428-4	2009	Gag-specific IFN-gamma-producing CD4+ T cell responses were detected in 261/373 (70%) subjects, with the Gag responders having a significantly lower viral load and higher CD4 count than those with no detectable Gag response (p&lt;0.0001 for both parameters).	Glycosaminoglycans	0-3	interferon gamma	Homo sapiens	13-22
19352428-4	2009	Gag-specific IFN-gamma-producing CD4+ T cell responses were detected in 261/373 (70%) subjects, with the Gag responders having a significantly lower viral load and higher CD4 count than those with no detectable Gag response (p&lt;0.0001 for both parameters).	Glycosaminoglycans	0-3	CD4 molecule	Homo sapiens	33-36
19352428-4	2009	Gag-specific IFN-gamma-producing CD4+ T cell responses were detected in 261/373 (70%) subjects, with the Gag responders having a significantly lower viral load and higher CD4 count than those with no detectable Gag response (p&lt;0.0001 for both parameters).	Glycosaminoglycans	0-3	CD4 molecule	Homo sapiens	171-174
19352428-4	2009	Gag-specific IFN-gamma-producing CD4+ T cell responses were detected in 261/373 (70%) subjects, with the Gag responders having a significantly lower viral load and higher CD4 count than those with no detectable Gag response (p&lt;0.0001 for both parameters).	Glycosaminoglycans	105-108	interferon gamma	Homo sapiens	13-22
19352428-4	2009	Gag-specific IFN-gamma-producing CD4+ T cell responses were detected in 261/373 (70%) subjects, with the Gag responders having a significantly lower viral load and higher CD4 count than those with no detectable Gag response (p&lt;0.0001 for both parameters).	Glycosaminoglycans	105-108	CD4 molecule	Homo sapiens	171-174
19352428-4	2009	Gag-specific IFN-gamma-producing CD4+ T cell responses were detected in 261/373 (70%) subjects, with the Gag responders having a significantly lower viral load and higher CD4 count than those with no detectable Gag response (p&lt;0.0001 for both parameters).	Glycosaminoglycans	105-108	interferon gamma	Homo sapiens	13-22
19352428-4	2009	Gag-specific IFN-gamma-producing CD4+ T cell responses were detected in 261/373 (70%) subjects, with the Gag responders having a significantly lower viral load and higher CD4 count than those with no detectable Gag response (p&lt;0.0001 for both parameters).	Glycosaminoglycans	105-108	CD4 molecule	Homo sapiens	171-174
19352428-6	2009	The ELISPOT screening identified 33 CD4+ peptides targeted by 18/32 patients (56%), with 27 of the 33 peptides located in the Gag region.	Glycosaminoglycans	126-129	CD4 molecule	Homo sapiens	36-39
19352428-8	2009	CONCLUSIONS/SIGNIFICANCE: These data indicate that in chronic untreated clade C HIV-1 infection, IFN-gamma-secreting Gag-specific CD4+ T cell responses are immunodominant, directed at multiple distinct epitopes, and associated with viral control.	Glycosaminoglycans	117-120	interferon gamma	Homo sapiens	97-106
19352428-8	2009	CONCLUSIONS/SIGNIFICANCE: These data indicate that in chronic untreated clade C HIV-1 infection, IFN-gamma-secreting Gag-specific CD4+ T cell responses are immunodominant, directed at multiple distinct epitopes, and associated with viral control.	Glycosaminoglycans	117-120	CD4 molecule	Homo sapiens	130-133
19100702-2	2008	Using two-photon imaging of tumor-infiltrating T lymphocytes, we found that CD44, a receptor for extracellular matrix proteins and glycosaminoglycans, was crucial for interstitial T cell navigation and, consequently, efficient tumor cell screening.	Glycosaminoglycans	131-149	CD44 molecule (Indian blood group)	Homo sapiens	76-80
18760403-6	2008	Interestingly, bioclinical data analyses revealed significant correlation between GAG or ENV antigenemia (a protein causing dysimmune inflammatory effects) and C-reactive protein (CRP) levels (a systemic inflammation biomarker).	Glycosaminoglycans	82-85	C-reactive protein	Homo sapiens	160-178
18760403-6	2008	Interestingly, bioclinical data analyses revealed significant correlation between GAG or ENV antigenemia (a protein causing dysimmune inflammatory effects) and C-reactive protein (CRP) levels (a systemic inflammation biomarker).	Glycosaminoglycans	82-85	C-reactive protein	Homo sapiens	180-183
19053244-7	2008	Our findings, which suggest that interference with the TSG101-Gag interaction by cyclic peptides may be of practical use in the treatment of HIV infections, identify a specific cyclic peptide that reduces VLP release by this mechanism; they also demonstrate that the efficiency of interference with protein-protein interactions by cyclic peptides can be enhanced by tagging the peptides with translocation-promoting sequences.	Glycosaminoglycans	62-65	tumor susceptibility 101	Homo sapiens	55-61
18988796-2	2008	Another proteoglycan that may influence elastogenesis is biglycan, which possesses two GAG chains.	Glycosaminoglycans	87-90	biglycan	Rattus norvegicus	57-65
19068144-4	2008	We therefore analyzed the impact of platelet derived glycosaminoglycans on the immobilization of the chemokine CCL5 (RANTES) on human microvascular endothelial cells and their influence on CCL5-CCR5 interactions.	Glycosaminoglycans	53-71	C-C motif chemokine ligand 5	Homo sapiens	111-115
19068144-4	2008	We therefore analyzed the impact of platelet derived glycosaminoglycans on the immobilization of the chemokine CCL5 (RANTES) on human microvascular endothelial cells and their influence on CCL5-CCR5 interactions.	Glycosaminoglycans	53-71	C-C motif chemokine ligand 5	Homo sapiens	117-123
18820257-0	2008	TSG-6 transfers proteins between glycosaminoglycans via a Ser28-mediated covalent catalytic mechanism.	Glycosaminoglycans	33-51	TNF alpha induced protein 6	Homo sapiens	0-5
18820257-1	2008	Studies of the interaction between Bikunin proteins, tumor necrosis factor-stimulated gene-6 protein (TSG-6), and glycosaminoglycans have revealed a unique catalytic activity where TSG-6/heavy chain 2 transfer heavy chain subunits between glycosaminoglycan chains.	Glycosaminoglycans	114-132	alpha-1-microglobulin/bikunin precursor	Homo sapiens	35-42
18820257-1	2008	Studies of the interaction between Bikunin proteins, tumor necrosis factor-stimulated gene-6 protein (TSG-6), and glycosaminoglycans have revealed a unique catalytic activity where TSG-6/heavy chain 2 transfer heavy chain subunits between glycosaminoglycan chains.	Glycosaminoglycans	114-132	TNF alpha induced protein 6	Homo sapiens	53-100
18820257-1	2008	Studies of the interaction between Bikunin proteins, tumor necrosis factor-stimulated gene-6 protein (TSG-6), and glycosaminoglycans have revealed a unique catalytic activity where TSG-6/heavy chain 2 transfer heavy chain subunits between glycosaminoglycan chains.	Glycosaminoglycans	114-132	TNF alpha induced protein 6	Homo sapiens	102-107
18820257-1	2008	Studies of the interaction between Bikunin proteins, tumor necrosis factor-stimulated gene-6 protein (TSG-6), and glycosaminoglycans have revealed a unique catalytic activity where TSG-6/heavy chain 2 transfer heavy chain subunits between glycosaminoglycan chains.	Glycosaminoglycans	114-132	TNF alpha induced protein 6	Homo sapiens	181-186
18820257-1	2008	Studies of the interaction between Bikunin proteins, tumor necrosis factor-stimulated gene-6 protein (TSG-6), and glycosaminoglycans have revealed a unique catalytic activity where TSG-6/heavy chain 2 transfer heavy chain subunits between glycosaminoglycan chains.	Glycosaminoglycans	114-131	alpha-1-microglobulin/bikunin precursor	Homo sapiens	35-42
18820257-1	2008	Studies of the interaction between Bikunin proteins, tumor necrosis factor-stimulated gene-6 protein (TSG-6), and glycosaminoglycans have revealed a unique catalytic activity where TSG-6/heavy chain 2 transfer heavy chain subunits between glycosaminoglycan chains.	Glycosaminoglycans	114-131	TNF alpha induced protein 6	Homo sapiens	53-100
18820257-1	2008	Studies of the interaction between Bikunin proteins, tumor necrosis factor-stimulated gene-6 protein (TSG-6), and glycosaminoglycans have revealed a unique catalytic activity where TSG-6/heavy chain 2 transfer heavy chain subunits between glycosaminoglycan chains.	Glycosaminoglycans	114-131	TNF alpha induced protein 6	Homo sapiens	102-107
18820257-1	2008	Studies of the interaction between Bikunin proteins, tumor necrosis factor-stimulated gene-6 protein (TSG-6), and glycosaminoglycans have revealed a unique catalytic activity where TSG-6/heavy chain 2 transfer heavy chain subunits between glycosaminoglycan chains.	Glycosaminoglycans	114-131	TNF alpha induced protein 6	Homo sapiens	181-186
18988796-10	2008	These findings suggest that the GAG chains of biglycan serve as inhibitors of elastin synthesis and assembly, and that biglycan can act as an important modulator of the composition of the extracellular matrix of blood vessels.	Glycosaminoglycans	32-35	biglycan	Rattus norvegicus	46-54
18988796-10	2008	These findings suggest that the GAG chains of biglycan serve as inhibitors of elastin synthesis and assembly, and that biglycan can act as an important modulator of the composition of the extracellular matrix of blood vessels.	Glycosaminoglycans	32-35	elastin	Rattus norvegicus	78-85
18796646-3	2008	A major effect of the glycosaminoglycan binding may be on the quaternary structure of SDF-1, which has been controversially reported as a monomer or a dimer.	Glycosaminoglycans	22-39	C-X-C motif chemokine ligand 12	Homo sapiens	86-91
18717819-2	2008	A recent microarray assay notes that expression of the UDP-glucose dehydrogenase (UGDH) gene, participating in glycosaminoglycan synthesis, shows high correlation with LMP2A levels in NPC biopsies.	Glycosaminoglycans	111-128	UDP-glucose 6-dehydrogenase	Homo sapiens	55-80
18717819-2	2008	A recent microarray assay notes that expression of the UDP-glucose dehydrogenase (UGDH) gene, participating in glycosaminoglycan synthesis, shows high correlation with LMP2A levels in NPC biopsies.	Glycosaminoglycans	111-128	UDP-glucose 6-dehydrogenase	Homo sapiens	82-86
18717819-2	2008	A recent microarray assay notes that expression of the UDP-glucose dehydrogenase (UGDH) gene, participating in glycosaminoglycan synthesis, shows high correlation with LMP2A levels in NPC biopsies.	Glycosaminoglycans	111-128	LMP2A	Human gammaherpesvirus 4	168-173
18717819-3	2008	This study extends the finding and demonstrates that the UGDH transcript and protein quantities, the enzyme activity, and glycosaminoglycan contents increase in LMP2A overexpressed human embryonic kidney 293 (HEK293) cells.	Glycosaminoglycans	122-139	LMP2A	Human gammaherpesvirus 4	161-166
18812191-0	2008	Heparin-like glycosaminoglycans prevent the infection of measles virus in SLAM-negative cell lines.	Glycosaminoglycans	13-31	signaling lymphocytic activation molecule family member 1	Homo sapiens	74-78
18812191-7	2008	Taken together, our results suggest that HP-like glycosaminoglycans bind to the H protein of MV and play a key role in the infection of SLAM-negative cells.	Glycosaminoglycans	49-67	signaling lymphocytic activation molecule family member 1	Homo sapiens	136-140
18798279-1	2008	Heparanase is an endoglycosidase that specifically cleaves heparan sulfate side chains, a class of glycosaminoglycans abundantly present in the extracellular matrix and on the cell surface.	Glycosaminoglycans	99-117	heparanase	Homo sapiens	0-10
19179755-1	2008	The LHX3 gene encodes LIM homeodomain class transcription factors that have important roles to play in pituitary and nervous system development.On the one hand,mutations of LHX3 are associated with deficiencies of growth hormone (GH),prolactin (PRL),luteotrophic hormone (LH),follicle-stimulating hormone (FSH)and thyroid- stimulating hormone (TSH);on the other hand,mutations of LHX3 are also associated with combined pituitary hormone deficiency (CPHD) diseases in human and animal models.To date,few polymorphisms of the bovine LHX3 gene have been reported.In this study,polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP)and DNA sequencing methods were employed to screen the genetic variations within the bovine LHX3 gene in 802 Chinese indigenous cattle.The results revealed three novel single-nucleotide polymorphisms (SNPs): AY923832: g.7553G &gt;A, 7631C&gt;T and 7668C&gt;G.Among them,a synonymous mutation of exon II was identified: GAG ((Glu)&gt; GAA (Glu) at position 72 aa (AY923832:g.7553G&gt;A) of LHX3 ((403aa) in the four Chinese bovine breeds.Significant statistical differences in genotypic frequencies for exon II and its flanking region of the LHX3 gene implied that the polymorphic locus was significantly associated with cattle breeds by the X2-test (X2=68.975,df=6, P &lt;0.001).Hence,the three novel SNPs not only extend the spectrum of genetic variations of the bovine LHX3 gene, but could also possibly contribute to conducting association analysis and evaluating these as genetic markers in bovine breeding and genetics,and CPHD detection.	Glycosaminoglycans	969-972	LIM homeobox 3	Homo sapiens	4-8
18849196-2	2008	In a previous report, we demonstrated that recombinant BCG (rBCG) expressing the full-length gag gene of simian immunodeficiency virus (SIV) (rBCG-SIVgag) induced Gag-specific delayed-type hypersensitivity, T cell proliferation, gamma interferon (IFN gamma), and serum IgG responses in guinea pigs immunized intradermally (i.d.)	Glycosaminoglycans	93-96	interferon gamma	Homo sapiens	247-256
18849196-2	2008	In a previous report, we demonstrated that recombinant BCG (rBCG) expressing the full-length gag gene of simian immunodeficiency virus (SIV) (rBCG-SIVgag) induced Gag-specific delayed-type hypersensitivity, T cell proliferation, gamma interferon (IFN gamma), and serum IgG responses in guinea pigs immunized intradermally (i.d.)	Glycosaminoglycans	163-166	interferon gamma	Homo sapiens	247-256
18849196-6	2008	To learn this, we examined Gag-specific IgG production in sera and Gag-specific IFN gamma mRNA expression in peripheral blood mononuclear cells (PBMC) in guinea pigs vaccinated with rBCG-SIVgag i.d.	Glycosaminoglycans	67-70	interferon gamma	Homo sapiens	80-89
18849196-10	2008	The enhancement of IFN gamma mRNA expression by in vitro restimulation with Gag antigen was also detected in PBMC from the two immunization groups throughout the 3-year observation period.	Glycosaminoglycans	76-79	interferon gamma	Homo sapiens	19-28
18849196-14	2008	and oral inoculations of rBCG-SIVgag elicit stable, strong, Gag-specific serum IgG production while exhibiting the different kinetics of Gag-specific IFN gamma responses between i.d.	Glycosaminoglycans	137-140	interferon gamma	Homo sapiens	150-159
18720384-8	2008	Fluorescence correlation spectroscopy method using fluoresceinamine-labeled GAG revealed that the oversulfated GAGs have a high affinity for BMP-4.	Glycosaminoglycans	76-79	bone morphogenetic protein 4	Mus musculus	141-146
18720384-8	2008	Fluorescence correlation spectroscopy method using fluoresceinamine-labeled GAG revealed that the oversulfated GAGs have a high affinity for BMP-4.	Glycosaminoglycans	111-115	bone morphogenetic protein 4	Mus musculus	141-146
19179755-1	2008	The LHX3 gene encodes LIM homeodomain class transcription factors that have important roles to play in pituitary and nervous system development.On the one hand,mutations of LHX3 are associated with deficiencies of growth hormone (GH),prolactin (PRL),luteotrophic hormone (LH),follicle-stimulating hormone (FSH)and thyroid- stimulating hormone (TSH);on the other hand,mutations of LHX3 are also associated with combined pituitary hormone deficiency (CPHD) diseases in human and animal models.To date,few polymorphisms of the bovine LHX3 gene have been reported.In this study,polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP)and DNA sequencing methods were employed to screen the genetic variations within the bovine LHX3 gene in 802 Chinese indigenous cattle.The results revealed three novel single-nucleotide polymorphisms (SNPs): AY923832: g.7553G &gt;A, 7631C&gt;T and 7668C&gt;G.Among them,a synonymous mutation of exon II was identified: GAG ((Glu)&gt; GAA (Glu) at position 72 aa (AY923832:g.7553G&gt;A) of LHX3 ((403aa) in the four Chinese bovine breeds.Significant statistical differences in genotypic frequencies for exon II and its flanking region of the LHX3 gene implied that the polymorphic locus was significantly associated with cattle breeds by the X2-test (X2=68.975,df=6, P &lt;0.001).Hence,the three novel SNPs not only extend the spectrum of genetic variations of the bovine LHX3 gene, but could also possibly contribute to conducting association analysis and evaluating these as genetic markers in bovine breeding and genetics,and CPHD detection.	Glycosaminoglycans	969-972	LIM homeobox 3	Homo sapiens	173-177
19179755-1	2008	The LHX3 gene encodes LIM homeodomain class transcription factors that have important roles to play in pituitary and nervous system development.On the one hand,mutations of LHX3 are associated with deficiencies of growth hormone (GH),prolactin (PRL),luteotrophic hormone (LH),follicle-stimulating hormone (FSH)and thyroid- stimulating hormone (TSH);on the other hand,mutations of LHX3 are also associated with combined pituitary hormone deficiency (CPHD) diseases in human and animal models.To date,few polymorphisms of the bovine LHX3 gene have been reported.In this study,polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP)and DNA sequencing methods were employed to screen the genetic variations within the bovine LHX3 gene in 802 Chinese indigenous cattle.The results revealed three novel single-nucleotide polymorphisms (SNPs): AY923832: g.7553G &gt;A, 7631C&gt;T and 7668C&gt;G.Among them,a synonymous mutation of exon II was identified: GAG ((Glu)&gt; GAA (Glu) at position 72 aa (AY923832:g.7553G&gt;A) of LHX3 ((403aa) in the four Chinese bovine breeds.Significant statistical differences in genotypic frequencies for exon II and its flanking region of the LHX3 gene implied that the polymorphic locus was significantly associated with cattle breeds by the X2-test (X2=68.975,df=6, P &lt;0.001).Hence,the three novel SNPs not only extend the spectrum of genetic variations of the bovine LHX3 gene, but could also possibly contribute to conducting association analysis and evaluating these as genetic markers in bovine breeding and genetics,and CPHD detection.	Glycosaminoglycans	969-972	LIM homeobox 3	Homo sapiens	173-177
19179755-1	2008	The LHX3 gene encodes LIM homeodomain class transcription factors that have important roles to play in pituitary and nervous system development.On the one hand,mutations of LHX3 are associated with deficiencies of growth hormone (GH),prolactin (PRL),luteotrophic hormone (LH),follicle-stimulating hormone (FSH)and thyroid- stimulating hormone (TSH);on the other hand,mutations of LHX3 are also associated with combined pituitary hormone deficiency (CPHD) diseases in human and animal models.To date,few polymorphisms of the bovine LHX3 gene have been reported.In this study,polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP)and DNA sequencing methods were employed to screen the genetic variations within the bovine LHX3 gene in 802 Chinese indigenous cattle.The results revealed three novel single-nucleotide polymorphisms (SNPs): AY923832: g.7553G &gt;A, 7631C&gt;T and 7668C&gt;G.Among them,a synonymous mutation of exon II was identified: GAG ((Glu)&gt; GAA (Glu) at position 72 aa (AY923832:g.7553G&gt;A) of LHX3 ((403aa) in the four Chinese bovine breeds.Significant statistical differences in genotypic frequencies for exon II and its flanking region of the LHX3 gene implied that the polymorphic locus was significantly associated with cattle breeds by the X2-test (X2=68.975,df=6, P &lt;0.001).Hence,the three novel SNPs not only extend the spectrum of genetic variations of the bovine LHX3 gene, but could also possibly contribute to conducting association analysis and evaluating these as genetic markers in bovine breeding and genetics,and CPHD detection.	Glycosaminoglycans	969-972	LIM homeobox 3	Bos taurus	173-177
19179755-1	2008	The LHX3 gene encodes LIM homeodomain class transcription factors that have important roles to play in pituitary and nervous system development.On the one hand,mutations of LHX3 are associated with deficiencies of growth hormone (GH),prolactin (PRL),luteotrophic hormone (LH),follicle-stimulating hormone (FSH)and thyroid- stimulating hormone (TSH);on the other hand,mutations of LHX3 are also associated with combined pituitary hormone deficiency (CPHD) diseases in human and animal models.To date,few polymorphisms of the bovine LHX3 gene have been reported.In this study,polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP)and DNA sequencing methods were employed to screen the genetic variations within the bovine LHX3 gene in 802 Chinese indigenous cattle.The results revealed three novel single-nucleotide polymorphisms (SNPs): AY923832: g.7553G &gt;A, 7631C&gt;T and 7668C&gt;G.Among them,a synonymous mutation of exon II was identified: GAG ((Glu)&gt; GAA (Glu) at position 72 aa (AY923832:g.7553G&gt;A) of LHX3 ((403aa) in the four Chinese bovine breeds.Significant statistical differences in genotypic frequencies for exon II and its flanking region of the LHX3 gene implied that the polymorphic locus was significantly associated with cattle breeds by the X2-test (X2=68.975,df=6, P &lt;0.001).Hence,the three novel SNPs not only extend the spectrum of genetic variations of the bovine LHX3 gene, but could also possibly contribute to conducting association analysis and evaluating these as genetic markers in bovine breeding and genetics,and CPHD detection.	Glycosaminoglycans	969-972	LIM homeobox 3	Bos taurus	173-177
19179755-1	2008	The LHX3 gene encodes LIM homeodomain class transcription factors that have important roles to play in pituitary and nervous system development.On the one hand,mutations of LHX3 are associated with deficiencies of growth hormone (GH),prolactin (PRL),luteotrophic hormone (LH),follicle-stimulating hormone (FSH)and thyroid- stimulating hormone (TSH);on the other hand,mutations of LHX3 are also associated with combined pituitary hormone deficiency (CPHD) diseases in human and animal models.To date,few polymorphisms of the bovine LHX3 gene have been reported.In this study,polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP)and DNA sequencing methods were employed to screen the genetic variations within the bovine LHX3 gene in 802 Chinese indigenous cattle.The results revealed three novel single-nucleotide polymorphisms (SNPs): AY923832: g.7553G &gt;A, 7631C&gt;T and 7668C&gt;G.Among them,a synonymous mutation of exon II was identified: GAG ((Glu)&gt; GAA (Glu) at position 72 aa (AY923832:g.7553G&gt;A) of LHX3 ((403aa) in the four Chinese bovine breeds.Significant statistical differences in genotypic frequencies for exon II and its flanking region of the LHX3 gene implied that the polymorphic locus was significantly associated with cattle breeds by the X2-test (X2=68.975,df=6, P &lt;0.001).Hence,the three novel SNPs not only extend the spectrum of genetic variations of the bovine LHX3 gene, but could also possibly contribute to conducting association analysis and evaluating these as genetic markers in bovine breeding and genetics,and CPHD detection.	Glycosaminoglycans	969-972	LIM homeobox 3	Bos taurus	173-177
19179755-1	2008	The LHX3 gene encodes LIM homeodomain class transcription factors that have important roles to play in pituitary and nervous system development.On the one hand,mutations of LHX3 are associated with deficiencies of growth hormone (GH),prolactin (PRL),luteotrophic hormone (LH),follicle-stimulating hormone (FSH)and thyroid- stimulating hormone (TSH);on the other hand,mutations of LHX3 are also associated with combined pituitary hormone deficiency (CPHD) diseases in human and animal models.To date,few polymorphisms of the bovine LHX3 gene have been reported.In this study,polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP)and DNA sequencing methods were employed to screen the genetic variations within the bovine LHX3 gene in 802 Chinese indigenous cattle.The results revealed three novel single-nucleotide polymorphisms (SNPs): AY923832: g.7553G &gt;A, 7631C&gt;T and 7668C&gt;G.Among them,a synonymous mutation of exon II was identified: GAG ((Glu)&gt; GAA (Glu) at position 72 aa (AY923832:g.7553G&gt;A) of LHX3 ((403aa) in the four Chinese bovine breeds.Significant statistical differences in genotypic frequencies for exon II and its flanking region of the LHX3 gene implied that the polymorphic locus was significantly associated with cattle breeds by the X2-test (X2=68.975,df=6, P &lt;0.001).Hence,the three novel SNPs not only extend the spectrum of genetic variations of the bovine LHX3 gene, but could also possibly contribute to conducting association analysis and evaluating these as genetic markers in bovine breeding and genetics,and CPHD detection.	Glycosaminoglycans	969-972	LIM homeobox 3	Bos taurus	173-177
19179755-1	2008	The LHX3 gene encodes LIM homeodomain class transcription factors that have important roles to play in pituitary and nervous system development.On the one hand,mutations of LHX3 are associated with deficiencies of growth hormone (GH),prolactin (PRL),luteotrophic hormone (LH),follicle-stimulating hormone (FSH)and thyroid- stimulating hormone (TSH);on the other hand,mutations of LHX3 are also associated with combined pituitary hormone deficiency (CPHD) diseases in human and animal models.To date,few polymorphisms of the bovine LHX3 gene have been reported.In this study,polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP)and DNA sequencing methods were employed to screen the genetic variations within the bovine LHX3 gene in 802 Chinese indigenous cattle.The results revealed three novel single-nucleotide polymorphisms (SNPs): AY923832: g.7553G &gt;A, 7631C&gt;T and 7668C&gt;G.Among them,a synonymous mutation of exon II was identified: GAG ((Glu)&gt; GAA (Glu) at position 72 aa (AY923832:g.7553G&gt;A) of LHX3 ((403aa) in the four Chinese bovine breeds.Significant statistical differences in genotypic frequencies for exon II and its flanking region of the LHX3 gene implied that the polymorphic locus was significantly associated with cattle breeds by the X2-test (X2=68.975,df=6, P &lt;0.001).Hence,the three novel SNPs not only extend the spectrum of genetic variations of the bovine LHX3 gene, but could also possibly contribute to conducting association analysis and evaluating these as genetic markers in bovine breeding and genetics,and CPHD detection.	Glycosaminoglycans	969-972	LIM homeobox 3	Bos taurus	173-177
18805795-4	2008	We show that PEDF coprecipitation with glycosaminoglycans in media conditioned by human retinoblastoma Y-79 cells decreased after pretreatments with hyaluronidase, implying an association between HA and PEDF.	Glycosaminoglycans	39-57	serpin family F member 1	Homo sapiens	13-17
18497712-3	2008	In rat venules stimulated with proinflammatory substances ex vivo, the GAG-containing proteoglycan, syndecan-1, is shed from the endothelium.	Glycosaminoglycans	71-74	syndecan 1	Rattus norvegicus	100-110
19244744-2	2008	Recent research of TSG101 has revealed that TSG101 aids HIV-1 budding from infected cells by attaching to Gag.	Glycosaminoglycans	106-109	tumor susceptibility 101	Homo sapiens	19-25
19244744-2	2008	Recent research of TSG101 has revealed that TSG101 aids HIV-1 budding from infected cells by attaching to Gag.	Glycosaminoglycans	106-109	tumor susceptibility 101	Homo sapiens	44-50
18788910-4	2008	Production of MIP-1beta, IL-2, TNF-alpha, and CD107 expression by CD8(+) T cells in response to Gag and Nef optimal peptide pools was analyzed using polychromatic flow cytometry in nine HIV-infected individuals followed for 12 months after discontinuation of antiretroviral therapy.	Glycosaminoglycans	96-99	C-C motif chemokine ligand 4	Homo sapiens	14-23
18975307-8	2008	RESULTS: IL-1alpha caused cleavage of aggrecan in cultured human articular cartilage explants, with release of GAG and aggrecan fragments containing ARGS and AGEG neoepitopes.	Glycosaminoglycans	111-114	interleukin 1 alpha	Homo sapiens	9-18
18786170-7	2008	Thus, these glycosaminoglycans bind to SPACR in a different manner than to sialoproteoglycan associated with cones and rods.	Glycosaminoglycans	12-30	interphotoreceptor matrix proteoglycan 1	Homo sapiens	39-44
18715646-9	2008	Taken together these results reinforce the case for the occupation of some of the seven arms of C4BP in a multivalent interaction with DNA or surface bound glycosaminoglycans while other arms engage C4b or C3b.	Glycosaminoglycans	156-174	complement component 4 binding protein alpha	Homo sapiens	96-100
18826339-5	2008	After 3 weeks, the histological and biochemical analysis of the CMP/PEODA gel revealed twice as much glycosaminoglycan and collagen contents as in control PEODA hydrogels.	Glycosaminoglycans	101-118	matrilin 1	Homo sapiens	64-73
18765417-2	2008	The formation of GAG-side chains (glycosylation) is catalysed by xylosyltransferase-1 (XT-1).	Glycosaminoglycans	17-20	xylosyltransferase 1	Rattus norvegicus	65-85
18765417-2	2008	The formation of GAG-side chains (glycosylation) is catalysed by xylosyltransferase-1 (XT-1).	Glycosaminoglycans	17-20	xylosyltransferase 1	Rattus norvegicus	87-91
18765417-4	2008	A continuous 2-week delivery of DNAXTas near the rostral border of a peripheral nerve graft bridging the transected dorsal columns in the thoracic spinal cord resulted in an 81% decrease in XT-1 mRNA, an average of 1.4-fold reduction in GAG-side chains of chondroitin sulphate or heparan sulphate-PGs and 2.2-fold reduction in neurocan and brevican core proteins in scar tissue.	Glycosaminoglycans	237-240	xylosyltransferase 1	Rattus norvegicus	190-194
18624285-5	2008	The presence of glycosaminoglycan chains was demonstrated for a subset of the core proteins (lumican, biglycan, and decorin) using lyase digestion.	Glycosaminoglycans	16-33	biglycan	Homo sapiens	102-110
18624285-5	2008	The presence of glycosaminoglycan chains was demonstrated for a subset of the core proteins (lumican, biglycan, and decorin) using lyase digestion.	Glycosaminoglycans	16-33	decorin	Homo sapiens	116-123
18684837-6	2008	Given its elevated transcriptional activity and the presence of a full-length Gag open reading frame, the 22q11.21 HML-2 provirus may also significantly contribute to Gag protein and thus particle production in Tera-1 cells.	Glycosaminoglycans	78-81	C-type lectin domain containing 10A	Homo sapiens	115-120
18684837-6	2008	Given its elevated transcriptional activity and the presence of a full-length Gag open reading frame, the 22q11.21 HML-2 provirus may also significantly contribute to Gag protein and thus particle production in Tera-1 cells.	Glycosaminoglycans	167-170	C-type lectin domain containing 10A	Homo sapiens	115-120
18479789-2	2008	The p24 Gag protein was selected for analysis, since previous studies of the same cohort of patients had shown that almost 80% of these individuals responded to Gag peptides of subtypes A, B and/or C. A large number of Gag antigen-specific responses were recorded.	Glycosaminoglycans	8-11	transmembrane p24 trafficking protein 2	Homo sapiens	4-7
18479789-2	2008	The p24 Gag protein was selected for analysis, since previous studies of the same cohort of patients had shown that almost 80% of these individuals responded to Gag peptides of subtypes A, B and/or C. A large number of Gag antigen-specific responses were recorded.	Glycosaminoglycans	161-164	transmembrane p24 trafficking protein 2	Homo sapiens	4-7
18479789-2	2008	The p24 Gag protein was selected for analysis, since previous studies of the same cohort of patients had shown that almost 80% of these individuals responded to Gag peptides of subtypes A, B and/or C. A large number of Gag antigen-specific responses were recorded.	Glycosaminoglycans	161-164	transmembrane p24 trafficking protein 2	Homo sapiens	4-7
19035406-5	2008	Biological GAG samples were exhaustively digested using lyase enzymes, the disaccharide products and standards were derivatized with the fluorophore 2-aminoacridone and subjected to reversed polarity CE-LIF detection.	Glycosaminoglycans	11-14	LIF interleukin 6 family cytokine	Homo sapiens	203-206
18959744-2	2008	PrP binds glycosaminoglycan (GAG) and divalent cations, such as Cu(2+) and Zn(2+).	Glycosaminoglycans	10-27	proline rich protein 2-like 1	Rattus norvegicus	0-3
18959744-2	2008	PrP binds glycosaminoglycan (GAG) and divalent cations, such as Cu(2+) and Zn(2+).	Glycosaminoglycans	29-32	proline rich protein 2-like 1	Rattus norvegicus	0-3
18959744-3	2008	Here, we report our findings that GAG and Cu(2+) promote the aggregation of recombinant human PrP (rPrP).	Glycosaminoglycans	34-37	prion protein	Homo sapiens	94-97
18959744-3	2008	Here, we report our findings that GAG and Cu(2+) promote the aggregation of recombinant human PrP (rPrP).	Glycosaminoglycans	34-37	proline rich protein 2-like 1	Rattus norvegicus	99-103
18959744-5	2008	In the presence of either GAG or Cu(2+), mutant rPrPs with eight or ten octapeptide repeats are more aggregation prone, exhibit faster kinetics and form larger aggregates than wild-type PrP.	Glycosaminoglycans	26-29	proline rich protein 2-like 1	Rattus norvegicus	49-52
18959744-9	2008	Furthermore, aggregation of rPrP in the presence of GAG is blocked with anti-PrP mAbs, whereas none of the tested anti-PrP mAbs block Cu(2+)-promoted aggregation.	Glycosaminoglycans	52-55	proline rich protein 2-like 1	Rattus norvegicus	28-32
18959744-9	2008	Furthermore, aggregation of rPrP in the presence of GAG is blocked with anti-PrP mAbs, whereas none of the tested anti-PrP mAbs block Cu(2+)-promoted aggregation.	Glycosaminoglycans	52-55	proline rich protein 2-like 1	Rattus norvegicus	29-32
18959744-9	2008	Furthermore, aggregation of rPrP in the presence of GAG is blocked with anti-PrP mAbs, whereas none of the tested anti-PrP mAbs block Cu(2+)-promoted aggregation.	Glycosaminoglycans	52-55	proline rich protein 2-like 1	Rattus norvegicus	77-80
18959744-11	2008	Therefore, although binding of either GAG or Cu(2+) promotes the aggregation of rPrP, their aggregation processes are different, suggesting multiple pathways of rPrP aggregation.	Glycosaminoglycans	38-41	proline rich protein 2-like 1	Rattus norvegicus	80-84
18959744-11	2008	Therefore, although binding of either GAG or Cu(2+) promotes the aggregation of rPrP, their aggregation processes are different, suggesting multiple pathways of rPrP aggregation.	Glycosaminoglycans	38-41	proline rich protein 2-like 1	Rattus norvegicus	161-165
19039992-1	2008	DYTI dystonia (DYT1-D, early-onset torsion dystonia) is caused by a GAG deletion in the DYTI gene.	Glycosaminoglycans	68-71	torsin family 1 member A	Homo sapiens	15-19
18788910-4	2008	Production of MIP-1beta, IL-2, TNF-alpha, and CD107 expression by CD8(+) T cells in response to Gag and Nef optimal peptide pools was analyzed using polychromatic flow cytometry in nine HIV-infected individuals followed for 12 months after discontinuation of antiretroviral therapy.	Glycosaminoglycans	96-99	CD8a molecule	Homo sapiens	66-69
18456345-2	2008	The anti-HSV mode of action of Lf and Lfcin is assumed to involve, in part, their interaction with the cell surface glycosaminoglycan heparan sulfate, thereby blocking of viral entry.	Glycosaminoglycans	116-133	lactotransferrin	Homo sapiens	38-43
18554504-6	2008	GAG contents also increased after PTHrP treatment.	Glycosaminoglycans	0-3	parathyroid hormone like hormone	Homo sapiens	34-39
18433381-1	2008	The transcription factor SOX9 (Sry-type high-mobility-group box 9) is expressed in all chondrocytes and is essential for the expression of aggrecan, which during biosynthesis is substituted with more than 10 times its weight of CS (chondroitin sulfate) and is secreted by chondrocytes to form the characteristic GAG (glycosaminoglycan)-rich ECM (extracellular matrix) of cartilage.	Glycosaminoglycans	312-315	SRY-box transcription factor 9	Homo sapiens	25-29
18433381-1	2008	The transcription factor SOX9 (Sry-type high-mobility-group box 9) is expressed in all chondrocytes and is essential for the expression of aggrecan, which during biosynthesis is substituted with more than 10 times its weight of CS (chondroitin sulfate) and is secreted by chondrocytes to form the characteristic GAG (glycosaminoglycan)-rich ECM (extracellular matrix) of cartilage.	Glycosaminoglycans	312-315	SRY-box transcription factor 9	Homo sapiens	31-65
18433381-1	2008	The transcription factor SOX9 (Sry-type high-mobility-group box 9) is expressed in all chondrocytes and is essential for the expression of aggrecan, which during biosynthesis is substituted with more than 10 times its weight of CS (chondroitin sulfate) and is secreted by chondrocytes to form the characteristic GAG (glycosaminoglycan)-rich ECM (extracellular matrix) of cartilage.	Glycosaminoglycans	317-334	SRY-box transcription factor 9	Homo sapiens	25-29
18433381-1	2008	The transcription factor SOX9 (Sry-type high-mobility-group box 9) is expressed in all chondrocytes and is essential for the expression of aggrecan, which during biosynthesis is substituted with more than 10 times its weight of CS (chondroitin sulfate) and is secreted by chondrocytes to form the characteristic GAG (glycosaminoglycan)-rich ECM (extracellular matrix) of cartilage.	Glycosaminoglycans	317-334	SRY-box transcription factor 9	Homo sapiens	31-65
18433381-4	2008	Retroviral SOX9 transduction of passaged chondrocytes increased the endogenous rate of GAG synthesis and the total capacity for GAG synthesis assessed in monolayer culture with beta-xyloside.	Glycosaminoglycans	87-90	SRY-box transcription factor 9	Homo sapiens	11-15
18433381-4	2008	Retroviral SOX9 transduction of passaged chondrocytes increased the endogenous rate of GAG synthesis and the total capacity for GAG synthesis assessed in monolayer culture with beta-xyloside.	Glycosaminoglycans	128-131	SRY-box transcription factor 9	Homo sapiens	11-15
18768520-1	2008	The glycosaminoglycan chondroitin sulfate is significantly increased in the peritumoral stroma of prostate tumors compared with normal stroma and is an independent predictor of prostate-specific antigen (PSA) relapse following radical prostatectomy.	Glycosaminoglycans	4-21	kallikrein related peptidase 3	Homo sapiens	177-208
18768520-2	2008	In this study, we determined whether specific alterations in the sulfation pattern of glycosaminoglycan chains in clinically organ-confined prostate cancer are associated with PSA relapse.	Glycosaminoglycans	86-103	kallikrein related peptidase 3	Homo sapiens	176-179
18549827-2	2008	A GAG-repeat polymorphism in the 5" UTR of the gene coding for the catalytic subunit of GCL (GCLC) has been associated with altered GSH levels in vitro.	Glycosaminoglycans	2-5	glutamate-cysteine ligase catalytic subunit	Homo sapiens	93-97
18461555-7	2008	Thus, results implicated CNP-3/NPR-B signaling in pre-chondrogenic mesenchymal condensation, glycosaminoglycan synthesis and late differentiation of chondrocytes in the process of endochondral ossification.	Glycosaminoglycans	93-110	C-type natriuretic peptide 3	Gallus gallus	25-30
18461555-7	2008	Thus, results implicated CNP-3/NPR-B signaling in pre-chondrogenic mesenchymal condensation, glycosaminoglycan synthesis and late differentiation of chondrocytes in the process of endochondral ossification.	Glycosaminoglycans	93-110	natriuretic peptide receptor 2	Homo sapiens	31-36
18710930-7	2008	In comparison with CXCL8(1-77), CXCL8(1-77)Cit(5) had reduced affinity for glycosaminoglycans and induced less CXCR2-dependent calcium signaling and extracellular signal-regulated kinase 1/2 phosphorylation.	Glycosaminoglycans	75-93	interleukin-8	Oryctolagus cuniculus	32-37
18562528-5	2008	We found that increased genital tumor necrosis factor alpha (TNF-alpha) and interleukin-10 (IL-10) levels correlated significantly with levels of Gag-specific CD8(+) T cells at the cervix.	Glycosaminoglycans	146-149	tumor necrosis factor	Homo sapiens	61-70
18613275-1	2008	BACKGROUND: Mucopolysaccharidosis I (MPS I) is a lysosomal storage disease due to alpha-L-iduronidase (IDUA) deficiency that results in the accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	156-174	iduronidase, alpha-L	Mus musculus	82-101
18613275-1	2008	BACKGROUND: Mucopolysaccharidosis I (MPS I) is a lysosomal storage disease due to alpha-L-iduronidase (IDUA) deficiency that results in the accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	156-174	iduronidase, alpha-L	Mus musculus	103-107
18613275-1	2008	BACKGROUND: Mucopolysaccharidosis I (MPS I) is a lysosomal storage disease due to alpha-L-iduronidase (IDUA) deficiency that results in the accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	176-179	iduronidase, alpha-L	Mus musculus	82-101
18613275-1	2008	BACKGROUND: Mucopolysaccharidosis I (MPS I) is a lysosomal storage disease due to alpha-L-iduronidase (IDUA) deficiency that results in the accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	176-179	iduronidase, alpha-L	Mus musculus	103-107
18282772-8	2008	Expression of a Matn1 or Matn3 cDNA maintained and further enhanced chondrogenesis of SFBs as shown by increased cartilaginous matrix areas, elevated amount of GAG, and stimulated expression of chondrogenic markers.	Glycosaminoglycans	160-163	matrilin 1	Homo sapiens	16-21
18282772-8	2008	Expression of a Matn1 or Matn3 cDNA maintained and further enhanced chondrogenesis of SFBs as shown by increased cartilaginous matrix areas, elevated amount of GAG, and stimulated expression of chondrogenic markers.	Glycosaminoglycans	160-163	matrilin 3	Homo sapiens	25-30
18499864-1	2008	The hyaluronic acid receptor for endocytosis (HARE)/ Stabilin-2 is the primary systemic scavenger receptor for hyaluronan (HA), the chondroitin sulfates (CS), dermatan sulfate (DS), and nonglycosaminoglycan (GAG) ligands such as acetylated low-density lipoprotein (AcLDL), pro-collagen propeptides, and advanced glycation end products.	Glycosaminoglycans	208-211	stabilin 2	Homo sapiens	46-50
18538941-1	2008	DYT1 dystonia is caused by a single GAG deletion in exon 5 of TOR1A, the gene encoding torsinA, a putative chaperone protein.	Glycosaminoglycans	36-39	torsin family 1, member A	Rattus norvegicus	0-4
18538941-1	2008	DYT1 dystonia is caused by a single GAG deletion in exon 5 of TOR1A, the gene encoding torsinA, a putative chaperone protein.	Glycosaminoglycans	36-39	torsin family 1, member A	Rattus norvegicus	62-67
18538941-1	2008	DYT1 dystonia is caused by a single GAG deletion in exon 5 of TOR1A, the gene encoding torsinA, a putative chaperone protein.	Glycosaminoglycans	36-39	torsin family 1, member A	Rattus norvegicus	87-94
18620491-3	2008	All 12 viruses conserved both an H87Q mutation in the cyclophilin A-binding site of Gag p24 (capsid) and a T23N mutation in the cysteine-rich domain of Tat protein.	Glycosaminoglycans	84-87	transmembrane p24 trafficking protein 2	Homo sapiens	88-91
18672964-6	2008	RESULTS: Treatment with FGF-2, dexamethasone, or both increased pellet collagen type II content, total glycosaminoglycan content, and mRNA expression of aggrecan.	Glycosaminoglycans	103-120	fibroblast growth factor 2	Equus caballus	24-29
18631141-4	2008	In addition, the IRES extends to the gag coding region for all these viruses and this leads to the synthesis of shorter isoforms of the Gag polyprotein from downstream initiation codons.	Glycosaminoglycans	37-40	Pr55(Gag)	Human immunodeficiency virus 1	136-139
18543353-9	2008	pex2 ZPEG239 showed a mutation in codon GAG for Glu(201) to a nonsense mutation, TAG.	Glycosaminoglycans	40-43	peroxisome biogenesis factor 2	Cricetulus griseus	0-4
18499864-1	2008	The hyaluronic acid receptor for endocytosis (HARE)/ Stabilin-2 is the primary systemic scavenger receptor for hyaluronan (HA), the chondroitin sulfates (CS), dermatan sulfate (DS), and nonglycosaminoglycan (GAG) ligands such as acetylated low-density lipoprotein (AcLDL), pro-collagen propeptides, and advanced glycation end products.	Glycosaminoglycans	208-211	stabilin 2	Homo sapiens	53-63
18547105-7	2008	We conclude that glycosaminoglycans in the extracellular matrix have the capacity to promote coacervation at low concentrations of tropoelastin.	Glycosaminoglycans	17-35	elastin	Homo sapiens	131-143
18411283-10	2008	First, the potential of CXCL11-(5-73) to compete active CXCL11 from glycosaminoglycans might lead to the formation of an antagonistic haptotactic chemokine gradient.	Glycosaminoglycans	68-86	C-X-C motif chemokine ligand 11	Homo sapiens	24-30
18411283-11	2008	Second, upon further truncation, MMPs disperse the CXCL11 gradients in a novel way by proteolytic loss of a COOH-terminal GAG binding site.	Glycosaminoglycans	122-125	matrix metallopeptidase 9	Homo sapiens	33-37
18411283-11	2008	Second, upon further truncation, MMPs disperse the CXCL11 gradients in a novel way by proteolytic loss of a COOH-terminal GAG binding site.	Glycosaminoglycans	122-125	C-X-C motif chemokine ligand 11	Homo sapiens	51-57
18601454-0	2008	P188 reduces cell death and IGF-I reduces GAG release following single-impact loading of articular cartilage.	Glycosaminoglycans	42-45	IGFI	Bos taurus	28-33
18601454-14	2008	The combination did not perform better than either individual treatment; however, following low impact at 1 week, P188 reduced cell death by 75% compared to no treatment and IGF-I decreased GAG release from the tissue by 49%.	Glycosaminoglycans	190-193	IGFI	Bos taurus	174-179
18524827-4	2008	The present study compared MV protein A27, which has a role in virus attachment to glycosaminoglycans on the cell surface, to L1 with respect to immunogenicity and protection.	Glycosaminoglycans	83-101	immunoglobulin kappa variable 3-20	Homo sapiens	38-41
18554245-2	2008	The HLA-B*3713 allele differs from the closest matching allele B*370101 by one nucleotide substitutions in exon 3 at nt 527(T--&gt;A), resulting in an amino acid change from Val (GTG) to Glu (GAG) at codon 152.	Glycosaminoglycans	192-195	major histocompatibility complex, class I, B	Homo sapiens	4-9
18554245-2	2008	The HLA-B*3713 allele differs from the closest matching allele B*370101 by one nucleotide substitutions in exon 3 at nt 527(T--&gt;A), resulting in an amino acid change from Val (GTG) to Glu (GAG) at codon 152.	Glycosaminoglycans	192-195	gamma-glutamyltransferase 1	Homo sapiens	179-182
18683151-7	2008	It had one nucleotide change from the closest matching allele B*460101 at nucleotide 527 (A to T) in exon 3, resulting in an amino acid change from E (GAG) to V (GTG) at codon 176.	Glycosaminoglycans	151-154	gamma-glutamyltransferase 1	Homo sapiens	162-165
18479957-6	2008	Elastin fragmentation and aortic dilatation are severe at 6 months, which is temporally associated with marked increases in mRNA and enzyme activity for two elastin-degrading proteins, matrix metalloproteinase-12 (MMP-12) and cathepsin S. Upregulation of these genes likely involves activation of STAT proteins, which may be induced by structural stress to smooth muscle cells from accumulation of glycosaminoglycans in lysosomes.	Glycosaminoglycans	398-416	elastin	Mus musculus	0-7
18580692-2	2008	It is caused by a deficiency in the lysosomal enzyme iduronate-2-sulfatase, and in affected patients glycosaminoglycan accumulates in lysosomes of various tissues and organs and contributes to the pathophysiology of Hunter syndrome.	Glycosaminoglycans	101-118	iduronate 2-sulfatase	Homo sapiens	53-74
18691535-5	2008	Total collagen and GAG content were detected at their highest levels in the hydrogel scaffold with TGF beta-3.	Glycosaminoglycans	19-22	transforming growth factor beta-3	Oryctolagus cuniculus	99-109
18509682-3	2008	Proteoglycans (PG) consisting of low and high sulfated glycosaminoglycans (GAG) are the main components of articular cartilage matrix, and their synthesis is increased by insulin in growth plate cartilage.	Glycosaminoglycans	55-73	insulin	Homo sapiens	171-178
18509682-3	2008	Proteoglycans (PG) consisting of low and high sulfated glycosaminoglycans (GAG) are the main components of articular cartilage matrix, and their synthesis is increased by insulin in growth plate cartilage.	Glycosaminoglycans	75-78	insulin	Homo sapiens	171-178
18479957-6	2008	Elastin fragmentation and aortic dilatation are severe at 6 months, which is temporally associated with marked increases in mRNA and enzyme activity for two elastin-degrading proteins, matrix metalloproteinase-12 (MMP-12) and cathepsin S. Upregulation of these genes likely involves activation of STAT proteins, which may be induced by structural stress to smooth muscle cells from accumulation of glycosaminoglycans in lysosomes.	Glycosaminoglycans	398-416	elastin	Mus musculus	157-164
18479957-6	2008	Elastin fragmentation and aortic dilatation are severe at 6 months, which is temporally associated with marked increases in mRNA and enzyme activity for two elastin-degrading proteins, matrix metalloproteinase-12 (MMP-12) and cathepsin S. Upregulation of these genes likely involves activation of STAT proteins, which may be induced by structural stress to smooth muscle cells from accumulation of glycosaminoglycans in lysosomes.	Glycosaminoglycans	398-416	matrix metallopeptidase 12	Mus musculus	185-212
18525269-1	2008	In the present study, we assessed whether Gag-specific interferon (IFN)-gamma secreting responses correlate with the rate of disease progression as defined by the annual rate of CD4 decline.	Glycosaminoglycans	42-45	CD4 molecule	Homo sapiens	178-181
18360285-4	2008	Host CCL3L1 copy number correlated negatively with viral load (r=-0.239, P=0.045), as did magnitudes of Gag CD4 (r=-0.362, P=0.002) and CD8 (r=-0.261, P=0.028) T-cell responses.	Glycosaminoglycans	104-107	CD4 molecule	Homo sapiens	108-111
18360285-6	2008	CCL3L1 copy number greater than or equal to the population median of 5 was significantly associated with increased magnitude of CD4 Gag responses (P=0.017), and women who had CD4 and CD8 Gag-specific responses had significantly lower viral loads (P=0.004) and higher CCL3L1 copy number (P=0.015) than those women with only CD8 Gag-specific responses.	Glycosaminoglycans	132-135	C-C motif chemokine ligand 3 like 1	Homo sapiens	0-6
18360285-6	2008	CCL3L1 copy number greater than or equal to the population median of 5 was significantly associated with increased magnitude of CD4 Gag responses (P=0.017), and women who had CD4 and CD8 Gag-specific responses had significantly lower viral loads (P=0.004) and higher CCL3L1 copy number (P=0.015) than those women with only CD8 Gag-specific responses.	Glycosaminoglycans	132-135	CD4 molecule	Homo sapiens	128-131
18579773-4	2008	Properdin binding was facilitated by the glycosaminoglycan chains of surface proteoglycans.	Glycosaminoglycans	41-58	complement factor properdin	Homo sapiens	0-9
18525269-2	2008	Although neither the breadth nor the magnitude of the proteome-wide HIV-specific IFN-gamma response correlated with viral load or rate of CD4 decline, the preferential targeting of Gag is associated with slower annual CD4 T cell decline.	Glycosaminoglycans	181-184	CD4 molecule	Homo sapiens	218-221
18523584-6	2008	In contrast when cells were transfected with DNA vectors requiring nuclear transcription and processing of gag mRNA, codon optimization resulted in a very large enhancement of Gag production.	Glycosaminoglycans	176-179	Pr55(Gag)	Human immunodeficiency virus 1	107-110
18523305-8	2008	The K3R/Q102N mutant of S100A11 retained the capacity to bind to RAGE and chondrocytes but lost the capacity to signal via the p38 MAPK pathway or induce chondrocyte hypertrophy and glycosaminoglycans release.	Glycosaminoglycans	182-200	S100 calcium binding protein A11	Mus musculus	24-31
18574264-2	2008	UFH is a heterogeneous mixture of glycosaminoglycans that bind to antithrombin via a unique pentasaccharide sequence and catalyze the inactivation of thrombin factor Xa and other clotting factors.	Glycosaminoglycans	34-52	serpin family C member 1	Homo sapiens	66-78
19707363-1	2008	Mucopolysaccharidosis type II (MPS II, Hunter syndrome) is a heterogeneous, progressive X-linked recessively inherited lysosomal storage disease that is caused by a deficiency of the enzyme iduronate-2-sulfatase, resulting in abnormal tissue accumulation of the glycosaminoglycans, dermatan sulfate and heparan sulfate.	Glycosaminoglycans	262-280	iduronate 2-sulfatase	Homo sapiens	190-211
18574264-2	2008	UFH is a heterogeneous mixture of glycosaminoglycans that bind to antithrombin via a unique pentasaccharide sequence and catalyze the inactivation of thrombin factor Xa and other clotting factors.	Glycosaminoglycans	34-52	coagulation factor II, thrombin	Homo sapiens	70-78
18574264-2	2008	UFH is a heterogeneous mixture of glycosaminoglycans that bind to antithrombin via a unique pentasaccharide sequence and catalyze the inactivation of thrombin factor Xa and other clotting factors.	Glycosaminoglycans	34-52	coagulation factor X	Homo sapiens	159-168
21136869-1	2008	Primary torsion dystonia is an autosomal-dominantly inherited, neurodevelopmental movement disorder caused by a GAG deletion (DeltaGAG) in the DYT1 gene, encoding torsinA.	Glycosaminoglycans	112-115	torsin family 1, member A (torsin A)	Mus musculus	143-147
18367522-9	2008	These results indicate that MA sequences within the Gag moiety of the v-Abl protein contribute to proper localization by playing a dominant role in trafficking of the v-Abl molecule.	Glycosaminoglycans	52-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-75
18367522-9	2008	These results indicate that MA sequences within the Gag moiety of the v-Abl protein contribute to proper localization by playing a dominant role in trafficking of the v-Abl molecule.	Glycosaminoglycans	52-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-172
18255119-2	2008	Previously, we provided genetic and biochemical evidence indicating that Env packaging into simian immunodeficiency virus (SIV) particles is mediated by the association of the Env cytoplasmic domain (CD) with the matrix (MA) domain of Gag.	Glycosaminoglycans	235-238	envelope protein	Simian immunodeficiency virus	73-76
18255119-6	2008	Our results strongly support the notion that the association between the SIV MA and Env CD plays a central role in the process of SIV Env incorporation into Gag-made particles.	Glycosaminoglycans	157-160	envelope protein	Simian immunodeficiency virus	84-87
18255119-6	2008	Our results strongly support the notion that the association between the SIV MA and Env CD plays a central role in the process of SIV Env incorporation into Gag-made particles.	Glycosaminoglycans	157-160	envelope protein	Simian immunodeficiency virus	134-137
18396123-4	2008	After two weeks on enzyme replacement therapy (ERT) with idursulfase (IDS), the excretion of GAG was decreased to 36.2 ng/nmol/creatinine and the liver and spleen volumes were reduced to normal limits.	Glycosaminoglycans	93-96	iduronate 2-sulfatase	Homo sapiens	57-68
21136869-1	2008	Primary torsion dystonia is an autosomal-dominantly inherited, neurodevelopmental movement disorder caused by a GAG deletion (DeltaGAG) in the DYT1 gene, encoding torsinA.	Glycosaminoglycans	112-115	torsin family 1, member A (torsin A)	Mus musculus	163-170
18406133-2	2008	The Gag polyprotein is composed of three folded polypeptides (MA, CA, and NC) and three smaller peptides (SP1, SP2, and p6) that function together to coordinate membrane binding and Gag-Gag lattice interactions in immature virions.	Glycosaminoglycans	4-7	Sp2 transcription factor	Homo sapiens	111-114
18285341-3	2008	To determine if expression of ASB and GALNS impacts on glycosaminoglycans (GAGs) and proteoglycans beyond their association with the mucopolysaccharidoses, we modified the expression of ASB and GALNS by overexpression and by silencing with small interference RNA in MCF-7 cells.	Glycosaminoglycans	55-73	arylsulfatase B	Homo sapiens	30-33
18267113-3	2008	This study investigated the signaling pathways evoked by TGF-beta1 and IGF-1 that mediated chondrogenic differentiation in adult rat bone-marrow derived MSCs in (i) monolayer on plastic and (ii) a 3D collagen-GAG scaffold.	Glycosaminoglycans	209-212	transforming growth factor, beta 1	Rattus norvegicus	57-66
18267113-3	2008	This study investigated the signaling pathways evoked by TGF-beta1 and IGF-1 that mediated chondrogenic differentiation in adult rat bone-marrow derived MSCs in (i) monolayer on plastic and (ii) a 3D collagen-GAG scaffold.	Glycosaminoglycans	209-212	insulin-like growth factor 1	Rattus norvegicus	71-76
18267113-5	2008	Similarly, when the MSCs were seeded onto a collagen-GAG scaffold and treated with TGF-beta1, the chondrogenic differentiation was dependent upon p38.	Glycosaminoglycans	53-56	transforming growth factor, beta 1	Rattus norvegicus	83-92
18267113-5	2008	Similarly, when the MSCs were seeded onto a collagen-GAG scaffold and treated with TGF-beta1, the chondrogenic differentiation was dependent upon p38.	Glycosaminoglycans	53-56	mitogen activated protein kinase 14	Rattus norvegicus	146-149
18267113-8	2008	When MSCs were seeded onto the collagen-GAG scaffold and exposed to IGF-1, PI3K was required for chondrogenesis.	Glycosaminoglycans	40-43	insulin-like growth factor 1	Rattus norvegicus	68-73
18191978-5	2008	The resulting CypA-Nef protein enhanced the infectivity of Nef-defective HIV-1 particles and was specifically incorporated into the virions via association with Gag during particle assembly.	Glycosaminoglycans	161-164	peptidylprolyl isomerase A	Homo sapiens	14-18
18191978-5	2008	The resulting CypA-Nef protein enhanced the infectivity of Nef-defective HIV-1 particles and was specifically incorporated into the virions via association with Gag during particle assembly.	Glycosaminoglycans	161-164	Nef	Human immunodeficiency virus 1	19-22
18191978-6	2008	Pharmacologic or genetic inhibition of CypA-Nef binding to Gag prevented incorporation of CypA-Nef into virions and inhibited infectivity enhancement.	Glycosaminoglycans	59-62	peptidylprolyl isomerase A	Homo sapiens	39-43
18191978-6	2008	Pharmacologic or genetic inhibition of CypA-Nef binding to Gag prevented incorporation of CypA-Nef into virions and inhibited infectivity enhancement.	Glycosaminoglycans	59-62	S100 calcium binding protein B	Homo sapiens	44-47
18191978-6	2008	Pharmacologic or genetic inhibition of CypA-Nef binding to Gag prevented incorporation of CypA-Nef into virions and inhibited infectivity enhancement.	Glycosaminoglycans	59-62	peptidylprolyl isomerase A	Homo sapiens	90-94
18191978-6	2008	Pharmacologic or genetic inhibition of CypA-Nef binding to Gag prevented incorporation of CypA-Nef into virions and inhibited infectivity enhancement.	Glycosaminoglycans	59-62	S100 calcium binding protein B	Homo sapiens	95-98
18382677-0	2008	The p12 domain is unstructured in a murine leukemia virus p12-CA(N) Gag construct.	Glycosaminoglycans	68-71	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	4-7
18382677-0	2008	The p12 domain is unstructured in a murine leukemia virus p12-CA(N) Gag construct.	Glycosaminoglycans	68-71	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	58-61
18174362-8	2008	Binding of radiolabeled CXCL4 to L1.2 CXCR3 transfectants was of low affinity and appeared to be mediated chiefly by glycosaminoglycans (GAGs), as no specific CXCL4 binding was observed in GAG-deficient 745-Chinese hamster ovary cells stably expressing CXCR3.	Glycosaminoglycans	117-135	platelet factor 4	Homo sapiens	24-29
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
18158310-1	2008	Reduced activity of beta4-galactosyltransferase 7 (beta4GalT-7), an enzyme involved in synthesizing the glycosaminoglycan linkage region of proteoglycans, is associated with the progeroid form of Ehlers-Danlos syndrome (EDS).	Glycosaminoglycans	104-121	beta-1,4-galactosyltransferase 7	Homo sapiens	20-49
18158310-1	2008	Reduced activity of beta4-galactosyltransferase 7 (beta4GalT-7), an enzyme involved in synthesizing the glycosaminoglycan linkage region of proteoglycans, is associated with the progeroid form of Ehlers-Danlos syndrome (EDS).	Glycosaminoglycans	104-121	beta-1,4-galactosyltransferase 7	Homo sapiens	51-62
18174362-8	2008	Binding of radiolabeled CXCL4 to L1.2 CXCR3 transfectants was of low affinity and appeared to be mediated chiefly by glycosaminoglycans (GAGs), as no specific CXCL4 binding was observed in GAG-deficient 745-Chinese hamster ovary cells stably expressing CXCR3.	Glycosaminoglycans	117-135	skull development traits QTL 1	Mus musculus	33-37
18174362-8	2008	Binding of radiolabeled CXCL4 to L1.2 CXCR3 transfectants was of low affinity and appeared to be mediated chiefly by glycosaminoglycans (GAGs), as no specific CXCL4 binding was observed in GAG-deficient 745-Chinese hamster ovary cells stably expressing CXCR3.	Glycosaminoglycans	137-140	platelet factor 4	Homo sapiens	24-29
18174362-8	2008	Binding of radiolabeled CXCL4 to L1.2 CXCR3 transfectants was of low affinity and appeared to be mediated chiefly by glycosaminoglycans (GAGs), as no specific CXCL4 binding was observed in GAG-deficient 745-Chinese hamster ovary cells stably expressing CXCR3.	Glycosaminoglycans	137-140	skull development traits QTL 1	Mus musculus	33-37
18223258-9	2008	TGF-beta increased [(3)H]glucosamine incorporation into glycosaminoglycans by 180% and [(35)S]Met/Cys incorporation into proteoglycan core proteins by 35% with both effects completely inhibited by SB431542.	Glycosaminoglycans	56-74	transforming growth factor beta 1	Homo sapiens	0-8
18299128-1	2008	A single GAG deletion in Exon 5 of the TOR1A gene is associated with a form of early-onset primary dystonia showing less than 40% penetrance.	Glycosaminoglycans	9-12	torsin family 1, member A (torsin A)	Mus musculus	39-44
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
18256192-2	2008	HSPGs are composed of a core protein covalently linked to glycosaminoglycan (GAG) sugar chains that bind and modulate the signaling efficiency of many ligands, including Hedgehog (Hh), Wingless (Wg) and Bone morphogenetic proteins (BMPs).	Glycosaminoglycans	58-75	hedgehog	Drosophila melanogaster	170-178
17672828-1	2008	MPS VI (mucopolysaccharidosis type VI) is a lysosomal storage disease in which deficient activity of the enzyme N-acetylgalactosamine 4-sulfatase [ASB (arylsulfatase B)] impairs the stepwise degradation of the GAG (glycosaminoglycan) dermatan sulfate.	Glycosaminoglycans	210-213	arylsulfatase B	Homo sapiens	112-145
17672828-1	2008	MPS VI (mucopolysaccharidosis type VI) is a lysosomal storage disease in which deficient activity of the enzyme N-acetylgalactosamine 4-sulfatase [ASB (arylsulfatase B)] impairs the stepwise degradation of the GAG (glycosaminoglycan) dermatan sulfate.	Glycosaminoglycans	210-213	arylsulfatase B	Homo sapiens	147-150
17672828-1	2008	MPS VI (mucopolysaccharidosis type VI) is a lysosomal storage disease in which deficient activity of the enzyme N-acetylgalactosamine 4-sulfatase [ASB (arylsulfatase B)] impairs the stepwise degradation of the GAG (glycosaminoglycan) dermatan sulfate.	Glycosaminoglycans	210-213	arylsulfatase B	Homo sapiens	152-167
18223258-6	2008	In human VSMC, TGF-beta increased [(35)S]sulfate incorporation into proteoglycans associated with a 19% increase in glycosaminoglycan (GAG) chain size by size exclusion chromatography.	Glycosaminoglycans	116-133	transforming growth factor beta 1	Homo sapiens	15-23
18223258-6	2008	In human VSMC, TGF-beta increased [(35)S]sulfate incorporation into proteoglycans associated with a 19% increase in glycosaminoglycan (GAG) chain size by size exclusion chromatography.	Glycosaminoglycans	135-138	transforming growth factor beta 1	Homo sapiens	15-23
18683686-6	2008	RESULTS: The GAG percentage in the culture fluid of the TNF-alpha was 57.1% +/- 2.0%, significantly higher than those of the control and TNF-alpha + PAR groups (P = 0.001 and 0.02).	Glycosaminoglycans	13-16	tumor necrosis factor	Homo sapiens	56-65
18165227-7	2008	A genetic interaction of dbeta3GalTII with Drosophila beta1,4-galactoslyltransferase 7 (dbeta4GalT7) or with six genes that encode enzymes contributing to the synthesis of glycosaminoglycans indicated that dbeta3GalTII is involved in heparan sulfate synthesis for wing and eye development.	Glycosaminoglycans	172-190	beta-1,3-Galactosyltransferase II	Drosophila melanogaster	25-37
18256192-2	2008	HSPGs are composed of a core protein covalently linked to glycosaminoglycan (GAG) sugar chains that bind and modulate the signaling efficiency of many ligands, including Hedgehog (Hh), Wingless (Wg) and Bone morphogenetic proteins (BMPs).	Glycosaminoglycans	77-80	hedgehog	Drosophila melanogaster	170-178
18256192-4	2008	We find that a stage-specific block to GAG synthesis prevents HSPG expression during establishment of the BMP activity gradient that is crucial for dorsal embryonic patterning.	Glycosaminoglycans	39-42	decapentaplegic	Drosophila melanogaster	106-109
18195034-1	2008	Both decorin-binding proteins (DbpA and DbpB) of the Lyme disease spirochete Borrelia burgdorferi bind decorin and glycosaminoglycans, two important building blocks of proteoglycans that are abundantly found in the extracellular matrix (ECM) and connective tissues as well as on cell surfaces of mammals.	Glycosaminoglycans	115-133	Y-box binding protein 3	Homo sapiens	31-35
18156656-1	2008	Dermatan sulfate is a glycosaminoglycan that selectively inhibits the action of thrombin through interaction with heparin cofactor II.	Glycosaminoglycans	22-39	coagulation factor II, thrombin	Bos taurus	80-88
18156656-1	2008	Dermatan sulfate is a glycosaminoglycan that selectively inhibits the action of thrombin through interaction with heparin cofactor II.	Glycosaminoglycans	22-39	serpin family D member 1	Bos taurus	114-133
18195034-1	2008	Both decorin-binding proteins (DbpA and DbpB) of the Lyme disease spirochete Borrelia burgdorferi bind decorin and glycosaminoglycans, two important building blocks of proteoglycans that are abundantly found in the extracellular matrix (ECM) and connective tissues as well as on cell surfaces of mammals.	Glycosaminoglycans	115-133	Y-box binding protein 1	Homo sapiens	40-44
18437909-1	2008	OBJECTIVE: To investigate the frequency of GAG deletion in the DYT1 gene among early onset primary dystonia patients in China.	Glycosaminoglycans	43-46	torsin family 1 member A	Homo sapiens	63-67
19096623-3	2008	When intervertebral disc cells were cultured with TGF-beta1 or L-ascorbic acid, the production level of sulfated glycosaminoglycan (sGAG) was estimated by dimethyl methyleneblue (DMMB) assay.	Glycosaminoglycans	113-130	transforming growth factor beta 1	Homo sapiens	50-59
18437909-3	2008	RESULTS: The GAG deletion mutation which results in Glu302del in exon 5 of the DYT1 gene was found in 5 patients.	Glycosaminoglycans	13-16	torsin family 1 member A	Homo sapiens	79-83
18437909-6	2008	CONCLUSIONS: The GAG deletion in the DYT1 gene is common amongst early onset primary torsion dystonia patients in China.	Glycosaminoglycans	17-20	torsin family 1 member A	Homo sapiens	37-41
17950619-1	2008	Testican-2 is a member of the testican group of brain extracellular proteoglycans where a 45 kDa modular protein core is composed of a follistatin-like domain, a calcium-binding domain, a thyroglobulin type-1 (Tg1) domain and an acid C-terminal region with glycosaminoglycan attachment sites.	Glycosaminoglycans	257-274	SPARC (osteonectin), cwcv and kazal like domains proteoglycan 2	Homo sapiens	0-10
17404809-6	2008	By day 28, constructs cultured in the presence of TGF-beta3 exhibited significant increase in sulfated glycosaminoglycan and total collagen content up to 65 and 300%, respectively.	Glycosaminoglycans	103-120	transforming growth factor beta 3	Homo sapiens	50-59
18200630-5	2008	Up-regulation of HO-1 by cobalt protoporphyrin IX significantly reduced glycosaminoglycan degradation elicited by IL-1beta in OA cartilage explants but increased glycosaminoglycan synthesis and the expression of collagen II in OA chondrocytes in primary culture, as determined by radiometric procedures, immunoblotting and immunocytochemistry.	Glycosaminoglycans	72-89	heme oxygenase 1	Homo sapiens	17-21
18200630-5	2008	Up-regulation of HO-1 by cobalt protoporphyrin IX significantly reduced glycosaminoglycan degradation elicited by IL-1beta in OA cartilage explants but increased glycosaminoglycan synthesis and the expression of collagen II in OA chondrocytes in primary culture, as determined by radiometric procedures, immunoblotting and immunocytochemistry.	Glycosaminoglycans	72-89	interleukin 1 beta	Homo sapiens	114-122
18200630-5	2008	Up-regulation of HO-1 by cobalt protoporphyrin IX significantly reduced glycosaminoglycan degradation elicited by IL-1beta in OA cartilage explants but increased glycosaminoglycan synthesis and the expression of collagen II in OA chondrocytes in primary culture, as determined by radiometric procedures, immunoblotting and immunocytochemistry.	Glycosaminoglycans	162-179	heme oxygenase 1	Homo sapiens	17-21
18065761-7	2008	The formation of cis and trans dimers of the TSPN-1 domain with relatively short segments of heparin further enhances the ability of TSP-1 to participate in high affinity binding to glycosaminoglycans.	Glycosaminoglycans	182-200	thrombospondin 1	Homo sapiens	133-138
17974491-8	2008	RESULTS: Biochemical assays revealed an elevated sulfated glycosaminoglycan (GAG)/DNA ratio in mouse IVD cells that were cultured in the presence of various concentrations of mouse GDF-5(mGDF-5) protein.	Glycosaminoglycans	77-80	growth differentiation factor 5	Mus musculus	181-186
17974491-8	2008	RESULTS: Biochemical assays revealed an elevated sulfated glycosaminoglycan (GAG)/DNA ratio in mouse IVD cells that were cultured in the presence of various concentrations of mouse GDF-5(mGDF-5) protein.	Glycosaminoglycans	77-80	growth differentiation factor 5	Mus musculus	187-193
18319625-9	2008	We also found that microinjection of anti-gag antibodies inhibited the migration of CAS-/-v-Crk MEFs.	Glycosaminoglycans	42-45	breast cancer anti-estrogen resistance 1	Mus musculus	84-87
18319625-9	2008	We also found that microinjection of anti-gag antibodies inhibited the migration of CAS-/-v-Crk MEFs.	Glycosaminoglycans	42-45	v-crk avian sarcoma virus CT10 oncogene homolog	Mus musculus	92-95
18238796-1	2008	OBJECTIVES: To investigate the mechanisms by which cytokines and 17beta-oestradiol (17beta-E2) modulate gene expression and activity of uridine diphosphoglucose dehydrogenase (UGDH), a key enzyme of GAG synthesis in articular chondrocytes.	Glycosaminoglycans	199-202	UDP-glucose 6-dehydrogenase	Oryctolagus cuniculus	136-174
18238796-1	2008	OBJECTIVES: To investigate the mechanisms by which cytokines and 17beta-oestradiol (17beta-E2) modulate gene expression and activity of uridine diphosphoglucose dehydrogenase (UGDH), a key enzyme of GAG synthesis in articular chondrocytes.	Glycosaminoglycans	199-202	UDP-glucose 6-dehydrogenase	Oryctolagus cuniculus	176-180
18247611-1	2008	The structure of an intact glycosaminoglycan (GAG) chain of the bikunin proteoglycan (PG) was analyzed using a combined top-down and bottom-up sequencing strategy.	Glycosaminoglycans	27-44	alpha-1-microglobulin/bikunin precursor	Homo sapiens	64-71
18247611-1	2008	The structure of an intact glycosaminoglycan (GAG) chain of the bikunin proteoglycan (PG) was analyzed using a combined top-down and bottom-up sequencing strategy.	Glycosaminoglycans	46-49	alpha-1-microglobulin/bikunin precursor	Homo sapiens	64-71
18247611-10	2008	FTICR-MS analysis of a size-uniform fraction of bikunin GAG mixture obtained by preparative polyacrylamide gel electrophoresis, allowed the determination of chain length and number of sulfo groups in the intact GAGs.	Glycosaminoglycans	56-59	alpha-1-microglobulin/bikunin precursor	Homo sapiens	48-55
18301747-7	2008	Deleting gp150, by contrast, frees MuHV-4 from GAG dependence.	Glycosaminoglycans	47-50	integrin subunit beta 4	Homo sapiens	9-14
18301747-8	2008	This implies that GAGs normally displace gp150 to allow GAG-independent cell binding.	Glycosaminoglycans	18-21	integrin subunit beta 4	Homo sapiens	41-46
18301747-9	2008	But the gp150 GAG interaction is weak, and so would seem unlikely to make an effective first contact.	Glycosaminoglycans	14-17	integrin subunit beta 4	Homo sapiens	8-13
18301747-11	2008	Here we relate the seemingly disconnected gp70 and gp150 GAG interactions by showing that the MuHV-4 gH/gL also binds to GAGs.	Glycosaminoglycans	57-60	integrin subunit beta 4	Homo sapiens	51-56
18301747-13	2008	Thus, there was redundancy in GAG binding between gp70 and gH/gL.	Glycosaminoglycans	30-33	embigin	Homo sapiens	50-54
18301747-16	2008	MuHV-4 GAG dependence is consequently two-fold: gp70 or gH/gL binding provides virions with a vital first foothold, and gp150 is then engaged to reveal GAG-independent binding.	Glycosaminoglycans	7-10	embigin	Homo sapiens	48-52
18301747-16	2008	MuHV-4 GAG dependence is consequently two-fold: gp70 or gH/gL binding provides virions with a vital first foothold, and gp150 is then engaged to reveal GAG-independent binding.	Glycosaminoglycans	7-10	integrin subunit beta 4	Homo sapiens	120-125
18065761-9	2008	This association would enable glycosaminoglycans to cluster TSP-1.	Glycosaminoglycans	30-48	thrombospondin 1	Homo sapiens	60-65
17961072-5	2008	Heparan sulfate, a glycosaminoglycan, is highly abundant in the ECM and tightly binds EC-SOD.	Glycosaminoglycans	19-36	superoxide dismutase 3, extracellular	Mus musculus	86-92
18250460-6	2008	Mice primed with a single administration of rLm-gag by any route and then boosted with rAd5-gag intramuscularly exhibited abundant Gag-specific CD8 T cells in spleen and vaginal lamina propria.	Glycosaminoglycans	131-134	melanoma antigen	Mus musculus	48-51
18250460-6	2008	Mice primed with a single administration of rLm-gag by any route and then boosted with rAd5-gag intramuscularly exhibited abundant Gag-specific CD8 T cells in spleen and vaginal lamina propria.	Glycosaminoglycans	131-134	melanoma antigen	Mus musculus	92-95
18284325-5	2008	Following treatment cessation, there was an immediate increase in viral load followed by an increase in the magnitude of CD4(+) Gag-specific responses.	Glycosaminoglycans	128-131	CD4 molecule	Homo sapiens	121-124
18275276-4	2008	RESULTS: CD8+ T cells from both controller groups preferentially target Gag over other proteins in the context of diverse HLA class I alleles, whereas responses are more broadly distributed in persons with progressive infection.	Glycosaminoglycans	72-75	CD8a molecule	Homo sapiens	9-12
18158320-5	2008	There are two putative heparin-binding domains (HBDs) within the OPN molecule, which may bind both heparin and heparin-like glycosaminoglycans such as syndecan.	Glycosaminoglycans	124-142	secreted phosphoprotein 1	Mus musculus	65-68
17935853-6	2008	We will cover features of cathepsin K structure, cellular and tissue distribution, substrate specificity, and regulation (pH, propeptide, glycosaminoglycans, oxidants), and its putative roles in physiological or pathophysiological processes.	Glycosaminoglycans	138-156	cathepsin K	Homo sapiens	26-37
17980161-1	2008	Versican, a large chondroitin sulphate proteoglycan and hyaluronan (HA), a non-sulphated glycosaminoglycan are major constituents of the pericellular matrix.	Glycosaminoglycans	89-106	versican	Homo sapiens	0-8
18082196-13	2008	Loss of the glycosaminoglycan layer was associated with a loss of biglycan and perlecan on the luminal layer.	Glycosaminoglycans	12-29	biglycan	Homo sapiens	66-74
18245410-1	2008	Mucopolysaccharidosis II, also known as Hunter syndrome, is a rare, X-linked disorder caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase, which catalyzes a step in the catabolism of glycosaminoglycans.	Glycosaminoglycans	200-218	iduronate 2-sulfatase	Homo sapiens	133-154
18023272-2	2008	Recently, we and others provided first evidence that XT-II is capable of initiating the biosynthesis of glycosaminoglycan chains in proteoglycans.	Glycosaminoglycans	104-121	xylosyltransferase 2	Homo sapiens	53-58
18023272-4	2008	Furthermore, biochemical characterization of XT-II showed that this enzyme was strongly inhibited by nucleotides and glycosaminoglycans.	Glycosaminoglycans	117-135	xylosyltransferase 2	Homo sapiens	45-50
19024627-3	2008	Specific inhibition of the final rate-limiting step in Gag processing by bevirimat prevents release of mature capsid protein from its precursor (CA-SP1), resulting in the production of immature, non-infectious virus particles.	Glycosaminoglycans	55-58	caspase 1	Homo sapiens	145-151
18316776-6	2008	Direct sequencing of the AVP-NPII gene showed a heterozygous GAG deletion mutation in exon 2, which results in in-frame deletion of glutamic acid (c.232_234delGAG; p.Glu78del).	Glycosaminoglycans	61-64	arginine vasopressin	Homo sapiens	25-33
18468239-5	2008	Heparin, one of the soluble glycosaminoglycans (GAGs), inhibited PDX-1 internalization, while chondroitin sulfate A, B, and C caused only very limited inhibition.	Glycosaminoglycans	28-46	pancreatic and duodenal homeobox 1	Homo sapiens	65-70
18836230-6	2008	Mechanical stimulation of normal chondrocytes resulted in increased GAG synthesis that was blocked by the presence of antibodies to alpha5 and alphaVbeta5 integrins and CD47.	Glycosaminoglycans	68-71	CD47 molecule	Homo sapiens	169-173
18468239-5	2008	Heparin, one of the soluble glycosaminoglycans (GAGs), inhibited PDX-1 internalization, while chondroitin sulfate A, B, and C caused only very limited inhibition.	Glycosaminoglycans	48-52	pancreatic and duodenal homeobox 1	Homo sapiens	65-70
18468239-8	2008	PDX-1 internalization was significantly reduced in both pgs A-745 mutant cells, which are defective in a enzyme that initiates GAG synthesis, and pgs B-618 cells, which produce about 15% of the amount of GAGs synthesized by wild-type cells.	Glycosaminoglycans	127-130	pancreatic and duodenal homeobox 1	Homo sapiens	0-5
18468239-8	2008	PDX-1 internalization was significantly reduced in both pgs A-745 mutant cells, which are defective in a enzyme that initiates GAG synthesis, and pgs B-618 cells, which produce about 15% of the amount of GAGs synthesized by wild-type cells.	Glycosaminoglycans	204-208	pancreatic and duodenal homeobox 1	Homo sapiens	0-5
18097036-5	2008	Week 30 LN from IL-15-treated animals had significantly increased Gag-specific CD8+ T cell numbers, whereas total cell, lymphocyte, and CD4+ T cell numbers were reduced.	Glycosaminoglycans	66-69	interleukin 15	Homo sapiens	16-21
17706452-2	2008	The aim of the present study was to examine the possible participation of various glycosaminoglycans, i.e. chondroitin sulfate, dermatan sulfate and heparin on basal and FGF-2-induced growth of WM9 and M5 human metastatic melanoma cells.	Glycosaminoglycans	82-100	fibroblast growth factor 2	Homo sapiens	170-175
17706452-3	2008	Exogenous glycosaminoglycans mildly inhibited WM9 cell"s proliferation, which was abolished by FGF-2.	Glycosaminoglycans	10-28	fibroblast growth factor 2	Homo sapiens	95-100
17706452-9	2008	In this study, we show that chondroitin/dermatan sulfate-containing proteoglycans, likely in cooperation with heparan sulfate, participate in metastatic melanoma cell FGF-2-induced mitogenic response, which represents a novel finding and establishes the central role of sulfated glycosaminoglycans on melanoma growth.	Glycosaminoglycans	279-297	fibroblast growth factor 2	Homo sapiens	167-172
18585473-2	2008	In the present work the interaction of glycosaminoglycans with PHEX has been investigated by affinity chromatography, circular dichroism, protein intrinsic fluorescence analysis, hydrolysis of FRET substrates flow cytometry and confocal microscopy.	Glycosaminoglycans	39-57	phosphate regulating endopeptidase homolog X-linked	Homo sapiens	63-67
18585473-4	2008	Circular dichroism spectra and intrinsic fluorescence analysis showed that PHEX is protected by glycosaminoglycans against thermal denaturation.	Glycosaminoglycans	96-114	phosphate regulating endopeptidase homolog X-linked	Homo sapiens	75-79
17955027-4	2008	After systemic or intramuscular (IM) administration of AAV, therapeutic levels of circulating ARSB are achieved, resulting in skeletal improvements and significant decrease in glycosaminoglycan (GAG) storage, inflammation and apoptosis (despite a neutralizing immune response to ARSB in MPS VI rats).	Glycosaminoglycans	176-193	arylsulfatase B	Rattus norvegicus	94-98
17955027-4	2008	After systemic or intramuscular (IM) administration of AAV, therapeutic levels of circulating ARSB are achieved, resulting in skeletal improvements and significant decrease in glycosaminoglycan (GAG) storage, inflammation and apoptosis (despite a neutralizing immune response to ARSB in MPS VI rats).	Glycosaminoglycans	195-198	arylsulfatase B	Rattus norvegicus	94-98
17516498-3	2007	Here, we investigated the role of HSPG glycosaminoglycan (GAG) side chains on BMP signaling and found increased total and HSPG-specific GAG chain levels and dysregulation in HSPG modulation of BMP signaling in FOP lymphoblastoid cells (LCLs).	Glycosaminoglycans	39-56	syndecan 2	Homo sapiens	34-38
18974782-4	2008	In subjects not on ART, the percentage of rectal Gag-specific CD8+ T-cells capable of 3, 4 or 5 simultaneous effector functions was significantly related to blood CD4 count and inversely related to plasma viral load (PVL) (p&lt;0.05).	Glycosaminoglycans	49-52	CD8a molecule	Homo sapiens	62-65
18974782-4	2008	In subjects not on ART, the percentage of rectal Gag-specific CD8+ T-cells capable of 3, 4 or 5 simultaneous effector functions was significantly related to blood CD4 count and inversely related to plasma viral load (PVL) (p&lt;0.05).	Glycosaminoglycans	49-52	CD4 molecule	Homo sapiens	163-166
18974782-9	2008	CONCLUSIONS: The polyfunctionality of rectal Gag-specific CD8+ T-cells appears to be related to blood CD4 count and inversely related to PVL.	Glycosaminoglycans	45-48	CD8a molecule	Homo sapiens	58-61
18974782-9	2008	CONCLUSIONS: The polyfunctionality of rectal Gag-specific CD8+ T-cells appears to be related to blood CD4 count and inversely related to PVL.	Glycosaminoglycans	45-48	CD4 molecule	Homo sapiens	102-105
17516498-3	2007	Here, we investigated the role of HSPG glycosaminoglycan (GAG) side chains on BMP signaling and found increased total and HSPG-specific GAG chain levels and dysregulation in HSPG modulation of BMP signaling in FOP lymphoblastoid cells (LCLs).	Glycosaminoglycans	39-56	bone morphogenetic protein 1	Homo sapiens	78-81
17516498-3	2007	Here, we investigated the role of HSPG glycosaminoglycan (GAG) side chains on BMP signaling and found increased total and HSPG-specific GAG chain levels and dysregulation in HSPG modulation of BMP signaling in FOP lymphoblastoid cells (LCLs).	Glycosaminoglycans	39-56	bone morphogenetic protein 1	Homo sapiens	193-196
17516498-3	2007	Here, we investigated the role of HSPG glycosaminoglycan (GAG) side chains on BMP signaling and found increased total and HSPG-specific GAG chain levels and dysregulation in HSPG modulation of BMP signaling in FOP lymphoblastoid cells (LCLs).	Glycosaminoglycans	58-61	syndecan 2	Homo sapiens	34-38
18571697-10	2008	Chemically cleaved glycosaminoglycan (GAG) chains analyzed by SDS-PAGE and size exclusion chromatography were larger for proteoglycans from thrombin treated cells.	Glycosaminoglycans	19-36	coagulation factor II, thrombin	Homo sapiens	140-148
18571697-10	2008	Chemically cleaved glycosaminoglycan (GAG) chains analyzed by SDS-PAGE and size exclusion chromatography were larger for proteoglycans from thrombin treated cells.	Glycosaminoglycans	38-41	coagulation factor II, thrombin	Homo sapiens	140-148
18571697-17	2008	Thus, thrombin has actions on VSMCs which increase the length and modify the sulfation pattern of GAG chains on proteoglycans in a manner that would enhance the binding of LDL.	Glycosaminoglycans	98-101	coagulation factor II, thrombin	Homo sapiens	6-14
18160657-3	2007	We have successfully decreased the amount of CSPG GAG produced by astrocytes by targeting chondroitin polymerizing factor (ChPF), a key enzyme in the CSPG biosynthetic pathway.	Glycosaminoglycans	50-53	chondroitin polymerizing factor	Rattus norvegicus	90-121
18160657-3	2007	We have successfully decreased the amount of CSPG GAG produced by astrocytes by targeting chondroitin polymerizing factor (ChPF), a key enzyme in the CSPG biosynthetic pathway.	Glycosaminoglycans	50-53	chondroitin polymerizing factor	Rattus norvegicus	123-127
17516498-3	2007	Here, we investigated the role of HSPG glycosaminoglycan (GAG) side chains on BMP signaling and found increased total and HSPG-specific GAG chain levels and dysregulation in HSPG modulation of BMP signaling in FOP lymphoblastoid cells (LCLs).	Glycosaminoglycans	58-61	bone morphogenetic protein 1	Homo sapiens	78-81
17516498-3	2007	Here, we investigated the role of HSPG glycosaminoglycan (GAG) side chains on BMP signaling and found increased total and HSPG-specific GAG chain levels and dysregulation in HSPG modulation of BMP signaling in FOP lymphoblastoid cells (LCLs).	Glycosaminoglycans	136-139	syndecan 2	Homo sapiens	122-126
18160010-7	2007	The levels of osteocalcin were also significantly reduced by p55-gag treatment, while gp120 also increased PPARgamma activity.	Glycosaminoglycans	65-68	bone gamma-carboxyglutamate protein	Homo sapiens	14-25
17516498-3	2007	Here, we investigated the role of HSPG glycosaminoglycan (GAG) side chains on BMP signaling and found increased total and HSPG-specific GAG chain levels and dysregulation in HSPG modulation of BMP signaling in FOP lymphoblastoid cells (LCLs).	Glycosaminoglycans	136-139	syndecan 2	Homo sapiens	122-126
19662133-5	2007	The addition of the growth factors IGF-I (100 ng/mL) and TGF-beta1 (10 ng/mL) during the alginate culture and the absence of any growth factors during the high-density cell culture led to significantly higher GAG to DNA ratios and Young"s Moduli of the constructs compared to other combinations.	Glycosaminoglycans	209-212	insulin like growth factor 1	Homo sapiens	35-40
19662133-5	2007	The addition of the growth factors IGF-I (100 ng/mL) and TGF-beta1 (10 ng/mL) during the alginate culture and the absence of any growth factors during the high-density cell culture led to significantly higher GAG to DNA ratios and Young"s Moduli of the constructs compared to other combinations.	Glycosaminoglycans	209-212	transforming growth factor beta 1	Homo sapiens	57-66
17985932-10	2007	Glycosaminoglycan binding by IGFBPs can affect their IGF binding although the effects appear to differ among different IGFBPs; here, we found that heparin bound to the IGF-I.N-BP-2.C-BP-2 ternary complex, but did not cause it to dissociate.	Glycosaminoglycans	0-17	insulin like growth factor binding protein 1	Homo sapiens	29-35
17985932-10	2007	Glycosaminoglycan binding by IGFBPs can affect their IGF binding although the effects appear to differ among different IGFBPs; here, we found that heparin bound to the IGF-I.N-BP-2.C-BP-2 ternary complex, but did not cause it to dissociate.	Glycosaminoglycans	0-17	insulin like growth factor binding protein 1	Homo sapiens	119-125
17985932-10	2007	Glycosaminoglycan binding by IGFBPs can affect their IGF binding although the effects appear to differ among different IGFBPs; here, we found that heparin bound to the IGF-I.N-BP-2.C-BP-2 ternary complex, but did not cause it to dissociate.	Glycosaminoglycans	0-17	insulin like growth factor 1	Homo sapiens	168-173
17985932-10	2007	Glycosaminoglycan binding by IGFBPs can affect their IGF binding although the effects appear to differ among different IGFBPs; here, we found that heparin bound to the IGF-I.N-BP-2.C-BP-2 ternary complex, but did not cause it to dissociate.	Glycosaminoglycans	0-17	NUBP iron-sulfur cluster assembly factor 2, cytosolic	Homo sapiens	174-180
18056413-3	2007	DTDST imports sulfate for the modification of glycosaminoglycans.	Glycosaminoglycans	46-64	solute carrier family 26 member 2	Homo sapiens	0-5
18160010-7	2007	The levels of osteocalcin were also significantly reduced by p55-gag treatment, while gp120 also increased PPARgamma activity.	Glycosaminoglycans	65-68	H3 histone pseudogene 44	Homo sapiens	61-64
18160010-9	2007	The ability of MSCs to develop into functioning OBs was also affected by the presence of HIV proteins, with p55-gag inducing a decrease in osteogenesis, while rev induced an increase.	Glycosaminoglycans	112-115	H3 histone pseudogene 44	Homo sapiens	108-111
17916040-4	2007	ADAS chondrogenesis was assessed using Alcian Blue staining for proteoglycans and quantification of sulfated glycosaminoglycans.	Glycosaminoglycans	109-127	alkylglycerone phosphate synthase	Mus musculus	0-4
17561366-3	2007	IL-1 plays a role in the synthesis, degradation and degree of sulphatation of ECM components such as glycosaminoglycans.	Glycosaminoglycans	101-119	interleukin 1 alpha	Homo sapiens	0-4
17561366-3	2007	IL-1 plays a role in the synthesis, degradation and degree of sulphatation of ECM components such as glycosaminoglycans.	Glycosaminoglycans	101-119	multimerin 1	Homo sapiens	78-81
17561366-4	2007	Also, continuous changes in the ECM involve enzymes such as beta-N-acetyl-d-glucosaminidase (beta-NAG) and beta-d-glucuronidase (beta-GLU) which act on different GAG classes and collagen fibers.	Glycosaminoglycans	162-165	multimerin 1	Homo sapiens	32-35
17561366-4	2007	Also, continuous changes in the ECM involve enzymes such as beta-N-acetyl-d-glucosaminidase (beta-NAG) and beta-d-glucuronidase (beta-GLU) which act on different GAG classes and collagen fibers.	Glycosaminoglycans	162-165	glucuronidase beta	Homo sapiens	107-127
17561366-4	2007	Also, continuous changes in the ECM involve enzymes such as beta-N-acetyl-d-glucosaminidase (beta-NAG) and beta-d-glucuronidase (beta-GLU) which act on different GAG classes and collagen fibers.	Glycosaminoglycans	162-165	glucuronidase beta	Homo sapiens	129-137
17561366-12	2007	IL-1 acts on osteoblasts with decreases in GAG synthesis and alkaline phosphatase activity, while beta-NAG increases.	Glycosaminoglycans	43-46	interleukin 1 alpha	Homo sapiens	0-4
17982709-2	2007	We therefore investigated the presence of urinary IL-6 in patients with BPS/IC to find a possible correlation with the symptoms before and after glycosaminoglycan substitution therapy.	Glycosaminoglycans	145-162	interleukin 6	Homo sapiens	50-54
18008010-5	2007	rAAV vector-induced CD8(+) T cells proliferated poorly, produced low levels of IFN-gamma in response to gag stimulation, and upregulated immunoinhibitory molecules.	Glycosaminoglycans	104-107	CD8a molecule	Homo sapiens	20-23
17881456-8	2007	Gag-specific CD4+ T-cell responses were minimal to undetectable in the first 6 months of pediatric infection.	Glycosaminoglycans	0-3	CD4 molecule	Homo sapiens	13-16
17982668-7	2007	Inhibition of glycosaminoglycan sulphation resulted in a significant increase in cancer cell adhesion and a reduction in cell migration, together with upregulated expression of focal adhesion kinase and paxillin.	Glycosaminoglycans	14-31	protein tyrosine kinase 2	Bos taurus	177-198
17982668-7	2007	Inhibition of glycosaminoglycan sulphation resulted in a significant increase in cancer cell adhesion and a reduction in cell migration, together with upregulated expression of focal adhesion kinase and paxillin.	Glycosaminoglycans	14-31	paxillin	Bos taurus	203-211
18277681-8	2007	The GAG quantification also showed a positive result in both the cell culture systems and the NP cells at Passage 3 transfected with Ad/hTGF-beta1 had a much higher GAG content than the controls (P &lt; 0.05).	Glycosaminoglycans	4-7	transforming growth factor beta 1	Homo sapiens	136-146
18277681-8	2007	The GAG quantification also showed a positive result in both the cell culture systems and the NP cells at Passage 3 transfected with Ad/hTGF-beta1 had a much higher GAG content than the controls (P &lt; 0.05).	Glycosaminoglycans	165-168	transforming growth factor beta 1	Homo sapiens	136-146
18006807-5	2007	We show that overexpression of MMP-1 and MMP-8 in the human soft tissue sarcoma HSTS26T leads to a significant depletion of tumor-sulfated glycosaminoglycans.	Glycosaminoglycans	139-157	matrix metallopeptidase 1	Homo sapiens	31-36
17870532-1	2007	The synthesis of simple, non-sugar glycosaminoglycan (GAG) mimics has been achieved and the analogues evaluated for their ability to inhibit the activation of the MET receptor by hepatocyte growth factor/scatter factor (HGF/SF).	Glycosaminoglycans	54-57	hepatocyte growth factor	Homo sapiens	220-226
18006807-5	2007	We show that overexpression of MMP-1 and MMP-8 in the human soft tissue sarcoma HSTS26T leads to a significant depletion of tumor-sulfated glycosaminoglycans.	Glycosaminoglycans	139-157	matrix metallopeptidase 8	Homo sapiens	41-46
17804609-7	2007	Glycosaminoglycan, including heparan sulfate, synthesis was inhibited in both hIAPP transgenic and nontransgenic islets (the latter is a control that does not develop amyloid), while O-linked protein glycosylation was also decreased, and WAS-406 treatment tended to decrease islet viability in nontransgenic islets.	Glycosaminoglycans	0-17	islet amyloid polypeptide	Homo sapiens	78-83
17804410-8	2007	Furthermore, activation of TRPV4 in concert with insulin activity in ATDC5 cells or in concert with bone morphogenetic protein-2 in C3H10T1/2 cells promoted synthesis of sulfated glycosaminoglycan, but activation of TRPV4 had no effect alone.	Glycosaminoglycans	179-196	transient receptor potential cation channel, subfamily V, member 4	Mus musculus	27-32
17920451-1	2007	Mucopolysaccharidosis type I (MPS-I or Hurler syndrome) is an inherited deficiency of the lysosomal glycosaminoglycan (GAG)-degrading enzyme alpha-l-iduronidase (IDUA) in which GAG accumulation causes progressive multi-system dysfunction and death.	Glycosaminoglycans	119-122	iduronidase, alpha-L	Mus musculus	141-160
17936096-8	2007	We therefore conclude that since 3-OST-3A is able to bind also non-substrate GAG ligands with high affinity, discrimination among ligands is triggered by protein oligomerisation.	Glycosaminoglycans	77-80	heparan sulfate-glucosamine 3-sulfotransferase 3A1	Homo sapiens	33-41
17920451-1	2007	Mucopolysaccharidosis type I (MPS-I or Hurler syndrome) is an inherited deficiency of the lysosomal glycosaminoglycan (GAG)-degrading enzyme alpha-l-iduronidase (IDUA) in which GAG accumulation causes progressive multi-system dysfunction and death.	Glycosaminoglycans	119-122	iduronidase, alpha-L	Mus musculus	162-166
17920451-1	2007	Mucopolysaccharidosis type I (MPS-I or Hurler syndrome) is an inherited deficiency of the lysosomal glycosaminoglycan (GAG)-degrading enzyme alpha-l-iduronidase (IDUA) in which GAG accumulation causes progressive multi-system dysfunction and death.	Glycosaminoglycans	177-180	iduronidase, alpha-L	Mus musculus	141-160
17920451-1	2007	Mucopolysaccharidosis type I (MPS-I or Hurler syndrome) is an inherited deficiency of the lysosomal glycosaminoglycan (GAG)-degrading enzyme alpha-l-iduronidase (IDUA) in which GAG accumulation causes progressive multi-system dysfunction and death.	Glycosaminoglycans	177-180	iduronidase, alpha-L	Mus musculus	162-166
18040638-8	2007	At 6 weeks, OP-1 increased GAG accumulation dose-dependently in the presence or absence of TGFbeta1, and the GAG content was the highest after combined treatment with 200 ng OP-1 and TGFbeta1.	Glycosaminoglycans	27-30	bone morphogenetic protein 7	Homo sapiens	12-16
18174963-3	2007	Results of the randomized, double-blind, placebo-controlled phase II/III clinical trial of idursulfase demonstrated that weekly infusions of idursulfase increase walking distance and improve pulmonary function as well as reduce organ size and urinary glycosaminoglycans (GAGs) excretion in MPS II patients.	Glycosaminoglycans	251-269	iduronate 2-sulfatase	Homo sapiens	91-102
18174963-3	2007	Results of the randomized, double-blind, placebo-controlled phase II/III clinical trial of idursulfase demonstrated that weekly infusions of idursulfase increase walking distance and improve pulmonary function as well as reduce organ size and urinary glycosaminoglycans (GAGs) excretion in MPS II patients.	Glycosaminoglycans	251-269	iduronate 2-sulfatase	Homo sapiens	141-152
18001203-2	2007	Chondroitinase catalyzes the cleavage of glycosaminoglycans (GAGs) from the core proteins of chondroitin sulfate proteoglycans (CSPGs).	Glycosaminoglycans	41-59	galactosamine (N-acetyl)-6-sulfatase	Rattus norvegicus	0-14
18001203-12	2007	This demonstrates that expression patterns of CSPGs in contusion injury are similar to those surrounding surgical hemisection lesions and demonstrates that the sensory and motor function enhancing effects of chondroitinase are likely due to removal of GAG chains rather than reduction in CSPG content.	Glycosaminoglycans	252-255	galactosamine (N-acetyl)-6-sulfatase	Rattus norvegicus	208-222
17804494-0	2007	Escape from the dominant HLA-B27-restricted cytotoxic T-lymphocyte response in Gag is associated with a dramatic reduction in human immunodeficiency virus type 1 replication.	Glycosaminoglycans	79-82	major histocompatibility complex, class I, B	Homo sapiens	25-32
17876721-2	2007	I2S catalyses a step in the catabolism of glycosaminoglycans (GAGs) dermatan sulfate and heparan sulfate, and when it is deficient or absent GAGs accumulate in tissues and organs.	Glycosaminoglycans	42-60	iduronate 2-sulfatase	Homo sapiens	0-3
17699580-2	2007	We have recently shown that Gag-specific CD8+ T cells recognize simian immunodeficiency virus-infected cells at 2 h postinfection, whereas Env-specific CD8+ T cells do not recognize infected cells until much later in infection.	Glycosaminoglycans	28-31	CD8a molecule	Homo sapiens	41-44
18040638-8	2007	At 6 weeks, OP-1 increased GAG accumulation dose-dependently in the presence or absence of TGFbeta1, and the GAG content was the highest after combined treatment with 200 ng OP-1 and TGFbeta1.	Glycosaminoglycans	109-112	bone morphogenetic protein 7	Homo sapiens	174-178
18040638-8	2007	At 6 weeks, OP-1 increased GAG accumulation dose-dependently in the presence or absence of TGFbeta1, and the GAG content was the highest after combined treatment with 200 ng OP-1 and TGFbeta1.	Glycosaminoglycans	109-112	transforming growth factor beta 1	Homo sapiens	183-191
17644521-5	2007	This allosteric coupling between RCL positioning and occupancy of the CBG steroid-binding site, which resembles the ligand (glycosamino-glycan)-dependent activation of the thrombin inhibitory serpins heparin cofactor II and anti-thrombin RCLs, ensures both optimal recognition of CBG by target proteinases and efficient release of steroid to sites of action.	Glycosaminoglycans	124-142	serpin family A member 6	Rattus norvegicus	70-73
18025279-7	2007	The fact that RANTES/CCL5-induced migration and invasion of Huh7 cells are both strongly inhibited by anti-CCR1 antibodies and heparin, as well as by beta-d-xyloside treatment of the cells, suggests that CCR1 and glycosaminoglycans are involved in these events.	Glycosaminoglycans	213-231	C-C motif chemokine ligand 5	Homo sapiens	14-20
18025279-7	2007	The fact that RANTES/CCL5-induced migration and invasion of Huh7 cells are both strongly inhibited by anti-CCR1 antibodies and heparin, as well as by beta-d-xyloside treatment of the cells, suggests that CCR1 and glycosaminoglycans are involved in these events.	Glycosaminoglycans	213-231	C-C motif chemokine ligand 5	Homo sapiens	21-25
18025279-7	2007	The fact that RANTES/CCL5-induced migration and invasion of Huh7 cells are both strongly inhibited by anti-CCR1 antibodies and heparin, as well as by beta-d-xyloside treatment of the cells, suggests that CCR1 and glycosaminoglycans are involved in these events.	Glycosaminoglycans	213-231	MIR7-3 host gene	Homo sapiens	60-64
18025279-7	2007	The fact that RANTES/CCL5-induced migration and invasion of Huh7 cells are both strongly inhibited by anti-CCR1 antibodies and heparin, as well as by beta-d-xyloside treatment of the cells, suggests that CCR1 and glycosaminoglycans are involved in these events.	Glycosaminoglycans	213-231	C-C motif chemokine receptor 1	Homo sapiens	204-208
18025279-8	2007	We then show by surface plasmon resonance that synthetic glycosaminoglycan mimetics, OTR4120 or OTR4131, directly bind to RANTES/CCL5.	Glycosaminoglycans	57-74	C-C motif chemokine ligand 5	Homo sapiens	122-128
18025279-8	2007	We then show by surface plasmon resonance that synthetic glycosaminoglycan mimetics, OTR4120 or OTR4131, directly bind to RANTES/CCL5.	Glycosaminoglycans	57-74	C-C motif chemokine ligand 5	Homo sapiens	129-133
18025279-10	2007	Therefore, targeting the RANTES-glycosaminoglycan interaction could be a new therapeutic approach for human hepatocellular carcinoma.	Glycosaminoglycans	32-49	C-C motif chemokine ligand 5	Homo sapiens	25-31
18025279-0	2007	Glycosaminoglycans and their synthetic mimetics inhibit RANTES-induced migration and invasion of human hepatoma cells.	Glycosaminoglycans	0-18	C-C motif chemokine ligand 5	Homo sapiens	56-62
18025279-1	2007	The CC-chemokine regulated on activation, normal T-cell expressed, and presumably secreted (RANTES)/CCL5 mediates its biological activities through activation of G protein-coupled receptors, CCR1, CCR3, or CCR5, and binds to glycosaminoglycans.	Glycosaminoglycans	225-243	C-C motif chemokine ligand 5	Homo sapiens	92-98
18025279-1	2007	The CC-chemokine regulated on activation, normal T-cell expressed, and presumably secreted (RANTES)/CCL5 mediates its biological activities through activation of G protein-coupled receptors, CCR1, CCR3, or CCR5, and binds to glycosaminoglycans.	Glycosaminoglycans	225-243	C-C motif chemokine ligand 5	Homo sapiens	100-104
18025279-1	2007	The CC-chemokine regulated on activation, normal T-cell expressed, and presumably secreted (RANTES)/CCL5 mediates its biological activities through activation of G protein-coupled receptors, CCR1, CCR3, or CCR5, and binds to glycosaminoglycans.	Glycosaminoglycans	225-243	C-C motif chemokine receptor 1	Homo sapiens	191-195
18025279-1	2007	The CC-chemokine regulated on activation, normal T-cell expressed, and presumably secreted (RANTES)/CCL5 mediates its biological activities through activation of G protein-coupled receptors, CCR1, CCR3, or CCR5, and binds to glycosaminoglycans.	Glycosaminoglycans	225-243	C-C motif chemokine receptor 3	Homo sapiens	197-201
18025279-1	2007	The CC-chemokine regulated on activation, normal T-cell expressed, and presumably secreted (RANTES)/CCL5 mediates its biological activities through activation of G protein-coupled receptors, CCR1, CCR3, or CCR5, and binds to glycosaminoglycans.	Glycosaminoglycans	225-243	C-C motif chemokine receptor 5	Homo sapiens	206-210
18025279-4	2007	RANTES/CCL5 binding to these cells depends on CCR1 and glycosaminoglycans.	Glycosaminoglycans	55-73	C-C motif chemokine ligand 5	Homo sapiens	0-6
18025279-4	2007	RANTES/CCL5 binding to these cells depends on CCR1 and glycosaminoglycans.	Glycosaminoglycans	55-73	C-C motif chemokine ligand 5	Homo sapiens	7-11
17644521-5	2007	This allosteric coupling between RCL positioning and occupancy of the CBG steroid-binding site, which resembles the ligand (glycosamino-glycan)-dependent activation of the thrombin inhibitory serpins heparin cofactor II and anti-thrombin RCLs, ensures both optimal recognition of CBG by target proteinases and efficient release of steroid to sites of action.	Glycosaminoglycans	124-142	coagulation factor II	Rattus norvegicus	172-180
17644521-5	2007	This allosteric coupling between RCL positioning and occupancy of the CBG steroid-binding site, which resembles the ligand (glycosamino-glycan)-dependent activation of the thrombin inhibitory serpins heparin cofactor II and anti-thrombin RCLs, ensures both optimal recognition of CBG by target proteinases and efficient release of steroid to sites of action.	Glycosaminoglycans	124-142	serpin family D member 1	Rattus norvegicus	200-219
17644521-5	2007	This allosteric coupling between RCL positioning and occupancy of the CBG steroid-binding site, which resembles the ligand (glycosamino-glycan)-dependent activation of the thrombin inhibitory serpins heparin cofactor II and anti-thrombin RCLs, ensures both optimal recognition of CBG by target proteinases and efficient release of steroid to sites of action.	Glycosaminoglycans	124-142	coagulation factor II	Rattus norvegicus	229-237
17644521-5	2007	This allosteric coupling between RCL positioning and occupancy of the CBG steroid-binding site, which resembles the ligand (glycosamino-glycan)-dependent activation of the thrombin inhibitory serpins heparin cofactor II and anti-thrombin RCLs, ensures both optimal recognition of CBG by target proteinases and efficient release of steroid to sites of action.	Glycosaminoglycans	124-142	serpin family A member 6	Rattus norvegicus	280-283
17767562-2	2007	The B*4609 allele has one nucleotide change from the closest matching allele B*460101 resulting in an amino acid change from E (GAG) to V (GTG) at codon 176.	Glycosaminoglycans	128-131	gamma-glutamyltransferase 1	Homo sapiens	139-142
17878372-3	2007	The ratio of Bcl-2+ Gag-specific CD8+ T cells to caspase-3+ Gag-specific CD8+ T cells was higher in the vaccinated-protected animals compared with unprotected monkeys.	Glycosaminoglycans	20-23	BCL2 apoptosis regulator	Homo sapiens	13-18
17878372-3	2007	The ratio of Bcl-2+ Gag-specific CD8+ T cells to caspase-3+ Gag-specific CD8+ T cells was higher in the vaccinated-protected animals compared with unprotected monkeys.	Glycosaminoglycans	20-23	CD8a molecule	Homo sapiens	33-36
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
17634219-10	2007	The results indicate that both gag-dependent particle budding and cleavage of p2E are required to activate the SI phenotype of TR1.3 and W102G viruses.	Glycosaminoglycans	31-34	taste receptor, type 1, member 1	Mus musculus	127-130
17893201-2	2007	We report that CD8+ T cell responses specific for Gag and, in particular, the immunodominant p24 epitope KK10 correlate with control of HIV-1 replication in human histocompatibility leukocyte antigen (HLA)-B27 patients.	Glycosaminoglycans	50-53	CD8a molecule	Homo sapiens	15-18
17893201-2	2007	We report that CD8+ T cell responses specific for Gag and, in particular, the immunodominant p24 epitope KK10 correlate with control of HIV-1 replication in human histocompatibility leukocyte antigen (HLA)-B27 patients.	Glycosaminoglycans	50-53	major histocompatibility complex, class I, B	Homo sapiens	163-207
17644519-6	2007	In studies of glycosaminoglycan binding, MIP-1beta-A10C binds to a heparin-Sepharose column as tightly as the wild type protein and more tightly than monomeric variants.	Glycosaminoglycans	14-31	C-C motif chemokine ligand 4	Homo sapiens	41-50
17706843-3	2007	Immunization of Balb/c mice with a single intraperitoneal injection of J200 elicited strong Gag-specific CD8 responses, as measured by intracellular IFN-gamma staining and flow cytometry analysis.	Glycosaminoglycans	92-95	interferon gamma	Mus musculus	149-158
17623663-6	2007	Furthermore, transfection of mutated syndecan-2 lacking glycosaminoglycan attachment sites into highly metastatic cells did not have any suppressive effect on MMP-2 activation, suggesting that this suppression was mediated by the heparan sulfate side chains of syndecan-2.	Glycosaminoglycans	56-73	syndecan 2	Homo sapiens	37-47
17626017-1	2007	The longer splice isoforms of vascular endothelial growth factor-A (VEGF-A), including mouse VEGF164, contain a highly basic heparin-binding domain (HBD), which imparts the ability of these isoforms to be deposited in the heparan sulfate-rich extracellular matrix and to interact with the prototype sulfated glycosaminoglycan, heparin.	Glycosaminoglycans	308-325	vascular endothelial growth factor A	Mus musculus	30-66
17626017-1	2007	The longer splice isoforms of vascular endothelial growth factor-A (VEGF-A), including mouse VEGF164, contain a highly basic heparin-binding domain (HBD), which imparts the ability of these isoforms to be deposited in the heparan sulfate-rich extracellular matrix and to interact with the prototype sulfated glycosaminoglycan, heparin.	Glycosaminoglycans	308-325	vascular endothelial growth factor A	Mus musculus	68-74
17635914-7	2007	For XT-I we found an increased expression in parallel with an elevated chondroitin sulfate-GAG content after incubation with TGF-beta(1) and after mechanical stretch.	Glycosaminoglycans	91-94	xylosyltransferase 1	Homo sapiens	4-8
17785808-4	2007	Previous studies from our laboratory demonstrated that hyaluronan (HA), a large glycosaminoglycan, abundant in the extracellular matrix and on the cell surface, caused a marked increase of IL-2-induced VLS in the lungs and liver of C57BL/6 mice.	Glycosaminoglycans	80-97	interleukin 2	Mus musculus	189-193
17580303-9	2007	Inhibition of attachment of glycosaminoglycans to the core proteins of proteoglycans by beta-d-xylosides also reduced incorporation of LTBP1 into the ECM.	Glycosaminoglycans	28-46	latent transforming growth factor beta binding protein 1	Homo sapiens	135-140
17673669-6	2007	Furthermore, induction of Wnt/beta-catenin signaling by LiCl enhances chondrogenesis in pericyte pellet cultures in the presence of transforming growth factor-beta3, as demonstrated by increased Sox-9 expression and glycosaminoglycan accumulation into the matrix.	Glycosaminoglycans	216-233	catenin beta 1	Homo sapiens	30-42
17673669-7	2007	In contrast, transduction of pericytes with a recombinant adenovirus encoding dominant-negative T-cell factor-4 (RAd/dnTCF), which blocks Wnt/beta-catenin signaling, inhibited chondrogenesis, leading to reduced Sox-9 and type II collagen expression and less glycosaminoglycan accumulation.	Glycosaminoglycans	258-275	transcription factor 7 like 2	Homo sapiens	96-111
17673669-7	2007	In contrast, transduction of pericytes with a recombinant adenovirus encoding dominant-negative T-cell factor-4 (RAd/dnTCF), which blocks Wnt/beta-catenin signaling, inhibited chondrogenesis, leading to reduced Sox-9 and type II collagen expression and less glycosaminoglycan accumulation.	Glycosaminoglycans	258-275	RRAD, Ras related glycolysis inhibitor and calcium channel regulator	Homo sapiens	113-116
17635914-7	2007	For XT-I we found an increased expression in parallel with an elevated chondroitin sulfate-GAG content after incubation with TGF-beta(1) and after mechanical stretch.	Glycosaminoglycans	91-94	transforming growth factor beta 1	Homo sapiens	125-136
17635914-9	2007	Usage of XT-I small interfering RNA could specifically block the increased XT-I expression under mechanical stress and resulted in a significantly reduced chondroitin sulfate-GAG content.	Glycosaminoglycans	175-178	xylosyltransferase 1	Homo sapiens	9-13
17635914-14	2007	Specific blocking of XT-I expression confirmed that XT-I catalyzes a rate-limiting step during fibrotic GAG biosynthesis.	Glycosaminoglycans	104-107	xylosyltransferase 1	Homo sapiens	21-25
17635914-14	2007	Specific blocking of XT-I expression confirmed that XT-I catalyzes a rate-limiting step during fibrotic GAG biosynthesis.	Glycosaminoglycans	104-107	xylosyltransferase 1	Homo sapiens	52-56
17458871-2	2007	ARSB is a lysosomal enzyme involved in the degradation of the glycosaminoglycans (GAG) dermatan and chondroitin sulfate.	Glycosaminoglycans	62-80	arylsulfatase B	Homo sapiens	0-4
17922662-4	2007	A change of expression level of decorin correlated with expression of D-glucuronyl-C5-epimerase, a key enzyme responsible for the biosynthesis of idurone-containing glycosaminoglycans, possessing antimitotic activity.	Glycosaminoglycans	165-183	glucuronic acid epimerase	Homo sapiens	70-95
17596313-0	2007	Gag influences transformation by Abelson murine leukemia virus and suppresses nuclear localization of the v-Abl protein.	Glycosaminoglycans	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-111
17596313-2	2007	Although the Gag-derived myristoylation signal targets the v-Abl protein to the plasma membrane, the protein contains the entire MA and p12 sequences and a small number of CA-derived residues.	Glycosaminoglycans	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-64
17596313-6	2007	Although all of the mutant proteins retained kinase activity, those defective in transformation were reduced in their ability to activate Erk, suggesting a role for Gag sequences in v-Abl signaling.	Glycosaminoglycans	165-168	mitogen-activated protein kinase 1	Homo sapiens	138-141
17596313-6	2007	Although all of the mutant proteins retained kinase activity, those defective in transformation were reduced in their ability to activate Erk, suggesting a role for Gag sequences in v-Abl signaling.	Glycosaminoglycans	165-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-187
17596313-7	2007	Immunofluorescence analysis revealed that a v-Abl protein retaining only the first 34 amino acids of Gag localized to the nucleus.	Glycosaminoglycans	101-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
17596313-8	2007	These data indicate that Gag sequences are important for normal v-Abl signaling and that they suppress nuclear localization of the molecule.	Glycosaminoglycans	25-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
17458871-2	2007	ARSB is a lysosomal enzyme involved in the degradation of the glycosaminoglycans (GAG) dermatan and chondroitin sulfate.	Glycosaminoglycans	82-85	arylsulfatase B	Homo sapiens	0-4
17458871-3	2007	ARSB mutations reduce enzyme function and GAG degradation, causing lysosomal storage and urinary excretion of these partially degraded substrates.	Glycosaminoglycans	42-45	arylsulfatase B	Homo sapiens	0-4
17658885-0	2007	Glycosaminoglycans as naturally occurring combinatorial libraries: developing a mass spectrometry-based strategy for characterization of anti-thrombin interaction with low molecular weight heparin and heparin oligomers.	Glycosaminoglycans	0-18	coagulation factor II, thrombin	Homo sapiens	142-150
17609268-5	2007	Mice encode an antiviral restriction factor called Fv1 (for Friend virus susceptibility gene 1), which is active against murine leukemia virus and related to endogenous gag sequences.	Glycosaminoglycans	169-172	Friend virus susceptibility 1	Mus musculus	51-54
17704393-12	2007	These data indicate that glypican-1 function requires the GAG chain attachment sites for myogenic satellite cell FGF2 responsiveness during proliferation and to affect the process of differentiation.	Glycosaminoglycans	58-61	glypican-1	Meleagris gallopavo	25-35
17704393-12	2007	These data indicate that glypican-1 function requires the GAG chain attachment sites for myogenic satellite cell FGF2 responsiveness during proliferation and to affect the process of differentiation.	Glycosaminoglycans	58-61	fibroblast growth factor 2	Meleagris gallopavo	113-117
17588949-11	2007	In summary, our data indicate that COMP/TSP5 is an aggrecan-binding protein, and this interaction is regulated by the calcium-sensitive conformation of COMP/TSP5; interaction of COMP with aggrecan can be mediated through the GAG side chains on aggrecan and the "signature domain" of COMP/TSP5.	Glycosaminoglycans	225-228	cartilage oligomeric matrix protein	Homo sapiens	40-44
17588949-11	2007	In summary, our data indicate that COMP/TSP5 is an aggrecan-binding protein, and this interaction is regulated by the calcium-sensitive conformation of COMP/TSP5; interaction of COMP with aggrecan can be mediated through the GAG side chains on aggrecan and the "signature domain" of COMP/TSP5.	Glycosaminoglycans	225-228	cartilage oligomeric matrix protein	Homo sapiens	157-161
17588949-11	2007	In summary, our data indicate that COMP/TSP5 is an aggrecan-binding protein, and this interaction is regulated by the calcium-sensitive conformation of COMP/TSP5; interaction of COMP with aggrecan can be mediated through the GAG side chains on aggrecan and the "signature domain" of COMP/TSP5.	Glycosaminoglycans	225-228	cartilage oligomeric matrix protein	Homo sapiens	157-161
17681480-1	2007	Mucopolysaccharidosis type IIIA (MPS IIIA) is a specific lysosomal storage disorder caused by an enzyme deficiency in sulphamidase, which is required for the degradation of heparan sulphate glycosaminoglycan (gag).	Glycosaminoglycans	209-212	N-sulfoglucosamine sulfohydrolase (sulfamidase)	Mus musculus	118-130
17615585-4	2007	Enhanced CD4+ T cell responses were stimulated when Gag was redirected into the lysosomal pathway via the targeting signal derived from lysosome-associated membrane protein-1 (LAMP-1).	Glycosaminoglycans	52-55	CD4 molecule	Homo sapiens	9-12
17697350-11	2007	Progrado was exceptionally effective in reducing both basal and IL-1beta induced glycosaminoglycan release from human cartilage explants at concentrations that also directly blocked the gelatinolytic activity of MMP-2 and MMP-9.	Glycosaminoglycans	81-98	interleukin 1 beta	Homo sapiens	64-72
17725421-6	2007	Only 52% of the Nef peptides and 64% of the Gag peptides that elicited a CTL response contained sequence motifs thought to be required for binding by the HLA-A or -B alleles found in the corresponding patient.	Glycosaminoglycans	44-47	major histocompatibility complex, class I, A	Homo sapiens	154-165
17610078-2	2007	In Drosophila, mutations in the tout velu (ttv) gene, a homolog of the mammalian EXT1 tumor suppressor gene, leads to abrogation of glycosaminoglycan (GAG) biosynthesis.	Glycosaminoglycans	132-149	exostosin glycosyltransferase 1	Homo sapiens	81-85
17610078-2	2007	In Drosophila, mutations in the tout velu (ttv) gene, a homolog of the mammalian EXT1 tumor suppressor gene, leads to abrogation of glycosaminoglycan (GAG) biosynthesis.	Glycosaminoglycans	151-154	exostosin glycosyltransferase 1	Homo sapiens	81-85
17610078-6	2007	The hEXT1 gene was able to rescue a ttv null mutant to adulthood and restore GAG biosynthesis.	Glycosaminoglycans	77-80	exostosin glycosyltransferase 1	Homo sapiens	4-9
17573353-4	2007	Pharmacological inhibition of Rac1 expression in micromass culture resulted in reduced mRNA levels of the chondrogenic markers collagen II and aggrecan, and decreased accumulation of glycosaminoglycans.	Glycosaminoglycans	183-201	Rac family small GTPase 1	Mus musculus	30-34
17635118-1	2007	The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).	Glycosaminoglycans	302-305	TNF alpha induced protein 6	Homo sapiens	36-41
17635118-1	2007	The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).	Glycosaminoglycans	302-305	TNF alpha induced protein 6	Homo sapiens	58-98
17635118-1	2007	The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).	Glycosaminoglycans	302-305	CYCS pseudogene 39	Homo sapiens	151-154
17635118-1	2007	The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).	Glycosaminoglycans	302-305	CYCS pseudogene 38	Homo sapiens	159-162
17635118-1	2007	The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).	Glycosaminoglycans	302-305	TNF alpha induced protein 6	Homo sapiens	208-213
17635118-1	2007	The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).	Glycosaminoglycans	302-305	TNF alpha induced protein 6	Homo sapiens	208-213
17635118-1	2007	The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).	Glycosaminoglycans	307-324	TNF alpha induced protein 6	Homo sapiens	36-41
17635118-1	2007	The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).	Glycosaminoglycans	307-324	TNF alpha induced protein 6	Homo sapiens	58-98
17635118-1	2007	The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).	Glycosaminoglycans	307-324	CYCS pseudogene 39	Homo sapiens	151-154
17635118-1	2007	The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).	Glycosaminoglycans	307-324	CYCS pseudogene 38	Homo sapiens	159-162
17635118-1	2007	The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).	Glycosaminoglycans	307-324	TNF alpha induced protein 6	Homo sapiens	208-213
17635118-1	2007	The inflammation-associated protein TSG-6 (the product of tumour necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-alpha-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).	Glycosaminoglycans	307-324	TNF alpha induced protein 6	Homo sapiens	208-213
17222823-0	2007	Enhanced production of p24 Gag protein in HIV-1-infected rat cells fused with uninfected human cells.	Glycosaminoglycans	27-30	transmembrane p24 trafficking protein 2	Homo sapiens	23-26
17662008-0	2007	Copaxone interferes with the PrP Sc-GAG interaction.	Glycosaminoglycans	36-39	major prion protein	Cricetulus griseus	29-32
17615585-4	2007	Enhanced CD4+ T cell responses were stimulated when Gag was redirected into the lysosomal pathway via the targeting signal derived from lysosome-associated membrane protein-1 (LAMP-1).	Glycosaminoglycans	52-55	lysosomal associated membrane protein 1	Homo sapiens	136-174
17615585-4	2007	Enhanced CD4+ T cell responses were stimulated when Gag was redirected into the lysosomal pathway via the targeting signal derived from lysosome-associated membrane protein-1 (LAMP-1).	Glycosaminoglycans	52-55	lysosomal associated membrane protein 1	Homo sapiens	176-182
17615585-5	2007	Rhesus DC transfected with lysosome-targeted gag encoding an escape mutation in an immunodominant CTL epitope stimulated CD4+ and CD8+ T cell responses of almost equivalent magnitude directed towards undefined epitopes outside of the mutated region.	Glycosaminoglycans	45-48	CD4 molecule	Homo sapiens	121-124
17615585-5	2007	Rhesus DC transfected with lysosome-targeted gag encoding an escape mutation in an immunodominant CTL epitope stimulated CD4+ and CD8+ T cell responses of almost equivalent magnitude directed towards undefined epitopes outside of the mutated region.	Glycosaminoglycans	45-48	CD8a molecule	Homo sapiens	130-133
17646643-2	2007	An inherited deficiency of beta-glucuronidase (GUS) causes mucopolysaccharidosis type VII that is characterized by increased systemic and CNS storage of glycosaminoglycans.	Glycosaminoglycans	153-171	glucuronidase, beta	Mus musculus	47-50
17651433-0	2007	The glycosaminoglycan chain of decorin plays an important role in collagen fibril formation at the early stages of fibrillogenesis.	Glycosaminoglycans	4-21	decorin	Homo sapiens	31-38
17651433-2	2007	In patients with a variant of Ehlers-Danlos syndrome, about half of the secreted decorin lacks the single glycosaminoglycan side chain.	Glycosaminoglycans	106-123	decorin	Homo sapiens	81-88
17545188-4	2007	This site, Gag-30, lies within p17, the gag-encoded matrix protein.	Glycosaminoglycans	11-14	family with sequence similarity 72 member B	Homo sapiens	31-34
17545188-4	2007	This site, Gag-30, lies within p17, the gag-encoded matrix protein.	Glycosaminoglycans	40-43	family with sequence similarity 72 member B	Homo sapiens	31-34
17538883-3	2007	This escape was associated with the development of mutations in 2 HLA-B*57-restricted CD8(+) T cell Gag epitopes, reversion of the drug-resistance mutation M184V, and reversion of a novel polymorphism in Vpu.	Glycosaminoglycans	100-103	major histocompatibility complex, class I, B	Homo sapiens	66-71
17470431-4	2007	Our data indicate that this interaction is mediated largely through the binding of glycosaminoglycans (specifically chondroitin 6-sulfate) of aggrecan to binding sites in the thrombospondin type 1 motif and spacer domains of ADAMTS-4 to form a complex with an improved binding affinity for TIMP-3 over free ADAMTS-4.	Glycosaminoglycans	83-101	ADAM metallopeptidase with thrombospondin type 1 motif 4	Homo sapiens	225-233
17470431-4	2007	Our data indicate that this interaction is mediated largely through the binding of glycosaminoglycans (specifically chondroitin 6-sulfate) of aggrecan to binding sites in the thrombospondin type 1 motif and spacer domains of ADAMTS-4 to form a complex with an improved binding affinity for TIMP-3 over free ADAMTS-4.	Glycosaminoglycans	83-101	TIMP metallopeptidase inhibitor 3	Homo sapiens	290-296
17470431-4	2007	Our data indicate that this interaction is mediated largely through the binding of glycosaminoglycans (specifically chondroitin 6-sulfate) of aggrecan to binding sites in the thrombospondin type 1 motif and spacer domains of ADAMTS-4 to form a complex with an improved binding affinity for TIMP-3 over free ADAMTS-4.	Glycosaminoglycans	83-101	ADAM metallopeptidase with thrombospondin type 1 motif 4	Homo sapiens	307-315
17437056-1	2007	The xylosyltransferases I and II (XT-I, XT-II, EC 2.4.2.26) catalyze the transfer of xylose from UDP-xylose to selected serine residues in the proteoglycan core protein, which is the initial and ratelimiting step in glycosaminoglycan biosynthesis.	Glycosaminoglycans	216-233	xylosyltransferase 1	Homo sapiens	4-32
17360715-11	2007	The data support a causal link between H402Y and age-related macular degeneration in which variation at position 402 modulates the response of factor H to age-related changes in the glycosaminoglycan composition and apoptotic activity of the macula.	Glycosaminoglycans	182-199	complement factor H	Homo sapiens	143-151
17573534-8	2007	Using constructs of PrP, we show that this regulatory effect of PrP(C) on the beta-secretase cleavage of APP required the localization of PrP(C) to cholesterol-rich lipid rafts and was mediated by the N-terminal polybasic region of PrP(C) via interaction with glycosaminoglycans.	Glycosaminoglycans	260-278	prion protein	Homo sapiens	20-23
17573534-8	2007	Using constructs of PrP, we show that this regulatory effect of PrP(C) on the beta-secretase cleavage of APP required the localization of PrP(C) to cholesterol-rich lipid rafts and was mediated by the N-terminal polybasic region of PrP(C) via interaction with glycosaminoglycans.	Glycosaminoglycans	260-278	prion protein	Homo sapiens	64-70
17573534-8	2007	Using constructs of PrP, we show that this regulatory effect of PrP(C) on the beta-secretase cleavage of APP required the localization of PrP(C) to cholesterol-rich lipid rafts and was mediated by the N-terminal polybasic region of PrP(C) via interaction with glycosaminoglycans.	Glycosaminoglycans	260-278	prion protein	Homo sapiens	138-144
17573534-8	2007	Using constructs of PrP, we show that this regulatory effect of PrP(C) on the beta-secretase cleavage of APP required the localization of PrP(C) to cholesterol-rich lipid rafts and was mediated by the N-terminal polybasic region of PrP(C) via interaction with glycosaminoglycans.	Glycosaminoglycans	260-278	prion protein	Homo sapiens	138-144
17547695-4	2007	The individual expression of MLV Env resulted in its accumulation in LE in contrast to RD114 Env that required the presence of gamma retroviral Gag proteins.	Glycosaminoglycans	144-147	endogenous retrovirus group W member 1, envelope	Homo sapiens	93-96
17503336-1	2007	A GAG deletion in the DYT1 gene is a major cause of early-onset dystonia, but clinical disease expression occurs in only 30% of mutation carriers.	Glycosaminoglycans	2-5	torsin family 1 member A	Homo sapiens	22-26
17503336-2	2007	To gain insight into genetic factors that may influence penetrance, we evaluated three DYT1 single-nucleotide polymorphisms, including D216H, a coding-sequence variation that moderates the effects of the DYT1 GAG deletion in cellular models.	Glycosaminoglycans	209-212	torsin family 1 member A	Homo sapiens	204-208
17437056-1	2007	The xylosyltransferases I and II (XT-I, XT-II, EC 2.4.2.26) catalyze the transfer of xylose from UDP-xylose to selected serine residues in the proteoglycan core protein, which is the initial and ratelimiting step in glycosaminoglycan biosynthesis.	Glycosaminoglycans	216-233	xylosyltransferase 1	Homo sapiens	34-38
17437056-1	2007	The xylosyltransferases I and II (XT-I, XT-II, EC 2.4.2.26) catalyze the transfer of xylose from UDP-xylose to selected serine residues in the proteoglycan core protein, which is the initial and ratelimiting step in glycosaminoglycan biosynthesis.	Glycosaminoglycans	216-233	xylosyltransferase 2	Homo sapiens	40-45
17277974-1	2007	Chondroitin 4-sulfate (C4S) is a bioactive glycosaminoglycan with inductive properties in bone and tissue regeneration.	Glycosaminoglycans	43-60	complement C4A (Rodgers blood group)	Homo sapiens	0-26
17539945-0	2007	Clinical characteristics of carriers of a GAG deletion in the DYT1 gene amongst Polish patients with primary dystonia.	Glycosaminoglycans	42-45	torsin family 1 member A	Homo sapiens	62-66
17539945-3	2007	We assessed the frequency of the GAG deletion in the DYT1 gene in a group of 61 Polish probands with clinical diagnosis of primary dystonia.	Glycosaminoglycans	33-36	torsin family 1 member A	Homo sapiens	53-57
17428861-2	2007	HIV-1 harbors a PTAP-type L domain in the p6 region of Gag that engages an endosomal budding machinery through Tsg101.	Glycosaminoglycans	55-58	tumor susceptibility 101	Homo sapiens	111-117
17344302-9	2007	In patients not on antiretroviral therapy, the magnitude of Gag-specific responses, as a percentage of CD8(+) T cells, was greater in the rectal mucosa than in PBMC (P = 0.054); however, the breakdown of responding cells into specific functional categories was similar in both sites.	Glycosaminoglycans	60-63	CD8a molecule	Homo sapiens	103-106
17517600-0	2007	Polycystic disease caused by deficiency in xylosyltransferase 2, an initiating enzyme of glycosaminoglycan biosynthesis.	Glycosaminoglycans	89-106	xylosyltransferase 2	Homo sapiens	43-63
17376899-2	2007	Following infection, the majority (&gt;95%) of Gag-specific CD8 T cells expressed PD-1, and the level of PD-1 expression per cell increased over time.	Glycosaminoglycans	47-50	CD8a molecule	Homo sapiens	60-63
17376899-2	2007	Following infection, the majority (&gt;95%) of Gag-specific CD8 T cells expressed PD-1, and the level of PD-1 expression per cell increased over time.	Glycosaminoglycans	47-50	programmed cell death 1	Homo sapiens	82-86
17376899-2	2007	Following infection, the majority (&gt;95%) of Gag-specific CD8 T cells expressed PD-1, and the level of PD-1 expression per cell increased over time.	Glycosaminoglycans	47-50	programmed cell death 1	Homo sapiens	105-109
17459751-1	2007	Mucopolysaccharidosis II (MPS II; Hunter syndrome) is an X-linked metabolic disorder caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase (I2S), which catalyzes the catabolism of glycosaminoglycans (GAG) by cleaving the O-linked sulfate from dermatan sulfate and heparan sulfate.	Glycosaminoglycans	195-213	iduronate 2-sulfatase	Mus musculus	132-153
17459751-1	2007	Mucopolysaccharidosis II (MPS II; Hunter syndrome) is an X-linked metabolic disorder caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase (I2S), which catalyzes the catabolism of glycosaminoglycans (GAG) by cleaving the O-linked sulfate from dermatan sulfate and heparan sulfate.	Glycosaminoglycans	195-213	iduronate 2-sulfatase	Mus musculus	155-158
17459751-1	2007	Mucopolysaccharidosis II (MPS II; Hunter syndrome) is an X-linked metabolic disorder caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase (I2S), which catalyzes the catabolism of glycosaminoglycans (GAG) by cleaving the O-linked sulfate from dermatan sulfate and heparan sulfate.	Glycosaminoglycans	215-218	iduronate 2-sulfatase	Mus musculus	132-153
17459751-1	2007	Mucopolysaccharidosis II (MPS II; Hunter syndrome) is an X-linked metabolic disorder caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase (I2S), which catalyzes the catabolism of glycosaminoglycans (GAG) by cleaving the O-linked sulfate from dermatan sulfate and heparan sulfate.	Glycosaminoglycans	215-218	iduronate 2-sulfatase	Mus musculus	155-158
17459751-3	2007	The purpose of the studies presented here was to describe some of the preclinical development of idursulfase using the I2S knock-out mouse model of MPS II designed to study the effect of dose and various dosing regimens of idursulfase on urine and tissue GAG levels.	Glycosaminoglycans	255-258	iduronate 2-sulfatase	Homo sapiens	97-108
17459751-3	2007	The purpose of the studies presented here was to describe some of the preclinical development of idursulfase using the I2S knock-out mouse model of MPS II designed to study the effect of dose and various dosing regimens of idursulfase on urine and tissue GAG levels.	Glycosaminoglycans	255-258	iduronate 2-sulfatase	Homo sapiens	223-234
17459751-6	2007	Results showed that idursulfase, at several doses and at several dosing frequencies, caused a reduction in tissue and urine GAG levels in a dose-dependent manner.	Glycosaminoglycans	124-127	iduronate 2-sulfatase	Homo sapiens	20-31
17459751-7	2007	These studies also demonstrated that after IV administration, idursulfase is biologically active in the IdS-KO mouse model and is transported to key target tissues, reaching the lysosomes in an active form, and degrading the accumulated GAG.	Glycosaminoglycans	237-240	iduronate 2-sulfatase	Homo sapiens	62-73
17434638-5	2007	Chondrocyte macroaggregates presented long survival time and good viability; constructs fabricated using both techniques can develop into tissues with characteristic structure of native cartilage, glycosaminoglycans as well as type II collagen were highly produced in the ECM of engineered cartilages.	Glycosaminoglycans	197-215	multimerin 1	Homo sapiens	272-275
17217338-7	2007	Affinity chromatography studies using CS isolated from aggrecan indicate that the catalytic domain of MT3-MMP and the C-terminal domain of MMP-2 directly bind to the GAG.	Glycosaminoglycans	166-169	matrix metallopeptidase 16	Homo sapiens	102-109
17217338-1	2007	We previously reported that CS (chondroitin sulfate) GAG (glycosaminoglycan), expressed on MCSP (melanoma-specific CS proteoglycan), is important for regulating MT3-MMP [membrane-type 3 MMP (matrix metalloproteinase)]-mediated human melanoma invasion and gelatinolytic activity in vitro.	Glycosaminoglycans	53-56	chondroitin sulfate proteoglycan 4	Homo sapiens	91-95
17217338-7	2007	Affinity chromatography studies using CS isolated from aggrecan indicate that the catalytic domain of MT3-MMP and the C-terminal domain of MMP-2 directly bind to the GAG.	Glycosaminoglycans	166-169	matrix metallopeptidase 2	Homo sapiens	139-144
17217338-1	2007	We previously reported that CS (chondroitin sulfate) GAG (glycosaminoglycan), expressed on MCSP (melanoma-specific CS proteoglycan), is important for regulating MT3-MMP [membrane-type 3 MMP (matrix metalloproteinase)]-mediated human melanoma invasion and gelatinolytic activity in vitro.	Glycosaminoglycans	53-56	chondroitin sulfate proteoglycan 4	Homo sapiens	97-130
17471004-4	2007	Specific molecules such as glycosaminoglycans and proteoglycans that affect the conformation and stability of beta(2)-m and amyloid fibrils are considered to have significant effects on the formation and deposition of amyloid fibrils.	Glycosaminoglycans	27-45	beta-2-microglobulin	Homo sapiens	110-119
17217338-1	2007	We previously reported that CS (chondroitin sulfate) GAG (glycosaminoglycan), expressed on MCSP (melanoma-specific CS proteoglycan), is important for regulating MT3-MMP [membrane-type 3 MMP (matrix metalloproteinase)]-mediated human melanoma invasion and gelatinolytic activity in vitro.	Glycosaminoglycans	53-56	matrix metallopeptidase 16	Homo sapiens	161-168
17217338-1	2007	We previously reported that CS (chondroitin sulfate) GAG (glycosaminoglycan), expressed on MCSP (melanoma-specific CS proteoglycan), is important for regulating MT3-MMP [membrane-type 3 MMP (matrix metalloproteinase)]-mediated human melanoma invasion and gelatinolytic activity in vitro.	Glycosaminoglycans	58-75	chondroitin sulfate proteoglycan 4	Homo sapiens	91-95
17217338-1	2007	We previously reported that CS (chondroitin sulfate) GAG (glycosaminoglycan), expressed on MCSP (melanoma-specific CS proteoglycan), is important for regulating MT3-MMP [membrane-type 3 MMP (matrix metalloproteinase)]-mediated human melanoma invasion and gelatinolytic activity in vitro.	Glycosaminoglycans	58-75	chondroitin sulfate proteoglycan 4	Homo sapiens	97-130
17217338-1	2007	We previously reported that CS (chondroitin sulfate) GAG (glycosaminoglycan), expressed on MCSP (melanoma-specific CS proteoglycan), is important for regulating MT3-MMP [membrane-type 3 MMP (matrix metalloproteinase)]-mediated human melanoma invasion and gelatinolytic activity in vitro.	Glycosaminoglycans	58-75	matrix metallopeptidase 16	Homo sapiens	161-168
17315042-6	2007	The sustained level of IGF-1 overexpression resulted in significantly higher amounts of tissue formation, chondrocyte-like cells, GAG accumulation, and type II collagen production, compared to control scaffolds.	Glycosaminoglycans	130-133	insulin like growth factor 1	Homo sapiens	23-28
17417949-7	2007	Further studies demonstrated that 5-mM RGDS chondrogenic cultures had greater gene expression for aggrecan and collagen II in conjunction with producing twice as much glycosaminoglycan as 0-mM chondrogenic cultures and 7 times that of control cultures.	Glycosaminoglycans	167-184	ral guanine nucleotide dissociation stimulator	Homo sapiens	39-43
17344295-4	2007	In particular, some investigators have reported that APOBEC3G interacts directly with the nucleocapsid (NC) subunit of Gag, while others have found that an RNA intermediate is required for Gag-APOBEC3G interactions.	Glycosaminoglycans	119-122	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	53-61
17344295-4	2007	In particular, some investigators have reported that APOBEC3G interacts directly with the nucleocapsid (NC) subunit of Gag, while others have found that an RNA intermediate is required for Gag-APOBEC3G interactions.	Glycosaminoglycans	189-192	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	193-201
17344295-7	2007	Specifically, Gag constructs containing only the N-terminal region of NC packaged minimal amounts of APOBEC3G, while significant levels of APOBEC3G packaging were achieved with Gag constructs containing the basic linker region of NC.	Glycosaminoglycans	177-180	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	139-147
17344295-8	2007	Furthermore, membrane-binding experiments revealed that the basic linker region was essential for the membrane association of APOBEC3G in a Gag-APOBEC3G complex.	Glycosaminoglycans	140-143	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	126-134
17344295-8	2007	Furthermore, membrane-binding experiments revealed that the basic linker region was essential for the membrane association of APOBEC3G in a Gag-APOBEC3G complex.	Glycosaminoglycans	140-143	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	144-152
17344295-10	2007	Regions of APOBEC3G-Gag colocalization at the plasma membrane were detected that were distinct from the punctate cytoplasmic bodies where APOBEC3G accumulates within the cell.	Glycosaminoglycans	20-23	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	11-19
17344295-11	2007	Together, our results indicate that APOBEC3G multimerizes in an RNA-dependent fashion and that RNA-APOBEC3G multimers are recruited to the plasma membrane and subsequently into virion particles by Gag.	Glycosaminoglycans	197-200	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	36-44
17344295-11	2007	Together, our results indicate that APOBEC3G multimerizes in an RNA-dependent fashion and that RNA-APOBEC3G multimers are recruited to the plasma membrane and subsequently into virion particles by Gag.	Glycosaminoglycans	197-200	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	99-107
17344296-6	2007	A transient CD8(+) cell depletion experiment 3 years postinfection resulted in transient reappearance of plasma viremia in these two animals, suggesting involvement of the SIV non-Gag-specific CTLs in the chronic SIV control.	Glycosaminoglycans	180-183	CD8a molecule	Homo sapiens	12-15
17344299-0	2007	In vivo fitness costs of different Gag CD8 T-cell escape mutant simian-human immunodeficiency viruses for macaques.	Glycosaminoglycans	35-38	CD8a molecule	Homo sapiens	39-42
17344299-2	2007	Escape kinetics of three simian immunodeficiency virus Gag CTL epitopes in pigtail macaques were variable; those of KP9 and AF9 were faster than those of KW9.	Glycosaminoglycans	55-58	MLLT3 super elongation complex subunit	Homo sapiens	124-127
17456603-7	2007	Accordingly, all mutant rPrPs bind more GAG, and GAG promotes the aggregation of mutant rPrPs more efficiently than wild-type recombinant normal cellular PrP (rPrP(C)).	Glycosaminoglycans	40-43	prion protein	Rattus norvegicus	25-28
17456603-7	2007	Accordingly, all mutant rPrPs bind more GAG, and GAG promotes the aggregation of mutant rPrPs more efficiently than wild-type recombinant normal cellular PrP (rPrP(C)).	Glycosaminoglycans	40-43	prion protein	Rattus norvegicus	24-28
17456603-9	2007	Importantly, brain-derived PrP from transgenic mice, which express a pathogenic mutant with nine extra octapeptide repeats, also binds more strongly to GAG than wild-type PrP(C).	Glycosaminoglycans	152-155	prion protein	Mus musculus	27-30
17311010-1	2007	Mucopolysaccharidosis I (MPS I) is caused by deficient alpha-L-iduronidase (IDUA) activity and results in the accumulation of glycosaminoglycans and multisystemic disease.	Glycosaminoglycans	126-144	iduronidase, alpha-L	Mus musculus	55-74
17311010-1	2007	Mucopolysaccharidosis I (MPS I) is caused by deficient alpha-L-iduronidase (IDUA) activity and results in the accumulation of glycosaminoglycans and multisystemic disease.	Glycosaminoglycans	126-144	iduronidase, alpha-L	Mus musculus	76-80
17126871-4	2007	Our studies revealed that the amount of the A3G incorporated into Deltavif virions was proportional to the level of its expression in the viral producing cells, and the ratio of the A3G to Gag in the Deltavif virions produced from activated human peripheral blood mononuclear cells (PBMC) was approximately 1:439.	Glycosaminoglycans	189-192	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	44-47
17379830-4	2007	PN-1 bound to the cell surface through interactions with glycosaminoglycans, is an efficient inhibitor of thrombin and controls thrombin-induced cell responses.	Glycosaminoglycans	57-75	serpin family E member 2	Homo sapiens	0-4
17126871-5	2007	Based on previous estimates of the stoichiometry of HIV-1 Gag in virions (1400-5000), we conclude that approximately 7 (+/-4) molecules of A3G are incorporated into Deltavif virions produced from human PBMCs.	Glycosaminoglycans	58-61	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	139-142
17397292-8	2007	RESULTS: Cultures treated with MMP-13 or IL-1alpha had increased media GAG concentration at 48 and 96 hours.	Glycosaminoglycans	71-74	matrix metallopeptidase 13	Equus caballus	31-37
17039513-9	2007	The platelet GPIIb/IIIa receptor antagonist (XV459) might be of potential benefit in the management of thrombotic thrombocytopenia produced by heparin and/or related glycosaminoglycans.	Glycosaminoglycans	166-184	integrin subunit alpha 2b	Homo sapiens	13-18
17343367-1	2007	Although the thrombin/thrombomodulin complex is considered the physiological activator of protein C, factor Xa (f.Xa) can also activate protein C in a reaction that is potentiated by glycosaminoglycans.	Glycosaminoglycans	183-201	coagulation factor X	Homo sapiens	101-110
17397292-8	2007	RESULTS: Cultures treated with MMP-13 or IL-1alpha had increased media GAG concentration at 48 and 96 hours.	Glycosaminoglycans	71-74	interleukin 1 alpha	Equus caballus	41-50
17233629-5	2007	We suggest that MPG-induced clustering of the glycosaminoglycan platform constitutes the "onset" of the cellular uptake mechanism, thereby increasing membrane dynamics and membrane fusion processes.	Glycosaminoglycans	46-63	N-methylpurine DNA glycosylase	Homo sapiens	16-19
17403366-1	2007	At the endothelial cell surface, binding of chylomicrons and lipoprotein lipase (LpL), the major enzyme involved in the processing of these triglyceride-rich lipoproteins, is thought to involve electrostatic interactions with glycosaminoglycans.	Glycosaminoglycans	226-244	lipoprotein lipase	Homo sapiens	61-79
17403366-1	2007	At the endothelial cell surface, binding of chylomicrons and lipoprotein lipase (LpL), the major enzyme involved in the processing of these triglyceride-rich lipoproteins, is thought to involve electrostatic interactions with glycosaminoglycans.	Glycosaminoglycans	226-244	lipoprotein lipase	Homo sapiens	81-84
17156989-7	2007	Cell surface proteoglycans may promote the attachment, as cells deficient in glycosaminoglycan biosynthesis adhere less well to matrilin-3.	Glycosaminoglycans	77-94	matrilin 3	Homo sapiens	128-138
17381672-1	2007	The aim of the study was to investigate the expression levels of endothelin-1 (ET-1) and ET(A) and ET(B) receptors (ET(A)-R and ET(B)-R) in porcine mitral valves and associate the transcription levels to age, leaflet location and deposition of mucopolysaccharides (MPS).	Glycosaminoglycans	244-263	endothelin-1	Sus scrofa	65-77
17381672-1	2007	The aim of the study was to investigate the expression levels of endothelin-1 (ET-1) and ET(A) and ET(B) receptors (ET(A)-R and ET(B)-R) in porcine mitral valves and associate the transcription levels to age, leaflet location and deposition of mucopolysaccharides (MPS).	Glycosaminoglycans	244-263	endothelin-1	Sus scrofa	79-83
17381672-1	2007	The aim of the study was to investigate the expression levels of endothelin-1 (ET-1) and ET(A) and ET(B) receptors (ET(A)-R and ET(B)-R) in porcine mitral valves and associate the transcription levels to age, leaflet location and deposition of mucopolysaccharides (MPS).	Glycosaminoglycans	244-263	endothelin receptor type A	Sus scrofa	89-94
17154173-10	2007	In addition, the data suggest that surface CS GAG chains were involved in P-selectin mediated adhesion of the 4T1 cells to murine platelets and human umbilical vein endothelial cells.	Glycosaminoglycans	46-49	selectin, platelet	Mus musculus	74-84
17384231-7	2007	However, mutations in the S2 subsite pocket of cathepsin L alone without engineering of binding sites to chondroitin sulfate are not sufficient to generate a cathepsin K-like collagenase, emphasizing the pivotal role of the complex formation between glycosaminoglycans and cathepsin K for its unique collagenolytic activity.	Glycosaminoglycans	250-268	cathepsin L	Homo sapiens	47-58
17389019-2	2007	Nucleotide sequence analysis showed the presence of a new HLA-A*02 allele identical to HLA-A*02010101 except for a non-synonymous nucleotide exchange in exon 4 modifying codon 232 from GAG (Glu) to GAC (Asp).	Glycosaminoglycans	185-188	major histocompatibility complex, class I, A	Homo sapiens	58-63
17145755-1	2007	The hyaluronic acid (HA) receptor for endocytosis (HARE; also designated stabilin-2 and FEEL-2) mediates systemic clearance of glycosaminoglycans from the circulatory and lymphatic systems via coated pit-mediated uptake.	Glycosaminoglycans	127-145	lymphatic vessel endothelial hyaluronan receptor 1	Homo sapiens	4-33
17000001-6	2007	A non-GAG-binding but receptor agonistic form of the chemokine CCL7 can inhibit leukocyte recruitment in response to a diverse range of chemokines in vitro and in vivo.	Glycosaminoglycans	6-9	C-C motif chemokine ligand 7	Homo sapiens	63-67
17124008-2	2007	Overall, the addition of TGF-beta1 increased cell viability, extracellular matrix (ECM) gene expression, matrix synthesis, and sulfated glycosaminoglycan content over basal construct medium.	Glycosaminoglycans	136-153	transforming growth factor beta 1	Bos taurus	25-34
17352757-0	2007	Release of basic fibroblast growth factor from a crosslinked glycosaminoglycan hydrogel promotes wound healing.	Glycosaminoglycans	61-78	fibroblast growth factor 2	Mus musculus	11-41
17189265-1	2007	Human xylosyltransferase I (XT-I) initiates the biosynthesis of the glycosaminoglycan (GAG) linkage tetrasaccharide in proteoglycans.	Glycosaminoglycans	68-85	xylosyltransferase 1	Homo sapiens	6-26
17189265-1	2007	Human xylosyltransferase I (XT-I) initiates the biosynthesis of the glycosaminoglycan (GAG) linkage tetrasaccharide in proteoglycans.	Glycosaminoglycans	68-85	xylosyltransferase 1	Homo sapiens	28-32
17189265-1	2007	Human xylosyltransferase I (XT-I) initiates the biosynthesis of the glycosaminoglycan (GAG) linkage tetrasaccharide in proteoglycans.	Glycosaminoglycans	87-91	xylosyltransferase 1	Homo sapiens	6-26
17189265-1	2007	Human xylosyltransferase I (XT-I) initiates the biosynthesis of the glycosaminoglycan (GAG) linkage tetrasaccharide in proteoglycans.	Glycosaminoglycans	87-91	xylosyltransferase 1	Homo sapiens	28-32
17189265-4	2007	Transfection of the xylosyltransferase-deficient Chinese hamster ovary mutant pgsA-745 with XT-I or XT-II coding cDNA completely restored GAG biosynthesis.	Glycosaminoglycans	138-141	xylosyltransferase 1	Homo sapiens	92-96
17189265-4	2007	Transfection of the xylosyltransferase-deficient Chinese hamster ovary mutant pgsA-745 with XT-I or XT-II coding cDNA completely restored GAG biosynthesis.	Glycosaminoglycans	138-141	xylosyltransferase 2	Homo sapiens	100-105
17206488-7	2007	Organization of elastin and collagen in engineered arteries may have been partially hindered by high concentrations of sulfated glycosaminoglycans.	Glycosaminoglycans	128-146	elastin	Homo sapiens	16-23
17312176-3	2007	In this study, we examined the suppressive function of the Gag-specific IL-10-positive CD8+ T cells.	Glycosaminoglycans	59-62	interleukin 10	Homo sapiens	72-77
17185020-8	2007	RESULTS: Urinary glycosaminoglycans were reduced within 2 weeks of initiating idursulfase and were decreased 49% after 48 weeks of treatment (P&lt;0.0001).	Glycosaminoglycans	17-35	iduronate 2-sulfatase	Homo sapiens	78-89
17345556-3	2007	DEVELOPMENT: A preclinical trial in a knockout mouse showed a decrease in glycosaminoglycans, both in urine and in tissues, following treatment with idursulfase.	Glycosaminoglycans	74-92	iduronate 2-sulfatase	Homo sapiens	149-160
17345556-4	2007	In a randomised, double-blind, placebo-controlled clinical study in phase I/II conducted in 12 patients with Hunter syndrome, treatment with idursulfase displayed a good safety profile and also a decrease in the excretion of glycosaminoglycans and cases of visceromegaly.	Glycosaminoglycans	225-243	iduronate 2-sulfatase	Homo sapiens	141-152
17145755-1	2007	The hyaluronic acid (HA) receptor for endocytosis (HARE; also designated stabilin-2 and FEEL-2) mediates systemic clearance of glycosaminoglycans from the circulatory and lymphatic systems via coated pit-mediated uptake.	Glycosaminoglycans	127-145	stabilin 2	Homo sapiens	51-55
17145755-1	2007	The hyaluronic acid (HA) receptor for endocytosis (HARE; also designated stabilin-2 and FEEL-2) mediates systemic clearance of glycosaminoglycans from the circulatory and lymphatic systems via coated pit-mediated uptake.	Glycosaminoglycans	127-145	stabilin 2	Homo sapiens	73-83
17145755-1	2007	The hyaluronic acid (HA) receptor for endocytosis (HARE; also designated stabilin-2 and FEEL-2) mediates systemic clearance of glycosaminoglycans from the circulatory and lymphatic systems via coated pit-mediated uptake.	Glycosaminoglycans	127-145	stabilin 2	Homo sapiens	88-94
17049328-1	2007	Osteoclast inhibitory lectin (OCIL) is a type II C-type lectin and binds NK cell-associated receptor Nkrp1d and sulfated glycosaminoglycans.	Glycosaminoglycans	121-139	C-type lectin domain family 2, member d	Mus musculus	0-28
17265493-8	2007	Chondrocytes sorted for brighter CD49c or CD44 signal expression produced tissues with higher levels of GAG per DNA (up to 1.4-fold) and type II collagen messenger RNA (up to 3.4-fold) than did unsorted cells.	Glycosaminoglycans	104-107	CD44 molecule (Indian blood group)	Homo sapiens	42-46
17049328-1	2007	Osteoclast inhibitory lectin (OCIL) is a type II C-type lectin and binds NK cell-associated receptor Nkrp1d and sulfated glycosaminoglycans.	Glycosaminoglycans	121-139	C-type lectin domain family 2, member d	Mus musculus	30-34
17180725-5	2007	In vivo studies in mice were carried out to evaluate the immune responses obtained to his-tag Gag p24 bound to Ni-NPs.	Glycosaminoglycans	94-97	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	98-101
17097365-9	2007	Our patient was a heterozygote carrier of GAG--&gt;GAC mutation (Glu 768 Asp) in exon 13, codon 768 of the RET proto-oncogene.	Glycosaminoglycans	42-45	ret proto-oncogene	Homo sapiens	107-110
16979922-1	2007	Mucopolysaccharidosis I (MPS I) due to deficient alpha-L-iduronidase (IDUA) activity results in accumulation of glycosaminoglycans in many cells.	Glycosaminoglycans	112-130	iduronidase, alpha-L	Mus musculus	49-68
16979922-1	2007	Mucopolysaccharidosis I (MPS I) due to deficient alpha-L-iduronidase (IDUA) activity results in accumulation of glycosaminoglycans in many cells.	Glycosaminoglycans	112-130	iduronidase, alpha-L	Mus musculus	70-74
16908205-11	2007	A decrease in either GAG sulfation or CS content diminished bACs" response to Wnt3a (approximately 40% and 37% of control, respectively).	Glycosaminoglycans	21-24	solute carrier family 27 member 5	Homo sapiens	60-65
16908205-11	2007	A decrease in either GAG sulfation or CS content diminished bACs" response to Wnt3a (approximately 40% and 37% of control, respectively).	Glycosaminoglycans	21-24	Wnt family member 3A	Homo sapiens	78-83
16965923-5	2007	When compared to untreated defects, higher scores were observed with IGF-1-treated defects for the six markers of neo-surface repair: neo-surface morphology, cartilage thickness, surface regularity, chondrocyte clustering, and the chondrocyte/glycosaminoglycan content of the neo-surface and the cartilage surrounding the defect.	Glycosaminoglycans	243-260	insulin-like growth factor I	Oryctolagus cuniculus	69-74
17180725-7	2007	The optimal binding ratio his-tag GFP and his-tag Gag p24 to Ni-NPs was found to be 1:33.7 and 1:35.4 w/w, respectively.	Glycosaminoglycans	50-53	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	54-57
17180725-9	2007	The in vivo studies demonstrated enhanced serum IgG and IgG2a responses to his-tag Gag p24 bound to Ni-NPs compared to protein adjuvanted with Alum or adsorbed on the surface of control NTA-NPs.	Glycosaminoglycans	83-86	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	87-90
17229838-7	2007	Presentation was diverse, because we identified eight different gag peptides that were recognized via DEC-205 in 11 individuals studied consecutively.	Glycosaminoglycans	64-67	lymphocyte antigen 75	Homo sapiens	102-109
17145752-4	2007	Interestingly, Ser-62 of proMBP is substituted with a glycosaminoglycan (GAG) chain, possibly a heparan sulfate type, and the PAPP-A.proMBP complex is unable to bind to the cell surface.	Glycosaminoglycans	54-71	proteoglycan 2, pro eosinophil major basic protein	Homo sapiens	25-31
17145752-4	2007	Interestingly, Ser-62 of proMBP is substituted with a glycosaminoglycan (GAG) chain, possibly a heparan sulfate type, and the PAPP-A.proMBP complex is unable to bind to the cell surface.	Glycosaminoglycans	54-71	pappalysin 1	Homo sapiens	126-132
17145752-5	2007	We show here that proMBP detaches surface-bound PAPP-A in a process that depends on the proMBP GAG and also on the formation of intermolecular disulfide bonds between PAPP-A and proMBP.	Glycosaminoglycans	95-98	proteoglycan 2, pro eosinophil major basic protein	Homo sapiens	18-24
17145752-5	2007	We show here that proMBP detaches surface-bound PAPP-A in a process that depends on the proMBP GAG and also on the formation of intermolecular disulfide bonds between PAPP-A and proMBP.	Glycosaminoglycans	95-98	pappalysin 1	Homo sapiens	48-54
30743745-1	2007	Mucopolysaccharidosis type II (Hunter syndrome) is a lysosomal storage disorder caused by deficiency of iduronate-2-sulfatase leading to tissue accumulation of glycosaminoglycans.	Glycosaminoglycans	160-178	iduronate 2-sulfatase	Homo sapiens	104-125
17227588-2	2007	The disease is caused by a deficiency of the lysosomal enzyme sulphamidase and results in the storage of the glycosaminoglycan (GAG), heparan sulphate.	Glycosaminoglycans	109-126	N-sulfoglucosamine sulfohydrolase (sulfamidase)	Mus musculus	62-74
17227588-2	2007	The disease is caused by a deficiency of the lysosomal enzyme sulphamidase and results in the storage of the glycosaminoglycan (GAG), heparan sulphate.	Glycosaminoglycans	128-131	N-sulfoglucosamine sulfohydrolase (sulfamidase)	Mus musculus	62-74
17263645-0	2007	A synthetic gag p24 epitope chemically coupled to BSA through a decaalanine peptide enhances HIV type 1 serodiagnostic ability by several folds.	Glycosaminoglycans	12-15	transmembrane p24 trafficking protein 2	Homo sapiens	16-19
17143825-9	2007	CD8+ T cell levels specific for each pool of peptides were similar in both groups, but cells mainly contributing to HIV Gag-specific responses in coinfected patients were CCL4 positive and interferon-gamma negative, whereas for HIV-monoinfected subjects, the response was dominated by CCL4-positive and interferon-gamma-positive cells.	Glycosaminoglycans	120-123	C-C motif chemokine ligand 4	Homo sapiens	171-175
17143825-9	2007	CD8+ T cell levels specific for each pool of peptides were similar in both groups, but cells mainly contributing to HIV Gag-specific responses in coinfected patients were CCL4 positive and interferon-gamma negative, whereas for HIV-monoinfected subjects, the response was dominated by CCL4-positive and interferon-gamma-positive cells.	Glycosaminoglycans	120-123	interferon gamma	Homo sapiens	189-205
17143825-9	2007	CD8+ T cell levels specific for each pool of peptides were similar in both groups, but cells mainly contributing to HIV Gag-specific responses in coinfected patients were CCL4 positive and interferon-gamma negative, whereas for HIV-monoinfected subjects, the response was dominated by CCL4-positive and interferon-gamma-positive cells.	Glycosaminoglycans	120-123	C-C motif chemokine ligand 4	Homo sapiens	285-289
17143825-9	2007	CD8+ T cell levels specific for each pool of peptides were similar in both groups, but cells mainly contributing to HIV Gag-specific responses in coinfected patients were CCL4 positive and interferon-gamma negative, whereas for HIV-monoinfected subjects, the response was dominated by CCL4-positive and interferon-gamma-positive cells.	Glycosaminoglycans	120-123	interferon gamma	Homo sapiens	303-319
17105745-1	2007	DYT1 primary torsion dystonia is an autosomal dominant movement disorder due to a 3-bp GAG deletion in the TOR1A gene, which becomes manifest in only 30-40% of mutation carriers.	Glycosaminoglycans	87-90	torsin family 1 member A	Homo sapiens	0-4
17105745-1	2007	DYT1 primary torsion dystonia is an autosomal dominant movement disorder due to a 3-bp GAG deletion in the TOR1A gene, which becomes manifest in only 30-40% of mutation carriers.	Glycosaminoglycans	87-90	torsin family 1 member A	Homo sapiens	107-112
17194609-6	2007	Binding assays showed that the interaction of CCL2 with molecules present in trypomastigote forms is abolished by the addition of condroitin 6-sulphate, a glycosaminoglycan.	Glycosaminoglycans	155-172	chemokine (C-C motif) ligand 2	Mus musculus	46-50
17064891-1	2007	Sulfatase enzymes have important roles in metabolism of steroid hormones and of glycosaminoglycans (GAGs).	Glycosaminoglycans	80-98	arylsulfatase family member H	Homo sapiens	0-9
17222891-4	2007	All these glycosaminoglycans (GAGs) also inhibited thrombin-induced aggregation of washed platelets in the presence of antithrombin (AT) or heparin cofactor II (HCII) but not in their absence.	Glycosaminoglycans	10-28	coagulation factor II, thrombin	Homo sapiens	51-59
17173051-5	2007	Increasing breadth of Gag-specific responses was associated with decreasing viremia and increasing Env breadth with increasing viremia.	Glycosaminoglycans	22-25	endogenous retrovirus group K member 20	Homo sapiens	99-102
16891129-4	2007	RESULTS: Cell expansion with TFP enhanced glycosaminoglycan (GAG) deposition by all cell types (up to 4.1-fold) and messenger RNA expression of collagen type II by FPC and SMC (up to 472-fold) following pellet culture.	Glycosaminoglycans	42-59	inhibitor of carbonic anhydrase pseudogene	Homo sapiens	29-32
16891129-4	2007	RESULTS: Cell expansion with TFP enhanced glycosaminoglycan (GAG) deposition by all cell types (up to 4.1-fold) and messenger RNA expression of collagen type II by FPC and SMC (up to 472-fold) following pellet culture.	Glycosaminoglycans	61-64	inhibitor of carbonic anhydrase pseudogene	Homo sapiens	29-32
17365913-0	2007	Urinary glycosaminoglycan levels as a marker of renal amyloidosis in patients with familial Mediterranean fever.	Glycosaminoglycans	8-25	MEFV innate immuity regulator, pyrin	Homo sapiens	83-111
17259344-8	2007	These biological effects of SDF-1 were strongly inhibited by the CXCR4 antagonist AMD3100, by a glycosaminoglycan, heparin, as well as by beta-D-xyloside treatment of the cells, or by c-jun NH(2)-terminal kinase/stress-activated protein kinase inhibitor.	Glycosaminoglycans	96-113	C-X-C motif chemokine ligand 12	Homo sapiens	28-33
16919311-0	2007	Relative quantification of glycosaminoglycan-induced upregulation of TFPI-mRNA expression in vitro.	Glycosaminoglycans	27-44	tissue factor pathway inhibitor	Homo sapiens	69-73
17222891-4	2007	All these glycosaminoglycans (GAGs) also inhibited thrombin-induced aggregation of washed platelets in the presence of antithrombin (AT) or heparin cofactor II (HCII) but not in their absence.	Glycosaminoglycans	10-28	serpin family D member 1	Homo sapiens	161-165
17142960-6	2006	During the rolling interaction, which is mediated by L-selectin and sulfated glycans, lymphocytes receive activation signals from chemokines presented on the surface of HEV by heparan sulfate, a sulfated glycosaminoglycan, which leads to the activation of lymphocyte beta2 integrin.	Glycosaminoglycans	204-221	selectin, lymphocyte	Mus musculus	53-63
17020769-13	2006	Possible preferential binding of IGFBP-2 and its C- domain fragments to glycosaminoglycans in the acidic extracellular matrix (ECM) of tumours may be related to their roles in cancer.	Glycosaminoglycans	72-90	insulin like growth factor binding protein 2	Homo sapiens	33-40
17142960-6	2006	During the rolling interaction, which is mediated by L-selectin and sulfated glycans, lymphocytes receive activation signals from chemokines presented on the surface of HEV by heparan sulfate, a sulfated glycosaminoglycan, which leads to the activation of lymphocyte beta2 integrin.	Glycosaminoglycans	204-221	hemoglobin, beta adult minor chain	Mus musculus	267-272
17030874-3	2006	The generation of Gag-specific CD8(+) T cells was reported previously from a cynomolgus monkey infected with SHIV89.6P by taking advantage of a B-lymphoblastoid cell line transduced with a retroviral vector expressing simian immunodeficiency virus (SIV) Gag.	Glycosaminoglycans	18-21	CD8a molecule	Homo sapiens	31-34
16972247-6	2006	The inhibitory effects of FGF2 on FGFR3 expression and ALP activity are also mediated by the ERK pathway, although the effects of FGF2 on ColIalpha1 and OPN expression are mediated by GAGs and PKC activity.	Glycosaminoglycans	184-188	fibroblast growth factor 2	Rattus norvegicus	130-134
17176450-2	2006	This results in a single amino acid exchange depending on the closest related allele investigated, whether DRB*1103 codon 74 alanine (GCG) is changed to leucine (CTG) or DRB1*1125 codon 71 arginine (GAG) is replaced with glutamic acid.	Glycosaminoglycans	199-202	glucagon	Homo sapiens	134-137
16687179-8	2006	However, inhibition of p55 Gag processing by active-site inhibitors was enhanced when combined with P27, suggesting that P27 can affect protease function in maturing virions.	Glycosaminoglycans	27-30	dynactin subunit 6	Homo sapiens	121-124
17044753-1	2006	Mucopolysaccharidosis type I (MPS I) due to deficient alpha-L-iduronidase (IDUA) activity results in the accumulation of glycosaminoglycans (GAGs) in many of the cells of affected patients.	Glycosaminoglycans	121-139	alpha-L-iduronidase	Homo sapiens	54-73
17044753-1	2006	Mucopolysaccharidosis type I (MPS I) due to deficient alpha-L-iduronidase (IDUA) activity results in the accumulation of glycosaminoglycans (GAGs) in many of the cells of affected patients.	Glycosaminoglycans	121-139	iduronidase, alpha-L	Mus musculus	75-79
17044753-1	2006	Mucopolysaccharidosis type I (MPS I) due to deficient alpha-L-iduronidase (IDUA) activity results in the accumulation of glycosaminoglycans (GAGs) in many of the cells of affected patients.	Glycosaminoglycans	141-145	alpha-L-iduronidase	Homo sapiens	54-73
17044753-1	2006	Mucopolysaccharidosis type I (MPS I) due to deficient alpha-L-iduronidase (IDUA) activity results in the accumulation of glycosaminoglycans (GAGs) in many of the cells of affected patients.	Glycosaminoglycans	141-145	iduronidase, alpha-L	Mus musculus	75-79
17040958-1	2006	BACKGROUND: Xylosyltransferase I (XT-I), the key enzyme in the biosynthesis of glycosaminoglycan chains in proteoglycans, has increased activity in the blood serum of patients with connective tissue diseases.	Glycosaminoglycans	79-96	xylosyltransferase 1	Homo sapiens	12-32
17040958-1	2006	BACKGROUND: Xylosyltransferase I (XT-I), the key enzyme in the biosynthesis of glycosaminoglycan chains in proteoglycans, has increased activity in the blood serum of patients with connective tissue diseases.	Glycosaminoglycans	79-96	xylosyltransferase 1	Homo sapiens	34-38
17518673-5	2006	TGF-beta1 induced matrix contraction and enhanced collagen and sulfated glycosaminoglycan production, bFGF effectively increased cell proliferation, and HGF stimulated synthesis of hyaluronic acid and elastin with less collagen accumulation than other conditions.	Glycosaminoglycans	72-89	transforming growth factor beta 1	Homo sapiens	0-9
16982628-10	2006	Further proteolytic processing of sTEM5 leads to exposure of its RGD motif mediating endothelial cell survival by linking integrin alpha(v)beta3 to glycosaminoglycans.	Glycosaminoglycans	148-166	integrin subunit alpha V	Homo sapiens	122-144
17450675-9	2006	We found that any variation in GlcAT-I activity in chondrocytes or cartilage explants (overexpression, or repression with antisense RNA) affected the GAG content of cartilage.	Glycosaminoglycans	150-153	beta-1,3-glucuronyltransferase 3	Homo sapiens	31-38
17009243-11	2006	In OSM/IL-1beta- stimulated cocultures, cartilage sections demonstrated significant proteoglycan depletion that was paralleled by a significant increase in GAG release in supernatants.	Glycosaminoglycans	156-159	interleukin 1 beta	Homo sapiens	7-15
17009261-1	2006	OBJECTIVE: To determine whether interleukin-1alpha (IL-1alpha) induces tensile weakening of articular cartilage that is concomitant with the loss of glycosaminoglycans (GAGs) or the subsequent degradation of the collagen network.	Glycosaminoglycans	149-167	interleukin 1 alpha	Bos taurus	52-61
17009261-8	2006	CONCLUSION: IL-1alpha-induced degradation of cartilage results in tensile weakening that occurs subsequent to the depletion of GAG and concomitant with the degradation of the collagen network.	Glycosaminoglycans	127-130	interleukin 1 alpha	Bos taurus	12-21
16940047-2	2006	The crystal structure of MBP resembles that of the C-type lectin (CTL) superfamily, and recent data showed that MBP binds heparan sulfate glycosaminoglycan (GAG), with the CTL ligand-binding region as the binding site.	Glycosaminoglycans	157-160	myelin basic protein	Homo sapiens	25-28
16940047-2	2006	The crystal structure of MBP resembles that of the C-type lectin (CTL) superfamily, and recent data showed that MBP binds heparan sulfate glycosaminoglycan (GAG), with the CTL ligand-binding region as the binding site.	Glycosaminoglycans	157-160	myelin basic protein	Homo sapiens	112-115
16940047-4	2006	Using flow cytometry and site-directed mutagenesis, we demonstrate here that the MBP domain of pro-MBP binds to heparan sulfate GAG on the cell surface and that this is independent of GAG covalently bound to pro-MBP.	Glycosaminoglycans	128-131	myelin basic protein	Homo sapiens	81-84
16940047-4	2006	Using flow cytometry and site-directed mutagenesis, we demonstrate here that the MBP domain of pro-MBP binds to heparan sulfate GAG on the cell surface and that this is independent of GAG covalently bound to pro-MBP.	Glycosaminoglycans	128-131	proteoglycan 2, pro eosinophil major basic protein	Homo sapiens	95-102
16940047-5	2006	Eight basic residues located in the CTL ligand-binding region of MBP were hypothesized previously to mediate GAG binding, but we found that surface binding was not compromised by the substitution of these residues with alanine.	Glycosaminoglycans	109-112	myelin basic protein	Homo sapiens	65-68
17450675-10	2006	Interestingly, overexpression of this enzyme completely counteracted the GAG depletion produced by the proinflammatory cytokine interleukin 1-beta.	Glycosaminoglycans	73-76	interleukin 1 beta	Homo sapiens	128-146
16995857-4	2006	Our results confirm that glycosaminoglycans induced FGF-1 dimerization either in a cis or trans disposition with respect to the heparin chain is not an absolute requirement for biological activity.	Glycosaminoglycans	25-43	fibroblast growth factor 1	Homo sapiens	52-57
16983721-8	2006	Eotaxin-3 cell surface association was partially glycosaminoglycan (GAG) dependent, but was completely protein dependent, suggesting that eotaxin-3 associates with both GAG and cell surface proteins.	Glycosaminoglycans	49-66	C-C motif chemokine ligand 26	Homo sapiens	0-9
16983721-8	2006	Eotaxin-3 cell surface association was partially glycosaminoglycan (GAG) dependent, but was completely protein dependent, suggesting that eotaxin-3 associates with both GAG and cell surface proteins.	Glycosaminoglycans	68-71	C-C motif chemokine ligand 26	Homo sapiens	0-9
16983721-8	2006	Eotaxin-3 cell surface association was partially glycosaminoglycan (GAG) dependent, but was completely protein dependent, suggesting that eotaxin-3 associates with both GAG and cell surface proteins.	Glycosaminoglycans	169-172	C-C motif chemokine ligand 26	Homo sapiens	0-9
16983721-8	2006	Eotaxin-3 cell surface association was partially glycosaminoglycan (GAG) dependent, but was completely protein dependent, suggesting that eotaxin-3 associates with both GAG and cell surface proteins.	Glycosaminoglycans	169-172	C-C motif chemokine ligand 26	Homo sapiens	138-147
16873373-6	2006	In RNA interference flies, an analysis of the genetic interaction between dPAPST2 and genes that contribute to glycosaminoglycan synthesis suggested that dPAPST2 is involved in the glycosaminoglycan synthesis and the subsequent signaling.	Glycosaminoglycans	111-128	PAPS transporter 2	Drosophila melanogaster	74-81
16774908-1	2006	Beta-glucuronidase is a lysosomal enzyme that plays an essential role in normal turnover of glycosaminoglycans and remodeling of the extracellular matrix components in both physiological and inflammatory states.	Glycosaminoglycans	92-110	beta-glucuronidase	Bos taurus	0-18
16874761-1	2006	The GAG deletion in the DYT1 gene usually causes a typical form of primary torsion dystonia (PTD) with early onset in a limb, rapid generalization, and sparing of cranial-cervical muscles, but atypical phenotypes have often been reported.	Glycosaminoglycans	4-7	torsin family 1 member A	Homo sapiens	24-28
16873373-6	2006	In RNA interference flies, an analysis of the genetic interaction between dPAPST2 and genes that contribute to glycosaminoglycan synthesis suggested that dPAPST2 is involved in the glycosaminoglycan synthesis and the subsequent signaling.	Glycosaminoglycans	111-128	PAPS transporter 2	Drosophila melanogaster	154-161
16873373-6	2006	In RNA interference flies, an analysis of the genetic interaction between dPAPST2 and genes that contribute to glycosaminoglycan synthesis suggested that dPAPST2 is involved in the glycosaminoglycan synthesis and the subsequent signaling.	Glycosaminoglycans	181-198	PAPS transporter 2	Drosophila melanogaster	74-81
16873373-6	2006	In RNA interference flies, an analysis of the genetic interaction between dPAPST2 and genes that contribute to glycosaminoglycan synthesis suggested that dPAPST2 is involved in the glycosaminoglycan synthesis and the subsequent signaling.	Glycosaminoglycans	181-198	PAPS transporter 2	Drosophila melanogaster	154-161
16989614-0	2006	Impact of Gag sequence variability on level, phenotype, and function of anti-HIV Gag-specific CD8(+) cytotoxic T lymphocytes in untreated chronically HIV-infected patients.	Glycosaminoglycans	10-13	CD8a molecule	Homo sapiens	94-97
16784821-3	2006	Here, we found that the mRNA expression of EXT2, one of the crucial enzymes for heparan sulfate-glycosaminoglycan synthesis, was markedly up-regulated in injured hypoglossal motor neurons after axotomy.	Glycosaminoglycans	96-113	exostosin glycosyltransferase 2	Homo sapiens	43-47
16839828-6	2006	In contrast, incubation with the enzyme chondroitinase ABC resulted in a total removal of glycosaminoglycan from the samples, and a subsequent reduction in the extent of swelling.	Glycosaminoglycans	90-107	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	55-58
16972797-1	2006	Recently a novel plasma serine protease with high affinity to hyaluronic acid and glycosaminoglycans, such as heparin and heparan sulfate, has been described and termed hyaluronan-binding protease (HABP).	Glycosaminoglycans	82-100	hyaluronan binding protein 2	Homo sapiens	169-196
16690200-4	2006	In addition, the accumulated versican and decorin were markedly modified on both protein core and glycosaminoglycan (GAG) levels.	Glycosaminoglycans	98-115	versican	Homo sapiens	29-37
16690200-4	2006	In addition, the accumulated versican and decorin were markedly modified on both protein core and glycosaminoglycan (GAG) levels.	Glycosaminoglycans	98-115	decorin	Homo sapiens	42-49
16972797-1	2006	Recently a novel plasma serine protease with high affinity to hyaluronic acid and glycosaminoglycans, such as heparin and heparan sulfate, has been described and termed hyaluronan-binding protease (HABP).	Glycosaminoglycans	82-100	hyaluronan binding protein 2	Homo sapiens	198-202
16971807-4	2006	These cells not only express and secrete the HIV p24 antigen after electroporation with codon-optimized HIV-1 gag mRNA, but can also be used to in vitro reactivate Gag antigen-specific interferon-gamma-producing CD4 and CD8 autologous T-cells.	Glycosaminoglycans	164-167	interferon gamma	Homo sapiens	185-201
16914593-14	2006	CONCLUSION: TNFalpha and IL1 stimulate ICAM1 expression and GAG production, but have opposite effects on adipogenesis in OFs in vitro.	Glycosaminoglycans	60-63	tumor necrosis factor	Homo sapiens	12-20
16914593-14	2006	CONCLUSION: TNFalpha and IL1 stimulate ICAM1 expression and GAG production, but have opposite effects on adipogenesis in OFs in vitro.	Glycosaminoglycans	60-63	interleukin 1 alpha	Homo sapiens	25-28
16971807-4	2006	These cells not only express and secrete the HIV p24 antigen after electroporation with codon-optimized HIV-1 gag mRNA, but can also be used to in vitro reactivate Gag antigen-specific interferon-gamma-producing CD4 and CD8 autologous T-cells.	Glycosaminoglycans	164-167	CD4 molecule	Homo sapiens	212-215
16971807-4	2006	These cells not only express and secrete the HIV p24 antigen after electroporation with codon-optimized HIV-1 gag mRNA, but can also be used to in vitro reactivate Gag antigen-specific interferon-gamma-producing CD4 and CD8 autologous T-cells.	Glycosaminoglycans	164-167	CD8a molecule	Homo sapiens	220-223
16807236-2	2006	CCL5 binding to glycosaminoglycans (GAGs) on the cell surface or in extracellular matrix sequesters CCL5, thereby immobilizing CCL5 to provide the directional signal.	Glycosaminoglycans	16-34	C-C motif chemokine ligand 5	Homo sapiens	0-4
16807236-2	2006	CCL5 binding to glycosaminoglycans (GAGs) on the cell surface or in extracellular matrix sequesters CCL5, thereby immobilizing CCL5 to provide the directional signal.	Glycosaminoglycans	16-34	C-C motif chemokine ligand 5	Homo sapiens	100-104
16807236-2	2006	CCL5 binding to glycosaminoglycans (GAGs) on the cell surface or in extracellular matrix sequesters CCL5, thereby immobilizing CCL5 to provide the directional signal.	Glycosaminoglycans	16-34	C-C motif chemokine ligand 5	Homo sapiens	100-104
16807236-7	2006	We show that CCL5-CCR5-mediated apoptosis is dependent on cell surface GAG binding.	Glycosaminoglycans	71-74	C-C motif chemokine ligand 5	Homo sapiens	13-17
16807236-7	2006	We show that CCL5-CCR5-mediated apoptosis is dependent on cell surface GAG binding.	Glycosaminoglycans	71-74	C-C motif chemokine receptor 5	Homo sapiens	18-22
16807236-9	2006	Moreover, the non-GAG binding variant, (44AANA47)-CCL5, fails to induce apoptosis.	Glycosaminoglycans	18-21	C-C motif chemokine ligand 5	Homo sapiens	50-54
16807236-12	2006	Viewed altogether, these data suggest that CCL5-GAG binding and CCL5 aggregation are important for CCL5 activity in T cells, specifically in the context of CCR5-mediated apoptosis.	Glycosaminoglycans	48-51	C-C motif chemokine ligand 5	Homo sapiens	43-47
16807236-12	2006	Viewed altogether, these data suggest that CCL5-GAG binding and CCL5 aggregation are important for CCL5 activity in T cells, specifically in the context of CCR5-mediated apoptosis.	Glycosaminoglycans	48-51	C-C motif chemokine receptor 5	Homo sapiens	156-160
16890679-11	2006	Peak 1 consisted of macromolecular glycosaminoglycans whereas peaks 2 and 3 contained oligosaccharides.	Glycosaminoglycans	35-53	pseudopodium enriched atypical kinase 1	Homo sapiens	0-6
16773641-3	2006	The 14 patients (25%) with GAG deletion (904_906/907_909delGAG) in the DYT1 gene were compared with the remaining non-DYT1 patients.	Glycosaminoglycans	27-30	torsin family 1 member A	Homo sapiens	71-75
17225872-5	2006	We found an altered ECM production in CLP-SP fibroblasts that synthesized and secreted more glycosaminoglycans (GAGs) and fibronectin (FN) compared with N-SP cells.	Glycosaminoglycans	92-110	calmodulin like 3	Homo sapiens	38-41
17225872-5	2006	We found an altered ECM production in CLP-SP fibroblasts that synthesized and secreted more glycosaminoglycans (GAGs) and fibronectin (FN) compared with N-SP cells.	Glycosaminoglycans	112-116	calmodulin like 3	Homo sapiens	38-41
16961606-10	2006	Additionally, odiparcil-induced heparin cofactor II (HCII)-dependent antithrombin activity was shown to be a function of dermatan sulfate-like GAG production.	Glycosaminoglycans	143-146	serpin family D member 1	Rattus norvegicus	32-51
16961606-10	2006	Additionally, odiparcil-induced heparin cofactor II (HCII)-dependent antithrombin activity was shown to be a function of dermatan sulfate-like GAG production.	Glycosaminoglycans	143-146	serpin family D member 1	Rattus norvegicus	53-57
16945153-5	2006	Glycosaminoglycans (GAGs), such as heparin, can inhibit tumour growth; they have also shown antiviral effects and inhibition of AP1 transcriptional activity.	Glycosaminoglycans	0-18	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	128-131
16945153-8	2006	GAG-hed effects on AP1 binding to HPV18-LCR-DNA were tested by EMSA.	Glycosaminoglycans	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	19-22
16945153-13	2006	We also detected that GAG-hed prevents the binding of the transcription factor AP1 to the LCR.	Glycosaminoglycans	22-25	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	79-82
16945153-14	2006	CONCLUSION: Direct interaction of GAG-hed with the components of the AP1 complex and subsequent interference with its ability to correctly bind specific sites within the viral LCR may contribute to the inhibition of E6/E7 transcription and cell proliferation.	Glycosaminoglycans	34-37	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	69-72
16828054-0	2006	Characterization of osteoprotegerin binding to glycosaminoglycans by surface plasmon resonance: role in the interactions with receptor activator of nuclear factor kappaB ligand (RANKL) and RANK.	Glycosaminoglycans	47-65	TNF superfamily member 11	Homo sapiens	178-183
16828054-3	2006	As OPG contains a heparin-binding domain, the present study investigated the interactions between OPG and glycosaminoglycans (GAGs) by surface plasmon resonance and their involvement in the OPG functions.	Glycosaminoglycans	106-124	TNF receptor superfamily member 11b	Homo sapiens	3-6
16828054-3	2006	As OPG contains a heparin-binding domain, the present study investigated the interactions between OPG and glycosaminoglycans (GAGs) by surface plasmon resonance and their involvement in the OPG functions.	Glycosaminoglycans	106-124	TNF receptor superfamily member 11b	Homo sapiens	98-101
16828054-3	2006	As OPG contains a heparin-binding domain, the present study investigated the interactions between OPG and glycosaminoglycans (GAGs) by surface plasmon resonance and their involvement in the OPG functions.	Glycosaminoglycans	106-124	TNF receptor superfamily member 11b	Homo sapiens	98-101
16910828-5	2006	At baseline most patients presented a high level of CD8+ responses to different HIV peptide pools and 23% of them had CD4+ responses to Gag and/or Env.	Glycosaminoglycans	136-139	CD4 molecule	Homo sapiens	118-121
16730772-5	2006	Analysis of cellular immune responses revealed slower response rates in virus-specific IFN-gamma production to SIV Gag in the Depo-treated macaques.	Glycosaminoglycans	115-118	interferon gamma	Homo sapiens	87-96
16890533-5	2006	First, viral RNA (vRNA) blocks the binding of mA3 to Gag, resulting in the exclusion of mA3 from MLV virions.	Glycosaminoglycans	53-56	olfactory receptor family 2 subfamily B member 4	Mus musculus	46-49
16890533-5	2006	First, viral RNA (vRNA) blocks the binding of mA3 to Gag, resulting in the exclusion of mA3 from MLV virions.	Glycosaminoglycans	53-56	olfactory receptor family 2 subfamily B member 4	Mus musculus	88-91
16995783-2	2006	It is speculated that the inherent GAGs in acellular tissues may serve as a reservoir for loading basic fibroblast growth factor (bFGF) and promote angiogenesis and tissue regeneration.	Glycosaminoglycans	35-39	fibroblast growth factor 2	Bos taurus	130-134
16995783-3	2006	This study was therefore designed to investigate effects of the content of GAGs in acellular bovine pericardia on the binding of bFGF and its release profile in vitro while its stimulation in angiogenesis and tissue regeneration in vivo were evaluated subcutaneously in a rat model.	Glycosaminoglycans	75-79	fibroblast growth factor 2	Bos taurus	129-133
16995783-5	2006	The in vitro results indicated that a higher content of GAGs in the acellular tissue resulted in an increase in bFGF binding and in a more gradual and sustained release of the growth factor.	Glycosaminoglycans	56-60	fibroblast growth factor 2	Bos taurus	112-116
16995783-9	2006	In conclusion, the inherent GAGs present in acellular tissues may be used for binding and sustained release of bFGF to enhance angiogenesis and tissue regeneration.	Glycosaminoglycans	28-32	fibroblast growth factor 2	Bos taurus	111-115
16718701-1	2006	OBJECTIVE: A defect of the lysosomal enzyme alpha-L-iduronidase (IDUA) interrupts the degradation of glycosaminoglycans in mucopolysaccharidosis type I, causing severe neurological manifestations in children with Hurler"s syndrome.	Glycosaminoglycans	101-119	alpha-L-iduronidase	Homo sapiens	44-63
16718701-1	2006	OBJECTIVE: A defect of the lysosomal enzyme alpha-L-iduronidase (IDUA) interrupts the degradation of glycosaminoglycans in mucopolysaccharidosis type I, causing severe neurological manifestations in children with Hurler"s syndrome.	Glycosaminoglycans	101-119	alpha-L-iduronidase	Homo sapiens	65-69
16718701-7	2006	The delivery of IDUA to large areas, which could encompass the entire brain, prevented glycosaminoglycan and secondary ganglioside accumulations.	Glycosaminoglycans	87-104	alpha-L-iduronidase	Canis lupus familiaris	16-20
16736203-5	2006	The present work demonstrates that keratan sulfate (KS) in the glycosaminoglycan-binding region of disc aggrecan is confined to the KS-rich domain of the core protein and is not present in association with chondroitin sulfate (CS) in the CS1 and CS2 domains.	Glycosaminoglycans	63-80	myozenin 2	Homo sapiens	238-241
16868144-0	2006	Glycosaminoglycans increase levels of free and bioactive IGF-I in vitro.	Glycosaminoglycans	0-18	insulin like growth factor 1	Homo sapiens	57-62
16822580-1	2006	Hyaluronan is a straight chain, glycosaminoglycan polymer of the extracellular matrix composed of repeating units of the disaccharide [-D-glucuronic acid-beta1,3-N-acetyl-D-glucosamine-beta1,4-]n. Hyaluronan is synthesized in mammals by at least three synthases with products of varying chain lengths.	Glycosaminoglycans	32-49	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	154-161
16822580-1	2006	Hyaluronan is a straight chain, glycosaminoglycan polymer of the extracellular matrix composed of repeating units of the disaccharide [-D-glucuronic acid-beta1,3-N-acetyl-D-glucosamine-beta1,4-]n. Hyaluronan is synthesized in mammals by at least three synthases with products of varying chain lengths.	Glycosaminoglycans	32-49	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	185-192
16968160-5	2006	Further, diffusion coefficients of 2 probes, dextran (500 kDa) and bovine serum albumin (BSA), correlated well with GAG production.	Glycosaminoglycans	116-119	albumin	Homo sapiens	74-87
16617026-8	2006	GAG content in explants was higher in both HA groups at the beginning and the conclusion of the study compared to the IL-1beta-treated group.	Glycosaminoglycans	0-3	interleukin 1 beta	Canis lupus familiaris	118-126
16749903-10	2006	Gag and Env only co-localize at the trans-Golgi network, suggesting that Env-Gag interactions that are required for viral egress from the cell, occurs at this site.	Glycosaminoglycans	0-3	endogenous retrovirus group K member 20	Homo sapiens	73-76
16749903-10	2006	Gag and Env only co-localize at the trans-Golgi network, suggesting that Env-Gag interactions that are required for viral egress from the cell, occurs at this site.	Glycosaminoglycans	77-80	endogenous retrovirus group K member 20	Homo sapiens	8-11
16749903-10	2006	Gag and Env only co-localize at the trans-Golgi network, suggesting that Env-Gag interactions that are required for viral egress from the cell, occurs at this site.	Glycosaminoglycans	77-80	endogenous retrovirus group K member 20	Homo sapiens	73-76
16820603-1	2006	BACKGROUND: Marfan syndrome (MFS), a condition caused by fibrillin-1 gene mutation is associated with aortic aneurysm that shows elastic lamellae disruption, accumulation of glycosaminoglycans, and vascular smooth muscle cell (VSMC) apoptosis with minimal inflammatory response.	Glycosaminoglycans	174-192	fibrillin 1	Homo sapiens	57-68
16763549-5	2006	Glycosylation increased VEGF binding in both cell types, but the differential GAG composition of NRP1 mediates opposite responsiveness to VEGF in ECs and SMCs.	Glycosaminoglycans	78-81	PDGF- and VEGF-receptor related	Drosophila melanogaster	138-142
16763549-7	2006	These findings indicate that GAG modification of NRP1 plays a critical role in modulating VEGF signaling, and may provide new insights into physiological and pathological angiogenesis.	Glycosaminoglycans	29-32	PDGF- and VEGF-receptor related	Drosophila melanogaster	90-94
16819182-8	2006	In cartilage explants and chondroctyes treated by IL-1alpha, Aralia cordata showed the decrease of GAG and collagen degradation, decrease of MMPs (MMP-1, -3, -13) activity, and increase of TIMP-1 activity in a dose-dependent manner.	Glycosaminoglycans	99-102	interleukin-1 alpha	Oryctolagus cuniculus	50-59
16831093-6	2006	Before immunization (W0), anti-HIV CD4(+) T cell responses to Gag, Nef, and Env large peptides were detected in 7/23 (30%) analyzable patients.	Glycosaminoglycans	62-65	CD4 molecule	Homo sapiens	35-38
16847188-2	2006	Hyaluronan, a glycosaminoglycan component of the extracellular matrix, is a ligand for the transmembrane receptor CD44, which acts through multiple signaling pathways to influence cellular behavior.	Glycosaminoglycans	14-31	CD44 molecule (Indian blood group)	Homo sapiens	114-118
16766924-3	2006	METHODS: Patients with CBD, beryllium-sensitized subjects (BeS), and beryllium-exposed subjects without CBD were genotyped for the GCLC GAG trinucleotide repeat polymorphism (GCLC TNR), the GCLC-129 single nucleotide polymorphism (SNP), and the GCLM-588 SNP.	Glycosaminoglycans	136-139	glutamate-cysteine ligase catalytic subunit	Homo sapiens	131-135
16583246-8	2006	Glycosaminoglycan chains were of the dermatan/chondroitin sulfate type both in beta4GalT-7(Arg270Cys) and control cells, and epimerization was reduced for decorin and biglycan.	Glycosaminoglycans	0-17	beta-1,4-galactosyltransferase 7	Homo sapiens	79-90
16580800-5	2006	Also, in the group treated only with IL-1beta (11.9+/-0.3 microg), the amount of released GAG increased significantly compared to the control (7.9+/-0.1 microg) and the SFEA-treated group (7.8+/-0.4 microg).	Glycosaminoglycans	90-93	interleukin 1 beta	Homo sapiens	37-45
16709808-6	2006	Proteolytic cleavage of CCL20 occurs also with chemokine bound to glycosaminoglycans.	Glycosaminoglycans	66-84	C-C motif chemokine ligand 20	Homo sapiens	24-29
16763520-0	2006	Correlation between gag-specific CD8 T-cell responses, viral load, and CD4 count in HIV-1 infection is dependent on disease status.	Glycosaminoglycans	20-23	CD8a molecule	Homo sapiens	33-36
16763520-0	2006	Correlation between gag-specific CD8 T-cell responses, viral load, and CD4 count in HIV-1 infection is dependent on disease status.	Glycosaminoglycans	20-23	CD4 molecule	Homo sapiens	71-74
16763520-10	2006	Gag-specific CD8 responses may play differential roles in different stages of HIV-1 infection, and the maintenance of a threshold level of CD4 T-cells may contribute to mediate effective HIV-specific responses in natural control of HIV-1 infection.	Glycosaminoglycans	0-3	CD8a molecule	Homo sapiens	13-16
16815917-2	2006	Here, we develop phylogenetic and mutational approaches to identify critical residues involved in UDP-GlcA binding and enzyme activity of the human beta1,3-glucuronosyltransferase I (GlcAT-I), which plays a key role in glycosaminoglycan biosynthesis.	Glycosaminoglycans	219-236	beta-1,3-glucuronyltransferase 3	Homo sapiens	183-190
16740087-7	2006	RESULTS: IL-1beta-induced GAG loss from cartilage was significantly less in cocultures than in cartilage-only cultures.	Glycosaminoglycans	26-29	interleukin-1 beta	Equus caballus	9-17
16740087-10	2006	CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that synoviocytes secrete 1 or more mediators that preferentially protect matrix GAG metabolism from the degradative effects of IL-1beta.	Glycosaminoglycans	133-136	interleukin-1 beta	Equus caballus	180-188
16841290-6	2006	In vitro study showed that, compared to the scaffold, the scaffold/MS-TGF beta1 significantly augmented the proliferation of MSCs and GAG synthesis.	Glycosaminoglycans	134-137	transforming growth factor, beta 1	Mus musculus	70-79
17083064-1	2006	Angiotensin-converting enzyme (ACE) inhibitors may reduce urinary albumin excretion (UAE) by decreasing glomerular pressure and increasing glomerular charge selectivity through preservation of glycosaminoglycans.	Glycosaminoglycans	193-211	angiotensin I converting enzyme	Homo sapiens	0-29
17083064-1	2006	Angiotensin-converting enzyme (ACE) inhibitors may reduce urinary albumin excretion (UAE) by decreasing glomerular pressure and increasing glomerular charge selectivity through preservation of glycosaminoglycans.	Glycosaminoglycans	193-211	angiotensin I converting enzyme	Homo sapiens	31-34
16569486-6	2006	Insulin released from the matrices increased the wet weights of the cartilaginous cell-polymer constructs (up to 3.2-fold), the amount of GAG and collagen in the constructs (up to 2.4-fold and 3.2-fold, respectively) and the GAG and collagen content per cell (1.8-fold and 2.5-fold, respectively), compared to the control.	Glycosaminoglycans	138-141	insulin	Homo sapiens	0-7
16519915-3	2006	Responses to Gag p24 or to Pol were associated with lower proviral DNA load.	Glycosaminoglycans	13-16	transmembrane p24 trafficking protein 2	Homo sapiens	17-20
16699011-8	2006	Competition studies and time course experiments suggest that interactions of HCV with cell surface-resident glycosaminoglycans aid in efficient infection of Huh7 cells and that CD81 acts during a postattachment step.	Glycosaminoglycans	108-126	MIR7-3 host gene	Homo sapiens	157-161
16414141-7	2006	Microglia were transduced with SV(AT), carrying human alpha1-antitrypsin (alpha1AT), which blocks Env and Gag processing.	Glycosaminoglycans	106-109	serpin family A member 1	Homo sapiens	54-72
16414141-7	2006	Microglia were transduced with SV(AT), carrying human alpha1-antitrypsin (alpha1AT), which blocks Env and Gag processing.	Glycosaminoglycans	106-109	serpin family A member 1	Homo sapiens	74-82
16569486-6	2006	Insulin released from the matrices increased the wet weights of the cartilaginous cell-polymer constructs (up to 3.2-fold), the amount of GAG and collagen in the constructs (up to 2.4-fold and 3.2-fold, respectively) and the GAG and collagen content per cell (1.8-fold and 2.5-fold, respectively), compared to the control.	Glycosaminoglycans	225-228	insulin	Homo sapiens	0-7
16771647-0	2006	Effects of cross-linking type II collagen-GAG scaffolds on chondrogenesis in vitro: dynamic pore reduction promotes cartilage formation.	Glycosaminoglycans	42-45	collagen type II alpha 1 chain	Canis lupus familiaris	25-41
16682496-7	2006	Mutations in HLA-B*57-restricted Gag epitopes were present in all viruses from plasma but were rare in proviruses, suggesting powerful selective pressure acting at these epitopes.	Glycosaminoglycans	33-36	major histocompatibility complex, class I, B	Homo sapiens	13-18
16636519-1	2006	Mucopolysaccharidosis type VII (MPSVII) is a lysosomal storage disease resulted from a deficiency of the enzyme beta-glucuronidase (GUSB), which is necessary for degradation of glycosaminoglycans (GAGs).	Glycosaminoglycans	177-195	glucuronidase, beta	Mus musculus	132-136
16636519-1	2006	Mucopolysaccharidosis type VII (MPSVII) is a lysosomal storage disease resulted from a deficiency of the enzyme beta-glucuronidase (GUSB), which is necessary for degradation of glycosaminoglycans (GAGs).	Glycosaminoglycans	197-201	glucuronidase, beta	Mus musculus	132-136
16619193-4	2006	RESULTS: SIV Gag-specific GrB activity increased from 3.9- to 14.4-fold after infection, compared with that observed before infection.	Glycosaminoglycans	13-16	granzyme B	Homo sapiens	26-29
16517607-2	2006	Mutations in ML1 result in mucolipidosis type IV, a lysosomal storage disease characterized by the intracellular accumulation of enlarged vacuolar structures containing phospholipids, sphingolipids, and mucopolysaccharides.	Glycosaminoglycans	203-222	mucolipin 1	Mus musculus	13-16
16771647-2	2006	The objective of the present study was to investigate this relationship further using adult canine articular chondrocyte-seeded type II collagen-GAG scaffolds.	Glycosaminoglycans	145-148	collagen type II alpha 1 chain	Canis lupus familiaris	128-144
16442581-5	2006	These results suggest that the domain immediately C-terminal to the MHR is functionally involved in Gag-Gag and Gag/Gag-Pol interaction, and this supports the notion that Gag or Gag-Pol mutants blocked in assembly into virus particles can be rescued into virions provided they retain the domains that are able to interact with the Gag precursor.	Glycosaminoglycans	100-103	Gag-Pol	Human immunodeficiency virus 1	178-185
16442581-5	2006	These results suggest that the domain immediately C-terminal to the MHR is functionally involved in Gag-Gag and Gag/Gag-Pol interaction, and this supports the notion that Gag or Gag-Pol mutants blocked in assembly into virus particles can be rescued into virions provided they retain the domains that are able to interact with the Gag precursor.	Glycosaminoglycans	104-107	Gag-Pol	Human immunodeficiency virus 1	178-185
16442581-5	2006	These results suggest that the domain immediately C-terminal to the MHR is functionally involved in Gag-Gag and Gag/Gag-Pol interaction, and this supports the notion that Gag or Gag-Pol mutants blocked in assembly into virus particles can be rescued into virions provided they retain the domains that are able to interact with the Gag precursor.	Glycosaminoglycans	104-107	Gag-Pol	Human immunodeficiency virus 1	178-185
16442581-5	2006	These results suggest that the domain immediately C-terminal to the MHR is functionally involved in Gag-Gag and Gag/Gag-Pol interaction, and this supports the notion that Gag or Gag-Pol mutants blocked in assembly into virus particles can be rescued into virions provided they retain the domains that are able to interact with the Gag precursor.	Glycosaminoglycans	104-107	Gag-Pol	Human immunodeficiency virus 1	178-185
16442581-5	2006	These results suggest that the domain immediately C-terminal to the MHR is functionally involved in Gag-Gag and Gag/Gag-Pol interaction, and this supports the notion that Gag or Gag-Pol mutants blocked in assembly into virus particles can be rescued into virions provided they retain the domains that are able to interact with the Gag precursor.	Glycosaminoglycans	104-107	Gag-Pol	Human immunodeficiency virus 1	178-185
16442581-7	2006	Analysis by immunofluorescence staining indicated that the subcellular localization patterns shown by the Gag-Pol mutants were not fully compatible with their efficiency in being incorporated into virions, suggesting that the ability of Gag-Pol mutants to be incorporated into virions largely depends on their interactions with the Gag precursor.	Glycosaminoglycans	106-109	Gag-Pol	Human immunodeficiency virus 1	237-244
16377754-9	2006	The presence of both odd and even-length oligosaccharides suggests both endo-beta-glucuronidase and endo-N-acetylhexosaminidase activities toward both glycosaminoglycans.	Glycosaminoglycans	151-169	glucuronidase beta	Homo sapiens	77-95
16603065-13	2006	IL-1beta - induced degradation of cartilage matrix was quantified as glycosaminoglycan release.	Glycosaminoglycans	69-86	interleukin 1 beta	Homo sapiens	0-8
16533727-0	2006	The effects of glycosaminoglycans on thrombopoietin-induced megakaryocytopoiesis.	Glycosaminoglycans	15-33	thrombopoietin	Homo sapiens	37-51
16549978-3	2006	METHODS: We determined nucleotide sequences from the C2V3C3 and gp41 region of env and the p17 region of gag in viruses from the three infected individuals from whom specimens were available.	Glycosaminoglycans	105-108	family with sequence similarity 72 member B	Homo sapiens	91-94
16514625-4	2006	Achilles tendons from 16-week-old GDF-7 -/- mice contained 14% less GAG/DNA than did wild type littermates (p = 0.0481), although collagen content was comparable to controls.	Glycosaminoglycans	68-71	growth differentiation factor 7	Mus musculus	34-39
16796813-8	2006	35S labeling demonstrated an increased GAG synthesis in the presence of IGF1 (P&lt;0.001).	Glycosaminoglycans	39-42	insulin like growth factor 1	Homo sapiens	72-76
16537608-8	2006	The presence of chromosome 2 did not have consistent effects on the amount of unspliced viral RNA, whereas the amount of cell-associated Gag p55 was increased a fewfold.	Glycosaminoglycans	137-140	H3 histone pseudogene 44	Homo sapiens	141-144
16556679-4	2006	This multifunctional glycosaminoglycan also inhibited apoptosis induced by other agents, including staurosporin, broad-spectrum kinase inhibitor and thrombin.	Glycosaminoglycans	21-38	coagulation factor II, thrombin	Homo sapiens	149-157
16679673-9	2006	WB indeterminate results were largely due to non-specific reactivity to gag protein (p55).	Glycosaminoglycans	72-75	H3 histone pseudogene 44	Homo sapiens	85-88
16442624-7	2006	We also found that KCP binds to heparan sulfate and weakly to glycosaminoglycans at the surface of cells.	Glycosaminoglycans	62-80	kielin cysteine rich BMP regulator	Homo sapiens	19-22
16549525-4	2006	Clearance of glycosaminoglycans from chondrocytes was observed at a dose of 10 microg recombinant human N-acetylgalactosamine-4-sulfatase (rh4S), but greater clearance was observed with higher doses.	Glycosaminoglycans	13-31	arylsulfatase B	Homo sapiens	104-137
16418163-1	2006	UDP-glucose dehydrogenase (UGDH) supplies the cell with UDP-glucuronic acid (UDP-GlcUA), a precursor of glycosaminoglycan and proteoglycan synthesis.	Glycosaminoglycans	104-121	UDP-glucose 6-dehydrogenase S homeolog	Xenopus laevis	0-25
16406047-4	2006	However, one pediatric subject with late-stage infection displayed robust expansion of Gag 77-85-specific CD8 T cells which were perforin+ and lytic, but lacked expression of CD27 and IFNgamma.	Glycosaminoglycans	87-90	CD8a molecule	Homo sapiens	106-109
16507336-2	2006	Accumulating evidence suggests that regulation of the activity of one such aggrecanase, ADAMTS-4 (or Aggrecanase-1), involves post-translational C-terminal processing (truncation) which modulates both glycosaminoglycan (GAG)-binding affinity and enzymatic activity.	Glycosaminoglycans	201-218	ADAM metallopeptidase with thrombospondin type 1 motif 4	Homo sapiens	88-96
16373332-0	2006	Inhibition or activation of Apert syndrome FGFR2 (S252W) signaling by specific glycosaminoglycans.	Glycosaminoglycans	79-97	fibroblast growth factor receptor 2	Homo sapiens	43-48
16418163-1	2006	UDP-glucose dehydrogenase (UGDH) supplies the cell with UDP-glucuronic acid (UDP-GlcUA), a precursor of glycosaminoglycan and proteoglycan synthesis.	Glycosaminoglycans	104-121	UDP-glucose 6-dehydrogenase S homeolog	Xenopus laevis	27-31
16418163-10	2006	Our findings were confirmed by in vivo experiments where the silencing of xUGDH in X. laevis embryos decreased glycosaminoglycan synthesis causing severe embryonic malformations because of a defective gastrulation process.	Glycosaminoglycans	111-128	UDP-glucose 6-dehydrogenase S homeolog	Xenopus laevis	74-79
16421105-10	2006	Amino acid sequence alignment analysis showed that the Ser74-Gly75 dipeptide and its flanking regions are highly conserved among a wide range of species from caiman to the Homo sapiens, indicating that this glycosaminoglycan attachment domain has survived an extremely long period of evolution pressure, suggesting that the glycosaminoglycan may be critical for the basic biological functions of DMP1.	Glycosaminoglycans	207-224	dentin matrix acidic phosphoprotein 1	Homo sapiens	396-400
16507336-2	2006	Accumulating evidence suggests that regulation of the activity of one such aggrecanase, ADAMTS-4 (or Aggrecanase-1), involves post-translational C-terminal processing (truncation) which modulates both glycosaminoglycan (GAG)-binding affinity and enzymatic activity.	Glycosaminoglycans	201-218	ADAM metallopeptidase with thrombospondin type 1 motif 4	Homo sapiens	101-114
16507336-2	2006	Accumulating evidence suggests that regulation of the activity of one such aggrecanase, ADAMTS-4 (or Aggrecanase-1), involves post-translational C-terminal processing (truncation) which modulates both glycosaminoglycan (GAG)-binding affinity and enzymatic activity.	Glycosaminoglycans	220-223	ADAM metallopeptidase with thrombospondin type 1 motif 4	Homo sapiens	88-96
16507336-2	2006	Accumulating evidence suggests that regulation of the activity of one such aggrecanase, ADAMTS-4 (or Aggrecanase-1), involves post-translational C-terminal processing (truncation) which modulates both glycosaminoglycan (GAG)-binding affinity and enzymatic activity.	Glycosaminoglycans	220-223	ADAM metallopeptidase with thrombospondin type 1 motif 4	Homo sapiens	101-114
16507336-8	2006	Other TSR-1 domain-bearing truncated ADAMTS constructs demonstrating either positive GAG-binding ability (trADAMTS-9F649) or negligible GAG-affinity (trADAMTS-16F647 and trADAMTS-18F650) displayed comparably low aggrecanase activities.	Glycosaminoglycans	85-88	TSR1 ribosome maturation factor	Homo sapiens	6-11
16507336-8	2006	Other TSR-1 domain-bearing truncated ADAMTS constructs demonstrating either positive GAG-binding ability (trADAMTS-9F649) or negligible GAG-affinity (trADAMTS-16F647 and trADAMTS-18F650) displayed comparably low aggrecanase activities.	Glycosaminoglycans	136-139	TSR1 ribosome maturation factor	Homo sapiens	6-11
16023208-3	2006	We here characterize the interactions of murine FH (mFH) with C3b, glycosaminoglycans, and endothelial cells and compare these interactions with those of human FH (hFH).	Glycosaminoglycans	67-85	ferritin heavy polypeptide 1	Mus musculus	48-50
16419111-6	2006	The gag p24 region is subtype G, env gp41 IDR is subtype B, and pol IN is a B/G chimera.	Glycosaminoglycans	4-7	transmembrane p24 trafficking protein 2	Homo sapiens	8-11
16023208-3	2006	We here characterize the interactions of murine FH (mFH) with C3b, glycosaminoglycans, and endothelial cells and compare these interactions with those of human FH (hFH).	Glycosaminoglycans	67-85	ferritin heavy polypeptide 1	Mus musculus	52-55
16023208-3	2006	We here characterize the interactions of murine FH (mFH) with C3b, glycosaminoglycans, and endothelial cells and compare these interactions with those of human FH (hFH).	Glycosaminoglycans	67-85	complement factor H	Homo sapiens	53-55
16297422-6	2006	With one exception, all Bet- and/or Env-positive sera were also positive for Gag.	Glycosaminoglycans	77-80	delta/notch like EGF repeat containing	Homo sapiens	24-27
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
16475811-9	2006	By extension, the biochemical results herein suggest that tissue-selective deposition characteristic of the gelsolin amyloidoses is likely influenced by the extracellular localization of distinct glycosaminoglycans.	Glycosaminoglycans	196-214	gelsolin	Homo sapiens	108-116
16297422-6	2006	With one exception, all Bet- and/or Env-positive sera were also positive for Gag.	Glycosaminoglycans	77-80	endogenous retrovirus group K member 20	Homo sapiens	36-39
16225459-1	2006	Human XT-I (xylosyltransferase I; EC 2.4.2.26) initiates the biosynthesis of the glycosaminoglycan linkage region and is a diagnostic marker of an enhanced proteoglycan biosynthesis.	Glycosaminoglycans	81-98	xylosyltransferase 1	Homo sapiens	6-10
16225459-1	2006	Human XT-I (xylosyltransferase I; EC 2.4.2.26) initiates the biosynthesis of the glycosaminoglycan linkage region and is a diagnostic marker of an enhanced proteoglycan biosynthesis.	Glycosaminoglycans	81-98	xylosyltransferase 1	Homo sapiens	12-32
16387752-0	2006	Glycosaminoglycans inhibit the antibacterial activity of LL-37 in biological fluids.	Glycosaminoglycans	0-18	cathelicidin antimicrobial peptide	Homo sapiens	57-62
16321973-2	2006	This study provided biochemical data about the substrate specificity and activation of hK6 by glycosaminoglycans and by kosmotropic salts, which followed the Hofmeister series.	Glycosaminoglycans	94-112	kallikrein related peptidase 6	Homo sapiens	87-90
16387752-6	2006	A slot-binding assay was used to study the effects of inhibitors on the interaction between LL-37 and glycosaminoglycans.	Glycosaminoglycans	102-120	cathelicidin antimicrobial peptide	Homo sapiens	92-97
16387752-10	2006	The interaction between LL-37 and glycosaminoglycans was abrogated by the cationic polymers DEAE-dextran and chitosan, yielding increased activity of LL-37.	Glycosaminoglycans	34-52	cathelicidin antimicrobial peptide	Homo sapiens	24-29
16387752-10	2006	The interaction between LL-37 and glycosaminoglycans was abrogated by the cationic polymers DEAE-dextran and chitosan, yielding increased activity of LL-37.	Glycosaminoglycans	34-52	cathelicidin antimicrobial peptide	Homo sapiens	150-155
16257242-3	2006	In this Editorial review, a working model is presented which supports the view that one or more aggrecanases (ADAMTS 1, 4, 5, 8, 9, 15) are responsible for cleavage of the IGD with destructive loss of tissue GAG.	Glycosaminoglycans	208-211	ADAM metallopeptidase with thrombospondin type 1 motif 1	Homo sapiens	110-118
16570510-1	2006	Arylsulfatase B (ASB) hydrolyzes the desulfation of N-acetylgalactosamine-4-sulfate at the non-reducing terminal of glycosaminoglycans.	Glycosaminoglycans	116-134	arylsulfatase B	Mus musculus	0-15
16570510-1	2006	Arylsulfatase B (ASB) hydrolyzes the desulfation of N-acetylgalactosamine-4-sulfate at the non-reducing terminal of glycosaminoglycans.	Glycosaminoglycans	116-134	arylsulfatase B	Mus musculus	17-20
16280358-4	2006	Here granzyme B was delivered as a purified monomer, or in complex with either glycosaminoglycans or serglycin, and killing was evaluated.	Glycosaminoglycans	79-97	granzyme B	Homo sapiens	5-15
16257242-4	2006	In contrast, one or more metalloproteinases (MMPs) (MMP 1, 2, 3, 7, 8, 9, 10, 13, 14, 19, 20) are responsible for cleavage of the IGD (at Asn360-Phe361) within a separate pool of aggrecan, which does not bear GAG, because it has previously been C-terminally truncated in a separate slow turnover process.	Glycosaminoglycans	209-212	matrix metallopeptidase 1	Homo sapiens	45-49
16507142-2	2006	Binding of CXCL12 to glycosaminoglycans on endothelial cells (ECs) is supposed to be relevant to the regulation of leukocyte diapedesis and neoangiogenesis during inflammatory responses.	Glycosaminoglycans	21-39	C-X-C motif chemokine ligand 12	Homo sapiens	11-17
16394019-2	2006	We characterized the Gag-specific IL-10 responses by CD8+ T cells in HIV-1-positive volunteers from Uganda.	Glycosaminoglycans	21-24	interleukin 10	Homo sapiens	34-39
16394019-5	2006	Interestingly, the frequency of Gag-specific CD107a/b-, but not IFN-gamma-, positive cells was significantly lower in individuals with detectable IL-10-positive CD8+ T cells (p = 0.004).	Glycosaminoglycans	32-35	lysosomal associated membrane protein 1	Homo sapiens	45-51
16394019-5	2006	Interestingly, the frequency of Gag-specific CD107a/b-, but not IFN-gamma-, positive cells was significantly lower in individuals with detectable IL-10-positive CD8+ T cells (p = 0.004).	Glycosaminoglycans	32-35	interleukin 10	Homo sapiens	146-151
16394019-6	2006	Gag-specific IL-10-positive CD8+ T cells demonstrated a pattern of surface memory marker expression that is distinct compared with CD107a/b- and IFN-gamma-positive CD8+ T cell populations (p &lt; 0.0001).	Glycosaminoglycans	0-3	interleukin 10	Homo sapiens	13-18
16385517-7	2006	RESULTS: The glycosaminoglycan chondroitin sulfate, but not fibronectin or collagens, bound and released MCP-1 in a time-dependent manner.	Glycosaminoglycans	13-30	C-C motif chemokine ligand 2	Homo sapiens	105-110
16511250-3	2006	Here, a complex of the rhesus macaque MHC I molecule (Mamu-A*02) with human beta2m and an immunodominant SIV-Gag nonapeptide, GESNLKSLY (GY9), has been crystallized.	Glycosaminoglycans	109-112	major histocompatibility complex, class I, I	Macaca mulatta	38-43
16224775-6	2006	Because ChS was a heparin-like glycosaminoglycan (GAG), the ChS-Chito composite AECMs appeared to promote binding efficiency for basic fibroblast growth factor (bFGF).	Glycosaminoglycans	31-48	fibroblast growth factor 2	Homo sapiens	129-159
16696862-9	2006	Over 7 days, sphingomyelinase increased the release of newly synthesized sulphated glycosaminoglycan and collagen into the media, whereas inhibition of PKR in sphingomyelinase-treated cells reduced the level of newly synthesized sulphated glycosaminoglycan and collagen.	Glycosaminoglycans	239-256	eukaryotic translation initiation factor 2 alpha kinase 2	Bos taurus	152-155
17053321-9	2006	The combination of IGF-I and TGF-beta1 produced higher amounts of glycosaminoglycan than TGF-beta1 alone at 8 weeks.	Glycosaminoglycans	66-83	insulin like growth factor 1	Homo sapiens	19-24
17053321-9	2006	The combination of IGF-I and TGF-beta1 produced higher amounts of glycosaminoglycan than TGF-beta1 alone at 8 weeks.	Glycosaminoglycans	66-83	transforming growth factor beta 1	Homo sapiens	29-38
16368999-3	2006	Three surface-localized GAG-binding bacterial ligands, Bgp, DbpA, and DbpB, have been previously identified, but recent studies suggested that at least one additional GAG-binding ligand is expressed on the spirochetal surface when the spirochete is adapted to the mammalian host environment.	Glycosaminoglycans	24-27	bone gamma-carboxyglutamate protein	Homo sapiens	55-58
16368999-3	2006	Three surface-localized GAG-binding bacterial ligands, Bgp, DbpA, and DbpB, have been previously identified, but recent studies suggested that at least one additional GAG-binding ligand is expressed on the spirochetal surface when the spirochete is adapted to the mammalian host environment.	Glycosaminoglycans	24-27	Y-box binding protein 3	Homo sapiens	60-64
16368999-3	2006	Three surface-localized GAG-binding bacterial ligands, Bgp, DbpA, and DbpB, have been previously identified, but recent studies suggested that at least one additional GAG-binding ligand is expressed on the spirochetal surface when the spirochete is adapted to the mammalian host environment.	Glycosaminoglycans	24-27	Y-box binding protein 1	Homo sapiens	70-74
16368999-3	2006	Three surface-localized GAG-binding bacterial ligands, Bgp, DbpA, and DbpB, have been previously identified, but recent studies suggested that at least one additional GAG-binding ligand is expressed on the spirochetal surface when the spirochete is adapted to the mammalian host environment.	Glycosaminoglycans	167-170	bone gamma-carboxyglutamate protein	Homo sapiens	55-58
16224775-6	2006	Because ChS was a heparin-like glycosaminoglycan (GAG), the ChS-Chito composite AECMs appeared to promote binding efficiency for basic fibroblast growth factor (bFGF).	Glycosaminoglycans	50-53	fibroblast growth factor 2	Homo sapiens	129-159
16275036-1	2006	Mucopolysaccharidosis VII (MPS VII) is a lysosomal storage disease due to deficient activity of beta-glucuronidase (GUSB) that results in accumulation of glycosaminoglycans in many organs.	Glycosaminoglycans	154-172	glucuronidase beta	Canis lupus familiaris	96-114
16352538-8	2006	sNec1(123)-mediated entry was highly impaired by interference with the cell-binding activities of viral glycoproteins B and C. While gD has at least two functions, virus attachment to the cell and initiation of the virus entry process, our results demonstrate that the attachment function of gD is dispensable for entry provided that other means of attachment are available, such as gB and gC binding to cell surface glycosaminoglycans.	Glycosaminoglycans	417-435	atypical chemokine receptor 1 (Duffy blood group)	Homo sapiens	133-135
16365408-5	2006	A potential GAG-binding site was found in the C-terminal region of DcR3, and the mutation of three basic residues, i.e., K256, R258, and R259, to alanines abolished its ability to trigger cell adhesion.	Glycosaminoglycans	12-15	TNF receptor superfamily member 6b	Homo sapiens	67-71
16275036-1	2006	Mucopolysaccharidosis VII (MPS VII) is a lysosomal storage disease due to deficient activity of beta-glucuronidase (GUSB) that results in accumulation of glycosaminoglycans in many organs.	Glycosaminoglycans	154-172	glucuronidase beta	Canis lupus familiaris	116-120
16374054-0	2006	rd1 mouse retina shows imbalance in cellular distribution and levels of TIMP-1/MMP-9, TIMP-2/MMP-2 and sulfated glycosaminoglycans.	Glycosaminoglycans	112-130	phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide	Mus musculus	0-3
16338794-7	2005	This is consistent with the quantitative measurement of glycosaminoglycans, whereby a significant increase in GAG/DNA was noted in the co-treatment group.	Glycosaminoglycans	56-74	melanoma antigen	Mus musculus	110-113
16219767-1	2005	The related glycosaminoglycans heparin and heparan sulfate are essential for the activity of the fibroblast growth factor (FGF) family as they form an integral part of the signaling complex at the cell surface.	Glycosaminoglycans	12-30	fibroblast growth factor 1	Homo sapiens	123-126
16379605-10	2005	Gag p17 exhibited greater covariability and less diversity for HIV-1B than HIV-1C, raising the hypothesis that Gag p17 is highly immunodominant in HIV-1B and is especially important for HIV-1B vaccines.	Glycosaminoglycans	0-3	family with sequence similarity 72 member B	Homo sapiens	4-7
16379605-10	2005	Gag p17 exhibited greater covariability and less diversity for HIV-1B than HIV-1C, raising the hypothesis that Gag p17 is highly immunodominant in HIV-1B and is especially important for HIV-1B vaccines.	Glycosaminoglycans	0-3	family with sequence similarity 72 member B	Homo sapiens	115-118
16379605-10	2005	Gag p17 exhibited greater covariability and less diversity for HIV-1B than HIV-1C, raising the hypothesis that Gag p17 is highly immunodominant in HIV-1B and is especially important for HIV-1B vaccines.	Glycosaminoglycans	111-114	family with sequence similarity 72 member B	Homo sapiens	4-7
16379605-10	2005	Gag p17 exhibited greater covariability and less diversity for HIV-1B than HIV-1C, raising the hypothesis that Gag p17 is highly immunodominant in HIV-1B and is especially important for HIV-1B vaccines.	Glycosaminoglycans	111-114	family with sequence similarity 72 member B	Homo sapiens	115-118
16047167-16	2005	TGF-beta1 increased glycosaminoglycan secretions in the superficial zone populations and in the growth zone populations, whereas IGF-I produced an increase in glycosaminoglycan secretion only in the growth zone populations.	Glycosaminoglycans	20-37	transforming growth factor beta-1 proprotein	Capra hircus	0-9
16047167-16	2005	TGF-beta1 increased glycosaminoglycan secretions in the superficial zone populations and in the growth zone populations, whereas IGF-I produced an increase in glycosaminoglycan secretion only in the growth zone populations.	Glycosaminoglycans	159-176	insulin-like growth factor I	Capra hircus	129-134
15951190-2	2005	In addition, several lines of evidence suggest that glycosaminoglycans (GAGs) and in particular heparan sulfate (HS) may play a role in the PrP(C) to PrP(Sc) conversion process.	Glycosaminoglycans	52-70	prion protein	Mus musculus	140-143
16282500-0	2005	Tat(28-35)SL8-specific CD8+ T lymphocytes are more effective than Gag(181-189)CM9-specific CD8+ T lymphocytes at suppressing simian immunodeficiency virus replication in a functional in vitro assay.	Glycosaminoglycans	66-69	CD8a molecule	Homo sapiens	91-94
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
16288042-1	2005	Recently, we reported that the laminin alpha5 synthetic peptide A5G27 (RLVSYNGIIFFLK, residues 2,892-2,904) binds to the CD44 receptor of B16-F10 melanoma cells via the glycosaminoglycans on CD44 and inhibits tumor cell migration, invasion, and angiogenesis in a dominant-negative manner.	Glycosaminoglycans	169-187	laminin, alpha 5	Mus musculus	31-45
16317389-7	2005	Data from experiments with Chinese hamster ovary cells with altered glycosaminoglycan expression indicated that heparan sulfate and chondroitin sulfate (glycosaminoglycans on the syndecan-1 ectodomain) participated in bacterial interactions with mammalian cells.	Glycosaminoglycans	153-171	syndecan-1	Cricetulus griseus	179-189
16240131-2	2005	A novel 3-bp deletion encompassing the nucleotides GAG at positions 1,142 to 1,144 of exon 5 of the PANK2 gene was found in all patients.	Glycosaminoglycans	51-54	pantothenate kinase 2	Homo sapiens	100-105
16288042-1	2005	Recently, we reported that the laminin alpha5 synthetic peptide A5G27 (RLVSYNGIIFFLK, residues 2,892-2,904) binds to the CD44 receptor of B16-F10 melanoma cells via the glycosaminoglycans on CD44 and inhibits tumor cell migration, invasion, and angiogenesis in a dominant-negative manner.	Glycosaminoglycans	169-187	CD44 antigen	Mus musculus	121-125
16288042-3	2005	WiDr cells bound to the laminin A5G27 peptide via the heparin-like and chondroitin sulfate B glycosaminoglycan side chains of CD44.	Glycosaminoglycans	93-110	CD44 molecule (Indian blood group)	Homo sapiens	126-130
15878765-8	2005	With FGF-2, the morphology of the mandibular condyles changed and the GAG and collagen contents were reduced.	Glycosaminoglycans	70-73	fibroblast growth factor 2	Rattus norvegicus	5-10
16235176-6	2005	After adjustment for CD4(+) count, age, and log(10) viral load, African American children demonstrated significantly higher Gag responses (average, 486 spot-forming cells higher; P=.01) than Hispanic children; this was significantly driven by robust responses in African American girls near the age of puberty, many of whom carried the human leukocyte antigen class I B*58 allele.	Glycosaminoglycans	124-127	major histocompatibility complex, class I, B	Homo sapiens	342-369
15966019-1	2005	BACKGROUND: Hunter syndrome, mucopolysaccharidosis type II (MPS II), is a X-linked inherited disorder caused by the deficiency of the enzyme iduronate-2-sulfatase (IDS), involved in the lysosomal catabolism of the glycosaminoglycans (GAG) dermatan and heparan sulfate.	Glycosaminoglycans	214-232	iduronate 2-sulfatase	Mus musculus	141-162
16012778-7	2005	Spearman statistical analysis indicated that blood plasma concentrations of anti-U1 RNP and anti-Sm antibodies may correlate with PBMC transcript levels of HERV-E clone 4-1 gag sequence (R = 0.775, p &lt; 0.000001; R = 0.698, p &lt; 0.000001, respectively).	Glycosaminoglycans	173-176	small nuclear ribonucleoprotein U1 subunit 70	Homo sapiens	81-87
16140574-6	2005	Further analysis revealed that the gag-specific T-cells were predominantly targeting the HLA B27-restricted CTL epitope KRWIILGLNK (KK10).	Glycosaminoglycans	35-38	major histocompatibility complex, class I, B	Homo sapiens	89-96
15966019-1	2005	BACKGROUND: Hunter syndrome, mucopolysaccharidosis type II (MPS II), is a X-linked inherited disorder caused by the deficiency of the enzyme iduronate-2-sulfatase (IDS), involved in the lysosomal catabolism of the glycosaminoglycans (GAG) dermatan and heparan sulfate.	Glycosaminoglycans	214-232	iduronate 2-sulfatase	Mus musculus	164-167
15966019-1	2005	BACKGROUND: Hunter syndrome, mucopolysaccharidosis type II (MPS II), is a X-linked inherited disorder caused by the deficiency of the enzyme iduronate-2-sulfatase (IDS), involved in the lysosomal catabolism of the glycosaminoglycans (GAG) dermatan and heparan sulfate.	Glycosaminoglycans	234-237	iduronate 2-sulfatase	Mus musculus	141-162
15966019-1	2005	BACKGROUND: Hunter syndrome, mucopolysaccharidosis type II (MPS II), is a X-linked inherited disorder caused by the deficiency of the enzyme iduronate-2-sulfatase (IDS), involved in the lysosomal catabolism of the glycosaminoglycans (GAG) dermatan and heparan sulfate.	Glycosaminoglycans	234-237	iduronate 2-sulfatase	Mus musculus	164-167
16219698-5	2005	NHPs immunized with HIV Gag protein and a TLR7/8 agonist or a TLR9 ligand [CpG oligodeoxynucleotides (CpG ODN)] had significantly increased Gag-specific T helper 1 and antibody responses, compared with animals immunized with HIV Gag protein alone.	Glycosaminoglycans	24-27	toll like receptor 7	Homo sapiens	42-46
16219698-5	2005	NHPs immunized with HIV Gag protein and a TLR7/8 agonist or a TLR9 ligand [CpG oligodeoxynucleotides (CpG ODN)] had significantly increased Gag-specific T helper 1 and antibody responses, compared with animals immunized with HIV Gag protein alone.	Glycosaminoglycans	24-27	toll like receptor 9	Homo sapiens	62-66
15932347-3	2005	As MPO binds to glycosaminoglycans, oxidation of extracellular matrix and cell surfaces by HOCl may be localized to these materials.	Glycosaminoglycans	16-34	myeloperoxidase	Homo sapiens	3-6
15958243-0	2005	Injectable glycosaminoglycan hydrogels for controlled release of human basic fibroblast growth factor.	Glycosaminoglycans	11-28	fibroblast growth factor 2	Homo sapiens	71-101
15958243-4	2005	With as little as 1% (w/w) covalently bound heparin (relative to total glycosaminoglycan content), the rate of release of bFGF in vitro was substantially reduced.	Glycosaminoglycans	71-88	fibroblast growth factor 2	Homo sapiens	122-126
16213816-6	2005	LAR interacts with the glycosaminoglycan chains of Syndecan in vitro with nanomolar affinity.	Glycosaminoglycans	23-40	Leukocyte-antigen-related-like	Drosophila melanogaster	0-3
16213816-6	2005	LAR interacts with the glycosaminoglycan chains of Syndecan in vitro with nanomolar affinity.	Glycosaminoglycans	23-40	Syndecan	Drosophila melanogaster	51-59
16194844-4	2005	In particular, transforming growth factor beta 1 (TGFbeta1) acts on collagen fibres, glycosaminoglycan secretion and on the enzymes correlated to the turnover of glycosaminoglycans.	Glycosaminoglycans	85-102	transforming growth factor beta 1	Homo sapiens	15-48
16194844-4	2005	In particular, transforming growth factor beta 1 (TGFbeta1) acts on collagen fibres, glycosaminoglycan secretion and on the enzymes correlated to the turnover of glycosaminoglycans.	Glycosaminoglycans	85-102	transforming growth factor beta 1	Homo sapiens	50-58
16194844-4	2005	In particular, transforming growth factor beta 1 (TGFbeta1) acts on collagen fibres, glycosaminoglycan secretion and on the enzymes correlated to the turnover of glycosaminoglycans.	Glycosaminoglycans	162-180	transforming growth factor beta 1	Homo sapiens	15-48
16194844-4	2005	In particular, transforming growth factor beta 1 (TGFbeta1) acts on collagen fibres, glycosaminoglycan secretion and on the enzymes correlated to the turnover of glycosaminoglycans.	Glycosaminoglycans	162-180	transforming growth factor beta 1	Homo sapiens	50-58
16194844-8	2005	RESULTS: Our data show that TGFbeta1 significantly decreases 3H-thymidine and 3H-proline incorporation and increases (p &lt; or = 0.01) extracellular sulphated glycosaminoglycan synthesis.	Glycosaminoglycans	160-177	transforming growth factor beta 1	Homo sapiens	28-36
16159120-1	2005	Mass spectrometry, and specifically sequential stages of mass spectrometry (MSn), is an established tool for the analysis of carbohydrates, proteins, and more recently glycosaminoglycans.	Glycosaminoglycans	168-186	moesin	Homo sapiens	76-79
16014624-0	2005	A synthetic glycosaminoglycan mimetic binds vascular endothelial growth factor and modulates angiogenesis.	Glycosaminoglycans	12-29	vascular endothelial growth factor A	Homo sapiens	44-78
16159120-7	2005	Having a means, such as HOST, for automating the interpretation of the MSn data generated from glycosaminoglycans, provides a practical methodology for the future analysis of heparin/HS oligosaccharides of unknown structure.	Glycosaminoglycans	95-113	moesin	Homo sapiens	71-74
16023165-6	2005	Approximate twofold higher ELISPOT responses to Gag and Env epitopes were observed for IC48 animals than for IC1-90 animals at the peak post-MVA effector (P = 0.028) and late memory (P = 0.051) phases, respectively.	Glycosaminoglycans	48-51	ICR1 differentially methylated region	Homo sapiens	109-112
15947088-1	2005	In mucopolysaccharidosis-I (MPS-I), alpha-L-iduronidase deficiency leads to progressive heparan sulfate (HS) and dermatan sulfate (DS) glycosaminoglycan (GAG) accumulation.	Glycosaminoglycans	135-152	alpha-L-iduronidase	Homo sapiens	36-55
15947088-1	2005	In mucopolysaccharidosis-I (MPS-I), alpha-L-iduronidase deficiency leads to progressive heparan sulfate (HS) and dermatan sulfate (DS) glycosaminoglycan (GAG) accumulation.	Glycosaminoglycans	154-157	alpha-L-iduronidase	Homo sapiens	36-55
16027123-2	2005	The biological activity of granulocyte-macrophage colony-stimulating factor (GM-CSF) is modulated by the sulfated glycosaminoglycans (GAGs) heparan sulfate and heparin.	Glycosaminoglycans	114-132	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	77-83
16027123-4	2005	We have proposed previously that helix C, one of the four alpha-helices of human GM-CSF (hGM-CSF), contains a GAG-binding site in which positively charged residues are spatially positioned for interaction with the sulfate moieties of the GAGs (Wettreich, A., Sebollela, A., Carvalho, M. A., Azevedo, S. P., Borojevic, R., Ferreira, S. T., and Coelho-Sampaio, T. (1999) J. Biol.	Glycosaminoglycans	110-113	colony stimulating factor 2	Homo sapiens	81-87
16027123-4	2005	We have proposed previously that helix C, one of the four alpha-helices of human GM-CSF (hGM-CSF), contains a GAG-binding site in which positively charged residues are spatially positioned for interaction with the sulfate moieties of the GAGs (Wettreich, A., Sebollela, A., Carvalho, M. A., Azevedo, S. P., Borojevic, R., Ferreira, S. T., and Coelho-Sampaio, T. (1999) J. Biol.	Glycosaminoglycans	110-113	colony stimulating factor 2	Homo sapiens	89-96
16107729-6	2005	We also show that GrB-mediated cytotoxicity is abrogated by heparin and that target cells deficient in cell surface sulfate or glycosaminoglycans resist GrB.	Glycosaminoglycans	127-145	granzyme B	Homo sapiens	153-156
16076473-5	2005	When compared to detection of antigen-specific T cells via HLA tetramer/pentamer-based methods of T-cell staining in HIV gag peptide-specific human T cell lines the caspase 3 cleavage readout assay exhibited a comparable level of sensitivity with detection of CTL function at antigen-specific T-cell frequencies of 1:15,000 or lower.	Glycosaminoglycans	121-124	caspase 3	Homo sapiens	165-174
15908019-6	2005	Among the gD receptors, spinoculated GAG- HVEM cells showed restoration of HSV-1 entry compared to unspinoculated GAG+ HVEM cells.	Glycosaminoglycans	37-40	TNF receptor superfamily member 14	Homo sapiens	42-46
15908019-7	2005	In contrast, spinoculated GAG- nectin-1 cells showed less entry than unspinoculated GAG+ nectin-1 cells.	Glycosaminoglycans	26-29	nectin cell adhesion molecule 1	Homo sapiens	31-39
16123674-3	2005	Strong inverse correlations were observed between the percentage of CD4(+) T cells at almost every timepoint of the study and the levels of IgM (but not IgG and IgA) against Gag, Nef, and Rev (but not Tat) measured after, but not during, the primary peak of IgM response.	Glycosaminoglycans	174-177	CD4 molecule	Homo sapiens	68-71
15994821-5	2005	The only element with an ORF among gag, pro, pol, and env genes was the env ORF of the original ERV3 locus.	Glycosaminoglycans	35-38	endogenous retrovirus group W member 1, envelope	Homo sapiens	72-75
15980072-2	2005	Fibrillin-1 assembly into microfibrils and elastic fiber formation involves interactions with glycosaminoglycans.	Glycosaminoglycans	94-112	fibrillin 1	Homo sapiens	0-11
15985216-8	2005	Taken as a whole, our results demonstrate that there is a direct connection between the dependence of endostatin activity on heparin-like glycosaminoglycans and its ability to antagonize bFGF.	Glycosaminoglycans	138-156	collagen type XVIII alpha 1 chain	Homo sapiens	102-112
15985216-8	2005	Taken as a whole, our results demonstrate that there is a direct connection between the dependence of endostatin activity on heparin-like glycosaminoglycans and its ability to antagonize bFGF.	Glycosaminoglycans	138-156	fibroblast growth factor 2	Homo sapiens	187-191
16131312-6	2005	The intensity of memory Gag-specific CTL and the breadth of the CTL response at the beginning of treatment were significantly correlated with lower plasma viral load during treatment, independently of baseline plasma viral load, CD4+ counts, and age.	Glycosaminoglycans	24-27	CD4 molecule	Homo sapiens	229-232
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
15990567-6	2005	RESULTS: Absolute numbers, but not percentages, of Gag-specific IFN-gamma-, IL-2- or IFN-gamma/IL-2-producing CD4 T cells were increased in treated compared with untreated individuals up to 2 years after seroconversion.	Glycosaminoglycans	51-54	interferon gamma	Homo sapiens	64-73
15990567-6	2005	RESULTS: Absolute numbers, but not percentages, of Gag-specific IFN-gamma-, IL-2- or IFN-gamma/IL-2-producing CD4 T cells were increased in treated compared with untreated individuals up to 2 years after seroconversion.	Glycosaminoglycans	51-54	interleukin 2	Homo sapiens	95-99
15990567-6	2005	RESULTS: Absolute numbers, but not percentages, of Gag-specific IFN-gamma-, IL-2- or IFN-gamma/IL-2-producing CD4 T cells were increased in treated compared with untreated individuals up to 2 years after seroconversion.	Glycosaminoglycans	51-54	CD4 molecule	Homo sapiens	110-113
16002730-1	2005	A non-glycosaminoglycan (GAG)-binding variant of the pleiotropic chemokine CCL7 was generated by mutating to alanine the basic (B) amino acids within an identified (44)BXBXXB(49) GAG-binding motif.	Glycosaminoglycans	6-23	C-C motif chemokine ligand 7	Homo sapiens	75-79
16002730-1	2005	A non-glycosaminoglycan (GAG)-binding variant of the pleiotropic chemokine CCL7 was generated by mutating to alanine the basic (B) amino acids within an identified (44)BXBXXB(49) GAG-binding motif.	Glycosaminoglycans	25-28	C-C motif chemokine ligand 7	Homo sapiens	75-79
16002730-1	2005	A non-glycosaminoglycan (GAG)-binding variant of the pleiotropic chemokine CCL7 was generated by mutating to alanine the basic (B) amino acids within an identified (44)BXBXXB(49) GAG-binding motif.	Glycosaminoglycans	179-182	C-C motif chemokine ligand 7	Homo sapiens	75-79
15840581-1	2005	The high molecular mass glycosaminoglycan hyaluronan (HA) can become modified by the covalent attachment of heavy chains (HCs) derived from the serum protein inter-alpha-inhibitor (IalphaI), which is composed of three subunits (HC1, HC2 and bikunin) linked together via a chondroitin sulfate moiety.	Glycosaminoglycans	24-41	CYCS pseudogene 39	Homo sapiens	228-231
15840581-1	2005	The high molecular mass glycosaminoglycan hyaluronan (HA) can become modified by the covalent attachment of heavy chains (HCs) derived from the serum protein inter-alpha-inhibitor (IalphaI), which is composed of three subunits (HC1, HC2 and bikunin) linked together via a chondroitin sulfate moiety.	Glycosaminoglycans	24-41	CYCS pseudogene 38	Homo sapiens	233-236
15840581-1	2005	The high molecular mass glycosaminoglycan hyaluronan (HA) can become modified by the covalent attachment of heavy chains (HCs) derived from the serum protein inter-alpha-inhibitor (IalphaI), which is composed of three subunits (HC1, HC2 and bikunin) linked together via a chondroitin sulfate moiety.	Glycosaminoglycans	24-41	alpha-1-microglobulin/bikunin precursor	Homo sapiens	241-248
15763267-6	2005	In our studies, we focussed on the modulation of the GAG-binding molecules macrophage chemoattractant protein-1 (MCP-1) and vascular endothelial growth factor-164 (VEGF164) in the inflammatory reaction against subcutaneously implanted degradable cross-linked dermal sheep collagen discs in AO rats.	Glycosaminoglycans	53-56	C-C motif chemokine ligand 2	Rattus norvegicus	113-118
15763267-6	2005	In our studies, we focussed on the modulation of the GAG-binding molecules macrophage chemoattractant protein-1 (MCP-1) and vascular endothelial growth factor-164 (VEGF164) in the inflammatory reaction against subcutaneously implanted degradable cross-linked dermal sheep collagen discs in AO rats.	Glycosaminoglycans	53-56	vascular endothelial growth factor A	Rattus norvegicus	164-171
15936726-5	2005	Furthermore, we could demonstrate that the XT-I interacts strongly with heparin and that this glycosaminoglycan is a predominantly non-competitive inhibitor of the enzyme using the fragment bFGF (1-24) as xylose acceptor.	Glycosaminoglycans	94-111	xylosyltransferase 1	Homo sapiens	43-47
15936726-5	2005	Furthermore, we could demonstrate that the XT-I interacts strongly with heparin and that this glycosaminoglycan is a predominantly non-competitive inhibitor of the enzyme using the fragment bFGF (1-24) as xylose acceptor.	Glycosaminoglycans	94-111	fibroblast growth factor 2	Homo sapiens	190-194
16060838-5	2005	Sequence analysis of the gag-pol region (2.1 kb) from 21 discordant specimens in the gag-p24, env-C2V3 and -gp41 regions in 1985 and 1999-2000 further confirmed the complex recombinant patterns.	Glycosaminoglycans	25-28	transmembrane p24 trafficking protein 2	Homo sapiens	89-92
15972650-6	2005	We show further that the GAG-deficient hamster pgsA-745 cells that lack HS and the GAG-expressing parent CHO-K1 cells are both killed by NK cells, with killing of both cell lines inhibited to the same extent by anti-NKp30 mAb.	Glycosaminoglycans	25-28	natural cytotoxicity triggering receptor 3	Homo sapiens	216-221
15956565-6	2005	Moreover, this packaging in turn correlates with the differential ability of these APOBEC3 proteins to bind MLV Gag.	Glycosaminoglycans	112-115	apolipoprotein B mRNA editing enzyme, catalytic polypeptide 3	Mus musculus	83-90
15956565-7	2005	Together, these data suggest that MLV Gag has evolved to avoid binding, and hence virion packaging, of the cognate murine APOBEC3 protein but that MLV infectivity is still restricted by certain heterologous APOBEC3 proteins that retain this ability.	Glycosaminoglycans	38-41	apolipoprotein B mRNA editing enzyme, catalytic polypeptide 3	Mus musculus	122-129
15994821-5	2005	The only element with an ORF among gag, pro, pol, and env genes was the env ORF of the original ERV3 locus.	Glycosaminoglycans	35-38	endogenous retrovirus group 3 member 1, envelope	Homo sapiens	96-100
16113778-3	2005	The neutrophil-derived elastase, cathepsin G, proteinase-3 and heparin-binding protein are cationic, and it is hypothesized that their effects can be inhibited by electrostatic binding with certain anionic polymers such as glycosaminoglycans or functionalized dextrans.	Glycosaminoglycans	223-241	cathepsin G	Homo sapiens	33-44
16113778-3	2005	The neutrophil-derived elastase, cathepsin G, proteinase-3 and heparin-binding protein are cationic, and it is hypothesized that their effects can be inhibited by electrostatic binding with certain anionic polymers such as glycosaminoglycans or functionalized dextrans.	Glycosaminoglycans	223-241	proteinase 3	Homo sapiens	46-58
16113778-3	2005	The neutrophil-derived elastase, cathepsin G, proteinase-3 and heparin-binding protein are cationic, and it is hypothesized that their effects can be inhibited by electrostatic binding with certain anionic polymers such as glycosaminoglycans or functionalized dextrans.	Glycosaminoglycans	223-241	azurocidin 1	Homo sapiens	63-86
16026543-3	2005	The EXT1 and EXT2 genes are glycosyltransferases that function as hetero-oligomers in the Golgi to add repeating glycosaminoglycans (GAGs) to heparan sulfate (HS) chains.	Glycosaminoglycans	113-131	exostosin glycosyltransferase 1	Homo sapiens	4-8
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
16026543-3	2005	The EXT1 and EXT2 genes are glycosyltransferases that function as hetero-oligomers in the Golgi to add repeating glycosaminoglycans (GAGs) to heparan sulfate (HS) chains.	Glycosaminoglycans	113-131	exostosin glycosyltransferase 2	Homo sapiens	13-17
15872080-6	2005	All of the perlecan synthesized by wild-type fibroblasts contained heparin sulfate, indicating an altered substitution of glycosaminoglycans on Hspg2(Delta)(3/)(Delta)(3) perlecan.	Glycosaminoglycans	122-140	perlecan (heparan sulfate proteoglycan 2)	Mus musculus	144-149
15914054-7	2005	The three-dimensional structure of the C-domain of IGFBP-6 contains a thyroglobulin type 1 fold, and the IGF-II binding site is located in the proximal half of this domain adjacent to the glycosaminoglycan binding site.	Glycosaminoglycans	188-205	insulin like growth factor binding protein 6	Homo sapiens	51-58
15914054-7	2005	The three-dimensional structure of the C-domain of IGFBP-6 contains a thyroglobulin type 1 fold, and the IGF-II binding site is located in the proximal half of this domain adjacent to the glycosaminoglycan binding site.	Glycosaminoglycans	188-205	insulin like growth factor 2	Homo sapiens	105-111
15957976-2	2005	It is one of a group of glycosaminoglycan compounds that accelerate the inactivation of factor Xa by inducing a conformational change in antithrombin.	Glycosaminoglycans	24-41	coagulation factor X	Homo sapiens	88-97
15957976-2	2005	It is one of a group of glycosaminoglycan compounds that accelerate the inactivation of factor Xa by inducing a conformational change in antithrombin.	Glycosaminoglycans	24-41	serpin family C member 1	Homo sapiens	137-149
16075925-3	2005	In support of this, we recently found that intact Tg is present in orbital tissues of patients with GO, where it is complexed with glycosaminoglycans.	Glycosaminoglycans	131-149	thyroglobulin	Homo sapiens	50-52
15911774-9	2005	Although WT Bet efficiently preserved FFV infectivity and genome integrity, it sustained particle release and Gag processing only when fe3 was moderately expressed.	Glycosaminoglycans	110-113	Bet	Feline foamy virus	12-15
15788473-12	2005	In conclusion, specific GAG domains are differentially distributed in the normal human kidney and are likely involved in binding of effector molecules such as FGF-2.	Glycosaminoglycans	24-27	fibroblast growth factor 2	Homo sapiens	159-164
15897512-6	2005	Molecular genetic analysis also excluded linkage to the DYT6 locus and the GAG deletion in DYT1, suggesting at least one additional RDP gene.	Glycosaminoglycans	75-78	torsin family 1 member A	Homo sapiens	91-95
15919923-5	2005	SIV Gag-specific T-cell responses were detected in peripheral blood by MHC class I tetramer staining (peak, 0.07 to 0.2% CD8(+) T cells at week 2) and gamma interferon (IFN-gamma) enzyme-linked immunospot (ELISPOT) assays (peak, 50 to 250 spot forming cells/10(6) peripheral blood mononuclear cell at week 3).	Glycosaminoglycans	4-7	interferon gamma	Homo sapiens	151-178
15788411-4	2005	Using a combination of cell binding and internalization assays, granzyme B was found to exchange to sulfated glycosaminoglycans and, depending on the cell type, to higher affinity sites.	Glycosaminoglycans	109-127	granzyme B	Homo sapiens	64-74
15788411-5	2005	Apoptosis induced by purified granzyme B and cytotoxic T-cells was diminished in targets with reduced cell surface glycosaminoglycan content.	Glycosaminoglycans	115-132	granzyme B	Homo sapiens	30-40
15820486-5	2005	RESULTS: Abnormal increase in the aortic lipids -glycosaminoglycans levels (p&lt;0.001) in CCT-diet fed group was circumvented by the exogenous glycosaminoglycan (LMWH) treatment (p&lt;0.001).	Glycosaminoglycans	49-66	FLVCR heme transporter 2	Rattus norvegicus	91-94
15820770-2	2005	There are two known polymorphisms in exon 11 of the DBP gene resulting in amino acid variants: GAT--&gt;GAG substitution replaces aspartic acid by glutamic acid in codon 416; and ACG--&gt;AAG substitution in codon 420 leads to an exchange of threonine for lysine.	Glycosaminoglycans	104-107	D-box binding PAR bZIP transcription factor	Homo sapiens	52-55
15851016-6	2005	In the neonatally treated mice, the expressed IDUA activity resulted in decreased GAG storage, prevention of skeletal abnormalities, a more normal gross appearance, and improved survival.	Glycosaminoglycans	82-85	iduronidase, alpha-L	Mus musculus	46-50
15769549-5	2005	The inhibitory effect of glycosaminoglycans on the interaction between the first component of the complement cascade (C1q) and beta-amyloid shows a similar structure-activity relationship as on the serum amyloid P component-beta-amyloid interaction.	Glycosaminoglycans	25-43	complement C1q A chain	Homo sapiens	118-121
15866045-5	2005	Treatment with excess glycosaminoglycans and chondroitinase ABC resulted in the removal of cell surface Sema3A.	Glycosaminoglycans	22-40	sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3A	Mus musculus	104-110
15769549-6	2005	This suggests that glycosaminoglycans interfere with the binding site on beta-amyloid for serum amyloid P component and C1q.	Glycosaminoglycans	19-37	complement C1q A chain	Homo sapiens	120-123
15853909-3	2005	The new DQB1 allele, DQB1*0314, was differed from DQB1*0304 only at codon 46 (GAG--&gt;GGG), corresponding to non-synonymous amino acid change (Glu--&gt;Gly).	Glycosaminoglycans	78-81	major histocompatibility complex, class II, DQ beta 1	Homo sapiens	8-12
15853909-3	2005	The new DQB1 allele, DQB1*0314, was differed from DQB1*0304 only at codon 46 (GAG--&gt;GGG), corresponding to non-synonymous amino acid change (Glu--&gt;Gly).	Glycosaminoglycans	78-81	major histocompatibility complex, class II, DQ beta 1	Homo sapiens	21-25
15853909-3	2005	The new DQB1 allele, DQB1*0314, was differed from DQB1*0304 only at codon 46 (GAG--&gt;GGG), corresponding to non-synonymous amino acid change (Glu--&gt;Gly).	Glycosaminoglycans	78-81	major histocompatibility complex, class II, DQ beta 1	Homo sapiens	21-25
15821391-5	2005	Gag-specific T cells mainly secrete interleukin-2 in ESN and interferon-gamma in HIV patients.	Glycosaminoglycans	0-3	interleukin 2	Homo sapiens	36-49
15668233-1	2005	Many lines of evidence suggest an interaction between glycosaminoglycans (GAGs) and the PrP proteins as well as a possible role for GAGs in prion disease pathogenesis.	Glycosaminoglycans	54-72	major prion protein	Cricetulus griseus	88-91
15668233-2	2005	In this work, we sought to determine whether the PrP-GAG interaction affects the incorporation of PrP(Sc) (the scrapie isoform of PrP) to normal cells.	Glycosaminoglycans	53-56	major prion protein	Cricetulus griseus	98-101
15668233-2	2005	In this work, we sought to determine whether the PrP-GAG interaction affects the incorporation of PrP(Sc) (the scrapie isoform of PrP) to normal cells.	Glycosaminoglycans	53-56	major prion protein	Cricetulus griseus	98-101
15821391-5	2005	Gag-specific T cells mainly secrete interleukin-2 in ESN and interferon-gamma in HIV patients.	Glycosaminoglycans	0-3	interferon gamma	Homo sapiens	61-77
15780641-7	2005	RESULTS: FGF-2 at 5 ng/ml was found to substantially increase the biosynthetic activity of the cells and the accumulation of GAG.	Glycosaminoglycans	125-128	fibroblast growth factor 2	Canis lupus familiaris	9-14
15699048-0	2005	TSG-6 protein binding to glycosaminoglycans: formation of stable complexes with hyaluronan and binding to chondroitin sulfates.	Glycosaminoglycans	25-43	tumor necrosis factor alpha induced protein 6	Mus musculus	0-5
15814743-7	2005	Our results suggest that S. mansoni coinfection is associated with decreased Gag-specific CD8+ cytolytic T cell responses and increased number of Gag-specific IL-10 positive CD8+ T cells.	Glycosaminoglycans	146-149	interleukin 10	Homo sapiens	159-164
15593317-1	2005	A single GAG deletion in the DYT1 gene causes primary early-onset, generalized torsion dystonia.	Glycosaminoglycans	9-12	torsin family 1 member A	Homo sapiens	29-33
15699048-4	2005	Interactions between the isolated link module and hyaluronan have been studied extensively, but little is known about the binding of full-length TSG-6 protein to hyaluronan and other glycosaminoglycans.	Glycosaminoglycans	183-201	tumor necrosis factor alpha induced protein 6	Mus musculus	145-150
15644496-3	2005	Soluble glycosaminoglycans such as heparin and heparan sulfate bind gp120 via V3 and, possibly, a CD4-induced domain.	Glycosaminoglycans	8-26	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	68-80
15644496-3	2005	Soluble glycosaminoglycans such as heparin and heparan sulfate bind gp120 via V3 and, possibly, a CD4-induced domain.	Glycosaminoglycans	8-26	CD4 molecule	Homo sapiens	98-101
15644496-5	2005	Env also binds cell-surface glycosaminoglycans.	Glycosaminoglycans	28-46	endogenous retrovirus group K member 20	Homo sapiens	0-3
15556948-5	2005	In this study, we also showed that co-localization of Vpx with Gag precursor in the cytoplasm is a prerequisite for Vpx incorporation into virus particles.	Glycosaminoglycans	63-66	vpx protein	Simian immunodeficiency virus	54-57
15556948-5	2005	In this study, we also showed that co-localization of Vpx with Gag precursor in the cytoplasm is a prerequisite for Vpx incorporation into virus particles.	Glycosaminoglycans	63-66	vpx protein	Simian immunodeficiency virus	116-119
15795524-0	2005	Gag-p6 Tsg101 binding site duplications in maternal-infant HIV infection.	Glycosaminoglycans	0-3	tumor susceptibility 101	Homo sapiens	7-13
15997874-3	2005	Inoculation with various concentration of rBCG-pSO gag p55 generated satisfactory specific lymphocyte proliferation in dose escalation trials.	Glycosaminoglycans	51-54	membrane protein, palmitoylated	Mus musculus	55-58
15369688-1	2005	Our goal is to fabricate continuous sheets of elastin atop non-biodegradable hydrogels (hylans) containing crosslinked hyaluronan, a glycosaminoglycan.	Glycosaminoglycans	133-150	elastin	Rattus norvegicus	46-53
15369688-2	2005	Such elastin-hyaluronan composites may be useful to tissue engineer replacements for the glycosaminoglycan- and elastin-rich layers of the native aortic valve cusp.	Glycosaminoglycans	89-106	elastin	Rattus norvegicus	5-12
15461586-1	2005	XT-I (xylosyltransferase I) is the initial enzyme in the post-translational biosynthesis of glycosaminoglycan chains in proteoglycans.	Glycosaminoglycans	92-109	xylosyltransferase 1	Homo sapiens	0-4
15461586-1	2005	XT-I (xylosyltransferase I) is the initial enzyme in the post-translational biosynthesis of glycosaminoglycan chains in proteoglycans.	Glycosaminoglycans	92-109	xylosyltransferase 1	Homo sapiens	6-26
15579465-8	2005	Overall, these observations suggest that Cochlin contributes to elevated IOP in primary open angle glaucoma through altered interactions within the TM extracellular matrix, resulting in cell aggregation, mucopolysaccharide deposition, and significant obstruction of the aqueous humor circulation.	Glycosaminoglycans	204-222	cochlin	Mus musculus	41-48
15727892-6	2005	RESULTS: IL-1beta and LPS stimulated significant release of GAG, NO, PGE2 and MMP-3.	Glycosaminoglycans	60-63	interleukin-1 beta	Equus caballus	9-17
15496958-4	2005	Two CTL clones derived from one of the CTL lines were found to recognize epitopes from gag in the context of HLA-B(*)4403 and -B(*)4601, respectively.	Glycosaminoglycans	87-90	major histocompatibility complex, class I, B	Homo sapiens	109-114
15686348-2	2005	PEG was attached to a 67-amino acid fully synthetic CCL-5 (RANTES) analogue at its GAG binding site both to reduce aggregation and to increase the circulating lifetime.	Glycosaminoglycans	83-86	C-C motif chemokine ligand 5	Homo sapiens	52-57
15686348-2	2005	PEG was attached to a 67-amino acid fully synthetic CCL-5 (RANTES) analogue at its GAG binding site both to reduce aggregation and to increase the circulating lifetime.	Glycosaminoglycans	83-86	C-C motif chemokine ligand 5	Homo sapiens	59-65
15859521-0	2005	Defective glycosaminoglycan substitution of decorin in a patient with progeroid syndrome is a direct consequence of two point mutations in the galactosyltransferase I (beta4GalT-7) gene.	Glycosaminoglycans	10-27	beta-1,4-galactosyltransferase 7	Homo sapiens	143-166
15859521-0	2005	Defective glycosaminoglycan substitution of decorin in a patient with progeroid syndrome is a direct consequence of two point mutations in the galactosyltransferase I (beta4GalT-7) gene.	Glycosaminoglycans	10-27	beta-1,4-galactosyltransferase 7	Homo sapiens	168-179
15859521-2	2005	In a progeroid patient carrying two point mutations in beta4 galactosyltransferase I (beta4GalT-7) only 50% of the decorin core protein molecules are substituted with glycosaminoglycan chains.	Glycosaminoglycans	167-184	beta-1,4-galactosyltransferase 7	Homo sapiens	86-97
15859521-4	2005	Decorin was less efficiently substituted with glycosaminoglycan chains upon expression of beta4GalT-7(186D) compared to beta4GalT-7-expressing cells.	Glycosaminoglycans	46-63	beta-1,4-galactosyltransferase 7	Homo sapiens	90-101
15743859-9	2005	Both TGF-beta(1) and FGF-2 antagonized the stimulatory effects of IGF-I on GAG synthesis in the two types of cartilage.	Glycosaminoglycans	75-78	transforming growth factor, beta 1	Rattus norvegicus	5-16
15743859-9	2005	Both TGF-beta(1) and FGF-2 antagonized the stimulatory effects of IGF-I on GAG synthesis in the two types of cartilage.	Glycosaminoglycans	75-78	fibroblast growth factor 2	Rattus norvegicus	21-26
15743859-9	2005	Both TGF-beta(1) and FGF-2 antagonized the stimulatory effects of IGF-I on GAG synthesis in the two types of cartilage.	Glycosaminoglycans	75-78	insulin-like growth factor 1	Rattus norvegicus	66-71
15743473-5	2005	Various glycosaminoglycans, including HA, chondroitin sulfate, keratan sulfate, heparin, and heparan, were incubated with human antithrombin III in vitro.	Glycosaminoglycans	8-26	serpin family C member 1	Homo sapiens	128-144
15355933-10	2005	Finally, RANTES forms GAG-dependent complexes with the shed ectodomains of SD-1 and SD-4 as well as with those of CD44.	Glycosaminoglycans	22-25	C-C motif chemokine ligand 5	Homo sapiens	9-15
15355933-10	2005	Finally, RANTES forms GAG-dependent complexes with the shed ectodomains of SD-1 and SD-4 as well as with those of CD44.	Glycosaminoglycans	22-25	syndecan 1	Homo sapiens	75-79
15355933-10	2005	Finally, RANTES forms GAG-dependent complexes with the shed ectodomains of SD-1 and SD-4 as well as with those of CD44.	Glycosaminoglycans	22-25	CD44 molecule (Indian blood group)	Homo sapiens	114-118
15659549-5	2005	Furthermore, expression of the RING finger mutant hPOSH inhibits virus release and induces accumulation of intracellular Gag in normal cells.	Glycosaminoglycans	121-124	SH3 domain containing ring finger 1	Homo sapiens	50-55
15641080-6	2005	RESULTS: Antagonists of IL-1 and TNFalpha inhibited the increase in CII cleavage by collagenase as well as the increase in GAG release observed in OA cartilage compared with normal cartilage.	Glycosaminoglycans	123-126	interleukin 1 alpha	Homo sapiens	24-28
15641080-6	2005	RESULTS: Antagonists of IL-1 and TNFalpha inhibited the increase in CII cleavage by collagenase as well as the increase in GAG release observed in OA cartilage compared with normal cartilage.	Glycosaminoglycans	123-126	tumor necrosis factor	Homo sapiens	33-41
15641092-7	2005	The mean +/- SD synovial fluid GAG concentration in patients was 157 +/- 86 mug/ml and showed a positive correlation with the T1(Gd) (r = 0.49, P = 0.02).	Glycosaminoglycans	31-34	CD5 molecule	Homo sapiens	126-132
15641092-9	2005	In cartilage with a high GAG content (long T1(Gd)), more GAG is released into the synovial fluid, suggesting that cartilage quality is a factor to consider when interpreting cartilage biomarkers of metabolism.	Glycosaminoglycans	25-28	CD5 molecule	Homo sapiens	43-49
15641092-9	2005	In cartilage with a high GAG content (long T1(Gd)), more GAG is released into the synovial fluid, suggesting that cartilage quality is a factor to consider when interpreting cartilage biomarkers of metabolism.	Glycosaminoglycans	57-60	CD5 molecule	Homo sapiens	43-49
16283481-3	2005	Specifically, glycosaminoglycans bind HBGFs and activate HBGF receptors, including those for FGF-2 and VEGF-A.	Glycosaminoglycans	14-32	fibroblast growth factor 2	Homo sapiens	93-98
16283481-3	2005	Specifically, glycosaminoglycans bind HBGFs and activate HBGF receptors, including those for FGF-2 and VEGF-A.	Glycosaminoglycans	14-32	vascular endothelial growth factor A	Homo sapiens	103-109
15629535-2	2005	The p24 protein plays an active structural role in the Gag protein and in its mature form.	Glycosaminoglycans	55-58	transmembrane p24 trafficking protein 2	Homo sapiens	4-7
15537641-8	2005	Glycosaminoglycanases with assorted glycosaminoglycan (GAG) cleavage specificities coupled with Western analyses of the cleaved GAG "stubs" demonstrated that the DSP GAG attachments contain chondroitin 6-sulfate, but not keratan sulfate, heparan sulfate, chondroitin, or chondroitin 4-sulfate.	Glycosaminoglycans	55-58	dentin sialophosphoprotein	Sus scrofa	162-165
15537641-8	2005	Glycosaminoglycanases with assorted glycosaminoglycan (GAG) cleavage specificities coupled with Western analyses of the cleaved GAG "stubs" demonstrated that the DSP GAG attachments contain chondroitin 6-sulfate, but not keratan sulfate, heparan sulfate, chondroitin, or chondroitin 4-sulfate.	Glycosaminoglycans	128-131	dentin sialophosphoprotein	Sus scrofa	162-165
15537641-8	2005	Glycosaminoglycanases with assorted glycosaminoglycan (GAG) cleavage specificities coupled with Western analyses of the cleaved GAG "stubs" demonstrated that the DSP GAG attachments contain chondroitin 6-sulfate, but not keratan sulfate, heparan sulfate, chondroitin, or chondroitin 4-sulfate.	Glycosaminoglycans	128-131	dentin sialophosphoprotein	Sus scrofa	162-165
15537641-10	2005	We conclude that DSP is a proteoglycan and that GAG attachments are the predominant structural feature of porcine DSP.	Glycosaminoglycans	48-51	dentin sialophosphoprotein	Sus scrofa	114-117
15665640-7	2005	Over the year of follow-up, IFN-() production to gag persisted, responses to other HIV antigens increased, and markers of cellular activation did not change.	Glycosaminoglycans	49-52	interferon alpha 1	Homo sapiens	28-31
15686253-6	2005	The pellets cultured in DMEM/ITS+/TGF-beta1 were larger and contained significantly greater amounts of DNA and glycosaminoglycans.	Glycosaminoglycans	111-129	transforming growth factor beta 1	Homo sapiens	34-43
15580653-4	2005	The circulating gag-specific CD8(+) T cells in fresh blood reliably produced IFN-gamma but lacked IL-2 and high perforin levels and failed to expand significantly during culture with mature DC presenting HIV-1 gag peptides.	Glycosaminoglycans	16-19	CD8a molecule	Homo sapiens	29-32
15580653-4	2005	The circulating gag-specific CD8(+) T cells in fresh blood reliably produced IFN-gamma but lacked IL-2 and high perforin levels and failed to expand significantly during culture with mature DC presenting HIV-1 gag peptides.	Glycosaminoglycans	16-19	interferon gamma	Homo sapiens	77-86
15580653-4	2005	The circulating gag-specific CD8(+) T cells in fresh blood reliably produced IFN-gamma but lacked IL-2 and high perforin levels and failed to expand significantly during culture with mature DC presenting HIV-1 gag peptides.	Glycosaminoglycans	16-19	interleukin 2	Homo sapiens	98-102
15703491-1	2005	Mucopolysaccharidosis type I is a lysosomal disease due to mutations in the IDUA gene, resulting in deficiency of alpha-L-iduronidase and accumulation of glycosaminoglycans (GAGs).	Glycosaminoglycans	154-172	iduronidase, alpha-L	Mus musculus	76-80
15921168-0	2005	Hb Kurosaki [alpha7(A5)Lys -->Glu (AAG --> GAG)]: an alpha2-globin gene mutation found in Thailand.	Glycosaminoglycans	43-46	immunoglobulin kappa variable 2D-26	Homo sapiens	0-22
15921168-0	2005	Hb Kurosaki [alpha7(A5)Lys -->Glu (AAG --> GAG)]: an alpha2-globin gene mutation found in Thailand.	Glycosaminoglycans	43-46	hemoglobin subunit alpha 2	Homo sapiens	53-66
15921168-1	2005	Hb Kurosaki [alpha 7(A5)Lys --> Glu (AAG --> GAG)], has been found for the first time in Thailand.	Glycosaminoglycans	45-48	immunoglobulin kappa variable 2D-26	Homo sapiens	0-23
15921168-4	2005	Direct DNA sequence analysis of selectively amplified segments of the alpha1 and alpha2 genes showed that codon 7 of the alpha2-globin gene was heterozygous for AAG (Lys) and GAG (Glu).	Glycosaminoglycans	175-178	glycoprotein hormone subunit alpha 2	Homo sapiens	81-87
15921168-4	2005	Direct DNA sequence analysis of selectively amplified segments of the alpha1 and alpha2 genes showed that codon 7 of the alpha2-globin gene was heterozygous for AAG (Lys) and GAG (Glu).	Glycosaminoglycans	175-178	hemoglobin subunit alpha 2	Homo sapiens	121-134
15790028-6	2005	The "early" virus phenomenon, which is deprived of any mature structure or the ability to infect and does not contain mature Gag and Env proteins, illustrates that the proteolytic pressing of the Gag p55 precursor is not enough for the maturation of the virus and additional viral or cellular factors are needed for the virus to become infectious.	Glycosaminoglycans	196-199	H3 histone pseudogene 44	Homo sapiens	200-203
16435197-1	2005	Mucopolysaccharidosis I (MPS I) is a lysosomal disorder characterized by a deficiency of the enzyme alpha-L: -iduronidase (IDUA), which is responsible for the degradation of glycosaminoglycans (GAGs).	Glycosaminoglycans	174-192	iduronidase, alpha-L	Mus musculus	123-127
16435198-2	2005	The deficiency of alpha-L-iduronidase (EC 1.2.3.76), one of the enzymes responsible for the degradation of glycosaminoglycans, results in accumulation of heparan and dermatan sulphate in these patients.	Glycosaminoglycans	107-125	alpha-L-iduronidase	Homo sapiens	18-37
15680145-2	2005	Here, we screen a cohort of HIV-1-infected persons in the United States for CD8+ T lymphocyte (CTL) responses using Gag peptides based on the Clade C primary isolate DU422 and the consensus sequence for Clade B.	Glycosaminoglycans	116-119	CD8a molecule	Homo sapiens	76-79
15601778-2	2004	We investigate a therapeutic strategy based on stimulation of PG synthesis by gene transfer of the glycosaminoglycan (GAG)-synthesizing enzyme, beta1,3-glucuronosyltransferase-I (GlcAT-I) to promote cartilage repair.	Glycosaminoglycans	99-116	beta-1,3-glucuronyltransferase 3	Homo sapiens	179-186
15639641-6	2005	Addition of transforming growth factor beta-3 and insulin like growth factor-1 increased collagen II expression and GAG synthesis in these SOX9 transduced cell pellets.	Glycosaminoglycans	116-119	transforming growth factor beta 3	Homo sapiens	12-45
15639641-6	2005	Addition of transforming growth factor beta-3 and insulin like growth factor-1 increased collagen II expression and GAG synthesis in these SOX9 transduced cell pellets.	Glycosaminoglycans	116-119	SRY-box transcription factor 9	Homo sapiens	139-143
15744563-3	2005	We previously localized a particle release defect of the full-length endogenous-derived expression construct pCMV2enJS56A1 to the amino-terminal region of gag that incorporates the two variable regions VR1 and VR2, which harbor the main sequence differences between endogenous and exogenous JSRV in this part of gag.	Glycosaminoglycans	155-158	vault RNA 1-1	Homo sapiens	202-205
15744563-3	2005	We previously localized a particle release defect of the full-length endogenous-derived expression construct pCMV2enJS56A1 to the amino-terminal region of gag that incorporates the two variable regions VR1 and VR2, which harbor the main sequence differences between endogenous and exogenous JSRV in this part of gag.	Glycosaminoglycans	155-158	vault RNA 1-2	Homo sapiens	210-213
15744563-8	2005	These results point to a small number of amino acids lying outside of VR1 and VR2 that may be responsible for the particle defect of enJS56A1 Gag.	Glycosaminoglycans	142-145	vault RNA 1-1	Homo sapiens	70-73
15744563-8	2005	These results point to a small number of amino acids lying outside of VR1 and VR2 that may be responsible for the particle defect of enJS56A1 Gag.	Glycosaminoglycans	142-145	vault RNA 1-2	Homo sapiens	78-81
15585404-1	2005	Mucopolysaccharidosis I (MPS I) due to deficient alpha-L-iduronidase (IDUA) activity results in accumulation of glycosaminoglycans in many cells.	Glycosaminoglycans	112-130	iduronidase, alpha-L	Mus musculus	49-68
15585404-1	2005	Mucopolysaccharidosis I (MPS I) due to deficient alpha-L-iduronidase (IDUA) activity results in accumulation of glycosaminoglycans in many cells.	Glycosaminoglycans	112-130	iduronidase, alpha-L	Mus musculus	70-74
15601778-2	2004	We investigate a therapeutic strategy based on stimulation of PG synthesis by gene transfer of the glycosaminoglycan (GAG)-synthesizing enzyme, beta1,3-glucuronosyltransferase-I (GlcAT-I) to promote cartilage repair.	Glycosaminoglycans	118-121	beta-1,3-glucuronyltransferase 3	Homo sapiens	179-186
15601778-6	2004	Interestingly, GlcAT-I overexpression significantly enhanced GAG synthesis and deposition as evidenced by (35)S-sulfate incorporation, histology, estimation of GAG content, and fluorophore-assisted carbohydrate electrophoresis analysis.	Glycosaminoglycans	61-64	beta-1,3-glucuronyltransferase 3	Homo sapiens	15-22
15601778-6	2004	Interestingly, GlcAT-I overexpression significantly enhanced GAG synthesis and deposition as evidenced by (35)S-sulfate incorporation, histology, estimation of GAG content, and fluorophore-assisted carbohydrate electrophoresis analysis.	Glycosaminoglycans	160-163	beta-1,3-glucuronyltransferase 3	Homo sapiens	15-22
15601778-7	2004	Metabolic labeling and Western blot analyses further suggested that GlcAT-I expression led to an increase in the abundance rather than in the length of GAG chains.	Glycosaminoglycans	152-155	beta-1,3-glucuronyltransferase 3	Homo sapiens	68-75
15601778-10	2004	In concert, our investigations strongly indicated that GlcAT-I was able to control and reverse articular cartilage defects in terms of PG anabolism and GAG content associated with IL-1beta.	Glycosaminoglycans	152-155	beta-1,3-glucuronyltransferase 3	Homo sapiens	55-62
15603739-3	2004	The thrombospondin repeats of Sema5A physically interact with the glycosaminoglycan portion of both chondroitin sulfate proteoglycans (CSPGs) and heparan sulfate proteoglycans (HSPGs).	Glycosaminoglycans	66-83	semaphorin 5A	Homo sapiens	30-36
15493058-2	2004	Sulfatase substrates range from small cytosolic steroids, such as estrogen sulfate, to complex cell-surface carbohydrates, such as the glycosaminoglycans.	Glycosaminoglycans	135-153	arylsulfatase family member H	Homo sapiens	0-9
15324304-4	2004	When [35S]glycosaminoglycans formed from DSDS after incubation with [35S]PAPS and C4ST-1 were digested with chondroitinase ACII, a major part of the radioactivity was recovered in disaccharide fractions and the remainder distributed to tetrasaccharides and larger fractions, indicating that C4ST-1 mainly transferred sulphate to position 4 of the GalNAc residue located at the GlcA-GalNAc-GlcA sequence.	Glycosaminoglycans	10-28	carbohydrate sulfotransferase 11	Rattus norvegicus	82-88
15324304-4	2004	When [35S]glycosaminoglycans formed from DSDS after incubation with [35S]PAPS and C4ST-1 were digested with chondroitinase ACII, a major part of the radioactivity was recovered in disaccharide fractions and the remainder distributed to tetrasaccharides and larger fractions, indicating that C4ST-1 mainly transferred sulphate to position 4 of the GalNAc residue located at the GlcA-GalNAc-GlcA sequence.	Glycosaminoglycans	10-28	carbohydrate sulfotransferase 11	Rattus norvegicus	291-297
15324304-6	2004	On the other hand, when [35S]glycosaminoglycans formed from DSDS after incubation with [35S]PAPS and C6ST-1 were digested with chondroitinase ACII, a major part of the radioactivity was recovered in fractions larger than hexasaccharides, indicating that C6ST-1 transferred sulphate to the GalNAc residues located in the L-iduronic acid-rich region.	Glycosaminoglycans	29-47	carbohydrate sulfotransferase 3	Rattus norvegicus	101-107
15324304-6	2004	On the other hand, when [35S]glycosaminoglycans formed from DSDS after incubation with [35S]PAPS and C6ST-1 were digested with chondroitinase ACII, a major part of the radioactivity was recovered in fractions larger than hexasaccharides, indicating that C6ST-1 transferred sulphate to the GalNAc residues located in the L-iduronic acid-rich region.	Glycosaminoglycans	29-47	carbohydrate sulfotransferase 3	Rattus norvegicus	254-260
15530414-4	2004	Based on the histological staining of glycosaminoglycan using toluidine blue dye-binding method we found that CDMP-1 could initiate chondrogenic differentiation of MSCs as did TGF-beta1.	Glycosaminoglycans	38-55	growth differentiation factor 5	Homo sapiens	110-116
15530414-7	2004	This synergic chondrogenic effect of CDMP-1 together with TGF-beta1 was further confirmed by quantification of GAG using dimethylmethylene blue dye-binding assay and immunohistochemical analysis of the expression of cartilage-specific protein collagen II.	Glycosaminoglycans	111-114	growth differentiation factor 5	Homo sapiens	37-43
15530414-7	2004	This synergic chondrogenic effect of CDMP-1 together with TGF-beta1 was further confirmed by quantification of GAG using dimethylmethylene blue dye-binding assay and immunohistochemical analysis of the expression of cartilage-specific protein collagen II.	Glycosaminoglycans	111-114	transforming growth factor beta 1	Homo sapiens	58-67
15631022-9	2004	RESULTS: GAG content in control samples increased significantly during the study, whereas GAG content in 3-D constructs cultured with TNF-alpha or TNF-alpha plus TIMP did not increase.	Glycosaminoglycans	90-93	tumor necrosis factor	Canis lupus familiaris	134-143
15631022-9	2004	RESULTS: GAG content in control samples increased significantly during the study, whereas GAG content in 3-D constructs cultured with TNF-alpha or TNF-alpha plus TIMP did not increase.	Glycosaminoglycans	90-93	tumor necrosis factor	Canis lupus familiaris	147-156
15631022-10	2004	On day 9, GAG release from 3-D constructs cultured with TNF-alpha was significantly higher than that in other constructs.	Glycosaminoglycans	10-13	tumor necrosis factor	Canis lupus familiaris	56-65
15486944-8	2004	The deposition of glycosaminoglycan (GAG) and type II collagen and the expression of type II collagen mRNA were all higher for hMSC cultured on silk than on collagen scaffolds.	Glycosaminoglycans	18-35	musculin	Homo sapiens	127-131
15486944-8	2004	The deposition of glycosaminoglycan (GAG) and type II collagen and the expression of type II collagen mRNA were all higher for hMSC cultured on silk than on collagen scaffolds.	Glycosaminoglycans	37-40	musculin	Homo sapiens	127-131
15984338-16	2004	Two broadly cross-reactive Gag peptides were identified which stimulated only an interferon gamma response by CD4+ T lymphocytes, which indicated a T helper 1 response is needed for CTL stimulation.	Glycosaminoglycans	27-30	CD4 molecule	Homo sapiens	110-113
15564468-3	2004	The transmembrane protein Elp specifically interacts with N-terminal Gag sequences during morphogenesis.	Glycosaminoglycans	69-72	nuclear receptor subfamily 5 group A member 1	Homo sapiens	26-29
15308688-9	2004	The IGF-II binding site lies adjacent to surfaces likely to be involved in glycosaminoglycan binding of IGFBPs, which might explain their decreased IGF affinity when bound to glycosaminoglycans, and nuclear localization.	Glycosaminoglycans	75-92	insulin like growth factor 2	Homo sapiens	4-10
15693627-9	2004	For patients with known infection dates, the estimated dates of the coalescent events obtained using molecular clock calculations based on a newly developed Bayesian method in gag + env were in agreement with the actual infection dates.	Glycosaminoglycans	176-181	endogenous retrovirus group K member 20	Homo sapiens	182-185
15308688-9	2004	The IGF-II binding site lies adjacent to surfaces likely to be involved in glycosaminoglycan binding of IGFBPs, which might explain their decreased IGF affinity when bound to glycosaminoglycans, and nuclear localization.	Glycosaminoglycans	75-92	insulin like growth factor binding protein 6	Homo sapiens	104-110
15308688-9	2004	The IGF-II binding site lies adjacent to surfaces likely to be involved in glycosaminoglycan binding of IGFBPs, which might explain their decreased IGF affinity when bound to glycosaminoglycans, and nuclear localization.	Glycosaminoglycans	175-193	insulin like growth factor 2	Homo sapiens	4-10
15308688-9	2004	The IGF-II binding site lies adjacent to surfaces likely to be involved in glycosaminoglycan binding of IGFBPs, which might explain their decreased IGF affinity when bound to glycosaminoglycans, and nuclear localization.	Glycosaminoglycans	175-193	insulin like growth factor binding protein 6	Homo sapiens	104-110
15294915-1	2004	Human xylosyltransferase I (XT-I) is the initial enzyme involved in the biosynthesis of the glycosaminoglycan linker region in proteoglycans.	Glycosaminoglycans	92-109	xylosyltransferase 1	Homo sapiens	6-26
15474298-6	2004	An interesting microsatellite is the CTC/GAG repeat which, as double-stranded (DS) DNA, bound specificity protein 1 (SP1) with high affinity, formed triplexes in vitro and displayed differences in SP1 binding and triplex formation capacity for repeats with distinct numbers of repeat units.	Glycosaminoglycans	41-44	Sp1 transcription factor	Homo sapiens	94-115
15294915-1	2004	Human xylosyltransferase I (XT-I) is the initial enzyme involved in the biosynthesis of the glycosaminoglycan linker region in proteoglycans.	Glycosaminoglycans	92-109	xylosyltransferase 1	Homo sapiens	28-32
15383330-3	2004	Deletions within the syndecan-1 ectodomain (S1ED) implicate an active site within the core protein between the glycosaminoglycan attachment region and the transmembrane domain.	Glycosaminoglycans	111-128	syndecan 1	Homo sapiens	21-31
15292227-6	2004	Four mutants (Asp51, Lys52, Lys145/Thr147/Trp148, Asp234) showed normal increased rates of inhibition by HCII-glycosaminoglycans, whereas four mutants (Trp50, Glu202, Glu229, Arg233) remained resistant to inhibition by HCII with glycosaminoglycans.	Glycosaminoglycans	110-128	serpin family D member 1	Homo sapiens	105-109
15292227-8	2004	Collectively, our results support a "double bridge" mechanism for HCII inhibition of thrombin in the presence of glycosaminoglycans, which relies in part on ternary complex formation but is primarily dominated by an allosteric process involving contact of the "hirudin-like" domain of HCII with thrombin exosite-1.	Glycosaminoglycans	113-131	serpin family D member 1	Homo sapiens	66-70
15292227-8	2004	Collectively, our results support a "double bridge" mechanism for HCII inhibition of thrombin in the presence of glycosaminoglycans, which relies in part on ternary complex formation but is primarily dominated by an allosteric process involving contact of the "hirudin-like" domain of HCII with thrombin exosite-1.	Glycosaminoglycans	113-131	coagulation factor II, thrombin	Homo sapiens	85-93
15292227-8	2004	Collectively, our results support a "double bridge" mechanism for HCII inhibition of thrombin in the presence of glycosaminoglycans, which relies in part on ternary complex formation but is primarily dominated by an allosteric process involving contact of the "hirudin-like" domain of HCII with thrombin exosite-1.	Glycosaminoglycans	113-131	serpin family D member 1	Homo sapiens	285-289
15292227-8	2004	Collectively, our results support a "double bridge" mechanism for HCII inhibition of thrombin in the presence of glycosaminoglycans, which relies in part on ternary complex formation but is primarily dominated by an allosteric process involving contact of the "hirudin-like" domain of HCII with thrombin exosite-1.	Glycosaminoglycans	113-131	coagulation factor II, thrombin	Homo sapiens	295-303
15613921-2	2004	Here we show that HPRG adsorbed to a glycosaminoglycan (GAG) surface also binds Plg with a Kd value of 0.7 micromol/l.	Glycosaminoglycans	56-59	histidine rich glycoprotein	Homo sapiens	18-22
15613921-2	2004	Here we show that HPRG adsorbed to a glycosaminoglycan (GAG) surface also binds Plg with a Kd value of 0.7 micromol/l.	Glycosaminoglycans	56-59	plasminogen	Homo sapiens	80-83
15613921-2	2004	Here we show that HPRG adsorbed to a glycosaminoglycan (GAG) surface also binds Plg with a Kd value of 0.7 micromol/l.	Glycosaminoglycans	37-54	histidine rich glycoprotein	Homo sapiens	18-22
15613921-4	2004	Specifically, Plg complexed with HPRG on a GAG surface is more readily activated by tissue-type Plg activator than free Plg, with a 10-fold difference in apparent catalytic efficiency (kcat/Km).	Glycosaminoglycans	43-46	plasminogen	Homo sapiens	14-17
15613921-2	2004	Here we show that HPRG adsorbed to a glycosaminoglycan (GAG) surface also binds Plg with a Kd value of 0.7 micromol/l.	Glycosaminoglycans	37-54	plasminogen	Homo sapiens	80-83
15613921-4	2004	Specifically, Plg complexed with HPRG on a GAG surface is more readily activated by tissue-type Plg activator than free Plg, with a 10-fold difference in apparent catalytic efficiency (kcat/Km).	Glycosaminoglycans	43-46	histidine rich glycoprotein	Homo sapiens	33-37
15613921-4	2004	Specifically, Plg complexed with HPRG on a GAG surface is more readily activated by tissue-type Plg activator than free Plg, with a 10-fold difference in apparent catalytic efficiency (kcat/Km).	Glycosaminoglycans	43-46	plasminogen	Homo sapiens	96-99
15613921-4	2004	Specifically, Plg complexed with HPRG on a GAG surface is more readily activated by tissue-type Plg activator than free Plg, with a 10-fold difference in apparent catalytic efficiency (kcat/Km).	Glycosaminoglycans	43-46	plasminogen	Homo sapiens	96-99
15613921-5	2004	HPRG also augments the increase in Plg activation caused by fibrinogen fragments either in solution or on GAG surfaces.	Glycosaminoglycans	106-109	histidine rich glycoprotein	Homo sapiens	0-4
15613921-5	2004	HPRG also augments the increase in Plg activation caused by fibrinogen fragments either in solution or on GAG surfaces.	Glycosaminoglycans	106-109	plasminogen	Homo sapiens	35-38
15281096-6	2004	PN-1 secreted by smooth muscle cells remained essentially associated to cell-surface glycosaminoglycans and was released from the cell surface by heparin.	Glycosaminoglycans	85-103	serpin family E member 2	Rattus norvegicus	0-4
15295619-3	2004	MPS VII is one of LSDs and caused by deficiency of beta-glucuronidase (GUSB), resulting in accumulation of glycosaminoglycans (GAGs) in brain.	Glycosaminoglycans	107-125	glucuronidase, beta	Mus musculus	71-75
15203110-5	2004	Heparin, heparan sulfate and dermatan sulfate, at various HARP to glycosaminoglycan ratios, partially protect HARP from plasmin degradation.	Glycosaminoglycans	66-83	pleiotrophin	Homo sapiens	110-114
15203110-5	2004	Heparin, heparan sulfate and dermatan sulfate, at various HARP to glycosaminoglycan ratios, partially protect HARP from plasmin degradation.	Glycosaminoglycans	66-83	plasminogen	Homo sapiens	120-127
15363109-6	2004	Vpr virion packaging was normal when amino acid #1-23 of the Gag p6 domain was preserved.	Glycosaminoglycans	61-64	Vpr	Human immunodeficiency virus 1	0-3
15452250-3	2004	The interacting region of HIV-2 Gag is located in the conserved matrix and capsid domains, while both the RS (arginine-serine-rich) domain and the KS (kinase) domain of PRP4 are able to bind to HIV-2 Gag.	Glycosaminoglycans	32-35	pre-mRNA processing factor 4B	Homo sapiens	169-173
15452250-8	2004	We hypothesize that as Gag accumulates in the cell, down regulation of splicing occurs through reduced phosphorylation of SF2.	Glycosaminoglycans	23-26	serine and arginine rich splicing factor 1	Homo sapiens	122-125
15363109-7	2004	Most importantly, Ala substitutions for Phe15, Arg16 and Phe17 in the context of amino acid #1-23 of the Gag p6 domain abolished Vpr virion packaging.	Glycosaminoglycans	105-108	Vpr	Human immunodeficiency virus 1	129-132
15383472-2	2004	UFH is a heterogeneous mixture of glycosaminoglycans that bind to antithrombin via a pentasaccharide, catalyzing the inactivation of thrombin and other clotting factors.	Glycosaminoglycans	34-52	serpin family C member 1	Homo sapiens	66-78
15320946-7	2004	Both the proliferation rate and glycosaminoglycan (GAG) production were significantly higher for scaffolds incorporating TGF-beta1 microspheres than for the control scaffolds without microspheres 10 days after incubation.	Glycosaminoglycans	32-49	LOW QUALITY PROTEIN: transforming growth factor beta-1	Oryctolagus cuniculus	121-130
15320946-7	2004	Both the proliferation rate and glycosaminoglycan (GAG) production were significantly higher for scaffolds incorporating TGF-beta1 microspheres than for the control scaffolds without microspheres 10 days after incubation.	Glycosaminoglycans	51-54	LOW QUALITY PROTEIN: transforming growth factor beta-1	Oryctolagus cuniculus	121-130
15383472-2	2004	UFH is a heterogeneous mixture of glycosaminoglycans that bind to antithrombin via a pentasaccharide, catalyzing the inactivation of thrombin and other clotting factors.	Glycosaminoglycans	34-52	coagulation factor II, thrombin	Homo sapiens	70-78
15208308-11	2004	We conclude that the 190-kDa hHARE can function independently of other hHARE isoforms to mediate the endocytosis of multiple glycosaminoglycans.	Glycosaminoglycans	125-143	stabilin 2	Homo sapiens	29-34
15485016-1	2004	OBJECTIVE: The tight skin (Tsk-1) mouse has been proposed as a model for systemic sclerosis on the basis of increased accumulation of collagen and glycosaminoglycans in the skin, and by the presence of serum autoantibodies.	Glycosaminoglycans	147-165	testis-specific serine kinase 1	Mus musculus	27-32
15311269-2	2004	Antithrombin circulates at a high concentration, but only becomes capable of efficient thrombin inhibition on interaction with heparin or related glycosaminoglycans.	Glycosaminoglycans	146-164	serpin family C member 1	Homo sapiens	0-12
15311269-2	2004	Antithrombin circulates at a high concentration, but only becomes capable of efficient thrombin inhibition on interaction with heparin or related glycosaminoglycans.	Glycosaminoglycans	146-164	coagulation factor II, thrombin	Homo sapiens	4-12
15569536-11	2004	An A5521G mutation (GAG--&gt;AAG) in the exon 38 was found in the proband and her diseased father, resulting in a characteristic change of NMMHC-A1841 (Glutamic acid--&gt;Arginine), which was not found in other members of the family and in normal controls.	Glycosaminoglycans	20-23	myosin heavy chain 9	Homo sapiens	139-146
15252057-8	2004	Based on our results, we propose that IL-8 dimerization functions as a negative regulator for the receptor function and as a positive regulator for binding to glycosaminoglycans and that both play a role in the neutrophil recruitment process.	Glycosaminoglycans	159-177	C-X-C motif chemokine ligand 8	Homo sapiens	38-42
15208308-11	2004	We conclude that the 190-kDa hHARE can function independently of other hHARE isoforms to mediate the endocytosis of multiple glycosaminoglycans.	Glycosaminoglycans	125-143	stabilin 2	Homo sapiens	71-76
15046906-6	2004	Both proliferation rate and glycosaminoglycan (GAG) production were significantly higher in the TGF-beta 1 microsphere-incorporated scaffolds than in the control scaffolds without microspheres.	Glycosaminoglycans	28-45	LOW QUALITY PROTEIN: transforming growth factor beta-1	Oryctolagus cuniculus	96-106
15210704-5	2004	Virus-like particles derived from constructs in which pol, env, and most of gag were deleted still contained high levels of cytidine deaminase activity; in addition, coimmunoprecipitation of APOBEC3G and HIV-1 Gag in the presence and absence of RNase A indicated that the two proteins do not interact directly but form an RNase-sensitive complex.	Glycosaminoglycans	210-213	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	191-199
15289379-1	2004	BACKGROUND: Mucopolysaccharidosis VII (MPS VII) is a lysosomal storage disease caused by deficient beta-glucuronidase (GUSB) activity resulting in defective catabolism of glycosaminoglycans (GAGs).	Glycosaminoglycans	171-189	glucuronidase beta	Canis lupus familiaris	119-123
15289379-1	2004	BACKGROUND: Mucopolysaccharidosis VII (MPS VII) is a lysosomal storage disease caused by deficient beta-glucuronidase (GUSB) activity resulting in defective catabolism of glycosaminoglycans (GAGs).	Glycosaminoglycans	191-195	glucuronidase beta	Canis lupus familiaris	119-123
15249198-3	2004	Insulin-induced accumulation of glycosaminoglycan and expression of chondrogenic differentiation markers, type II collagen, type X collagen, and aggrecan mRNA were inhibited by the MEK1/2 inhibitor (U0126) and the p38 MAP kinase inhibitor (SB203580).	Glycosaminoglycans	32-49	mitogen-activated protein kinase kinase 1	Mus musculus	181-187
15249198-3	2004	Insulin-induced accumulation of glycosaminoglycan and expression of chondrogenic differentiation markers, type II collagen, type X collagen, and aggrecan mRNA were inhibited by the MEK1/2 inhibitor (U0126) and the p38 MAP kinase inhibitor (SB203580).	Glycosaminoglycans	32-49	mitogen-activated protein kinase 14	Mus musculus	214-217
15249198-4	2004	Conversely, the JNK inhibitor (SP600125) enhanced the synthesis of glycosaminoglycan and expression of chondrogenic differentiation markers.	Glycosaminoglycans	67-84	mitogen-activated protein kinase 8	Mus musculus	16-19
15283994-1	2004	A GAG deletion in the gene (TOR1A) for torsinA is associated with childhood-onset generalized dystonia (DYT1).	Glycosaminoglycans	2-5	torsin family 1, member A	Rattus norvegicus	28-33
15283994-1	2004	A GAG deletion in the gene (TOR1A) for torsinA is associated with childhood-onset generalized dystonia (DYT1).	Glycosaminoglycans	2-5	torsin family 1, member A	Rattus norvegicus	39-46
15283994-1	2004	A GAG deletion in the gene (TOR1A) for torsinA is associated with childhood-onset generalized dystonia (DYT1).	Glycosaminoglycans	2-5	torsin family 1, member A	Rattus norvegicus	104-108
15247563-2	2004	Subtypes were assigned by heteroduplex mobility assay or sequencing of the p17/p24 region of gag and the V3/V4 region of env and by sequencing of the protease gene.	Glycosaminoglycans	93-96	family with sequence similarity 72 member B	Homo sapiens	75-78
15247563-2	2004	Subtypes were assigned by heteroduplex mobility assay or sequencing of the p17/p24 region of gag and the V3/V4 region of env and by sequencing of the protease gene.	Glycosaminoglycans	93-96	transmembrane p24 trafficking protein 2	Homo sapiens	79-82
15046906-6	2004	Both proliferation rate and glycosaminoglycan (GAG) production were significantly higher in the TGF-beta 1 microsphere-incorporated scaffolds than in the control scaffolds without microspheres.	Glycosaminoglycans	47-50	LOW QUALITY PROTEIN: transforming growth factor beta-1	Oryctolagus cuniculus	96-106
15481894-3	2004	After excluding most of the common Mediterranean mutations, the alpha2-globin gene was sequenced and found to have a point mutation in the heterozygous state that creates a premature stop signal for translation (GAG-->TAG or Glu-->Term) at codon 23.	Glycosaminoglycans	212-215	hemoglobin subunit alpha 2	Homo sapiens	64-77
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
15345313-3	2004	Continuous expression of Gag and Env proteins was detected in stably transduced BLCL, which induced Gag- or Env-specific T cell responses, as measured by both IFNgamma-ELISPOT and chromium release assays, upon in vitro stimulation of PBMC from the SHIV89.6P-infected monkeys.	Glycosaminoglycans	25-28	endogenous retrovirus group K member 20	Homo sapiens	108-111
15345313-3	2004	Continuous expression of Gag and Env proteins was detected in stably transduced BLCL, which induced Gag- or Env-specific T cell responses, as measured by both IFNgamma-ELISPOT and chromium release assays, upon in vitro stimulation of PBMC from the SHIV89.6P-infected monkeys.	Glycosaminoglycans	25-28	interferon gamma	Homo sapiens	159-167
15345313-3	2004	Continuous expression of Gag and Env proteins was detected in stably transduced BLCL, which induced Gag- or Env-specific T cell responses, as measured by both IFNgamma-ELISPOT and chromium release assays, upon in vitro stimulation of PBMC from the SHIV89.6P-infected monkeys.	Glycosaminoglycans	100-103	endogenous retrovirus group K member 20	Homo sapiens	33-36
15249683-11	2004	The results suggest that vWF domain A1 inhibits the cleavage of domain A2, and that inhibition can be relieved by interaction of domain A1 with platelet GPIbalpha or certain glycosaminoglycans.	Glycosaminoglycans	174-192	von Willebrand factor	Homo sapiens	25-28
15246272-4	2004	We found instead that nonactivated mixed glial cells expressed almost 10-fold less Gag protein, but more importantly, analysis of the intracellular Gag products in quiescent cells showed an aberrant p55/p24 Gag processing phenotype that appeared to be due to the premature activity of the viral protease.	Glycosaminoglycans	148-151	H3 histone pseudogene 44	Homo sapiens	199-202
15246272-4	2004	We found instead that nonactivated mixed glial cells expressed almost 10-fold less Gag protein, but more importantly, analysis of the intracellular Gag products in quiescent cells showed an aberrant p55/p24 Gag processing phenotype that appeared to be due to the premature activity of the viral protease.	Glycosaminoglycans	148-151	transmembrane p24 trafficking protein 2	Homo sapiens	203-206
15246272-4	2004	We found instead that nonactivated mixed glial cells expressed almost 10-fold less Gag protein, but more importantly, analysis of the intracellular Gag products in quiescent cells showed an aberrant p55/p24 Gag processing phenotype that appeared to be due to the premature activity of the viral protease.	Glycosaminoglycans	148-151	H3 histone pseudogene 44	Homo sapiens	199-202
15246272-4	2004	We found instead that nonactivated mixed glial cells expressed almost 10-fold less Gag protein, but more importantly, analysis of the intracellular Gag products in quiescent cells showed an aberrant p55/p24 Gag processing phenotype that appeared to be due to the premature activity of the viral protease.	Glycosaminoglycans	148-151	transmembrane p24 trafficking protein 2	Homo sapiens	203-206
15280800-3	2004	EC-SOD is a secretory, tetrameric glycoprotein containing copper and zinc, with a high affinity to certain glycosaminoglycans, such as heparin and heparan sulfate.	Glycosaminoglycans	107-125	superoxide dismutase 3	Homo sapiens	0-6
15256450-12	2004	Finally, attachment assays to A5G27 in the presence of soluble glycosaminoglycans (GAGs) identified the GAGs of CD44 as the binding sites for A5G27.	Glycosaminoglycans	63-81	CD44 antigen	Mus musculus	112-116
15138272-5	2004	In this study, HRG was shown to bind to most cell lines in a Zn(2+)-dependent manner, but failed to interact with the Chinese hamster ovary cell line pgsA-745, which lacks cell-surface glycosaminoglycans (GAGs).	Glycosaminoglycans	185-203	histidine-rich glycoprotein	Cricetulus griseus	15-18
15138272-6	2004	Subsequent treatment of GAG-positive Chinese hamster ovary cells with mammalian heparanase or bacterial heparinase III, but not chondroitinase ABC, abolished HRG binding.	Glycosaminoglycans	24-27	histidine rich glycoprotein	Homo sapiens	158-161
15138272-7	2004	Furthermore, blocking studies with various GAG species indicated that only heparin was a potent inhibitor of HRG binding.	Glycosaminoglycans	43-46	histidine rich glycoprotein	Homo sapiens	109-112
15078224-3	2004	Exposure of glycosaminoglycans to a MPO-H2O2-Cl- system or reagent HOCl generates long-lived chloramides [R-NCl-C(O)-R"] derived from the glycosamine N-acetyl functions.	Glycosaminoglycans	12-30	myeloperoxidase	Homo sapiens	36-39
15123656-4	2004	OCIL bound immobilized high molecular weight sulfated glycosaminoglycans, including fucoidan, lambda-carrageenan, and dextran sulfate, but not unsulfated dextran or sialated hyaluronic acid.	Glycosaminoglycans	54-72	C-type lectin domain family 2 member D	Homo sapiens	0-4
15563314-2	2004	One such marker, LYVE-1, the lymphatic receptor for the extracellular matrix mucopolysaccharide hyaluronan, has been a key component of many important studies on embryonic and tumour-induced lymphangiogenesis, and continues to be used for the detection and isolation of lymphatic endothelial cells.	Glycosaminoglycans	77-95	lymphatic vessel endothelial hyaluronan receptor 1	Homo sapiens	17-23
15123656-7	2004	However, the soluble forms of these low molecular weight glycosaminoglycans competed for OCIL binding of immobilized fucoidan (as did soluble fucoidan, dextran sulfate, and lambda-carrageenan), indicating that OCIL does recognize these carbohydrates.	Glycosaminoglycans	57-75	C-type lectin domain family 2 member D	Homo sapiens	89-93
15123656-7	2004	However, the soluble forms of these low molecular weight glycosaminoglycans competed for OCIL binding of immobilized fucoidan (as did soluble fucoidan, dextran sulfate, and lambda-carrageenan), indicating that OCIL does recognize these carbohydrates.	Glycosaminoglycans	57-75	C-type lectin domain family 2 member D	Homo sapiens	210-214
15123656-12	2004	Although the osteoclast inhibitory action of OCIL is independent of sugar recognition, we have found that OCIL, a lectin widely distributed, but notably localized in bone, skin, and other connective tissues, binds a range of physiologically important glycosaminoglycans, and this property may modulate OCIL actions upon other cells.	Glycosaminoglycans	251-269	C-type lectin domain family 2 member D	Homo sapiens	106-110
15123656-12	2004	Although the osteoclast inhibitory action of OCIL is independent of sugar recognition, we have found that OCIL, a lectin widely distributed, but notably localized in bone, skin, and other connective tissues, binds a range of physiologically important glycosaminoglycans, and this property may modulate OCIL actions upon other cells.	Glycosaminoglycans	251-269	C-type lectin domain family 2 member D	Homo sapiens	106-110
15126139-5	2004	Overall, the most beneficial growth factor was bFGF, which was most potent in increasing proliferation and GAG synthesis, and also effective in promoting collagen synthesis.	Glycosaminoglycans	107-110	fibroblast growth factor 2	Homo sapiens	47-51
15126139-7	2004	PDGF and bFGF were the most potent upregulators of GAG synthesis, producing 2-3 times more GAG than the control.	Glycosaminoglycans	51-54	fibroblast growth factor 2	Homo sapiens	9-13
15126139-7	2004	PDGF and bFGF were the most potent upregulators of GAG synthesis, producing 2-3 times more GAG than the control.	Glycosaminoglycans	91-94	fibroblast growth factor 2	Homo sapiens	9-13
15320789-0	2004	Novel human plasma proteins, IHRP (acute phase protein) and PHBP (serine protease), which bind to glycosaminoglycans.	Glycosaminoglycans	98-116	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	29-33
15186946-7	2004	The effect of glycosaminoglycan digestion in situ on medial SMC proliferation in response to a bolus injection of FGF-2 after injury was determined by measuring the percentage of SMC nuclei that incorporated 5-bromo-2"-deoxyuridine (BrdU) 48 h after injury.	Glycosaminoglycans	14-31	fibroblast growth factor 2	Rattus norvegicus	114-119
15320789-0	2004	Novel human plasma proteins, IHRP (acute phase protein) and PHBP (serine protease), which bind to glycosaminoglycans.	Glycosaminoglycans	98-116	hyaluronan binding protein 2	Homo sapiens	60-64
15320789-0	2004	Novel human plasma proteins, IHRP (acute phase protein) and PHBP (serine protease), which bind to glycosaminoglycans.	Glycosaminoglycans	98-116	coagulation factor II, thrombin	Homo sapiens	66-81
15272232-1	2004	Betaig-h3 (betaig-h3) is a secretory protein composed of fasciclin I-like repeats containing sequences that allows binding of integrins and glycosaminoglycans in vivo.	Glycosaminoglycans	140-158	transforming growth factor beta induced	Homo sapiens	0-9
15200483-2	2004	This cytokine, such as transforming growth factor-alpha (TGF-alpha), induces deposition of glycosaminoglycans (GAG), proteoglycans and collagen fibres in the ECM.	Glycosaminoglycans	91-109	tumor necrosis factor	Homo sapiens	23-55
15200483-2	2004	This cytokine, such as transforming growth factor-alpha (TGF-alpha), induces deposition of glycosaminoglycans (GAG), proteoglycans and collagen fibres in the ECM.	Glycosaminoglycans	91-109	transforming growth factor alpha	Homo sapiens	57-66
15200483-2	2004	This cytokine, such as transforming growth factor-alpha (TGF-alpha), induces deposition of glycosaminoglycans (GAG), proteoglycans and collagen fibres in the ECM.	Glycosaminoglycans	111-114	tumor necrosis factor	Homo sapiens	23-55
15200483-2	2004	This cytokine, such as transforming growth factor-alpha (TGF-alpha), induces deposition of glycosaminoglycans (GAG), proteoglycans and collagen fibres in the ECM.	Glycosaminoglycans	111-114	transforming growth factor alpha	Homo sapiens	57-66
15194752-8	2004	Assuming 1,200 to 2,500 Gag molecules per virion, this corresponds to 7 to 16 Env trimers per SIV239 virion particle.	Glycosaminoglycans	24-27	endogenous retrovirus group K member 20	Homo sapiens	78-81
15198666-5	2004	Initial experiments demonstrated that agrin N150 lacking GAG chains inhibited neurite outgrowth.	Glycosaminoglycans	57-60	agrin	Gallus gallus	38-43
15198666-9	2004	Our results suggest that there are two distinct mechanisms for neurite outgrowth inhibition by agrin, one that is GAG-dependent and one that is GAG-independent.	Glycosaminoglycans	114-117	agrin	Gallus gallus	95-100
15198666-9	2004	Our results suggest that there are two distinct mechanisms for neurite outgrowth inhibition by agrin, one that is GAG-dependent and one that is GAG-independent.	Glycosaminoglycans	144-147	agrin	Gallus gallus	95-100
15272232-1	2004	Betaig-h3 (betaig-h3) is a secretory protein composed of fasciclin I-like repeats containing sequences that allows binding of integrins and glycosaminoglycans in vivo.	Glycosaminoglycans	140-158	transforming growth factor beta induced	Homo sapiens	11-20
15044471-7	2004	After interaction with host GAG, soluble ACP enters ME180 cells and fractionates to the eukaryotic cell cytosol.	Glycosaminoglycans	28-31	NADH:ubiquinone oxidoreductase subunit AB1	Homo sapiens	41-44
15196911-3	2004	In the presence of glycosaminoglycans, AT and PCI had significantly reduced thrombin inhibition with Toggle-25, but it was only reduced 3-fold for HCII.	Glycosaminoglycans	19-37	coagulation factor II, thrombin	Homo sapiens	76-84
15196911-3	2004	In the presence of glycosaminoglycans, AT and PCI had significantly reduced thrombin inhibition with Toggle-25, but it was only reduced 3-fold for HCII.	Glycosaminoglycans	19-37	serpin family D member 1	Homo sapiens	147-151
15194051-1	2004	Human interferon-inducible protein 10 (IP-10; HGMW-approved gene symbol CXCL10) is an ELR(-) CXC chemokine that contains binding domains for both the chemokine receptor CXCR3 and glycosaminoglycans.	Glycosaminoglycans	179-197	C-X-C motif chemokine ligand 10	Homo sapiens	6-37
15242543-6	2004	Stimulations with five peptide pools for Gag and seven peptide pools for Env revealed epitopes for cellular immune responses throughout Gag and Env.	Glycosaminoglycans	136-139	endogenous retrovirus group K member 20	Homo sapiens	73-76
15194051-1	2004	Human interferon-inducible protein 10 (IP-10; HGMW-approved gene symbol CXCL10) is an ELR(-) CXC chemokine that contains binding domains for both the chemokine receptor CXCR3 and glycosaminoglycans.	Glycosaminoglycans	179-197	C-X-C motif chemokine ligand 10	Homo sapiens	39-44
15194051-1	2004	Human interferon-inducible protein 10 (IP-10; HGMW-approved gene symbol CXCL10) is an ELR(-) CXC chemokine that contains binding domains for both the chemokine receptor CXCR3 and glycosaminoglycans.	Glycosaminoglycans	179-197	C-X-C motif chemokine ligand 10	Homo sapiens	72-78
15194051-3	2004	Whether IP-10 exerts its angiostatic function through binding to CXCR3, glycosaminoglycans, or both, is not clear.	Glycosaminoglycans	72-90	C-X-C motif chemokine ligand 10	Homo sapiens	8-13
15194051-4	2004	To clarify this issue, we created expression constructs for mutants of IP-10 that exhibit partial (IP-10C) or total (IP-10C22) loss of binding to CXCR3 or loss of binding to glycosaminoglycans (IP-10H and IP-10C22H).	Glycosaminoglycans	174-192	C-X-C motif chemokine ligand 10	Homo sapiens	71-76
15140039-3	2004	These mutations are located at positions 527, 538, and 539 where a T, a C, and a T are substituted respectively, by an A, a T, and a G, leading to three aminoacidic substitutions at codon 152 from Valine to Glutamic Acid (GTG--&gt;GAG), at codon 155 from Histidine to Glutamine (CAC--&gt;CAG), and at codon 156 from Cysteine to Tryptophan (TGT--&gt;TGG).	Glycosaminoglycans	231-234	queuine tRNA-ribosyltransferase catalytic subunit 1	Homo sapiens	340-343
15135144-9	2004	The glycosaminoglycan (GAG) content of pellets obtained from CTR-expanded cells was not correlated with age.	Glycosaminoglycans	4-21	calcitonin receptor	Homo sapiens	61-64
15135144-9	2004	The glycosaminoglycan (GAG) content of pellets obtained from CTR-expanded cells was not correlated with age.	Glycosaminoglycans	23-26	calcitonin receptor	Homo sapiens	61-64
15135144-10	2004	Pellets from TFP-expanded cells reproducibly contained more GAG (up to 3.2-fold) than those from CTR-expanded cells only if donors were younger than 40.	Glycosaminoglycans	60-63	inhibitor of carbonic anhydrase pseudogene	Homo sapiens	13-16
15282658-5	2004	We propose that the main biological role of PF4 and the basis for its presence in the alpha granules of all known mammalian platelets is to neutralize surface heparan sulfate side-chains of glycosaminoglycans and to optimize thrombus development at sites of vascular injury.	Glycosaminoglycans	190-208	platelet factor 4	Homo sapiens	44-47
15282658-6	2004	In addition, the binding of PF4 to surface glycosaminoglycans may also underlie its angiostatic and proatherogenic properties.	Glycosaminoglycans	43-61	platelet factor 4	Homo sapiens	28-31
15044457-0	2004	Spacrcan binding to hyaluronan and other glycosaminoglycans.	Glycosaminoglycans	41-59	interphotoreceptor matrix proteoglycan 2	Mus musculus	0-8
15193918-3	2004	Human 293 cells transfected in vitro with LAMP/gag plasmids either in pcDNA3.1 or pITR produced much Gag protein in cell extracts (1.6 and 2.2 ng of Gag/mg of protein, respectively).	Glycosaminoglycans	101-104	lysosomal associated membrane protein 3	Homo sapiens	42-46
15193918-3	2004	Human 293 cells transfected in vitro with LAMP/gag plasmids either in pcDNA3.1 or pITR produced much Gag protein in cell extracts (1.6 and 2.2 ng of Gag/mg of protein, respectively).	Glycosaminoglycans	149-152	lysosomal associated membrane protein 3	Homo sapiens	42-46
15056609-3	2004	Our phenotypic and biochemical analyses reveal that HS levels are dramatically reduced in the absence of Sotv or its partner co-polymerase Tout velu (Ttv), suggesting that both copolymerases are essential for GAG synthesis.	Glycosaminoglycans	209-212	tout-velu	Drosophila melanogaster	139-148
15158613-1	2004	CD44 on leukocytes binds to its glycosaminoglycan (GAG) ligand, hyaluronic acid, and mediates the rolling of leukocytes on vascular endothelial cells.	Glycosaminoglycans	32-49	CD44 antigen	Mus musculus	0-4
15158613-1	2004	CD44 on leukocytes binds to its glycosaminoglycan (GAG) ligand, hyaluronic acid, and mediates the rolling of leukocytes on vascular endothelial cells.	Glycosaminoglycans	51-54	CD44 antigen	Mus musculus	0-4
15186532-3	2004	Analysis of gag-p24 region from 460 specimens indicated that 310 (67.4%) were A, 94 (20.4%) were D, 28 (6.1%) were C, 9 (2.0%) were A2, 8 (1.7%) were G, and 11 (2.4%) were unclassifiable.	Glycosaminoglycans	12-15	transmembrane p24 trafficking protein 2	Homo sapiens	16-19
15186532-9	2004	Comparison of amino acid sequences of gag-p24 and env-gp41 regions with the subtype A consensus sequence or Kenyan candidate vaccine antigen (HIVA) revealed minor variations in the immunodominant epitopes.	Glycosaminoglycans	38-41	transmembrane p24 trafficking protein 2	Homo sapiens	42-45
15118540-4	2004	The mechanism underlying this phenomenon depends on binding of the cationic PF4 to the anionic, vitamin K- dependent gamma-carboxyglutamic acid domain of protein C. The extent of PF4"s stimulation of APC generation is further increased by its interaction with the anionic glycosaminoglycan moiety that is variably expressed through posttranslational, O-linked glycosylation of thrombomodulin.	Glycosaminoglycans	272-289	platelet factor 4	Homo sapiens	76-79
15118540-4	2004	The mechanism underlying this phenomenon depends on binding of the cationic PF4 to the anionic, vitamin K- dependent gamma-carboxyglutamic acid domain of protein C. The extent of PF4"s stimulation of APC generation is further increased by its interaction with the anionic glycosaminoglycan moiety that is variably expressed through posttranslational, O-linked glycosylation of thrombomodulin.	Glycosaminoglycans	272-289	platelet factor 4	Homo sapiens	179-182
15265293-6	2004	TFP-expanded ear and nasal chondrocytes generated pellets of better quality than rib chondrocytes, as assessed by the significantly higher GAG/DNA content and collagen type II mRNA expression, and by the relative stain intensities for GAG and collagen types I and II.	Glycosaminoglycans	139-142	inhibitor of carbonic anhydrase pseudogene	Homo sapiens	0-3
14718373-2	2004	In a lysosomal storage disorder known as mucopolysaccharidosis I, caused by a deficiency of the exohydrolase alpha-l-iduronidase, fragments of two different glycosaminoglycans, dermatan sulfate and heparan sulfate, have been shown to accumulate.	Glycosaminoglycans	157-175	alpha-L-iduronidase	Homo sapiens	109-128
14718373-4	2004	The presence of odd and even oligosaccharides suggests both endo-beta-glucuronidase and endo-N-acetylhexosaminidase activities toward both glycosaminoglycans.	Glycosaminoglycans	139-157	glucuronidase beta	Homo sapiens	65-83
15174044-1	2004	Dynamic affinity capillary electrophoresis (ACE) was used for determining the binding constants between heparin-like glycosaminoglycans and the (96-110) heparin-binding domain of amyloid precursor protein (APP).	Glycosaminoglycans	117-135	amyloid beta precursor protein	Homo sapiens	179-204
15126635-0	2004	Nedd4.1-mediated ubiquitination and subsequent recruitment of Tsg101 ensure HTLV-1 Gag trafficking towards the multivesicular body pathway prior to virus budding.	Glycosaminoglycans	83-86	NEDD4 E3 ubiquitin protein ligase	Homo sapiens	0-5
15126635-0	2004	Nedd4.1-mediated ubiquitination and subsequent recruitment of Tsg101 ensure HTLV-1 Gag trafficking towards the multivesicular body pathway prior to virus budding.	Glycosaminoglycans	83-86	tumor susceptibility 101	Homo sapiens	62-68
15126635-2	2004	The Gag proteins of oncoretroviruses possess a PPxY motif that recruits a ubiquitin ligase from the Nedd4 family, whereas those of the human immunodeficiency virus interact through a PTAP motif with Tsg101, a protein of the ESCRT-1 complex.	Glycosaminoglycans	4-7	NEDD4 E3 ubiquitin protein ligase	Homo sapiens	100-105
15126635-2	2004	The Gag proteins of oncoretroviruses possess a PPxY motif that recruits a ubiquitin ligase from the Nedd4 family, whereas those of the human immunodeficiency virus interact through a PTAP motif with Tsg101, a protein of the ESCRT-1 complex.	Glycosaminoglycans	4-7	tumor susceptibility 101	Homo sapiens	199-205
15126635-5	2004	We show that Nedd4.1, but not Nedd4.2, is recruited by the PPPY motif of Gag and subsequently catalyzes Gag ubiquitination.	Glycosaminoglycans	73-76	NEDD4 E3 ubiquitin protein ligase	Homo sapiens	13-20
15126635-5	2004	We show that Nedd4.1, but not Nedd4.2, is recruited by the PPPY motif of Gag and subsequently catalyzes Gag ubiquitination.	Glycosaminoglycans	104-107	NEDD4 E3 ubiquitin protein ligase	Homo sapiens	13-20
15126635-6	2004	We also demonstrate that Gag interacts first with Nedd4.1 at the plasma membrane and then with Tsg101 in late endosomes/MVBs.	Glycosaminoglycans	25-28	NEDD4 E3 ubiquitin protein ligase	Homo sapiens	50-57
15126635-6	2004	We also demonstrate that Gag interacts first with Nedd4.1 at the plasma membrane and then with Tsg101 in late endosomes/MVBs.	Glycosaminoglycans	25-28	tumor susceptibility 101	Homo sapiens	95-101
15126635-8	2004	Our findings indicate that Nedd4.1 and Tsg101 act successively in the assembly process of HTLV-1 to ensure proper Gag trafficking through the endocytic pathway up to late endosomes where the late steps of retroviral release occur.	Glycosaminoglycans	114-117	NEDD4 E3 ubiquitin protein ligase	Homo sapiens	27-32
15126635-8	2004	Our findings indicate that Nedd4.1 and Tsg101 act successively in the assembly process of HTLV-1 to ensure proper Gag trafficking through the endocytic pathway up to late endosomes where the late steps of retroviral release occur.	Glycosaminoglycans	114-117	tumor susceptibility 101	Homo sapiens	39-45
15113892-8	2004	MHV-68-infected cells showed reduced surface GAG expression, suggesting that gp150 prevented virions from rebinding to infected cells after release by making MHV-68 infection GAG dependent.	Glycosaminoglycans	45-48	alanyl aminopeptidase, membrane	Homo sapiens	77-82
15113892-8	2004	MHV-68-infected cells showed reduced surface GAG expression, suggesting that gp150 prevented virions from rebinding to infected cells after release by making MHV-68 infection GAG dependent.	Glycosaminoglycans	175-178	alanyl aminopeptidase, membrane	Homo sapiens	77-82
15265293-6	2004	TFP-expanded ear and nasal chondrocytes generated pellets of better quality than rib chondrocytes, as assessed by the significantly higher GAG/DNA content and collagen type II mRNA expression, and by the relative stain intensities for GAG and collagen types I and II.	Glycosaminoglycans	235-238	inhibitor of carbonic anhydrase pseudogene	Homo sapiens	0-3
15067030-2	2004	In human histocompatibility leukocyte antigen (HLA)-B57+ HIV-infected persons, immune selection pressure leads to a mutation from alanine to proline at Gag residue 146 immediately preceding the NH2 terminus of a dominant HLA-B57-restricted epitope, ISPRTLNAW.	Glycosaminoglycans	152-155	major histocompatibility complex, class I, B	Homo sapiens	221-226
14729678-6	2004	Our data showed that a nuclear export sequence resides within a 70-amino acid domain in the C-terminal portion of the p10 region of Gag, and in vitro binding assays demonstrated that Gag interacts directly with CRM1.	Glycosaminoglycans	132-135	exportin 1	Homo sapiens	211-215
14729678-6	2004	Our data showed that a nuclear export sequence resides within a 70-amino acid domain in the C-terminal portion of the p10 region of Gag, and in vitro binding assays demonstrated that Gag interacts directly with CRM1.	Glycosaminoglycans	183-186	exportin 1	Homo sapiens	211-215
15081804-2	2004	A deficiency in alpha-L-iduronidase results in the lysosomal accumulation and urinary secretion of partially degraded glycosaminoglycans and is the cause of the lysosomal storage disorder mucopolysaccharidosis type I (MPS I; Hurler and Scheie syndromes; McKusick 25280).	Glycosaminoglycans	118-136	alpha-L-iduronidase	Homo sapiens	16-35
14707146-0	2004	Identification and characterization of a glycosaminoglycan recognition element of the C chemokine lymphotactin.	Glycosaminoglycans	41-58	X-C motif chemokine ligand 1	Homo sapiens	98-110
15064363-4	2004	We found that Ded1p interacts specifically and strongly with Gag, the L-A virus coat protein.	Glycosaminoglycans	61-64	DEAD-box ATP-dependent RNA helicase DED1	Saccharomyces cerevisiae S288C	14-19
15078180-3	2004	Evidence suggests that the formation of this complex involves a Gag/GagPol/viral genomic RNA complex interacting with a tRNA(Lys)/ LysRS complex, with Gag interacting with both GagPol and LysRS, and GagPol interacting with the tRNA(Lys).	Glycosaminoglycans	64-67	lysyl-tRNA synthetase 1	Homo sapiens	131-136
15078180-3	2004	Evidence suggests that the formation of this complex involves a Gag/GagPol/viral genomic RNA complex interacting with a tRNA(Lys)/ LysRS complex, with Gag interacting with both GagPol and LysRS, and GagPol interacting with the tRNA(Lys).	Glycosaminoglycans	64-67	lysyl-tRNA synthetase 1	Homo sapiens	188-193
15078180-4	2004	The interaction of Gag with LysRS is quite specific, does not require the presence of tRNA(Lys), and LysRS is believed to be the target that allows the specific packaging of tRNA(Lys) into the virion.	Glycosaminoglycans	19-22	lysyl-tRNA synthetase 1	Homo sapiens	28-33
15070984-2	2004	In the p17 coding region of the gag gene, a CRF02_AG-specific signature pattern was observed.	Glycosaminoglycans	32-35	family with sequence similarity 72 member B	Homo sapiens	7-10
15016855-7	2004	Animals that developed combined Th1- and Th2-like responses to Gag and Th2 dominant Env-specific responses were protected from disease progression.	Glycosaminoglycans	63-66	negative elongation factor complex member C/D	Homo sapiens	32-35
15066178-3	2004	PAPP-A adheres to mammalian cells by interactions with glycosaminoglycan (GAG), thus targeting the proteolytic activity of PAPP-A to the cell surface.	Glycosaminoglycans	74-77	pappalysin 1	Homo sapiens	0-6
15066178-3	2004	PAPP-A adheres to mammalian cells by interactions with glycosaminoglycan (GAG), thus targeting the proteolytic activity of PAPP-A to the cell surface.	Glycosaminoglycans	74-77	pappalysin 1	Homo sapiens	123-129
15066178-4	2004	Based on site-directed mutagenesis, we here delineate the PAPP-A GAG-binding site in the C-terminal modules CCP3 and CCP4.	Glycosaminoglycans	65-68	pappalysin 1	Homo sapiens	58-64
15066178-4	2004	Based on site-directed mutagenesis, we here delineate the PAPP-A GAG-binding site in the C-terminal modules CCP3 and CCP4.	Glycosaminoglycans	65-68	AGBL carboxypeptidase 3	Homo sapiens	108-112
15066178-4	2004	Based on site-directed mutagenesis, we here delineate the PAPP-A GAG-binding site in the C-terminal modules CCP3 and CCP4.	Glycosaminoglycans	65-68	AGBL carboxypeptidase 1	Homo sapiens	117-121
15033938-5	2004	Moreover, biotinylated SDF-1 directly binds in a glycosaminoglycans (GAGs)-dependent manner to electroblotted syndecan-4, and colocalization of SDF-1 with syndecan-4 was visualized by confocal microscopy.	Glycosaminoglycans	49-67	C-X-C motif chemokine ligand 12	Homo sapiens	23-28
15033938-5	2004	Moreover, biotinylated SDF-1 directly binds in a glycosaminoglycans (GAGs)-dependent manner to electroblotted syndecan-4, and colocalization of SDF-1 with syndecan-4 was visualized by confocal microscopy.	Glycosaminoglycans	49-67	syndecan 4	Homo sapiens	110-120
15033938-5	2004	Moreover, biotinylated SDF-1 directly binds in a glycosaminoglycans (GAGs)-dependent manner to electroblotted syndecan-4, and colocalization of SDF-1 with syndecan-4 was visualized by confocal microscopy.	Glycosaminoglycans	49-67	syndecan 4	Homo sapiens	155-165
14725807-7	2004	IGF-I increased glycosaminoglycan synthesis of both condylar and femoral cartilage.	Glycosaminoglycans	16-33	insulin-like growth factor 1	Rattus norvegicus	0-5
15117457-4	2004	Gag p17 and env-V3 nucleotide sequences of seroconvertors in our subjects were quite similar to the CS and conserved for at least 9 and 6 years postinfection, respectively.	Glycosaminoglycans	0-3	family with sequence similarity 72 member B	Homo sapiens	4-7
14751231-1	2004	Heparin/heparan sulfate-like glycosaminoglycans (HSGAGs) modulate the activity of the fibroblast growth factor (FGF) family of proteins.	Glycosaminoglycans	29-47	fibroblast growth factor 1	Mus musculus	112-115
15036459-1	2004	Mucopolysaccharide (YMP) of yam (Dioscorea batatas Decne) was tested for immunomodulatory activity in vitro.	Glycosaminoglycans	0-18	epithelial membrane protein 3	Mus musculus	20-23
14645229-2	2004	Here we demonstrate that complex formation with glycosaminoglycans (GAGs) is unique for cathepsin K among human papain-like cysteine proteases and that different GAGs compete for the binding to cathepsin K.	Glycosaminoglycans	48-66	cathepsin K	Homo sapiens	88-99
14980480-5	2004	Gag-specific CD8+ T-cells were found in separated IELs from the rectum, colon, jejunum, and vagina of most infected animals.	Glycosaminoglycans	0-3	CD8a molecule	Homo sapiens	13-16
14980480-7	2004	These Gag-specific IELs expressed the activation marker CD69 and produced IFN-gamma, suggesting an active immune response in this locale.	Glycosaminoglycans	6-9	CD69 molecule	Homo sapiens	56-60
14980480-7	2004	These Gag-specific IELs expressed the activation marker CD69 and produced IFN-gamma, suggesting an active immune response in this locale.	Glycosaminoglycans	6-9	interferon gamma	Homo sapiens	74-83
14645229-2	2004	Here we demonstrate that complex formation with glycosaminoglycans (GAGs) is unique for cathepsin K among human papain-like cysteine proteases and that different GAGs compete for the binding to cathepsin K.	Glycosaminoglycans	48-66	cathepsin K	Homo sapiens	194-205
14623881-12	2004	These data suggest that pgsG cells contain a labile form of GlcATI that causes conditional expression of glycosaminoglycans dependent on temperature.	Glycosaminoglycans	105-123	galactosylgalactosylxylosylprotein 3-beta-glucuronosyltransferase 3	Cricetulus griseus	60-66
14966466-2	2004	Heparan sulfate N-acetylglucosamine N-deacetylase/adenosine 3"-phosphate 5"-phosphosulfate: unsubstituted glucosamine N-sulfotransferase (NDST) is the key enzyme regulating sulfation of GAG chains.	Glycosaminoglycans	186-189	sulfotransferase family 1D, member 1	Rattus norvegicus	118-136
14960611-6	2004	DNA enzyme administration to TGF-beta-stimulated astrocytes in culture reduced specific GAG chains.	Glycosaminoglycans	88-91	transforming growth factor beta 1	Homo sapiens	29-37
14974582-1	2004	OBJECTIVE: To investigate the effects of insulin-like growth factor-II (IGF-II) on DNA and glycosaminoglycan (GAG) synthesis and the expression of matrix-related genes in equine articular cartilage explants and chondrocytes, respectively, with and without interleukin 1-beta (IL1-beta).	Glycosaminoglycans	91-108	insulin like growth factor 2	Equus caballus	41-78
14974582-1	2004	OBJECTIVE: To investigate the effects of insulin-like growth factor-II (IGF-II) on DNA and glycosaminoglycan (GAG) synthesis and the expression of matrix-related genes in equine articular cartilage explants and chondrocytes, respectively, with and without interleukin 1-beta (IL1-beta).	Glycosaminoglycans	110-113	insulin like growth factor 2	Equus caballus	41-78
14974582-8	2004	In cartilage explants conditioned with IL1-beta, IGF-II stimulated DNA and GAG synthesis at concentrations of 500 and 50 ng/mL, respectively.	Glycosaminoglycans	75-78	interleukin-1 beta	Equus caballus	39-47
14974582-8	2004	In cartilage explants conditioned with IL1-beta, IGF-II stimulated DNA and GAG synthesis at concentrations of 500 and 50 ng/mL, respectively.	Glycosaminoglycans	75-78	insulin like growth factor 2	Equus caballus	49-55
14974582-11	2004	CONCLUSIONS AND CLINICAL RELEVANCE: Insulin-like growth factor-II stimulated DNA and GAG synthesis in equine adult cartilage and may have potential application in vivo.	Glycosaminoglycans	85-88	insulin like growth factor 2	Equus caballus	36-65
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
15009704-7	2004	CD44, a cell surface receptor known to bind hyaluronan, not infrequently exists as a proteoglycan, decorated with various glycosaminoglycan chains including heparan sulfate and chondroitin sulfate, and as such can bind fibronectin.	Glycosaminoglycans	122-139	CD44 molecule (Indian blood group)	Homo sapiens	0-4
14966466-6	2004	Immunohistochemical studies were also performed with the use of monoclonal antibodies that react specifically with the N-sulfated portion of the GAG chain of HSPG and agrin, a major core protein of HSPG in glomerular basement membrane (GBM).	Glycosaminoglycans	145-148	syndecan 1	Rattus norvegicus	158-162
14966466-6	2004	Immunohistochemical studies were also performed with the use of monoclonal antibodies that react specifically with the N-sulfated portion of the GAG chain of HSPG and agrin, a major core protein of HSPG in glomerular basement membrane (GBM).	Glycosaminoglycans	145-148	syndecan 1	Rattus norvegicus	198-202
14966466-9	2004	Immunohistochemical studies revealed that staining for N-sulfated GAG chains of HSPG on GBM was markedly reduced on day 10 in PAN-treated rats but that staining for agrin was unchanged.	Glycosaminoglycans	66-69	syndecan 1	Rattus norvegicus	80-84
14698597-3	2004	Negatively charged surfaces were chosen to resemble physiological binding of GM-CSF to extracellular glycosaminoglycans, while modified positively charged surfaces may enhance GM-CSF adsorption due to electrostatic interaction.	Glycosaminoglycans	101-119	colony stimulating factor 2	Homo sapiens	77-83
14711988-2	2004	DYT1 dystonia is a form of primary dystonia caused by an in-frame GAG deletion (DeltaE302/3) in the TOR1A gene that encodes the endoplasmic reticulum luminal protein torsinA.	Glycosaminoglycans	66-69	torsin family 1 member A	Homo sapiens	0-4
14711988-2	2004	DYT1 dystonia is a form of primary dystonia caused by an in-frame GAG deletion (DeltaE302/3) in the TOR1A gene that encodes the endoplasmic reticulum luminal protein torsinA.	Glycosaminoglycans	66-69	torsin family 1 member A	Homo sapiens	100-105
14711988-2	2004	DYT1 dystonia is a form of primary dystonia caused by an in-frame GAG deletion (DeltaE302/3) in the TOR1A gene that encodes the endoplasmic reticulum luminal protein torsinA.	Glycosaminoglycans	66-69	torsin family 1 member A	Homo sapiens	166-173
14752287-1	2004	The interaction of antithrombin III (AT) with cell surface glycosaminoglycans is known to have an inhibitory effect on inflammatory processes.	Glycosaminoglycans	59-77	serpin family C member 1	Rattus norvegicus	19-35
14752287-7	2004	Thus, it appears that AT most likely reduces F-actin formation in neutrophil by binding to glycosaminoglycans (e.g., syndecan-4) on the neutrophil, thereby reducing neutrophil accumulation in the lung, which would in turn inhibit oxygen radical production in the lung.	Glycosaminoglycans	91-109	syndecan 4	Rattus norvegicus	117-127
14741150-2	2004	The CD8+ T-cell response to the dominant Gag(181-189) CM9 was quantitated in seven Mamu-A*01-positive macaques by tetramer staining, by ex vivo cytotoxic T-lymphocyte (CTL) activity, and by intracellular cytokine staining (ICS) with the specific Gag(181-189) CM9 peptide.	Glycosaminoglycans	41-44	CD8a molecule	Homo sapiens	4-7
14741150-3	2004	The overall CD8+ T-cell response to Gag was assessed using a peptide pool encompassing the entire Gag protein followed by measurement of TNF-alpha production in ICS assay.	Glycosaminoglycans	36-39	CD8a molecule	Homo sapiens	12-15
14741150-3	2004	The overall CD8+ T-cell response to Gag was assessed using a peptide pool encompassing the entire Gag protein followed by measurement of TNF-alpha production in ICS assay.	Glycosaminoglycans	36-39	tumor necrosis factor	Homo sapiens	137-146
14741150-3	2004	The overall CD8+ T-cell response to Gag was assessed using a peptide pool encompassing the entire Gag protein followed by measurement of TNF-alpha production in ICS assay.	Glycosaminoglycans	98-101	CD8a molecule	Homo sapiens	12-15
14570906-11	2004	Whereas Gag proteins localized to lipid rafts in cells expressing wt CD4 and RA5, gp120 accumulated in rafts in cells expressing wt CD4 but not RA5.	Glycosaminoglycans	8-11	RA5	Homo sapiens	77-80
14972565-0	2004	Inhibition of herpes simplex virus infection by lactoferrin is dependent on interference with the virus binding to glycosaminoglycans.	Glycosaminoglycans	115-133	lactotransferrin	Bos taurus	48-59
14695513-0	2004	The activation of fibroblast growth factors (FGFs) by glycosaminoglycans: influence of the sulfation pattern on the biological activity of FGF-1.	Glycosaminoglycans	54-72	fibroblast growth factor 1	Homo sapiens	139-144
14972565-2	2004	In the present work we investigated the mechanism of the antiviral activity of lactoferrin in mutant glycosaminoglycan (GAG)-deficient cells.	Glycosaminoglycans	101-118	lactotransferrin	Bos taurus	79-90
14972565-2	2004	In the present work we investigated the mechanism of the antiviral activity of lactoferrin in mutant glycosaminoglycan (GAG)-deficient cells.	Glycosaminoglycans	120-123	lactotransferrin	Bos taurus	79-90
14972565-3	2004	Bovine lactoferrin (BLf) was a strong inhibitor of HSV-1 infection in cells expressing either heparan sulfate (HS) or chondroitin sulfate (CS) or both, but was ineffective or less efficient in GAG-deficient cells or in cells treated with GAG-degrading enzymes.	Glycosaminoglycans	238-241	lactotransferrin	Bos taurus	7-18
14972565-5	2004	Finally, we demonstrated that lactoferrin bound directly to both HS and CS isolated from surfaces of the studied cells, as well as to commercial preparations of GAG chains.	Glycosaminoglycans	161-164	lactotransferrin	Bos taurus	30-41
14972565-6	2004	The results support the hypothesis that the inhibition of HSV-1 infectivity by lactoferrin is dependent on its interaction with cell surface GAG chains of HS and CS.	Glycosaminoglycans	141-144	lactotransferrin	Bos taurus	79-90
15663360-3	2004	Based on the amino acid sequence, the protein core of biglycan can be divided into six distinct domains: (1) a signal sequence, (2) a propeptide region, (3) a N-terminal glycosaminoglycan attachment region, (4) a cysteine loop, followed by (5) a leucine- rich repeat region domain (that makes up over 66% of the core protein), and (6) a final cysteine loop.	Glycosaminoglycans	170-187	biglycan	Homo sapiens	54-62
14684534-2	2004	CONCLUSION: The index of glycosaminoglycan distribution, T1(Gd), can exceed 500 msec (denoting high glycosaminoglycan) or can be less than 300 msec, with focal areas as low as 240 msec.	Glycosaminoglycans	25-42	CD5 molecule	Homo sapiens	57-63
14684534-2	2004	CONCLUSION: The index of glycosaminoglycan distribution, T1(Gd), can exceed 500 msec (denoting high glycosaminoglycan) or can be less than 300 msec, with focal areas as low as 240 msec.	Glycosaminoglycans	100-117	CD5 molecule	Homo sapiens	57-63
15133980-5	2004	Initial results show that TGF-beta 1 affected GAG expression compared to a control condition.	Glycosaminoglycans	46-49	transforming growth factor beta 1	Homo sapiens	26-36
15133980-9	2004	These data indicate that TNF-a and TGF-beta 1 play a role in the expression of GAG chains and sialic acids on the cell surface.	Glycosaminoglycans	79-82	tumor necrosis factor	Homo sapiens	25-30
15133980-9	2004	These data indicate that TNF-a and TGF-beta 1 play a role in the expression of GAG chains and sialic acids on the cell surface.	Glycosaminoglycans	79-82	transforming growth factor beta 1	Homo sapiens	35-45
14694155-5	2004	DEAE separation of total glycosaminoglycans (GAG) revealed a significant increase of GAG in the culture supernatant and decrease in the cell and matrix layer when podocytes were cultured for 72 h in the presence of AngII.	Glycosaminoglycans	25-43	angiotensinogen	Homo sapiens	215-220
15078125-1	2004	Heparin and other iduronic acid-containing glycosaminoglycans (GAG) such as dermatan sulfate exert their anticoagulant properties primarily by accelerating the rate of inhibition of the natural protease inhibitors antithrombin III (AT, which inhibits both factor Xa and thrombin) and heparin cofactor II (HCII, which selectively inhibits thrombin).	Glycosaminoglycans	43-61	serpin family C member 1	Homo sapiens	214-230
15078125-1	2004	Heparin and other iduronic acid-containing glycosaminoglycans (GAG) such as dermatan sulfate exert their anticoagulant properties primarily by accelerating the rate of inhibition of the natural protease inhibitors antithrombin III (AT, which inhibits both factor Xa and thrombin) and heparin cofactor II (HCII, which selectively inhibits thrombin).	Glycosaminoglycans	43-61	coagulation factor II, thrombin	Homo sapiens	218-226
15078125-1	2004	Heparin and other iduronic acid-containing glycosaminoglycans (GAG) such as dermatan sulfate exert their anticoagulant properties primarily by accelerating the rate of inhibition of the natural protease inhibitors antithrombin III (AT, which inhibits both factor Xa and thrombin) and heparin cofactor II (HCII, which selectively inhibits thrombin).	Glycosaminoglycans	43-61	serpin family D member 1	Homo sapiens	284-303
15078125-1	2004	Heparin and other iduronic acid-containing glycosaminoglycans (GAG) such as dermatan sulfate exert their anticoagulant properties primarily by accelerating the rate of inhibition of the natural protease inhibitors antithrombin III (AT, which inhibits both factor Xa and thrombin) and heparin cofactor II (HCII, which selectively inhibits thrombin).	Glycosaminoglycans	43-61	serpin family D member 1	Homo sapiens	305-309
15078125-1	2004	Heparin and other iduronic acid-containing glycosaminoglycans (GAG) such as dermatan sulfate exert their anticoagulant properties primarily by accelerating the rate of inhibition of the natural protease inhibitors antithrombin III (AT, which inhibits both factor Xa and thrombin) and heparin cofactor II (HCII, which selectively inhibits thrombin).	Glycosaminoglycans	43-61	coagulation factor II, thrombin	Homo sapiens	270-278
15078125-1	2004	Heparin and other iduronic acid-containing glycosaminoglycans (GAG) such as dermatan sulfate exert their anticoagulant properties primarily by accelerating the rate of inhibition of the natural protease inhibitors antithrombin III (AT, which inhibits both factor Xa and thrombin) and heparin cofactor II (HCII, which selectively inhibits thrombin).	Glycosaminoglycans	63-66	serpin family C member 1	Homo sapiens	214-230
15078125-1	2004	Heparin and other iduronic acid-containing glycosaminoglycans (GAG) such as dermatan sulfate exert their anticoagulant properties primarily by accelerating the rate of inhibition of the natural protease inhibitors antithrombin III (AT, which inhibits both factor Xa and thrombin) and heparin cofactor II (HCII, which selectively inhibits thrombin).	Glycosaminoglycans	63-66	coagulation factor II, thrombin	Homo sapiens	218-226
15078125-1	2004	Heparin and other iduronic acid-containing glycosaminoglycans (GAG) such as dermatan sulfate exert their anticoagulant properties primarily by accelerating the rate of inhibition of the natural protease inhibitors antithrombin III (AT, which inhibits both factor Xa and thrombin) and heparin cofactor II (HCII, which selectively inhibits thrombin).	Glycosaminoglycans	63-66	serpin family D member 1	Homo sapiens	284-303
15078125-1	2004	Heparin and other iduronic acid-containing glycosaminoglycans (GAG) such as dermatan sulfate exert their anticoagulant properties primarily by accelerating the rate of inhibition of the natural protease inhibitors antithrombin III (AT, which inhibits both factor Xa and thrombin) and heparin cofactor II (HCII, which selectively inhibits thrombin).	Glycosaminoglycans	63-66	serpin family D member 1	Homo sapiens	305-309
15078125-1	2004	Heparin and other iduronic acid-containing glycosaminoglycans (GAG) such as dermatan sulfate exert their anticoagulant properties primarily by accelerating the rate of inhibition of the natural protease inhibitors antithrombin III (AT, which inhibits both factor Xa and thrombin) and heparin cofactor II (HCII, which selectively inhibits thrombin).	Glycosaminoglycans	63-66	coagulation factor II, thrombin	Homo sapiens	270-278
15078125-3	2004	Whereas the binding site of heparin for AT is a unique pentasaccharide sequence contained in only about one third of the chains of this GAG, HCII-binding sequences of heparin and dermatan sulfate are less specific and contained in practically all the GAG chains.	Glycosaminoglycans	251-254	serpin family D member 1	Homo sapiens	141-145
14756373-6	2004	RESULTS: TA and IGF-1 in combination inhibited the IL-1-induced release of PG matrix components (glycosaminoglycan or GAG) from the articular cartilage, as well as producing a significant increase in GAG synthesis.	Glycosaminoglycans	97-114	insulin like growth factor 1	Equus caballus	16-21
14756373-6	2004	RESULTS: TA and IGF-1 in combination inhibited the IL-1-induced release of PG matrix components (glycosaminoglycan or GAG) from the articular cartilage, as well as producing a significant increase in GAG synthesis.	Glycosaminoglycans	118-121	insulin like growth factor 1	Equus caballus	16-21
14756373-6	2004	RESULTS: TA and IGF-1 in combination inhibited the IL-1-induced release of PG matrix components (glycosaminoglycan or GAG) from the articular cartilage, as well as producing a significant increase in GAG synthesis.	Glycosaminoglycans	200-203	insulin like growth factor 1	Equus caballus	16-21
15035435-1	2004	Recently we identified a plasma serine protease with a high affinity to glycosaminoglycans like heparin or hyaluronic acid, termed hyaluronan-binding protease (HABP).	Glycosaminoglycans	72-90	hyaluronan binding protein 2	Homo sapiens	160-164
15035435-8	2004	Heparin and heparan sulfate fully protected bFGF from complexation and cleavage by HABP, although these glycosaminoglycans are known to enhance the proteolytic activity of HABP.	Glycosaminoglycans	104-122	hyaluronan binding protein 2	Homo sapiens	172-176
14962227-5	2004	Nucleotide sequencing of amplified DNA revealed a novel mutation, Glu (GAG) to Gly (GGG) at residue 29, which normally undergoes gamma-carboxylation within the Gla domain of prothrombin.	Glycosaminoglycans	71-74	coagulation factor II, thrombin	Homo sapiens	174-185
14662788-1	2004	beta-Hexosaminidase (Hex) catalyzes the hydrolysis of terminal sugar residues from a number of substrates such as GM2 gangliosides, glycoproteins, glycolipids, and glycosaminoglycans.	Glycosaminoglycans	164-182	O-GlcNAcase	Rattus norvegicus	0-19
14662788-1	2004	beta-Hexosaminidase (Hex) catalyzes the hydrolysis of terminal sugar residues from a number of substrates such as GM2 gangliosides, glycoproteins, glycolipids, and glycosaminoglycans.	Glycosaminoglycans	164-182	O-GlcNAcase	Rattus norvegicus	5-8
14694155-5	2004	DEAE separation of total glycosaminoglycans (GAG) revealed a significant increase of GAG in the culture supernatant and decrease in the cell and matrix layer when podocytes were cultured for 72 h in the presence of AngII.	Glycosaminoglycans	45-48	angiotensinogen	Homo sapiens	215-220
14694155-5	2004	DEAE separation of total glycosaminoglycans (GAG) revealed a significant increase of GAG in the culture supernatant and decrease in the cell and matrix layer when podocytes were cultured for 72 h in the presence of AngII.	Glycosaminoglycans	85-88	angiotensinogen	Homo sapiens	215-220
14694155-7	2004	Qualitative analysis of HSPG, using gel filtration of HNO(2)-treated fractions, showed that AngII treatment decreased N-sulfation of HS-GAG side chains.	Glycosaminoglycans	136-139	angiotensinogen	Homo sapiens	92-97
14694164-0	2004	Glycosaminoglycans enhance the trifluoroethanol-induced extension of beta 2-microglobulin-related amyloid fibrils at a neutral pH.	Glycosaminoglycans	0-18	beta-2-microglobulin	Homo sapiens	69-89
14668432-6	2003	Combined with biochemical analysis of gag/env ratios in virions, these trimer counts allow calculation of the number of gag molecules per virion, yielding an average value of approximately 1400.	Glycosaminoglycans	120-123	endogenous retrovirus group K member 20	Homo sapiens	42-45
15697091-1	2004	Hemoglobin Q-India is a very rare alpha-chain structural variant caused by the mutation AAG--&gt;GAG (Asp--&gt;His) in the position of codon 64 of the alpha1 gene.	Glycosaminoglycans	97-100	adrenoceptor alpha 1D	Homo sapiens	151-157
13679381-5	2003	On the other hand, TGF-beta1 increases total GAG synthesis in immature, but not mature, cartilage (stimulates CS but not non-CS), age-independently decreases C6S:C4S (more C4S), and increases chondrocyte UDPGD activity in a manner inversely correlated with age.	Glycosaminoglycans	45-48	transforming growth factor beta 1	Homo sapiens	19-28
13679381-2	2003	However, how such stimuli, prototypically represented by transforming growth factor-beta1 (TGF-beta1) and IL-1alpha, modify GAG synthesis during aging of normal human articular cartilage is not known.	Glycosaminoglycans	124-127	transforming growth factor beta 1	Homo sapiens	57-89
13679381-2	2003	However, how such stimuli, prototypically represented by transforming growth factor-beta1 (TGF-beta1) and IL-1alpha, modify GAG synthesis during aging of normal human articular cartilage is not known.	Glycosaminoglycans	124-127	transforming growth factor beta 1	Homo sapiens	91-100
13679381-2	2003	However, how such stimuli, prototypically represented by transforming growth factor-beta1 (TGF-beta1) and IL-1alpha, modify GAG synthesis during aging of normal human articular cartilage is not known.	Glycosaminoglycans	124-127	interleukin 1 alpha	Homo sapiens	106-115
13679381-4	2003	We also show that IL-1alpha treatment reduces both total GAG and CS synthesis, decreases C6S:C4S ratios (less C6S), but fails to modify chondrocyte UDPGD activity at all ages.	Glycosaminoglycans	57-60	interleukin 1 alpha	Homo sapiens	18-27
14662882-6	2003	This vector, which belongs to a different serotype than the AdC68 virus, induces high frequencies of gag-specific CD8(+) T cells in mice including those pre-exposed to AdHu5 virus.	Glycosaminoglycans	101-104	CD8a molecule	Homo sapiens	114-117
14675751-2	2003	Here we report that the N-terminal inhibitory domain of tissue inhibitor of metalloproteinases 3 (N-TIMP-3), but not TIMP-1 or TIMP-2, inhibits glycosaminoglycan release from bovine nasal and porcine articular cartilage explants stimulated with interleukin-1alpha or retinoic acid in a dose-dependent manner.	Glycosaminoglycans	144-161	TIMP metallopeptidase inhibitor 3	Bos taurus	56-96
14675751-2	2003	Here we report that the N-terminal inhibitory domain of tissue inhibitor of metalloproteinases 3 (N-TIMP-3), but not TIMP-1 or TIMP-2, inhibits glycosaminoglycan release from bovine nasal and porcine articular cartilage explants stimulated with interleukin-1alpha or retinoic acid in a dose-dependent manner.	Glycosaminoglycans	144-161	TIMP metallopeptidase inhibitor 3	Bos taurus	100-106
14583446-3	2003	Homozygous Galns-/- mice have no detectable GALNS enzyme activity and show increased urinary glycosaminoglycan (GAGs) levels.	Glycosaminoglycans	93-110	galactosamine (N-acetyl)-6-sulfate sulfatase	Mus musculus	11-16
14654682-9	2003	The PBS/O3SLa interaction may regulate the processes of primer tRNA annealing, packaging and initiation of Gag translation through its involvement in leader tertiary structure.	Glycosaminoglycans	107-110	Src like adaptor	Homo sapiens	10-13
14506232-2	2003	Fibrillization of purified recombinant alpha-synuclein is inefficient in vitro but can be enhanced by the addition of various agents including glycosaminoglycans and polycations.	Glycosaminoglycans	143-161	synuclein alpha	Homo sapiens	39-54
12907439-5	2003	The stoichiometries were not affected by pentasaccharides, indicating that the inhibitory mechanism of antithrombin Cambridge II is perturbed only in the presence of a bridging glycosaminoglycan.	Glycosaminoglycans	177-194	serpin family C member 1	Homo sapiens	103-115
14632751-10	2003	CD4 cytokine responses to one Gag and two conserved Pol peptides correlated negatively with virus load.	Glycosaminoglycans	30-33	CD4 molecule	Homo sapiens	0-3
14634134-6	2003	The FAK-deficient mast cells had a reduction in the content of chondroitin/dermatan sulfate, the major glycosaminoglycan component of the granular matrix.	Glycosaminoglycans	103-120	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
14634134-11	2003	These results indicate that FAK plays a role in regulating the glycosaminoglycan content of the secretory granules and influences the cell surface morphology of mast cells.	Glycosaminoglycans	63-80	PTK2 protein tyrosine kinase 2	Mus musculus	28-31
14573704-6	2003	Consistent with the effect on Gag processing, we found that mutations conferring resistance to PA-457 map to the p25 to p24 cleavage site.	Glycosaminoglycans	30-33	transmembrane p24 trafficking protein 9	Homo sapiens	113-116
14596625-3	2003	The binding of glycosaminoglycans to factor Xa appears to be charge-dependent because affinity is correlated with degree of glycosaminoglycan sulfation.	Glycosaminoglycans	15-33	coagulation factor X	Homo sapiens	37-46
14596625-3	2003	The binding of glycosaminoglycans to factor Xa appears to be charge-dependent because affinity is correlated with degree of glycosaminoglycan sulfation.	Glycosaminoglycans	15-32	coagulation factor X	Homo sapiens	37-46
14596625-5	2003	In contrast, when Gla-domainless factor Xa was substituted for factor Xa, glycosaminoglycans bound with similar affinities in the absence and presence of Ca(2+).	Glycosaminoglycans	74-92	coagulation factor X	Homo sapiens	33-42
14596625-5	2003	In contrast, when Gla-domainless factor Xa was substituted for factor Xa, glycosaminoglycans bound with similar affinities in the absence and presence of Ca(2+).	Glycosaminoglycans	74-92	coagulation factor X	Homo sapiens	63-72
14596625-7	2003	The changes in fluorescence intensity of factor Xa when titrated with glycosaminoglycans suggest that glycosaminoglycans induce conformational changes in the active site environment of factor Xa.	Glycosaminoglycans	70-88	coagulation factor X	Homo sapiens	41-50
14596625-7	2003	The changes in fluorescence intensity of factor Xa when titrated with glycosaminoglycans suggest that glycosaminoglycans induce conformational changes in the active site environment of factor Xa.	Glycosaminoglycans	70-88	coagulation factor X	Homo sapiens	185-194
14596625-7	2003	The changes in fluorescence intensity of factor Xa when titrated with glycosaminoglycans suggest that glycosaminoglycans induce conformational changes in the active site environment of factor Xa.	Glycosaminoglycans	102-120	coagulation factor X	Homo sapiens	41-50
14596625-7	2003	The changes in fluorescence intensity of factor Xa when titrated with glycosaminoglycans suggest that glycosaminoglycans induce conformational changes in the active site environment of factor Xa.	Glycosaminoglycans	102-120	coagulation factor X	Homo sapiens	185-194
14596625-9	2003	Glycosaminoglycans influenced the ability of factor Xa to cleave chromogenic substrates and attenuated the capacity of factor Xa to activate factor VII.	Glycosaminoglycans	0-18	coagulation factor X	Homo sapiens	45-54
14596625-9	2003	Glycosaminoglycans influenced the ability of factor Xa to cleave chromogenic substrates and attenuated the capacity of factor Xa to activate factor VII.	Glycosaminoglycans	0-18	coagulation factor X	Homo sapiens	119-128
14596625-10	2003	The potency of glycosaminoglycans in these assays reflected their affinity for factor Xa.	Glycosaminoglycans	15-33	coagulation factor X	Homo sapiens	79-88
14596625-11	2003	These studies suggest that glycosaminoglycan binding perturbs exosites on the surface of factor Xa, potentially modifying interactions with cofactors or substrates.	Glycosaminoglycans	27-44	coagulation factor X	Homo sapiens	89-98
14596625-2	2003	To characterize this heparin-binding site, the extrinsic fluorescence of fluorescein-labeled, active site-blocked factor Xa was monitored as it was titrated with glycosaminoglycans of various sulfate content and chain length.	Glycosaminoglycans	162-180	coagulation factor X	Homo sapiens	114-123
14571181-0	2003	Evidence for Gag p24-specific CD4 T cells with reduced susceptibility to R5 HIV-1 infection in a UK cohort of HIV-exposed-seronegative subjects.	Glycosaminoglycans	13-16	transmembrane p24 trafficking protein 2	Homo sapiens	17-20
14571181-4	2003	Gag p24-specific and total Vbeta+ CD4 cells that expressed MIP-1beta, IFN-gamma and IL-2 were enumerated by intracytoplasmic cytokine staining.	Glycosaminoglycans	0-3	transmembrane p24 trafficking protein 2	Homo sapiens	4-7
14571181-4	2003	Gag p24-specific and total Vbeta+ CD4 cells that expressed MIP-1beta, IFN-gamma and IL-2 were enumerated by intracytoplasmic cytokine staining.	Glycosaminoglycans	0-3	C-C motif chemokine ligand 4	Homo sapiens	59-68
14571181-4	2003	Gag p24-specific and total Vbeta+ CD4 cells that expressed MIP-1beta, IFN-gamma and IL-2 were enumerated by intracytoplasmic cytokine staining.	Glycosaminoglycans	0-3	interferon gamma	Homo sapiens	70-79
14571181-4	2003	Gag p24-specific and total Vbeta+ CD4 cells that expressed MIP-1beta, IFN-gamma and IL-2 were enumerated by intracytoplasmic cytokine staining.	Glycosaminoglycans	0-3	interleukin 2	Homo sapiens	84-88
14575696-2	2003	PF4 also neutralizes heparan sulfate (HS), a glycosaminoglycan (GAG) present on the surface of endothelial cells, thereby possibly modulating an anticoagulant response.	Glycosaminoglycans	45-62	platelet factor 4	Homo sapiens	0-3
14575696-2	2003	PF4 also neutralizes heparan sulfate (HS), a glycosaminoglycan (GAG) present on the surface of endothelial cells, thereby possibly modulating an anticoagulant response.	Glycosaminoglycans	64-67	platelet factor 4	Homo sapiens	0-3
12904606-1	2003	Mucopolysaccharidosis type VI (MPS VI) is a lysosomal storage disease caused by a deficiency of arylsulfatase B (ASB) which has its function in the sequential degradation of glycosaminoglycans (GAG).	Glycosaminoglycans	174-192	arylsulfatase B	Mus musculus	113-116
14616355-3	2003	Interferon-alpha 2b normalizes the excessive synthesis of collagen, glycosaminoglycans and collagenase by keloidal fibroblasts, reduces recurrences following keloid excision, and enhances the expression of native p53 and apoptosis.	Glycosaminoglycans	68-86	interferon alpha 2	Homo sapiens	0-19
12799343-1	2003	Hybrid chondroitin/dermatan sulfate (CS/DS) glycosaminoglycan chains, derived from decorin secreted by human skin fibroblasts, were shown to interact with FGF-2, as did oligosaccharides derived therefrom by chondroitin B lyase digestion.	Glycosaminoglycans	44-61	fibroblast growth factor 2	Homo sapiens	155-160
14551349-13	2003	Heparin inhibited NF-kappaB activation in Ang II-stimulated MCs that expressed either normal or chemically altered GAG.	Glycosaminoglycans	115-118	nuclear factor kappa B subunit 1	Homo sapiens	18-27
14551349-13	2003	Heparin inhibited NF-kappaB activation in Ang II-stimulated MCs that expressed either normal or chemically altered GAG.	Glycosaminoglycans	115-118	angiotensinogen	Homo sapiens	42-48
14551349-14	2003	CONCLUSIONS: These findings suggest that alterations in HS-GAG chemistry or metabolism under pathological conditions, such as DN, may have direct functional consequences for the local effect of Ang II.	Glycosaminoglycans	59-62	angiotensinogen	Homo sapiens	194-200
12904606-1	2003	Mucopolysaccharidosis type VI (MPS VI) is a lysosomal storage disease caused by a deficiency of arylsulfatase B (ASB) which has its function in the sequential degradation of glycosaminoglycans (GAG).	Glycosaminoglycans	194-197	arylsulfatase B	Mus musculus	113-116
12933790-10	2003	Surprisingly, recognition of glycosaminoglycans (GAGs) other than HA by native or recombinant HARE was temperature-dependent.	Glycosaminoglycans	29-47	stabilin 2	Rattus norvegicus	94-98
12917413-1	2003	Brain-specific chondroitin sulfate (CS) proteoglycan (PG) DSD-1-PG/6B4-PG/phosphacan isolated from neonatal mouse brains exhibits neurite outgrowth-promoting activity toward embryonic rat and mouse hippocampal neurons in vitro through the so-called DSD-1 epitope embedded in its glycosaminoglycan side chains.	Glycosaminoglycans	279-296	protein tyrosine phosphatase, receptor type Z, polypeptide 1	Mus musculus	58-66
12917413-8	2003	In addition, chemical analysis of the glycosaminoglycan side chains of DSD-1-PG revealed the DS-type structures.	Glycosaminoglycans	38-55	protein tyrosine phosphatase, receptor type Z, polypeptide 1	Mus musculus	71-79
12933790-12	2003	These data suggest that temperature-induced conformational changes may alter the GAG specificity of HARE.	Glycosaminoglycans	81-84	stabilin 2	Rattus norvegicus	100-104
12829604-7	2003	Thus, exogenous CS GAGs blocked the EMR2-ligand interaction in a dose-dependent manner.	Glycosaminoglycans	19-23	adhesion G protein-coupled receptor E2	Homo sapiens	36-40
14637022-6	2003	This suggests that glycosaminoglycans (GAGs) are involved in RANTES binding to the PGs and that such bindings facilitate the subsequent interaction of RANTES with CCR5, on the MDM, characterized by low membrane expression of CCR5.	Glycosaminoglycans	19-37	C-C motif chemokine ligand 5	Homo sapiens	61-67
12834595-2	2003	In this study, isolated type I collagen fibrils, elastin fibres and chondroitin sulphate (CS) were used for the preparation of molecularly-defined collagen-elastin-glycosaminoglycan scaffolds.	Glycosaminoglycans	164-181	elastin	Homo sapiens	49-56
12834595-2	2003	In this study, isolated type I collagen fibrils, elastin fibres and chondroitin sulphate (CS) were used for the preparation of molecularly-defined collagen-elastin-glycosaminoglycan scaffolds.	Glycosaminoglycans	164-181	elastin	Homo sapiens	156-163
12834595-0	2003	Preparation and evaluation of molecularly-defined collagen-elastin-glycosaminoglycan scaffolds for tissue engineering.	Glycosaminoglycans	67-84	elastin	Homo sapiens	59-66
12805068-3	2003	Infection of monocyte-derived macrophages with laboratory-adapted HIV-1 or primary viral isolates in the continuous presence of anti-CCL2 antibody resulted in significantly lower p24 Gag antigen release with respect to control cultures.	Glycosaminoglycans	183-186	C-C motif chemokine ligand 2	Homo sapiens	133-137
12805068-4	2003	Interestingly, CCL2 neutralization did not affect the early steps of the HIV life cycle but resulted in the intracellular accumulation of p24 Gag antigen.	Glycosaminoglycans	142-145	C-C motif chemokine ligand 2	Homo sapiens	15-19
14527517-6	2003	Recombinant alpha-1 giardin displayed a Ca(2+)-dependent binding to glycosaminoglycans (GAGs), in particular heparan sulphate, a common GAG in the intestinal tract.	Glycosaminoglycans	68-86	adrenoceptor alpha 1D	Homo sapiens	12-19
14527517-6	2003	Recombinant alpha-1 giardin displayed a Ca(2+)-dependent binding to glycosaminoglycans (GAGs), in particular heparan sulphate, a common GAG in the intestinal tract.	Glycosaminoglycans	88-91	adrenoceptor alpha 1D	Homo sapiens	12-19
14653390-2	2003	METHODS: Collagen and glycosaminoglycan (GAG) synthesis were determined by radiolabeled precursors and biglycan expression by Northern blotting before and after adding IL-6.	Glycosaminoglycans	41-44	biglycan	Homo sapiens	103-111
14641413-9	2003	CD44 expression in ulcer type IC could explain the prolonged and stronger expression of GAG-binding growth factors that promote inflammation.	Glycosaminoglycans	88-91	CD44 molecule (Indian blood group)	Homo sapiens	0-4
14653390-4	2003	RESULTS: The results showed that IL-6 elicited an inhibitory effect on collagen and GAG levels in CLP fibroblasts by lowering hyaluronan and dermatan sulfate secretion.	Glycosaminoglycans	84-87	interleukin 6	Homo sapiens	33-37
12847110-7	2003	Our results suggest that N inhibits angiogenesis not by disrupting the HGF/c-met interaction but rather by interfering with the endothelial glycosaminoglycans, which are the secondary binding sites of HGF.	Glycosaminoglycans	140-158	hepatocyte growth factor	Homo sapiens	201-204
14512540-8	2003	Addition of exogenous IL-2 was sufficient to rescue in vitro proliferation of DR0101 class II Gag or Pol tetramer(+) or total-Gag-specific CD4(+) T cells.	Glycosaminoglycans	94-97	interleukin 2	Homo sapiens	22-26
12763925-2	2003	The propensity of chemokines such as CC chemokine ligand 5 (CCL5)/RANTES (regulated on activation, normal T cell expressed and secreted) to bind to glycosaminoglycans and to form higher order oligomers has been shown to be essential for its in vivo activity.	Glycosaminoglycans	148-166	C-C motif chemokine ligand 5	Homo sapiens	37-58
14505572-2	2003	Here, we characterize the ENU-induced mutation lazy mesoderm (lzme), which disrupts the single mouse gene encoding UDP-glucose dehydrogenase (Ugdh), an enzyme required for the synthesis of the glycosaminoglycan (GAG) side chains of proteoglycans.	Glycosaminoglycans	193-210	UDP-glucose dehydrogenase	Mus musculus	115-140
14505572-2	2003	Here, we characterize the ENU-induced mutation lazy mesoderm (lzme), which disrupts the single mouse gene encoding UDP-glucose dehydrogenase (Ugdh), an enzyme required for the synthesis of the glycosaminoglycan (GAG) side chains of proteoglycans.	Glycosaminoglycans	193-210	UDP-glucose dehydrogenase	Mus musculus	142-146
14505572-2	2003	Here, we characterize the ENU-induced mutation lazy mesoderm (lzme), which disrupts the single mouse gene encoding UDP-glucose dehydrogenase (Ugdh), an enzyme required for the synthesis of the glycosaminoglycan (GAG) side chains of proteoglycans.	Glycosaminoglycans	212-215	UDP-glucose dehydrogenase	Mus musculus	115-140
14505572-2	2003	Here, we characterize the ENU-induced mutation lazy mesoderm (lzme), which disrupts the single mouse gene encoding UDP-glucose dehydrogenase (Ugdh), an enzyme required for the synthesis of the glycosaminoglycan (GAG) side chains of proteoglycans.	Glycosaminoglycans	212-215	UDP-glucose dehydrogenase	Mus musculus	142-146
12968917-4	2003	This method has been applied to develop a synthesis of protected glucuronic acid 1, a key intermediate in the synthesis of glycosaminoglycans.	Glycosaminoglycans	123-141	mediator complex subunit 25	Homo sapiens	76-82
12763925-2	2003	The propensity of chemokines such as CC chemokine ligand 5 (CCL5)/RANTES (regulated on activation, normal T cell expressed and secreted) to bind to glycosaminoglycans and to form higher order oligomers has been shown to be essential for its in vivo activity.	Glycosaminoglycans	148-166	C-C motif chemokine ligand 5	Homo sapiens	60-64
12763925-2	2003	The propensity of chemokines such as CC chemokine ligand 5 (CCL5)/RANTES (regulated on activation, normal T cell expressed and secreted) to bind to glycosaminoglycans and to form higher order oligomers has been shown to be essential for its in vivo activity.	Glycosaminoglycans	148-166	C-C motif chemokine ligand 5	Homo sapiens	66-72
14499180-3	2003	Interleukin-1 beta acts as an important mediator of extracellular matrix changes where its activity is regulated by glycosaminoglycan composition.	Glycosaminoglycans	116-133	interleukin 1 beta	Bos taurus	0-18
14585207-8	2003	The analysis of Gag expression in murine cells transfected with CycT1 compared with human cells showed a 20-fold decrease in expression and a strong processing defect.	Glycosaminoglycans	16-19	cyclin T1	Mus musculus	64-69
12975293-0	2003	Frequency and phenotypic variability of the GAG deletion of the DYT1 gene in an unselected group of patients with dystonia.	Glycosaminoglycans	44-47	torsin family 1 member A	Homo sapiens	64-68
12975293-3	2003	OBJECTIVES: To investigate the prevalence of the GAG deletion in the DYT1 gene and the phenotypic variability in the general population by testing patients with different subtypes of dystonia from 4 different movement disorder outpatient clinics in Germany.	Glycosaminoglycans	49-52	torsin family 1 member A	Homo sapiens	69-73
12975293-5	2003	RESULTS: Six of the 256 patients did carry the GAG-deletion in the DYT1 gene.	Glycosaminoglycans	47-50	torsin family 1 member A	Homo sapiens	67-71
12954233-10	2003	Glycosaminoglycan (GAG) concentrations in 3-D constructs (GAG/weight) were significantly (P&lt;0.001) higher in groups without IL-1 beta than in those with IL-1 beta, on days 15 and 24.	Glycosaminoglycans	0-17	interleukin 1 beta	Canis lupus familiaris	127-136
12910476-2	2003	A quantitative cytochemical technique for uridine-diphospho glucose dehydrogenase (UDPGD) activity established that fibroblast-like cells on the intimal surface of the synovial lining made a specific contribution to maintaining these glycosaminoglycan levels.	Glycosaminoglycans	234-251	UDP-glucose 6-dehydrogenase	Homo sapiens	42-81
12910476-2	2003	A quantitative cytochemical technique for uridine-diphospho glucose dehydrogenase (UDPGD) activity established that fibroblast-like cells on the intimal surface of the synovial lining made a specific contribution to maintaining these glycosaminoglycan levels.	Glycosaminoglycans	234-251	UDP-glucose 6-dehydrogenase	Homo sapiens	83-88
14643300-2	2003	A novel HIV vaccine composed of plasmid DNA-encoding p55 gag formulated with poly-lactide-co-glycolide microparticles (PLG) and cetyl trimethyl ammonium bromide (CTAB) elicits both serum antibody titers and cytotoxic lymphocyte activity in mice at doses two orders of magnitude lower than those required for comparable response to plasmid DNA in saline.	Glycosaminoglycans	57-60	membrane protein, palmitoylated	Mus musculus	53-56
12773479-5	2003	Glycosaminoglycans removal from the cells by glycosaminidases treatment prevented RANTES binding to SD-1 and -4 and decreased RANTES binding to CCR5 on the CCR5-positive HeLa cells.	Glycosaminoglycans	0-18	C-C motif chemokine ligand 5	Homo sapiens	82-88
12773479-5	2003	Glycosaminoglycans removal from the cells by glycosaminidases treatment prevented RANTES binding to SD-1 and -4 and decreased RANTES binding to CCR5 on the CCR5-positive HeLa cells.	Glycosaminoglycans	0-18	CUP2Q35	Homo sapiens	100-111
12773479-5	2003	Glycosaminoglycans removal from the cells by glycosaminidases treatment prevented RANTES binding to SD-1 and -4 and decreased RANTES binding to CCR5 on the CCR5-positive HeLa cells.	Glycosaminoglycans	0-18	C-C motif chemokine ligand 5	Homo sapiens	126-132
12773479-5	2003	Glycosaminoglycans removal from the cells by glycosaminidases treatment prevented RANTES binding to SD-1 and -4 and decreased RANTES binding to CCR5 on the CCR5-positive HeLa cells.	Glycosaminoglycans	0-18	C-C motif chemokine receptor 5	Homo sapiens	144-148
12773479-5	2003	Glycosaminoglycans removal from the cells by glycosaminidases treatment prevented RANTES binding to SD-1 and -4 and decreased RANTES binding to CCR5 on the CCR5-positive HeLa cells.	Glycosaminoglycans	0-18	C-C motif chemokine receptor 5	Homo sapiens	156-160
12773479-6	2003	Removal of glycosaminoglycans by glycosaminidases treatment of the complexes, RANTES/SD-1/SD-4/+/-CCR5, immobilized on beads, reversed SD-1 and -4 bindings.	Glycosaminoglycans	11-29	C-C motif chemokine ligand 5	Homo sapiens	78-84
12773479-6	2003	Removal of glycosaminoglycans by glycosaminidases treatment of the complexes, RANTES/SD-1/SD-4/+/-CCR5, immobilized on beads, reversed SD-1 and -4 bindings.	Glycosaminoglycans	11-29	CUP2Q35	Homo sapiens	85-89
12773479-6	2003	Removal of glycosaminoglycans by glycosaminidases treatment of the complexes, RANTES/SD-1/SD-4/+/-CCR5, immobilized on beads, reversed SD-1 and -4 bindings.	Glycosaminoglycans	11-29	C-C motif chemokine receptor 5	Homo sapiens	98-102
12773479-6	2003	Removal of glycosaminoglycans by glycosaminidases treatment of the complexes, RANTES/SD-1/SD-4/+/-CCR5, immobilized on beads, reversed SD-1 and -4 bindings.	Glycosaminoglycans	11-29	CUP2Q35	Homo sapiens	135-146
13679195-5	2003	We measured in vitro the amount of glycosaminoglycans (GAGs) and the production of nitric oxide (NO) released into the culture medium of human articular cartilage treated with interleukin-1beta (IL-1beta), which promotes the cartilage destruction during articular disease.	Glycosaminoglycans	35-53	interleukin 1 beta	Homo sapiens	176-193
12915562-9	2003	Since TSG101 is crucial for HIV-1 release, this result suggests that the Gag-TSG101 interaction is responsible for the virus release function of the MPMV PSAP motif.	Glycosaminoglycans	73-76	prosaposin	Homo sapiens	154-158
12941902-6	2003	By contrast, dextran sulfate inhibited gp46-Fc binding to GAG-negative cells such as CHO 2244, CHO 2241, and Jurkat T cells weakly or not at all.	Glycosaminoglycans	58-61	serpin family H member 1	Homo sapiens	39-43
12954233-10	2003	Glycosaminoglycan (GAG) concentrations in 3-D constructs (GAG/weight) were significantly (P&lt;0.001) higher in groups without IL-1 beta than in those with IL-1 beta, on days 15 and 24.	Glycosaminoglycans	0-17	interleukin 1 beta	Canis lupus familiaris	156-165
12954233-10	2003	Glycosaminoglycan (GAG) concentrations in 3-D constructs (GAG/weight) were significantly (P&lt;0.001) higher in groups without IL-1 beta than in those with IL-1 beta, on days 15 and 24.	Glycosaminoglycans	19-22	interleukin 1 beta	Canis lupus familiaris	127-136
12954233-10	2003	Glycosaminoglycan (GAG) concentrations in 3-D constructs (GAG/weight) were significantly (P&lt;0.001) higher in groups without IL-1 beta than in those with IL-1 beta, on days 15 and 24.	Glycosaminoglycans	19-22	interleukin 1 beta	Canis lupus familiaris	156-165
12799382-5	2003	B/b130 is an underglycosylated isoform of BEHAB/brevican, lacking glycosaminoglycan chains as well as most of the sugars that invest B/b150.	Glycosaminoglycans	66-83	brevican	Rattus norvegicus	42-47
14588099-0	2003	Glycosaminoglycans provide a binding site for thyroglobulin in orbital tissues of patients with thyroid-associated ophthalmopathy.	Glycosaminoglycans	0-18	thyroglobulin	Homo sapiens	46-59
12905469-6	2003	In vitro digestion of human hyaline cartilage samples revealed that the dominant glycosidases, alone or in combination with MMPs, proved to be effective in depleting glycosaminoglycans (GAGs) from cartilage.	Glycosaminoglycans	166-184	matrix metallopeptidase 1	Homo sapiens	124-128
12886459-0	2003	Glycosaminoglycans affect the interaction of human plasma kallikrein with plasminogen, factor XII and inhibitors.	Glycosaminoglycans	0-18	kallikrein related peptidase 4	Homo sapiens	58-68
12886459-3	2003	The aim of the present study was to investigate the effect of glycosaminoglycans (30 to 250 micro/ml) on kallikrein activity on plasminogen and factor XII and on the inhibition of kallikrein by the plasma proteins C1-inhibitor and antithrombin.	Glycosaminoglycans	62-80	kallikrein related peptidase 4	Homo sapiens	105-115
12886459-4	2003	Almost all available glycosaminoglycans (heparin, heparan sulfate, bovine and tuna dermatan sulfate, chondroitin 4- and 6-sulfates) reduced (1.2 to 3.0 times) the catalytic efficiency of kallikrein (in a nanomolar range) on the hydrolysis of plasminogen (0.3 to 1.8 microM) and increased (1.9 to 7.7 times) the enzyme efficiency in factor XII (0.1 to 10 microM) activation.	Glycosaminoglycans	21-39	kallikrein related peptidase 4	Homo sapiens	187-197
12905469-6	2003	In vitro digestion of human hyaline cartilage samples revealed that the dominant glycosidases, alone or in combination with MMPs, proved to be effective in depleting glycosaminoglycans (GAGs) from cartilage.	Glycosaminoglycans	186-190	matrix metallopeptidase 1	Homo sapiens	124-128
12948739-1	2003	Mucopolysaccharidosis I is a lysosomal storage disorder caused by mutations in the IDUA gene, resulting in deficiency of alpha-L-iduronidase and accumulation of glycosaminoglycans.	Glycosaminoglycans	161-179	iduronidase, alpha-L	Mus musculus	83-87
12963107-1	2003	Beta-ig is a secretory protein embodied by fasciclin I-like repeats containing sequences that might bind integrins and glycosaminoglycans in vivo.	Glycosaminoglycans	119-137	transforming growth factor, beta induced	Mus musculus	0-7
12847218-3	2003	In particular, mac25/AGM interacted with not only the extracellular matrix proteins and glycosaminoglycans that are expressed in most blood vessels including HEVs, but also with some chemokines that are implicated in the regulation of lymphocyte trafficking, such as the secondary lymphoid-tissue chemokine (SLC; CCL21), IFN-gamma-inducible protein 10 (IP-10; CXCL10), and RANTES (CCL5).	Glycosaminoglycans	88-106	insulin like growth factor binding protein 7	Homo sapiens	15-20
13678446-6	2003	Glycosaminoglycan (GAG) and total collagen content of the hydrogels increased to 3.5% dry weight and 5.0% dry weight, respectively, in 6wk+TGF constructs.	Glycosaminoglycans	0-17	transforming growth factor beta-1 proprotein	Capra hircus	139-142
12847218-3	2003	In particular, mac25/AGM interacted with not only the extracellular matrix proteins and glycosaminoglycans that are expressed in most blood vessels including HEVs, but also with some chemokines that are implicated in the regulation of lymphocyte trafficking, such as the secondary lymphoid-tissue chemokine (SLC; CCL21), IFN-gamma-inducible protein 10 (IP-10; CXCL10), and RANTES (CCL5).	Glycosaminoglycans	88-106	C-C motif chemokine ligand 21	Homo sapiens	271-306
12847218-3	2003	In particular, mac25/AGM interacted with not only the extracellular matrix proteins and glycosaminoglycans that are expressed in most blood vessels including HEVs, but also with some chemokines that are implicated in the regulation of lymphocyte trafficking, such as the secondary lymphoid-tissue chemokine (SLC; CCL21), IFN-gamma-inducible protein 10 (IP-10; CXCL10), and RANTES (CCL5).	Glycosaminoglycans	88-106	C-C motif chemokine ligand 21	Homo sapiens	308-311
12847218-3	2003	In particular, mac25/AGM interacted with not only the extracellular matrix proteins and glycosaminoglycans that are expressed in most blood vessels including HEVs, but also with some chemokines that are implicated in the regulation of lymphocyte trafficking, such as the secondary lymphoid-tissue chemokine (SLC; CCL21), IFN-gamma-inducible protein 10 (IP-10; CXCL10), and RANTES (CCL5).	Glycosaminoglycans	88-106	C-C motif chemokine ligand 21	Homo sapiens	313-318
12847218-3	2003	In particular, mac25/AGM interacted with not only the extracellular matrix proteins and glycosaminoglycans that are expressed in most blood vessels including HEVs, but also with some chemokines that are implicated in the regulation of lymphocyte trafficking, such as the secondary lymphoid-tissue chemokine (SLC; CCL21), IFN-gamma-inducible protein 10 (IP-10; CXCL10), and RANTES (CCL5).	Glycosaminoglycans	88-106	C-X-C motif chemokine ligand 10	Homo sapiens	321-351
12847218-3	2003	In particular, mac25/AGM interacted with not only the extracellular matrix proteins and glycosaminoglycans that are expressed in most blood vessels including HEVs, but also with some chemokines that are implicated in the regulation of lymphocyte trafficking, such as the secondary lymphoid-tissue chemokine (SLC; CCL21), IFN-gamma-inducible protein 10 (IP-10; CXCL10), and RANTES (CCL5).	Glycosaminoglycans	88-106	C-X-C motif chemokine ligand 10	Homo sapiens	353-358
12847218-3	2003	In particular, mac25/AGM interacted with not only the extracellular matrix proteins and glycosaminoglycans that are expressed in most blood vessels including HEVs, but also with some chemokines that are implicated in the regulation of lymphocyte trafficking, such as the secondary lymphoid-tissue chemokine (SLC; CCL21), IFN-gamma-inducible protein 10 (IP-10; CXCL10), and RANTES (CCL5).	Glycosaminoglycans	88-106	C-X-C motif chemokine ligand 10	Homo sapiens	360-366
12847218-3	2003	In particular, mac25/AGM interacted with not only the extracellular matrix proteins and glycosaminoglycans that are expressed in most blood vessels including HEVs, but also with some chemokines that are implicated in the regulation of lymphocyte trafficking, such as the secondary lymphoid-tissue chemokine (SLC; CCL21), IFN-gamma-inducible protein 10 (IP-10; CXCL10), and RANTES (CCL5).	Glycosaminoglycans	88-106	C-C motif chemokine ligand 5	Homo sapiens	373-379
12730206-7	2003	First, the direct binding and competition experiments show that the carbohydrate recognition domain (CRD) of SP-D binds in a calcium dependent-manner to the sulfated N-acetyl galactosamine moiety of the glycosaminoglycan chain.	Glycosaminoglycans	203-220	surfactant protein D	Homo sapiens	109-113
12847218-3	2003	In particular, mac25/AGM interacted with not only the extracellular matrix proteins and glycosaminoglycans that are expressed in most blood vessels including HEVs, but also with some chemokines that are implicated in the regulation of lymphocyte trafficking, such as the secondary lymphoid-tissue chemokine (SLC; CCL21), IFN-gamma-inducible protein 10 (IP-10; CXCL10), and RANTES (CCL5).	Glycosaminoglycans	88-106	C-C motif chemokine ligand 5	Homo sapiens	381-385
12847218-9	2003	These results imply that mac25/AGM plays a multifunctional role, serving not only as an adhesion protein to interact with glycosaminoglycans and extracellular matrix proteins but also as a molecule to present chemokines so that lymphocytes extravasating through HEVs receive further directional cues subsequent to the luminal encounter with lymphoid chemokines.	Glycosaminoglycans	122-140	insulin like growth factor binding protein 7	Homo sapiens	25-30
12798179-1	2003	A newly developed capillary electrophoretic method using laser-induced fluorescence detection (CE-LIF) for the analysis of monosaccharides released from acid hydrolysis of glycosaminoglycans was studied.	Glycosaminoglycans	172-190	LIF interleukin 6 family cytokine	Homo sapiens	98-101
12682078-1	2003	UDP-glucose dehydrogenase (UGDH) is a key enzyme of the unique pathway for the synthesis of UDP-glucuronate, the substrate for the numerous glucuronosyl transferases, which act on the synthesis of glycosaminoglycans and glucuronidation reaction of xeno- and endobiotics.	Glycosaminoglycans	197-215	UDP-glucose 6-dehydrogenase	Homo sapiens	0-25
12926067-3	2003	Previous studies on glycosaminoglycan expression by THP-1 cells and peripheral blood mononuclear cells from healthy individuals showed that both cell types secrete mainly chondroitin sulfate PGs to the culture medium, whereas heparan sulfate PGs are mainly retarded at the cell membrane.	Glycosaminoglycans	20-37	GLI family zinc finger 2	Homo sapiens	52-57
12852860-4	2003	In the presence of Env, Gag is rerouted from lysosomes to transferrin-positive endosomes, and virion production becomes highly sensitive to drugs poisoning vesicular and endosomal traffic.	Glycosaminoglycans	24-27	endogenous retrovirus group K member 20	Homo sapiens	19-22
12852860-4	2003	In the presence of Env, Gag is rerouted from lysosomes to transferrin-positive endosomes, and virion production becomes highly sensitive to drugs poisoning vesicular and endosomal traffic.	Glycosaminoglycans	24-27	transferrin	Homo sapiens	58-69
12682078-1	2003	UDP-glucose dehydrogenase (UGDH) is a key enzyme of the unique pathway for the synthesis of UDP-glucuronate, the substrate for the numerous glucuronosyl transferases, which act on the synthesis of glycosaminoglycans and glucuronidation reaction of xeno- and endobiotics.	Glycosaminoglycans	197-215	UDP-glucose 6-dehydrogenase	Homo sapiens	27-31
12783425-1	2003	A three-nucleotide (GAG) deletion in the TOR1A gene is the most common cause of inherited dystonia, DYT1.	Glycosaminoglycans	20-23	torsin family 1 member A	Homo sapiens	41-46
12783425-1	2003	A three-nucleotide (GAG) deletion in the TOR1A gene is the most common cause of inherited dystonia, DYT1.	Glycosaminoglycans	20-23	torsin family 1 member A	Homo sapiens	100-104
12887056-5	2003	Cathepsin-predigested aggrecan complexes and cartilage provided suitable glycosaminoglycan fragments that allowed the formation of collagenolytically active cathepsin K complexes.	Glycosaminoglycans	73-90	cathepsin K	Bos taurus	157-168
12887056-7	2003	In summary, these results demonstrate that cathepsin K is capable to degrade aggrecan complexes at specific cleavage sites and that cathepsin K activity alone is sufficient to self-provide the glycosaminoglycan fragments required for the formation of its collagenolytically active complex.	Glycosaminoglycans	193-210	cathepsin K	Bos taurus	132-143
12692188-5	2003	TSG-6 is a member of the Link module superfamily and binds to hyaluronan (a vital component of extracellular matrix), as well as other glycosaminoglycans, via its Link module.	Glycosaminoglycans	135-153	TNF alpha induced protein 6	Homo sapiens	0-5
12626395-1	2003	We report ELISA studies of the glycosaminoglycan binding properties of recombinant human glial cell line-derived neurotrophic factor (GDNF).	Glycosaminoglycans	31-48	glial cell derived neurotrophic factor	Homo sapiens	89-132
12626395-1	2003	We report ELISA studies of the glycosaminoglycan binding properties of recombinant human glial cell line-derived neurotrophic factor (GDNF).	Glycosaminoglycans	31-48	glial cell derived neurotrophic factor	Homo sapiens	134-138
12626395-7	2003	Considered overall, these findings provide strong support for a hypothesis that the bioactivity of GDNF during prenatal development is essentially dependent on the binding of this growth factor to 2-O-sulfate-rich heparin-related glycosaminoglycan.	Glycosaminoglycans	230-247	glial cell derived neurotrophic factor	Homo sapiens	99-103
12771435-2	2003	An immunoblot analysis of the cell lysates transfected with DNA mutated in either the first (ZF1) or second (ZF2) motif showed that the amount of partially processed Gag products (Pr46) was greater than that produced by the wild-type (WT).	Glycosaminoglycans	166-169	zinc finger protein 274	Homo sapiens	109-112
12865952-5	2003	Antithrombin binds to endothelial glycosaminoglycans and then significantly increases anticoagulant activity.	Glycosaminoglycans	34-52	serpin family C member 1	Homo sapiens	0-12
12746900-11	2003	CONCLUSION: Interaction of the peptide V sequence in HBFN-f with glycosaminoglycans, such as those in CD44, plays an important role in HBFN-f-stimulated MMP production in articular cartilage.	Glycosaminoglycans	65-83	CD44 molecule (Indian blood group)	Homo sapiens	102-106
12598530-5	2003	The increase in VLDL binding results from an increase in the availability of HSPG sites as treatment with heparinase or competitors of glycosaminoglycan chain addition eliminated the augmented binding.	Glycosaminoglycans	135-152	syndecan 2	Homo sapiens	77-81
12571234-2	2003	IP-10 also binds to glycosaminoglycans (GAGs), an interaction thought to be important for its sequestration on endothelial and other cells.	Glycosaminoglycans	20-38	chemokine (C-X-C motif) ligand 10	Mus musculus	0-5
12571234-2	2003	IP-10 also binds to glycosaminoglycans (GAGs), an interaction thought to be important for its sequestration on endothelial and other cells.	Glycosaminoglycans	40-44	chemokine (C-X-C motif) ligand 10	Mus musculus	0-5
12600723-1	2003	Alzheimer"s disease (AD) literature indicates that glycosaminoglycans (GAGs) may prevent proteoglycan-induced amyloid-beta (Abeta) aggregation, decrease Abeta-induced tau-2 immunoreactivity, and increase the axonal growth and arborization of hippocampal neurons.	Glycosaminoglycans	51-69	amyloid beta precursor protein	Homo sapiens	124-129
12768169-7	2003	The most important mechanism responsible of the anti-inflammatory properties of AT is the binding to the glycosaminoglycans of the endothelial cells and the consequent release of prostacyclin.	Glycosaminoglycans	105-123	serpin family C member 1	Homo sapiens	80-82
12682278-4	2003	Furthermore, subjects with a severely depleted and phenotypically altered CD4(+) T cell compartment had circulating Gag-specific CD8(+) T cells with impaired IFN-gamma production.	Glycosaminoglycans	116-119	CD4 molecule	Homo sapiens	74-77
15969005-5	2003	The data of mutant clone DNA sequence showed that the amino acid of light chain gene of the parent anti-CD20 antibody (H47) was successful mutated as Ser (GAG)-Asn (CAG).	Glycosaminoglycans	155-158	keratin 20	Homo sapiens	104-108
12671990-1	2003	Most cases of early-onset torsion dystonia are caused by deletion of GAG in the coding region of the DYT1 gene encoding torsinA.	Glycosaminoglycans	69-72	torsin family 1, member A	Rattus norvegicus	101-105
12671990-1	2003	Most cases of early-onset torsion dystonia are caused by deletion of GAG in the coding region of the DYT1 gene encoding torsinA.	Glycosaminoglycans	69-72	torsin family 1, member A	Rattus norvegicus	120-127
12822816-1	2003	The question of whether a fetus carrying the GAG deletion on the DYT1 gene responsible for Oppenheim"s dystonia should be aborted is frequently raised.	Glycosaminoglycans	45-48	torsin family 1 member A	Homo sapiens	65-69
12726721-0	2003	Intragenic HIV-1 env sequences that enhance gag expression.	Glycosaminoglycans	44-47	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	17-20
12726721-4	2003	This element enhanced the expression of Gag when inserted together with Rev response element (RRE) into a truncated HIV-1 genome in the presence of Rev.	Glycosaminoglycans	40-43	Rev	Human immunodeficiency virus 1	72-75
12726721-4	2003	This element enhanced the expression of Gag when inserted together with Rev response element (RRE) into a truncated HIV-1 genome in the presence of Rev.	Glycosaminoglycans	40-43	Rev	Human immunodeficiency virus 1	148-151
12682278-4	2003	Furthermore, subjects with a severely depleted and phenotypically altered CD4(+) T cell compartment had circulating Gag-specific CD8(+) T cells with impaired IFN-gamma production.	Glycosaminoglycans	116-119	CD8a molecule	Homo sapiens	129-132
12654635-9	2003	These findings suggest that IL-8-glycosaminoglycan interactions determine the location where IL-8 binds in lung tissue and provides a site for the dimerization of IL-8, which increases the local concentration of IL-8 in the lungs.	Glycosaminoglycans	33-50	C-X-C motif chemokine ligand 8	Homo sapiens	28-32
12584198-6	2003	Transfection of sqv-6 restored xylosyltransferase activity to and rescued the glycosaminoglycan biosynthesis defect of a xylosyltransferase mutant hamster cell line.	Glycosaminoglycans	78-95	Protein xylosyltransferase;Xylosyltransferase sqv-6	Caenorhabditis elegans	16-21
12584198-9	2003	We conclude that C. elegans SQV-6 and SQV-2 likely act in concert with other SQV proteins to catalyze the stepwise formation of the proteoglycan core protein linkage tetrasaccharide GlcAbeta1,3Galbeta1, 3Galbeta1,4Xylbeta-O-(Ser), which is common to the two major types of glycosaminoglycans in vertebrates, chondroitin and heparan sulfate.	Glycosaminoglycans	273-291	Protein xylosyltransferase;Xylosyltransferase sqv-6	Caenorhabditis elegans	28-33
12584198-9	2003	We conclude that C. elegans SQV-6 and SQV-2 likely act in concert with other SQV proteins to catalyze the stepwise formation of the proteoglycan core protein linkage tetrasaccharide GlcAbeta1,3Galbeta1, 3Galbeta1,4Xylbeta-O-(Ser), which is common to the two major types of glycosaminoglycans in vertebrates, chondroitin and heparan sulfate.	Glycosaminoglycans	273-291	Beta-1,3-galactosyltransferase sqv-2	Caenorhabditis elegans	38-43
12654635-9	2003	These findings suggest that IL-8-glycosaminoglycan interactions determine the location where IL-8 binds in lung tissue and provides a site for the dimerization of IL-8, which increases the local concentration of IL-8 in the lungs.	Glycosaminoglycans	33-50	C-X-C motif chemokine ligand 8	Homo sapiens	93-97
12654635-9	2003	These findings suggest that IL-8-glycosaminoglycan interactions determine the location where IL-8 binds in lung tissue and provides a site for the dimerization of IL-8, which increases the local concentration of IL-8 in the lungs.	Glycosaminoglycans	33-50	C-X-C motif chemokine ligand 8	Homo sapiens	93-97
12654635-9	2003	These findings suggest that IL-8-glycosaminoglycan interactions determine the location where IL-8 binds in lung tissue and provides a site for the dimerization of IL-8, which increases the local concentration of IL-8 in the lungs.	Glycosaminoglycans	33-50	C-X-C motif chemokine ligand 8	Homo sapiens	93-97
12818259-0	2003	Additive thrombin inhibition by fast moving heparin and dermatan sulfate explains the anticoagulant effect of sulodexide, a natural mixture of glycosaminoglycans.	Glycosaminoglycans	143-161	coagulation factor II, thrombin	Homo sapiens	9-17
12653632-0	2003	Interaction between glial-cell-line-derived neurotrophic factor (GDNF) and 2-O-sulphated heparin-related glycosaminoglycans.	Glycosaminoglycans	105-123	glial cell line derived neurotrophic factor	Mus musculus	20-63
12653632-0	2003	Interaction between glial-cell-line-derived neurotrophic factor (GDNF) and 2-O-sulphated heparin-related glycosaminoglycans.	Glycosaminoglycans	105-123	glial cell line derived neurotrophic factor	Mus musculus	65-69
12670795-1	2003	Insulin-like growth factor-I (IGF-I) is an important stimulator of collagen and glycosaminoglycan (GAG) biosynthesis in tissues.	Glycosaminoglycans	80-97	insulin-like growth factor 1	Rattus norvegicus	0-28
12670795-1	2003	Insulin-like growth factor-I (IGF-I) is an important stimulator of collagen and glycosaminoglycan (GAG) biosynthesis in tissues.	Glycosaminoglycans	80-97	insulin-like growth factor 1	Rattus norvegicus	30-35
12511570-10	2003	Thus, all three glucuronyltransferases are likely involved in the synthesis of the GAG-protein linkage region in Drosophila, and DmGlcAT-BSI and -BSII appear to be involved in various GlcUA transfer reactions for the synthesis of proteoglycans, glycoproteins, and glycolipids.	Glycosaminoglycans	83-86	Glucuronyltransferase S	Drosophila melanogaster	129-150
12782143-7	2003	This finding is unexpected, as the accepted mechanism for degradation of syndecan HSPG following endocytosis is fragmentation of the protein core and glycosaminoglycan chains in endosomes, followed by delivery of the fragments to lysosomes.	Glycosaminoglycans	150-167	syndecan 2	Homo sapiens	82-86
12641447-2	2003	PEDF has been reported to bind to extracellular matrix (ECM) components such as collagens and glycosaminoglycans (GAGs).	Glycosaminoglycans	94-112	serpin family F member 1	Homo sapiens	0-4
12653715-5	2003	In the Russian family, we found a G to A transition at the first base of codon 402, resulting in a lysine substitution (GAG to AAG), designated E402K.	Glycosaminoglycans	120-123	N-methylpurine DNA glycosylase	Homo sapiens	127-130
12591953-1	2003	beta-Glucuronidase (GUSB) is a lysosomal enzyme important in the normal step-wise degradation of glycosaminoglycans.	Glycosaminoglycans	97-115	glucuronidase beta	Homo sapiens	0-18
12591953-1	2003	beta-Glucuronidase (GUSB) is a lysosomal enzyme important in the normal step-wise degradation of glycosaminoglycans.	Glycosaminoglycans	97-115	glucuronidase beta	Homo sapiens	20-24
12653715-6	2003	In the Colombian family, affected patients carried a missense mutation of codon 413, involving a transition from G to A causing a lysine substitution (GAG to AAG), designated E413K.	Glycosaminoglycans	151-154	N-methylpurine DNA glycosylase	Homo sapiens	158-161
12643279-7	2003	The region encompassing gag p17 to env C2-V3-C3 was amplified by the polymerase chain reaction followed by direct sequencing.	Glycosaminoglycans	24-27	family with sequence similarity 72 member B	Homo sapiens	28-31
12603746-5	2003	Three B. burgdorferi surface proteins, Bgp, DbpA and DbpB, have been demonstrated previously to bind to GAGs or to GAG-containing molecules, and we show here that recombinant derivatives of each of these proteins were able to bind to purified heparin and dermatan sulphate.	Glycosaminoglycans	104-108	Y-box binding protein 3	Homo sapiens	44-48
12603746-5	2003	Three B. burgdorferi surface proteins, Bgp, DbpA and DbpB, have been demonstrated previously to bind to GAGs or to GAG-containing molecules, and we show here that recombinant derivatives of each of these proteins were able to bind to purified heparin and dermatan sulphate.	Glycosaminoglycans	104-108	Y-box binding protein 1	Homo sapiens	53-57
12603746-5	2003	Three B. burgdorferi surface proteins, Bgp, DbpA and DbpB, have been demonstrated previously to bind to GAGs or to GAG-containing molecules, and we show here that recombinant derivatives of each of these proteins were able to bind to purified heparin and dermatan sulphate.	Glycosaminoglycans	104-107	Y-box binding protein 3	Homo sapiens	44-48
12603746-5	2003	Three B. burgdorferi surface proteins, Bgp, DbpA and DbpB, have been demonstrated previously to bind to GAGs or to GAG-containing molecules, and we show here that recombinant derivatives of each of these proteins were able to bind to purified heparin and dermatan sulphate.	Glycosaminoglycans	104-107	Y-box binding protein 1	Homo sapiens	53-57
12606025-0	2003	Heparin-like dextran derivatives as well as glycosaminoglycans inhibit the enzymatic activity of human cathepsin G.	Glycosaminoglycans	44-62	cathepsin G	Homo sapiens	103-114
12625842-0	2003	Glycosaminoglycans in human retinoblastoma cells: heparan sulfate, a modulator of the pigment epithelium-derived factor-receptor interactions.	Glycosaminoglycans	0-18	serpin family F member 1	Homo sapiens	86-119
12625842-1	2003	BACKGROUND: Pigment epithelium-derived factor (PEDF) has binding affinity for cell-surface receptors in retinoblastoma cells and for glycosaminoglycans.	Glycosaminoglycans	133-151	serpin family F member 1	Homo sapiens	12-45
12625842-1	2003	BACKGROUND: Pigment epithelium-derived factor (PEDF) has binding affinity for cell-surface receptors in retinoblastoma cells and for glycosaminoglycans.	Glycosaminoglycans	133-151	serpin family F member 1	Homo sapiens	47-51
12625842-2	2003	We investigated the effects of glycosaminoglycans on PEDF-receptor interactions.	Glycosaminoglycans	31-49	serpin family F member 1	Homo sapiens	53-57
12625842-4	2003	Using specific glycosaminoglycan degrading enzymes in spectrophotometric assays and PEDF-affinity chromatography, we detected heparin and heparan sulfate-like glycosaminoglycans in the Y-79 conditioned media, which had binding affinity for PEDF.	Glycosaminoglycans	15-32	serpin family F member 1	Homo sapiens	240-244
12625842-4	2003	Using specific glycosaminoglycan degrading enzymes in spectrophotometric assays and PEDF-affinity chromatography, we detected heparin and heparan sulfate-like glycosaminoglycans in the Y-79 conditioned media, which had binding affinity for PEDF.	Glycosaminoglycans	159-177	serpin family F member 1	Homo sapiens	240-244
12623288-8	2003	35SO(4)-decorin, which was present in TGF beta 1-treated cultures had an identical core protein, but a longer glycosaminoglycan chain than that of decorin in control cultures.	Glycosaminoglycans	110-127	transforming growth factor beta-1 proprotein	Canis lupus familiaris	38-48
12560570-4	2003	orf c is located between the 5" long terminal repeat and gag.	Glycosaminoglycans	57-60	hypothetical protein	Walleye dermal sarcoma virus	0-5
12594955-3	2003	When Rev activity level was reduced by virtue of amino acid alterations in the Rev protein sequence, infected cells were more resistant to anti-Gag and anti-Env CTL killing.	Glycosaminoglycans	144-147	Rev	Human immunodeficiency virus 1	5-8
12594955-3	2003	When Rev activity level was reduced by virtue of amino acid alterations in the Rev protein sequence, infected cells were more resistant to anti-Gag and anti-Env CTL killing.	Glycosaminoglycans	144-147	Rev	Human immunodeficiency virus 1	79-82
12552001-0	2003	Molluscum contagiosum virus interleukin-18 (IL-18) binding protein is secreted as a full-length form that binds cell surface glycosaminoglycans through the C-terminal tail and a furin-cleaved form with only the IL-18 binding domain.	Glycosaminoglycans	125-143	interleukin 18	Homo sapiens	28-42
12552001-0	2003	Molluscum contagiosum virus interleukin-18 (IL-18) binding protein is secreted as a full-length form that binds cell surface glycosaminoglycans through the C-terminal tail and a furin-cleaved form with only the IL-18 binding domain.	Glycosaminoglycans	125-143	interleukin 18	Homo sapiens	44-49
12596720-3	2003	In this study we genetically characterized a set of samples displaying the culture-negative phenotype by sequencing the nucleotides of three genomic regions: the p17 region of the gag gene, the C2V3C3 fragment of the env gene, and the nef gene.	Glycosaminoglycans	180-183	family with sequence similarity 72 member B	Homo sapiens	162-165
12609485-0	2003	TorsinA protein and neuropathology in early onset generalized dystonia with GAG deletion.	Glycosaminoglycans	76-79	torsin family 1 member A	Homo sapiens	0-7
12446672-6	2003	Transfection of the CSGalNAcT-1 gene into Chinese hamster ovary cells yielded a change of glycosaminoglycan composition, i.e. the replacement of heparan sulfate on a syndecan-4/fibroblast growth factor-1 chimera protein by chondroitin sulfate, however, transfection of the CSGalNAcT-2 gene did not.	Glycosaminoglycans	90-107	chondroitin sulfate N-acetylgalactosaminyltransferase 1	Cricetulus griseus	20-31
12446672-6	2003	Transfection of the CSGalNAcT-1 gene into Chinese hamster ovary cells yielded a change of glycosaminoglycan composition, i.e. the replacement of heparan sulfate on a syndecan-4/fibroblast growth factor-1 chimera protein by chondroitin sulfate, however, transfection of the CSGalNAcT-2 gene did not.	Glycosaminoglycans	90-107	syndecan-4	Cricetulus griseus	166-176
12446672-6	2003	Transfection of the CSGalNAcT-1 gene into Chinese hamster ovary cells yielded a change of glycosaminoglycan composition, i.e. the replacement of heparan sulfate on a syndecan-4/fibroblast growth factor-1 chimera protein by chondroitin sulfate, however, transfection of the CSGalNAcT-2 gene did not.	Glycosaminoglycans	90-107	fibroblast growth factor 1	Cricetulus griseus	177-203
12446672-6	2003	Transfection of the CSGalNAcT-1 gene into Chinese hamster ovary cells yielded a change of glycosaminoglycan composition, i.e. the replacement of heparan sulfate on a syndecan-4/fibroblast growth factor-1 chimera protein by chondroitin sulfate, however, transfection of the CSGalNAcT-2 gene did not.	Glycosaminoglycans	90-107	chondroitin sulfate N-acetylgalactosaminyltransferase 2	Cricetulus griseus	273-284
12527107-3	2003	Here we investigated whether galectin-1 (1) interacts with glycosaminoglycan (GAG) chains, (2) cross-links between ligands and facilitates the incorporation of GAGs, vitronectin and plasma fibronectin in the ECM of vascular SMCs.	Glycosaminoglycans	59-76	galectin 1	Homo sapiens	29-39
12527107-3	2003	Here we investigated whether galectin-1 (1) interacts with glycosaminoglycan (GAG) chains, (2) cross-links between ligands and facilitates the incorporation of GAGs, vitronectin and plasma fibronectin in the ECM of vascular SMCs.	Glycosaminoglycans	78-81	galectin 1	Homo sapiens	29-39
14618028-4	2003	We functionally evaluated CXCR3/CXCL10 and CXCR5/CXCL13 receptor/ligand pairs by analysing cell proliferation and the release of N-acetyl-beta-D-glucosaminidase (NAG), an enzyme that degrades glycosaminoglycans and hyaluronic acid.	Glycosaminoglycans	192-210	C-X-C motif chemokine receptor 3	Homo sapiens	26-31
12765780-3	2003	Bk carries a glycosaminoglycan (GAG) chain, which is linked by ester bonds to the heavy chains of I alpha I.	Glycosaminoglycans	13-30	alpha-1-microglobulin/bikunin precursor	Homo sapiens	0-2
12765780-3	2003	Bk carries a glycosaminoglycan (GAG) chain, which is linked by ester bonds to the heavy chains of I alpha I.	Glycosaminoglycans	32-35	alpha-1-microglobulin/bikunin precursor	Homo sapiens	0-2
12765780-4	2003	Furthermore, Bk, I alpha I and related components such as pre-alpha-inhibitor (P alpha I), all together making up the I alpha I family, present antiinflammatory and antimetastatic effects that hinge on this GAG chain.	Glycosaminoglycans	207-210	alpha-1-microglobulin/bikunin precursor	Homo sapiens	13-15
12765780-7	2003	268 (2001) 2717), we provided evidence that, during acute phase response, the GAG chain of Bk, which is a low-sulphated chondroitin-sulphate, increases in size according to the severity of the inflammatory disease.	Glycosaminoglycans	78-81	alpha-1-microglobulin/bikunin precursor	Homo sapiens	91-93
12765780-9	2003	In this work, we have more extensively analysed the GAG chain of Bk isolated from urine collected from a unique patient with septic shock.	Glycosaminoglycans	52-55	alpha-1-microglobulin/bikunin precursor	Homo sapiens	65-67
12765780-10	2003	Using MALDI-TOF-MS and HPLC analyses of chondrodisaccharides released by enzymatic digestion, we have demonstrated that the GAG chain is clearly modified; it consists of 20 +/- 5 disaccharide units vs. 14 +/- 3 for reference Bk originating from healthy donors.	Glycosaminoglycans	124-127	alpha-1-microglobulin/bikunin precursor	Homo sapiens	225-227
12765780-12	2003	Therefore, the non-sulphated region of the GAG chain, which is located towards its non-reducing end, where the heavy chains are positioned, is lengthened from 9 for reference Bk to 17 disaccharide units.	Glycosaminoglycans	43-46	alpha-1-microglobulin/bikunin precursor	Homo sapiens	175-177
14618028-4	2003	We functionally evaluated CXCR3/CXCL10 and CXCR5/CXCL13 receptor/ligand pairs by analysing cell proliferation and the release of N-acetyl-beta-D-glucosaminidase (NAG), an enzyme that degrades glycosaminoglycans and hyaluronic acid.	Glycosaminoglycans	192-210	O-GlcNAcase	Homo sapiens	129-160
12952196-4	2003	Both decorin and biglycan demonstrated a strong association for HAP, predominately facilitated through the glycosaminoglycan chains.	Glycosaminoglycans	107-124	biglycan	Homo sapiens	17-25
14979058-4	2003	TNF alpha and IL1 beta are major components of the inflammatory process: TNF alpha is an important stimulus of cells producing inflammatory mediators (cytokines, metalloproteinases, NO, PGE2,...) and IL1 beta mediates cartilage and bone destruction (via secretion of metalloproteinases, decrease synthesis of glycosaminoglycans...).	Glycosaminoglycans	309-327	tumor necrosis factor	Homo sapiens	0-9
14979058-4	2003	TNF alpha and IL1 beta are major components of the inflammatory process: TNF alpha is an important stimulus of cells producing inflammatory mediators (cytokines, metalloproteinases, NO, PGE2,...) and IL1 beta mediates cartilage and bone destruction (via secretion of metalloproteinases, decrease synthesis of glycosaminoglycans...).	Glycosaminoglycans	309-327	interleukin 1 beta	Homo sapiens	14-22
14979058-4	2003	TNF alpha and IL1 beta are major components of the inflammatory process: TNF alpha is an important stimulus of cells producing inflammatory mediators (cytokines, metalloproteinases, NO, PGE2,...) and IL1 beta mediates cartilage and bone destruction (via secretion of metalloproteinases, decrease synthesis of glycosaminoglycans...).	Glycosaminoglycans	309-327	tumor necrosis factor	Homo sapiens	73-82
14979058-4	2003	TNF alpha and IL1 beta are major components of the inflammatory process: TNF alpha is an important stimulus of cells producing inflammatory mediators (cytokines, metalloproteinases, NO, PGE2,...) and IL1 beta mediates cartilage and bone destruction (via secretion of metalloproteinases, decrease synthesis of glycosaminoglycans...).	Glycosaminoglycans	309-327	interleukin 1 beta	Homo sapiens	200-208
15043208-8	2003	Key area in the process include interactions with TSG101, L domain receptor which normally functions in the endosomal sorting pathway and with lipid rafts, a type of M domain receptor, which has been suggested to be the sites for effective concentration of Gag.	Glycosaminoglycans	257-260	tumor susceptibility 101	Homo sapiens	50-56
12583005-8	2003	Competitive solid phase assay showed that, among the glycosaminoglycans tested, heparin exhibits the highest affinity binding to bFGF (IC(50) = 6.4 nM).	Glycosaminoglycans	53-71	fibroblast growth factor 2	Homo sapiens	129-133
12560894-8	2003	The glycosaminoglycan content of the repair tissue was also significantly higher in the liposomal TGFbeta1 group than in the other groups.	Glycosaminoglycans	4-21	LOW QUALITY PROTEIN: transforming growth factor beta-1	Oryctolagus cuniculus	98-106
12634322-3	2003	The labeled glycosaminoglycans were fractionated by MK-agarose affinity chromatography to a weakly binding fraction, which was eluted by 0.5 M NaCl, and a strongly binding fraction, which was eluted by higher NaCl concentrations.	Glycosaminoglycans	12-30	midkine	Homo sapiens	52-54
12514214-2	2003	The extracellular domain of the NG2 core protein contains three subdomains: an N-terminal globular domain (domain 1), a central extended domain that has the sites for glycosaminoglycan (GAG) attachment (domain 2), and a juxtamembrane domain (domain 3).	Glycosaminoglycans	167-184	chondroitin sulfate proteoglycan 4	Homo sapiens	32-35
12514214-2	2003	The extracellular domain of the NG2 core protein contains three subdomains: an N-terminal globular domain (domain 1), a central extended domain that has the sites for glycosaminoglycan (GAG) attachment (domain 2), and a juxtamembrane domain (domain 3).	Glycosaminoglycans	186-189	chondroitin sulfate proteoglycan 4	Homo sapiens	32-35
12589770-4	2003	The deduced polypeptide sequence of mouse SPACRCAN contains a signal peptide at the N-terminal, seven N-link glycosylation sites, numerous potential O-linked glycosylation sites in a central mucin-like domain, two glycosaminoglycan attachment sites, five potential hyaluronan-binding motifs, two epidermal growth factor-like domains, and a hydrophobic stretch of 23 amino acids near the C-terminal.	Glycosaminoglycans	214-231	interphotoreceptor matrix proteoglycan 2	Mus musculus	42-50
12634322-0	2003	Glycosaminoglycan structures required for strong binding to midkine, a heparin-binding growth factor.	Glycosaminoglycans	0-17	midkine	Homo sapiens	60-67
12502804-6	2003	For Gag p24, a correlation was seen between better T-cell responses and lower plasma viral load.	Glycosaminoglycans	4-7	transmembrane p24 trafficking protein 2	Homo sapiens	8-11
12502804-8	2003	At the level of the HLA supertypes, a lower viral load was associated with higher T-cell responses to Gag p24 within the HLA A2, A24, B27, and B58 supertypes, in contrast to the absence of such a correlation within the HLA B44 supertype.	Glycosaminoglycans	102-105	transmembrane p24 trafficking protein 2	Homo sapiens	106-109
12502804-8	2003	At the level of the HLA supertypes, a lower viral load was associated with higher T-cell responses to Gag p24 within the HLA A2, A24, B27, and B58 supertypes, in contrast to the absence of such a correlation within the HLA B44 supertype.	Glycosaminoglycans	102-105	melanocortin 2 receptor accessory protein	Homo sapiens	134-137
12504576-6	2002	Both retroviruses were detected in the central nervous systems of some animals, either by culture or by direct antigen capture for p19 Gag in cerebrospinal fluid.	Glycosaminoglycans	135-138	interleukin 23 subunit alpha	Homo sapiens	131-134
14579589-0	2003	Recognition of glycosaminoglycans by midkine.	Glycosaminoglycans	15-33	midkine	Homo sapiens	37-44
12529415-0	2003	Interleukin-1beta induces glycosaminoglycan synthesis via the prostaglandin E2 pathway in cultured human cervical fibroblasts.	Glycosaminoglycans	26-43	interleukin 1 beta	Homo sapiens	0-17
12529415-1	2003	The aim of this study was to identify, in cultured human cervical fibroblasts, the mechanisms by which interleukin (IL)-1beta induces the synthesis of glycosaminoglycans (GAG) and to explore the putative role of prostaglandin E(2) (PGE(2)) in this process.	Glycosaminoglycans	151-169	interleukin 1 beta	Homo sapiens	103-125
12529415-1	2003	The aim of this study was to identify, in cultured human cervical fibroblasts, the mechanisms by which interleukin (IL)-1beta induces the synthesis of glycosaminoglycans (GAG) and to explore the putative role of prostaglandin E(2) (PGE(2)) in this process.	Glycosaminoglycans	171-174	interleukin 1 beta	Homo sapiens	103-125
12529415-2	2003	Exposure of the cells for 24 h to IL-1beta induced a significant (P &lt; 0.05) dose-dependent increase in GAG synthesis.	Glycosaminoglycans	106-109	interleukin 1 beta	Homo sapiens	34-42
12529415-5	2003	AH23848, the selective EP(4) receptor antagonist, completely abolished IL-1beta-induced GAG synthesis, whereas AH6809, an EP(2) receptor antagonist, had no effect on the stimulatory effects of IL-1beta.	Glycosaminoglycans	88-91	interleukin 1 beta	Homo sapiens	71-79
12529415-7	2003	In conclusion, these findings indicate that IL-1beta not only induced GAG synthesis by increasing COX-2 protein expression and the subsequent PGE(2) production but also enhanced the responsiveness of cervical fibroblasts to PGE(2) by selectively up-regulating EP(4) receptor mRNA expression.	Glycosaminoglycans	70-73	interleukin 1 beta	Homo sapiens	44-52
12529415-7	2003	In conclusion, these findings indicate that IL-1beta not only induced GAG synthesis by increasing COX-2 protein expression and the subsequent PGE(2) production but also enhanced the responsiveness of cervical fibroblasts to PGE(2) by selectively up-regulating EP(4) receptor mRNA expression.	Glycosaminoglycans	70-73	prostaglandin-endoperoxide synthase 2	Homo sapiens	98-103
15013278-0	2003	Prolonged bleeding time induced by anticoagulant glycosaminoglycans in dogs is associated with the inhibition of thrombin-induced platelet aggregation.	Glycosaminoglycans	49-67	coagulation factor II, thrombin	Homo sapiens	113-121
12529676-6	2003	Pretreatment of 4LHBMEC with glycosaminoglycan (GAG)-degrading enzymes or sodium chlorate demonstrated that SDF-1 bound to both HSPGs and CS/DSPGs in a sulfation-dependent manner, as determined with an SDF-1 antibody recognizing the CXCR4-binding site.	Glycosaminoglycans	29-46	C-X-C motif chemokine ligand 12	Homo sapiens	108-113
12529676-6	2003	Pretreatment of 4LHBMEC with glycosaminoglycan (GAG)-degrading enzymes or sodium chlorate demonstrated that SDF-1 bound to both HSPGs and CS/DSPGs in a sulfation-dependent manner, as determined with an SDF-1 antibody recognizing the CXCR4-binding site.	Glycosaminoglycans	48-51	C-X-C motif chemokine ligand 12	Homo sapiens	108-113
12441836-7	2002	Thyrotropin receptor antigen on fibroblasts diffusely in the body is causative in TAO and pretibial myxedema with even increased urinary secretion of glycosaminoglycans.	Glycosaminoglycans	150-168	thyroid stimulating hormone receptor	Homo sapiens	0-20
12490399-6	2002	Furthermore, we compared transduction efficiencies of vectors containing different portions of the BIV Gag coding region and found that the first 104 bp of gag contains a functional part of the BIV packaging signal.	Glycosaminoglycans	156-159	gag polyprotein	Bovine immunodeficiency virus	103-106
12482841-9	2002	Heparin-releasable TFPI likely represents only a small portion of the total TFPI on endothelium that remains attached to cell-surface glycosaminoglycans after cleavage of the GPI anchor by endogenous enzymes.	Glycosaminoglycans	134-152	tissue factor pathway inhibitor	Homo sapiens	19-23
12414995-3	2002	Here we show that GDNF requires glycosaminoglycans as well as the already-known components of its receptor complex, c-Ret and GFRalpha-1.	Glycosaminoglycans	32-50	glial cell derived neurotrophic factor	Rattus norvegicus	18-22
12490222-1	2002	Yam (Dioscorea batatas) mucopolysaccharide (YMP) was examined for the ability to induce secretory and cellular responses in murine peritoneal macrophages.	Glycosaminoglycans	24-42	epithelial membrane protein 3	Mus musculus	44-47
12489800-0	2002	Glycosaminoglycans affect the action of human plasma kallikrein on kininogen hydrolysis and inflammation.	Glycosaminoglycans	0-18	kallikrein B1	Homo sapiens	46-63
12489800-3	2002	BK generation may be influenced by several agents, and the aim of this work was to investigate the effect of glycosaminoglycans (GAGs) on human high-molecular-weight kininogen (HK) hydrolysis by huPK and on inflammation.	Glycosaminoglycans	109-127	kininogen 1	Homo sapiens	144-175
12466191-7	2002	IGFBP-2, -3, -5, and -6 have heparin-binding domains and can bind glycosaminoglycans.	Glycosaminoglycans	66-84	insulin like growth factor binding protein 2	Homo sapiens	0-23
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
12444145-10	2002	The Gag-specific IFN-gamma(+)IL-2(+) CD4 response also correlated positively with the percentage of Gag-specific IFN-gamma(+) CD8 T cells in these subjects.	Glycosaminoglycans	4-7	interleukin 2	Homo sapiens	29-33
12444145-4	2002	We compared the number/function of Gag p24-specific CD4 T cells in 17 HIV-infected long-term nonprogressors (LTNPs) infected for a median of 14.6 years with those of 16 slow progressors (SPs), also HIV infected for a median of 14 years but whose CD4 count had declined to &lt;500 cells/ micro l. Compared with SPs, LTNPs had higher numbers of specific CD4s that were double positive for IFN-gamma and IL-2 as well as CD28 and IL-2.	Glycosaminoglycans	35-38	CD4 molecule	Homo sapiens	52-55
12444145-10	2002	The Gag-specific IFN-gamma(+)IL-2(+) CD4 response also correlated positively with the percentage of Gag-specific IFN-gamma(+) CD8 T cells in these subjects.	Glycosaminoglycans	4-7	CD4 molecule	Homo sapiens	37-40
12444145-8	2002	The difference between LTNPs and SPs in the Gag p24 IFN-gamma(+)IL-2(+) response was maintained when responses to total Gag (p17 plus p24) were measured.	Glycosaminoglycans	44-47	transmembrane p24 trafficking protein 2	Homo sapiens	48-51
12444145-8	2002	The difference between LTNPs and SPs in the Gag p24 IFN-gamma(+)IL-2(+) response was maintained when responses to total Gag (p17 plus p24) were measured.	Glycosaminoglycans	44-47	interleukin 2	Homo sapiens	52-68
12444145-8	2002	The difference between LTNPs and SPs in the Gag p24 IFN-gamma(+)IL-2(+) response was maintained when responses to total Gag (p17 plus p24) were measured.	Glycosaminoglycans	44-47	transmembrane p24 trafficking protein 2	Homo sapiens	134-137
12444145-8	2002	The difference between LTNPs and SPs in the Gag p24 IFN-gamma(+)IL-2(+) response was maintained when responses to total Gag (p17 plus p24) were measured.	Glycosaminoglycans	120-123	interleukin 2	Homo sapiens	52-68
12444145-10	2002	The Gag-specific IFN-gamma(+)IL-2(+) CD4 response also correlated positively with the percentage of Gag-specific IFN-gamma(+) CD8 T cells in these subjects.	Glycosaminoglycans	4-7	interferon gamma	Homo sapiens	113-122
12444145-10	2002	The Gag-specific IFN-gamma(+)IL-2(+) CD4 response also correlated positively with the percentage of Gag-specific IFN-gamma(+) CD8 T cells in these subjects.	Glycosaminoglycans	4-7	CD8a molecule	Homo sapiens	126-129
12457961-6	2002	Immunoprecipitation analysis of 35S-pulse labeled, CAEV-infected goat synovial membrane (GSM) cells indicates that Rev-C is more abundant than is Gag at 12 h post-infection (PI); at later times PI Gag predominates.	Glycosaminoglycans	197-200	rev protein	Visna-maedi virus	115-118
12444145-9	2002	The percentage and absolute number of Gag-specific IFN-gamma(+)IL-2(+) but not of IFN-gamma(+)IL-2(-) CD4s correlated inversely with virus load.	Glycosaminoglycans	38-41	interferon gamma	Homo sapiens	51-60
12444145-9	2002	The percentage and absolute number of Gag-specific IFN-gamma(+)IL-2(+) but not of IFN-gamma(+)IL-2(-) CD4s correlated inversely with virus load.	Glycosaminoglycans	38-41	interleukin 2	Homo sapiens	63-67
12444145-10	2002	The Gag-specific IFN-gamma(+)IL-2(+) CD4 response also correlated positively with the percentage of Gag-specific IFN-gamma(+) CD8 T cells in these subjects.	Glycosaminoglycans	4-7	interferon gamma	Homo sapiens	17-26
12395090-8	2002	These results indicate that interaction with glycosaminoglycans such as heparin affects GDNF signal transduction positively.	Glycosaminoglycans	45-63	glial cell derived neurotrophic factor	Homo sapiens	88-92
12215432-1	2002	In mammals, the xylosylprotein beta4-galactosyltransferase termed beta4GalT7 (XgalT-1, EC ) participates in proteoglycan biosynthesis through the transfer of galactose to the xylose that initiates each glycosaminoglycan chain.	Glycosaminoglycans	202-219	beta-4-galactosyltransferase 7	Drosophila melanogaster	66-76
12431052-1	2002	The interaction of a series gag peptide analogues with human cyclophilin A (hCypA) have been studied employing molecular docking and 3D-QSAR approaches.	Glycosaminoglycans	28-31	peptidylprolyl isomerase A	Homo sapiens	76-81
12186633-1	2002	We used ELISA and flow cytometry to study the binding of prion protein PrP to glycosaminoglycans (GAGs).	Glycosaminoglycans	78-96	prion protein	Rattus norvegicus	71-74
12186633-1	2002	We used ELISA and flow cytometry to study the binding of prion protein PrP to glycosaminoglycans (GAGs).	Glycosaminoglycans	98-102	prion protein	Rattus norvegicus	71-74
12186633-2	2002	We found that recombinant human PrP (rPrP) binds GAGs including chondroitin sulphate A, chondroitin sulphate B, hyaluronic acid, and heparin.	Glycosaminoglycans	49-53	prion protein	Homo sapiens	32-35
12186633-2	2002	We found that recombinant human PrP (rPrP) binds GAGs including chondroitin sulphate A, chondroitin sulphate B, hyaluronic acid, and heparin.	Glycosaminoglycans	49-53	prion protein	Rattus norvegicus	37-41
12186633-3	2002	rPrP binding to GAGs occurs via the N-terminus, a region known to bind divalent cations.	Glycosaminoglycans	16-20	prion protein	Rattus norvegicus	0-4
12186633-4	2002	Additionally, rPrP binding to GAGs is enhanced in the presence of Cu2+ and Zn2+, but not Ca2+ and Mn2+.	Glycosaminoglycans	30-34	prion protein	Rattus norvegicus	14-18
12186633-7	2002	We found that GAGs specifically bind to a synthetic peptide corresponding to amino acid residues 23-35 in the N-terminus of rPrP.	Glycosaminoglycans	14-18	prion protein	Rattus norvegicus	124-128
12207034-5	2002	Transfected intact chimeric DCN(M1-Q153)-CSF-1(L241-S353), with two glycosaminoglycan chains, also contained almost exclusively d-glucuronate in chains at both sites, as did chimeras in which alanine was substituted for serine at either of the glycosaminoglycan attachment sites.	Glycosaminoglycans	68-85	decorin	Homo sapiens	28-31
12207034-5	2002	Transfected intact chimeric DCN(M1-Q153)-CSF-1(L241-S353), with two glycosaminoglycan chains, also contained almost exclusively d-glucuronate in chains at both sites, as did chimeras in which alanine was substituted for serine at either of the glycosaminoglycan attachment sites.	Glycosaminoglycans	68-85	colony stimulating factor 1	Homo sapiens	41-46
12207034-7	2002	C-terminal truncation constructs were prepared from the full-length chimera with an alanine substitution at the CSF-1 glycosaminoglycan attachment site.	Glycosaminoglycans	118-135	colony stimulating factor 1	Homo sapiens	112-117
12215437-8	2002	Thus, dermatan sulfate, the predominant glycosaminoglycan in skin, is the principle cofactor for FGF-7.	Glycosaminoglycans	40-57	fibroblast growth factor 7	Homo sapiens	97-102
12231358-2	2002	Successful cloning of the gene in man, mouse, cow and chicken has revealed the existence of at least four splice variants of versican, which differ in the size of the core protein and the number of glycosaminoglycan chains.	Glycosaminoglycans	198-215	versican	Gallus gallus	125-133
12124794-2	2002	This study describes a novel basic fibroblast growth factor-2 (FGF-2) delivery system synthesized by the conjugation of a structure-stabilizing polymer, hyaluronate (HA), with a sulfated glycosaminoglycan, heparin (HP), that has inherent specific binding sites for members of the FGF family.	Glycosaminoglycans	187-204	fibroblast growth factor 2	Homo sapiens	35-61
12244071-8	2002	These results showed that Drosophila encodes an ortholog of human beta4-galactosyltransferase-VII, also known as galactosyltransferase I, which participates in proteoglycan biosynthesis by transferring the first galactose to xylose in the linkage tetrasaccharide of glycosaminoglycan side chains.	Glycosaminoglycans	266-283	beta-1,4-galactosyltransferase 7	Homo sapiens	113-136
12244074-6	2002	In the SR91 myeloid cell line, the majority of CD44 sulfation was attributed to the glycosaminoglycan chondroitin sulfate.	Glycosaminoglycans	84-101	CD44 molecule (Indian blood group)	Homo sapiens	47-51
12124794-2	2002	This study describes a novel basic fibroblast growth factor-2 (FGF-2) delivery system synthesized by the conjugation of a structure-stabilizing polymer, hyaluronate (HA), with a sulfated glycosaminoglycan, heparin (HP), that has inherent specific binding sites for members of the FGF family.	Glycosaminoglycans	187-204	fibroblast growth factor 2	Homo sapiens	63-68
12124794-2	2002	This study describes a novel basic fibroblast growth factor-2 (FGF-2) delivery system synthesized by the conjugation of a structure-stabilizing polymer, hyaluronate (HA), with a sulfated glycosaminoglycan, heparin (HP), that has inherent specific binding sites for members of the FGF family.	Glycosaminoglycans	187-204	fibroblast growth factor 2	Homo sapiens	63-66
12351944-8	2002	The percentage of HIV-specific CD8 T cells also significantly correlated with the percentage of Gag-specific cytotoxicity measured by the traditional Cr release assay.	Glycosaminoglycans	96-99	CD8a molecule	Homo sapiens	31-34
12481989-0	2002	Multiple founder effects in Japanese families with primary torsion dystonia harboring the GAG deletion in the Tor1A (DYT1) gene.	Glycosaminoglycans	90-93	torsin family 1 member A	Homo sapiens	110-115
12481989-0	2002	Multiple founder effects in Japanese families with primary torsion dystonia harboring the GAG deletion in the Tor1A (DYT1) gene.	Glycosaminoglycans	90-93	torsin family 1 member A	Homo sapiens	117-121
12360559-6	2002	One family member, carrier of the GAG mutation on DYT1 gene and mother of the most severely affected individual, presented with a clinically established psychogenic movement disorder resembling dystonia initially diagnosed as a severe generalized PTD.	Glycosaminoglycans	34-37	torsin family 1 member A	Homo sapiens	50-54
12359050-5	2002	Sequencing of all coding exons of the p53 gene demonstrated only a neutral genetic polymorphism, i.e. a G-to-A substitution (GAG to GAA) at nucleotide position 13 432.	Glycosaminoglycans	125-128	tumor protein p53	Homo sapiens	38-41
12225748-10	2002	In a manner analogous to SL-3, we propose that conformational flexibility at this site may facilitate melting of the structure during Gag protein capture or genomic RNA dimerisation.	Glycosaminoglycans	134-137	matrix metallopeptidase 11	Homo sapiens	25-29
12217035-8	2002	Cell culture studies show that chondrocytes cultured in ELP coacervate maintain a rounded morphology and their chondrocytic phenotype, characterized by the synthesis of a significant amount of extracellular matrix composed of sulfated glycosaminoglycans and collagen.	Glycosaminoglycans	235-253	nuclear receptor subfamily 5 group A member 1	Homo sapiens	56-59
12228017-7	2002	IGF-I constructs contained increased amounts of glycosaminoglycans and collagen and confined-compression equilibrium moduli as compared with controls; all groups had subnormal cellularity.	Glycosaminoglycans	48-66	insulin like growth factor 1	Homo sapiens	0-5
12228017-8	2002	The amounts of glycosaminoglycans and collagen per unit DNA in IGF-I constructs were markedly higher than in constructs cultured in serum-supplemented medium or native cartilage.	Glycosaminoglycans	15-33	insulin like growth factor 1	Homo sapiens	63-68
13679662-1	2002	Dermatan sulphate (DS) is a glycosaminoglycan which selectively catalyzes the inactivation of thrombin by Heparin Cofactor II without interacting with Antithrombin III.	Glycosaminoglycans	28-45	coagulation factor II, thrombin	Homo sapiens	94-102
12169660-5	2002	HCII inhibits thrombin, the final protease of the coagulation cascade, in a glycosaminoglycan-dependent manner that involves the release of a sequestered hirudin-like N-terminal tail for interaction with thrombin.	Glycosaminoglycans	76-93	serpin family D member 1	Homo sapiens	0-4
12070165-5	2002	In vitro studies have identified five clusters of basic amino acids in delipidated apoB48 that bind negatively charged glycosaminoglycans.	Glycosaminoglycans	119-137	apolipoprotein B	Homo sapiens	83-89
12169660-5	2002	HCII inhibits thrombin, the final protease of the coagulation cascade, in a glycosaminoglycan-dependent manner that involves the release of a sequestered hirudin-like N-terminal tail for interaction with thrombin.	Glycosaminoglycans	76-93	coagulation factor II, thrombin	Homo sapiens	14-22
12169660-5	2002	HCII inhibits thrombin, the final protease of the coagulation cascade, in a glycosaminoglycan-dependent manner that involves the release of a sequestered hirudin-like N-terminal tail for interaction with thrombin.	Glycosaminoglycans	76-93	coagulation factor II, thrombin	Homo sapiens	204-212
12153565-4	2002	The newly found isoforms of biglycan have a smaller core protein substituted with smaller glycosaminoglycan chains, migrating on SDS/PAGE at between 110 and 200 kDa.	Glycosaminoglycans	90-107	biglycan	Homo sapiens	28-36
12000311-5	2002	In chlorate-treated, and hence sulphated, glycosaminoglycan-deficient cells, FGF-2 alone or in the presence of disaccharides did not stimulate DNA synthesis and it only elicited an early transient dual phosphorylation of p42/44 mitogen-activated protein kinase (MAPK).	Glycosaminoglycans	42-59	fibroblast growth factor 2	Rattus norvegicus	77-82
12171167-4	2002	Northern blot analysis was used to quantify the expression of COX-2 in first-passage cultures of equine articular chondrocytes propagated in media containing dexamethasone (DEX), phenylbutazone (PBZ), polysulfated glycosaminoglycan, and hyaluronan, each at concentrations of 10 and 100 microg/ml and each with or without reIL-1beta.	Glycosaminoglycans	214-231	cytochrome c oxidase subunit II	Equus caballus	62-67
12153565-10	2002	Structural analysis shows that these glycosaminoglycan chains contain a lower proportion of iduronic acid (61%) relative to glucuronic acid when compared to the glycosaminoglycan chain of the predominant form of biglycan (71%).	Glycosaminoglycans	161-178	biglycan	Homo sapiens	212-220
12413592-8	2002	In contrast, HCII does not require Arg(93), Arg(97) and Arg(101) of thrombin exosite-2 and further supports the hypothesis that HCII uses an allosteric process following glycosaminoglycan binding to inhibit thrombin.	Glycosaminoglycans	170-187	serpin family D member 1	Homo sapiens	13-17
12430897-5	2002	Ryudocan is a cell surface heparan sulfate proteoglycan, which bears heparin-like glycosaminoglycan (heparan sulfate) cahins, originally cloned from rat microvascular endothelial cells.	Glycosaminoglycans	82-99	syndecan 4	Mus musculus	0-8
12133622-6	2002	Such binding was dependent on cell surface glycosaminoglycans (GAGs) since it was reduced when macrophages or HeLa cells expressing or not CCR5 were first treated with GAG-specific enzymes.	Glycosaminoglycans	43-61	C-C motif chemokine receptor 5	Homo sapiens	139-143
12133622-6	2002	Such binding was dependent on cell surface glycosaminoglycans (GAGs) since it was reduced when macrophages or HeLa cells expressing or not CCR5 were first treated with GAG-specific enzymes.	Glycosaminoglycans	63-67	C-C motif chemokine receptor 5	Homo sapiens	139-143
12133622-6	2002	Such binding was dependent on cell surface glycosaminoglycans (GAGs) since it was reduced when macrophages or HeLa cells expressing or not CCR5 were first treated with GAG-specific enzymes.	Glycosaminoglycans	63-66	C-C motif chemokine receptor 5	Homo sapiens	139-143
12213118-5	2002	Polysulphated glycosaminoglycan reversed the concentration-related suppression of proteoglycan synthesis induced by interleukin-1beta.	Glycosaminoglycans	14-31	interleukin-1 beta	Equus caballus	116-133
12139612-4	2002	On Kupffer cells, CS protein predominantly recognizes chondroitin sulphate, whereas TRAP binding is glycosaminoglycan independent.	Glycosaminoglycans	100-117	TRAP	Homo sapiens	84-88
12201997-9	2002	Redifferentiation with SFM with IGF-I and TGFbeta-2 showed high collagen type II expression and high GAG/DNA production regardless of which expansion medium had been used.	Glycosaminoglycans	101-104	insulin like growth factor 1	Homo sapiens	32-37
12201997-9	2002	Redifferentiation with SFM with IGF-I and TGFbeta-2 showed high collagen type II expression and high GAG/DNA production regardless of which expansion medium had been used.	Glycosaminoglycans	101-104	transforming growth factor beta 2	Homo sapiens	42-51
12201999-3	2002	Addition of 100 ng/mL of BMP-2, BMP-12, or BMP-13 increased the total mass of the constructs relative to the controls by 121%, 80%, and 62%, respectively, which was accompanied by increases in the absolute amounts of collagen, glycosaminoglycans (GAG), and cells.	Glycosaminoglycans	227-245	bone morphogenetic protein 2	Bos taurus	25-30
12201999-3	2002	Addition of 100 ng/mL of BMP-2, BMP-12, or BMP-13 increased the total mass of the constructs relative to the controls by 121%, 80%, and 62%, respectively, which was accompanied by increases in the absolute amounts of collagen, glycosaminoglycans (GAG), and cells.	Glycosaminoglycans	227-245	growth differentiation factor 6	Bos taurus	43-49
12201999-3	2002	Addition of 100 ng/mL of BMP-2, BMP-12, or BMP-13 increased the total mass of the constructs relative to the controls by 121%, 80%, and 62%, respectively, which was accompanied by increases in the absolute amounts of collagen, glycosaminoglycans (GAG), and cells.	Glycosaminoglycans	247-250	bone morphogenetic protein 2	Bos taurus	25-30
12201999-3	2002	Addition of 100 ng/mL of BMP-2, BMP-12, or BMP-13 increased the total mass of the constructs relative to the controls by 121%, 80%, and 62%, respectively, which was accompanied by increases in the absolute amounts of collagen, glycosaminoglycans (GAG), and cells.	Glycosaminoglycans	247-250	growth differentiation factor 6	Bos taurus	43-49
12201999-4	2002	The addition of 100 ng/mL of BMP-2, BMP-12, or BMP-13 increased the weight percentage of GAG in the constructs by 27%, 18%, and 15%, and decreased the weight percent of total collagen to 63%, 89%, and 83% of controls, respectively.	Glycosaminoglycans	89-92	bone morphogenetic protein 2	Bos taurus	29-34
12201999-4	2002	The addition of 100 ng/mL of BMP-2, BMP-12, or BMP-13 increased the weight percentage of GAG in the constructs by 27%, 18%, and 15%, and decreased the weight percent of total collagen to 63%, 89%, and 83% of controls, respectively.	Glycosaminoglycans	89-92	growth differentiation factor 6	Bos taurus	47-53
11986319-1	2002	The human beta1,3-glucuronosyltransferase I (GlcAT-I) plays a key role in proteoglycan biosynthesis by catalyzing the transfer of glucuronic acid onto the trisaccharide-protein linkage structure Galbeta1,3Galbeta1,4Xylbeta-O-Ser, a prerequisite step for polymerization of glycosaminoglycan chains.	Glycosaminoglycans	272-289	beta-1,3-glucuronyltransferase 3	Homo sapiens	45-52
12413592-1	2002	Antithrombin (ATIII), heparin cofactor II (HCII) and protein C inhibitor (PCI; also named plasminogen activator inhibitor-3) are serine protease inhibitors (serpins) whose thrombin inhibition activity is accelerated in the presence of glycosaminoglycans.	Glycosaminoglycans	235-253	serpin family C member 1	Homo sapiens	0-12
12413592-1	2002	Antithrombin (ATIII), heparin cofactor II (HCII) and protein C inhibitor (PCI; also named plasminogen activator inhibitor-3) are serine protease inhibitors (serpins) whose thrombin inhibition activity is accelerated in the presence of glycosaminoglycans.	Glycosaminoglycans	235-253	serpin family C member 1	Homo sapiens	14-19
12413592-1	2002	Antithrombin (ATIII), heparin cofactor II (HCII) and protein C inhibitor (PCI; also named plasminogen activator inhibitor-3) are serine protease inhibitors (serpins) whose thrombin inhibition activity is accelerated in the presence of glycosaminoglycans.	Glycosaminoglycans	235-253	serpin family D member 1	Homo sapiens	22-41
12413592-1	2002	Antithrombin (ATIII), heparin cofactor II (HCII) and protein C inhibitor (PCI; also named plasminogen activator inhibitor-3) are serine protease inhibitors (serpins) whose thrombin inhibition activity is accelerated in the presence of glycosaminoglycans.	Glycosaminoglycans	235-253	serpin family D member 1	Homo sapiens	43-47
12413592-1	2002	Antithrombin (ATIII), heparin cofactor II (HCII) and protein C inhibitor (PCI; also named plasminogen activator inhibitor-3) are serine protease inhibitors (serpins) whose thrombin inhibition activity is accelerated in the presence of glycosaminoglycans.	Glycosaminoglycans	235-253	serpin family A member 5	Homo sapiens	53-72
12413592-1	2002	Antithrombin (ATIII), heparin cofactor II (HCII) and protein C inhibitor (PCI; also named plasminogen activator inhibitor-3) are serine protease inhibitors (serpins) whose thrombin inhibition activity is accelerated in the presence of glycosaminoglycans.	Glycosaminoglycans	235-253	serpin family A member 5	Homo sapiens	74-77
12413592-1	2002	Antithrombin (ATIII), heparin cofactor II (HCII) and protein C inhibitor (PCI; also named plasminogen activator inhibitor-3) are serine protease inhibitors (serpins) whose thrombin inhibition activity is accelerated in the presence of glycosaminoglycans.	Glycosaminoglycans	235-253	serpin family A member 5	Homo sapiens	90-123
12413592-1	2002	Antithrombin (ATIII), heparin cofactor II (HCII) and protein C inhibitor (PCI; also named plasminogen activator inhibitor-3) are serine protease inhibitors (serpins) whose thrombin inhibition activity is accelerated in the presence of glycosaminoglycans.	Glycosaminoglycans	235-253	coagulation factor II, thrombin	Homo sapiens	4-12
12413592-8	2002	In contrast, HCII does not require Arg(93), Arg(97) and Arg(101) of thrombin exosite-2 and further supports the hypothesis that HCII uses an allosteric process following glycosaminoglycan binding to inhibit thrombin.	Glycosaminoglycans	170-187	serpin family D member 1	Homo sapiens	128-132
12010802-8	2002	The observation that chemically modified AT III that lacks heparin-binding capacity had no effect on NF-kappaB activation supports the current understanding that the inhibitory potency of AT III depends on the interaction of AT III with heparinlike cell surface glycosaminoglycans.	Glycosaminoglycans	262-280	serpin family C member 1	Homo sapiens	188-194
12097281-2	2002	Analogs of syndecan-1 were produced by carbodiimide (EDAC) conjugation of glycosaminoglycan (GAG) chains to a protein scaffold, thereby generating synthetic proteoglycans that were evaluated for anticancer properties.	Glycosaminoglycans	74-91	syndecan 1	Mus musculus	11-21
12097281-2	2002	Analogs of syndecan-1 were produced by carbodiimide (EDAC) conjugation of glycosaminoglycan (GAG) chains to a protein scaffold, thereby generating synthetic proteoglycans that were evaluated for anticancer properties.	Glycosaminoglycans	93-96	syndecan 1	Mus musculus	11-21
12077357-0	2002	Midkine, a heparin-binding growth factor, promotes growth and glycosaminoglycan synthesis of endothelial cells through its action on smooth muscle cells in an artificial blood vessel model.	Glycosaminoglycans	62-79	midkine	Homo sapiens	0-7
12270764-12	2002	CONCLUSIONS: We conclude, therefore, that the apparent decrease in cTnT values by addition of heparin is a result of direct molecular interaction between the negatively charged glycosaminoglycan and clusters of basic residues within the sequence of the cardiac protein.	Glycosaminoglycans	177-194	troponin T2, cardiac type	Homo sapiens	67-71
12069613-0	2002	Inhibition of apolipoprotein E-related neurotoxicity by glycosaminoglycans and their oligosaccharides.	Glycosaminoglycans	56-74	apolipoprotein E	Homo sapiens	14-30
12069613-5	2002	The possibility that heparin inhibition of toxicity is mediated by a specific oligosaccharide sequence was investigated using a bioassay to determine the inhibition of apoE peptide toxicity by glycosaminoglycans and purified glycosaminoglycan oligosaccharides.	Glycosaminoglycans	193-211	apolipoprotein E	Homo sapiens	168-172
12010802-8	2002	The observation that chemically modified AT III that lacks heparin-binding capacity had no effect on NF-kappaB activation supports the current understanding that the inhibitory potency of AT III depends on the interaction of AT III with heparinlike cell surface glycosaminoglycans.	Glycosaminoglycans	262-280	serpin family C member 1	Homo sapiens	188-194
12010802-9	2002	This hypothesis was underscored by the finding that the AT III beta-isoform, known to have higher affinity for glycosaminoglycans, is more effective in preventing NF-kappaB transactivation than alpha-AT III.	Glycosaminoglycans	111-129	serpin family C member 1	Homo sapiens	56-62
12010802-9	2002	This hypothesis was underscored by the finding that the AT III beta-isoform, known to have higher affinity for glycosaminoglycans, is more effective in preventing NF-kappaB transactivation than alpha-AT III.	Glycosaminoglycans	111-129	nuclear factor kappa B subunit 1	Homo sapiens	163-172
12029153-4	2002	After intranasal immunization with a recombinant SeV expressing simian immunodeficiency virus Gag protein, SeV-Gag, robust gag expression was observed in the nasal mucosa and much lower but significant levels of gag expression were observed in the local retropharyngeal and submandibular lymph nodes (LN).	Glycosaminoglycans	123-126	melanoma antigen	Mus musculus	111-114
12036722-10	2002	Some extracellular glycosaminoglycans and serum interfere with 1,4-DHP-amphiphile-mediated transfection by destabilizing the amphiplexes.	Glycosaminoglycans	19-37	dihydropyrimidinase	Homo sapiens	67-70
12045489-2	2002	METHODS: Subpopulations of CD3 and intracellular p24 gag-positive cells in human lymphoid tissue infected ex vivo with X4 HIV-1 variant NL4-3 and R5 HIV-1 variant AD8 were analysed for expression of the T cell memory markers CD45RO and CD45RA, the T cell homing receptor for lymphoid tissue CD62L, and the HIV-1 coreceptors CCR5 and CXCR4.	Glycosaminoglycans	53-56	neurensin 1	Homo sapiens	49-52
12029153-4	2002	After intranasal immunization with a recombinant SeV expressing simian immunodeficiency virus Gag protein, SeV-Gag, robust gag expression was observed in the nasal mucosa and much lower but significant levels of gag expression were observed in the local retropharyngeal and submandibular lymph nodes (LN).	Glycosaminoglycans	212-215	melanoma antigen	Mus musculus	94-97
12023510-0	2002	Hypoxia differentially enhances the effects of transforming growth factor-beta isoforms on the synthesis and secretion of glycosaminoglycans by human lung fibroblasts.	Glycosaminoglycans	122-140	transforming growth factor beta 1	Homo sapiens	47-78
12023510-2	2002	In this study, we investigated the effect of hypoxia (3% O(2)) on TGF-beta-induced GAG synthesis by primary human pulmonary fibroblasts, established from lung biopsies.	Glycosaminoglycans	83-86	transforming growth factor beta 1	Homo sapiens	66-74
11856753-3	2002	Interestingly, D72N/Y73F/D75N rHCII had significantly enhanced thrombin inhibition without glycosaminoglycan (4-fold greater) and with heparin (6-fold greater), showing maximal activity at 2 microg/ml heparin compared with wild-type recombinant HCII (wt-rHCII) with maximal activity at 20 microg/ml heparin.	Glycosaminoglycans	91-108	serpin family D member 1	Homo sapiens	31-35
12021366-1	2002	Cell surface glycosaminoglycans (GAGs), in particular heparan sulfate (HS), have been proposed to mediate the attachment of human immunodeficiency virus type 1 (HIV-1) to target cells prior to virus entry, and both the viral gp120 envelope protein and virion-associated cyclophilin A (CypA) have been shown to directly interact with HS and its analogues.	Glycosaminoglycans	13-31	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	225-230
11856753-0	2002	Aspartic acid residues 72 and 75 and tyrosine-sulfate 73 of heparin cofactor II promote intramolecular interactions during glycosaminoglycan binding and thrombin inhibition.	Glycosaminoglycans	123-140	serpin family D member 1	Homo sapiens	60-79
11856753-8	2002	D72N/Y73F/D75N rHCII and D75K rHCII were significantly more active than wt-rHCII in a plasma-based thrombin inhibition assay with glycosaminoglycans.	Glycosaminoglycans	130-148	coagulation factor II, thrombin	Homo sapiens	99-107
11856753-9	2002	These results indicate that improved thrombin inhibition in the AR2 HCII mutants is mediated by enhanced interactions between the acidic domain and anion-binding exosite-1 of thrombin and that AR2 may be a "molecular rheostat" to promote thrombin inhibition in the presence of glycosaminoglycans.	Glycosaminoglycans	277-295	coagulation factor II, thrombin	Homo sapiens	37-45
11856753-9	2002	These results indicate that improved thrombin inhibition in the AR2 HCII mutants is mediated by enhanced interactions between the acidic domain and anion-binding exosite-1 of thrombin and that AR2 may be a "molecular rheostat" to promote thrombin inhibition in the presence of glycosaminoglycans.	Glycosaminoglycans	277-295	serpin family D member 1	Homo sapiens	68-72
11856753-9	2002	These results indicate that improved thrombin inhibition in the AR2 HCII mutants is mediated by enhanced interactions between the acidic domain and anion-binding exosite-1 of thrombin and that AR2 may be a "molecular rheostat" to promote thrombin inhibition in the presence of glycosaminoglycans.	Glycosaminoglycans	277-295	coagulation factor II, thrombin	Homo sapiens	175-183
11856753-9	2002	These results indicate that improved thrombin inhibition in the AR2 HCII mutants is mediated by enhanced interactions between the acidic domain and anion-binding exosite-1 of thrombin and that AR2 may be a "molecular rheostat" to promote thrombin inhibition in the presence of glycosaminoglycans.	Glycosaminoglycans	277-295	coagulation factor II, thrombin	Homo sapiens	175-183
11947905-6	2002	Gemfibrozil and another PPAR-alpha ligand, WY-14643, significantly inhibited basal and TGF-beta1 stimulated GAG synthesis.	Glycosaminoglycans	108-111	peroxisome proliferator activated receptor alpha	Homo sapiens	24-34
12042659-0	2002	Cyclosporin A and transforming growth factor beta modify the pattern of extracellular glycosaminoglycans without causing cytoskeletal changes in human gingival fibroblasts.	Glycosaminoglycans	86-104	transforming growth factor beta 1	Homo sapiens	0-49
12042659-3	2002	Transforming growth factor beta induces the deposition of glycosaminoglycans, proteoglycans, and collagen fibers in the extracellular matrix.	Glycosaminoglycans	58-76	transforming growth factor beta 1	Homo sapiens	0-31
12042659-4	2002	The aim of this study of normal and hypertrophic human gingival fibroblast cultures was to evaluate the cytoskeletal and extracellular changes in glycosaminoglycan secretion due to the presence of cyclosporin A and transforming growth factor beta.	Glycosaminoglycans	146-163	transforming growth factor beta 1	Homo sapiens	197-246
12042659-5	2002	The results showed that there is an increase in total and individual classes of extracellular glycosaminoglycans in the presence of cyclosporin A and transforming growth factor beta, but the action of the latter was significantly greater.	Glycosaminoglycans	94-112	transforming growth factor beta 1	Homo sapiens	132-181
12056850-3	2002	The recombinant human interleukin-1alpha (rhIL-1alpha, 5 ng/ml) was added to induce proteoglycan (PG) degradation and the degree of PG degradation was assessed by measuring the amount of glycosaminoglycan (GAG) released into the culture medium.	Glycosaminoglycans	187-204	interleukin 1 alpha	Homo sapiens	22-40
11947905-6	2002	Gemfibrozil and another PPAR-alpha ligand, WY-14643, significantly inhibited basal and TGF-beta1 stimulated GAG synthesis.	Glycosaminoglycans	108-111	transforming growth factor beta 1	Homo sapiens	87-96
11991744-3	2002	Cell attachment of the VLP is efficiently inhibited by soluble heparin and dextran sulfate and less efficiently abrogated by several other glycosaminoglycans (GAGs) including chondroitin sulfate A and chondroitin sulfate B (dermatan sulfate), as determined by deconvolution microscopic immunodetection of the viral gag protein and by quantitative binding studies of metabolically labeled (35)S-VLP.	Glycosaminoglycans	139-157	VHL like	Homo sapiens	23-26
12975603-3	2002	Biglycan contains two chondroitin sulfate glycosaminoglycan (GAG) chains attached near its NH(2) terminus making it different from decorin that has only one GAG chain.	Glycosaminoglycans	61-64	biglycan	Mus musculus	0-8
12975603-3	2002	Biglycan contains two chondroitin sulfate glycosaminoglycan (GAG) chains attached near its NH(2) terminus making it different from decorin that has only one GAG chain.	Glycosaminoglycans	157-160	biglycan	Mus musculus	0-8
12004255-7	2002	Antithrombin binds to specific pentasaccharides expressed on heparin, glycosaminoglycans, and related proteoglycans within the circulation and along endothelial surfaces.	Glycosaminoglycans	70-88	serpin family C member 1	Homo sapiens	0-12
11991744-3	2002	Cell attachment of the VLP is efficiently inhibited by soluble heparin and dextran sulfate and less efficiently abrogated by several other glycosaminoglycans (GAGs) including chondroitin sulfate A and chondroitin sulfate B (dermatan sulfate), as determined by deconvolution microscopic immunodetection of the viral gag protein and by quantitative binding studies of metabolically labeled (35)S-VLP.	Glycosaminoglycans	159-163	VHL like	Homo sapiens	23-26
11991744-5	2002	Furthermore, VLP adsorption onto several CHO cell lines variably deficient in cell surface GAG is significantly but incompletely abrogated.	Glycosaminoglycans	91-94	VHL like	Homo sapiens	13-16
11991744-8	2002	We conclude from these studies that the presence of Polybrene, the degree of sulfation of cell surface GAG, and possibly the presence of charged cell surface macromolecules create an electrostatic environment that promotes optimum binding of VLP to cells.	Glycosaminoglycans	103-106	VHL like	Homo sapiens	242-245
11991744-9	2002	Additionally, our results demonstrate that, in the absence of Polybrene, initial attachments of non-infectious, envelope protein-free VLP and probably mature infectious virus particles are mediated by interactions of the virus particles with cell surface heparan sulfate, and possibly with other GAG molecules.	Glycosaminoglycans	296-299	VHL like	Homo sapiens	134-137
12054609-9	2002	Mutational analysis and electrophoretic mobility shift assays (EMSA) showed that a GAG motif was responsible for mediating promoter activation in response to TFF2 stimulation.	Glycosaminoglycans	83-86	trefoil factor 2	Homo sapiens	158-162
11914485-5	2002	Comparison of these structures with the previous structure of TRAP bound to (GAGAU)(10)GAG RNA, in which the spacer nucleotides stack with each other close to the protein surface, shows that the RNA can adopt different conformations depending on the sequence of the spacer regions.	Glycosaminoglycans	77-80	TRAP	Homo sapiens	62-66
11948458-7	2002	TNF-alpha secreted by human monocytes, which may be present in the peritumoral area, increased cell proliferation and GAG accumulation and was, in turn, enhanced by TGF-beta1 treatment.	Glycosaminoglycans	118-121	tumor necrosis factor	Homo sapiens	0-9
11948458-7	2002	TNF-alpha secreted by human monocytes, which may be present in the peritumoral area, increased cell proliferation and GAG accumulation and was, in turn, enhanced by TGF-beta1 treatment.	Glycosaminoglycans	118-121	transforming growth factor beta 1	Homo sapiens	165-174
11944889-2	2002	Previously we suggested that Vif acts as a regulator of the viral protease (PR): It prevents the autoprocessing of Gag and Gag-Pol precursors until virus assembly, and it may control the PR activity in the preintegration complex at the early stage of infection.	Glycosaminoglycans	115-118	Vif	Human immunodeficiency virus 1	29-32
11853556-2	2002	Bovine nasal cartilage cultured with either IL-1beta or retinoic acid exhibited significant release of glycosaminoglycan (GAG).	Glycosaminoglycans	103-120	interleukin 1 beta	Bos taurus	44-52
12009333-3	2002	We have for the first time demonstrated that IGD cleavage by MMPs occurs during this late stage cartilage degeneration, both as a primary event in association with glycosaminoglycan (GAG) release from the tissue and secondarily in trimming of aggrecanase-generated G1 metabolites.	Glycosaminoglycans	164-181	matrix metallopeptidase 1	Homo sapiens	61-65
12009333-3	2002	We have for the first time demonstrated that IGD cleavage by MMPs occurs during this late stage cartilage degeneration, both as a primary event in association with glycosaminoglycan (GAG) release from the tissue and secondarily in trimming of aggrecanase-generated G1 metabolites.	Glycosaminoglycans	183-186	matrix metallopeptidase 1	Homo sapiens	61-65
12009333-9	2002	Collectively, these results suggest that C-terminal processing of aggrecan by MMPs may contribute to the depletion of cartilage GAG that leads to loss of tissue function in aging and disease.	Glycosaminoglycans	128-131	matrix metallopeptidase 1	Homo sapiens	78-82
11897032-9	2002	gag (p24/p7) sequence analysis of these variants confirmed the maintenance of the subtype G subclusters.	Glycosaminoglycans	0-3	transmembrane p24 trafficking protein 2	Homo sapiens	5-8
11903042-0	2002	Platelet-derived growth factor-BB-mediated glycosaminoglycan synthesis is transduced through Akt.	Glycosaminoglycans	43-60	AKT serine/threonine kinase 1	Homo sapiens	93-96
11903042-1	2002	Previously we have demonstrated that the phosphoinositide 3-kinase (PI-3K) signal-transduction pathway mediates platelet-derived growth factor (PDGF)-BB-induced glycosaminoglycan (GAG) synthesis in fetal lung fibroblasts.	Glycosaminoglycans	161-178	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	41-66
11903042-1	2002	Previously we have demonstrated that the phosphoinositide 3-kinase (PI-3K) signal-transduction pathway mediates platelet-derived growth factor (PDGF)-BB-induced glycosaminoglycan (GAG) synthesis in fetal lung fibroblasts.	Glycosaminoglycans	180-183	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	41-66
11903042-6	2002	Furthermore, expression of dominant-negative Akt abrogated endogenous Akt activity, Rab3D phosphorylation and GAG synthesis, whereas expression of constitutively activated Akt stimulated Rab3D phosphorylation and GAG synthesis in the absence of PDGF-BB.	Glycosaminoglycans	110-113	AKT serine/threonine kinase 1	Homo sapiens	45-48
11903042-6	2002	Furthermore, expression of dominant-negative Akt abrogated endogenous Akt activity, Rab3D phosphorylation and GAG synthesis, whereas expression of constitutively activated Akt stimulated Rab3D phosphorylation and GAG synthesis in the absence of PDGF-BB.	Glycosaminoglycans	213-216	AKT serine/threonine kinase 1	Homo sapiens	45-48
11903042-7	2002	Over-expression of wild-type PTEN (phosphatase and tensin homologue deleted in chromosome 10) inhibited Akt activity and concomitantly attenuated GAG synthesis in fibroblasts stimulated with PDGF-BB.	Glycosaminoglycans	146-149	phosphatase and tensin homolog	Homo sapiens	29-33
12067233-5	2002	GAGs and IGF-I treatments also affected IGF-I plasma and muscle levels.	Glycosaminoglycans	0-4	insulin-like growth factor 1	Mus musculus	40-45
12067233-6	2002	In wobbler mice there was a progressive reduction in IGF-I plasma levels that was prevented by IGF-I or GAGs alone and greatly increased, even above heterozygote levels, by the combination treatment.	Glycosaminoglycans	104-108	insulin-like growth factor 1	Mus musculus	53-58
11890696-1	2002	The glycosaminoglycans heparin and heparan sulfate (HS) bind to fibroblast growth factor FGF1 and promote its dimerization, a proposed prerequisite for binding to a cellular receptor and triggering mitogenic signals.	Glycosaminoglycans	4-22	fibroblast growth factor 1	Homo sapiens	89-93
11853556-2	2002	Bovine nasal cartilage cultured with either IL-1beta or retinoic acid exhibited significant release of glycosaminoglycan (GAG).	Glycosaminoglycans	122-125	interleukin 1 beta	Bos taurus	44-52
11853557-2	2002	In the present study, the release of glycosaminoglycan-containing components from bovine nasal cartilage cultured in the presence of interleukin-1beta, and from bovine nasal, fetal bovine epiphyseal and adult human articular cartilage cultured in the presence of retinoic acid, was accompanied by the loss of link protein and hyaluronate into the culture medium.	Glycosaminoglycans	37-54	interleukin 1 beta	Bos taurus	133-150
11880501-3	2002	Otospiralin is a novel 6.4 kDa protein of unknown function that shares a protein motif with the gag p30 core shell nucleocapsid protein of type C retroviruses.	Glycosaminoglycans	96-99	otospiralin	Cavia porcellus	0-11
11973627-3	2002	Mutation analyses for the GAG-deletion in the DYT1 gene were performed on 107 probands; and the mutation was detected in three.	Glycosaminoglycans	26-29	torsin family 1 member A	Homo sapiens	46-50
11836402-0	2002	Interaction of the CC-chemokine RANTES with glycosaminoglycans activates a p44/p42 mitogen-activated protein kinase-dependent signaling pathway and enhances human immunodeficiency virus type 1 infectivity.	Glycosaminoglycans	44-62	C-C motif chemokine ligand 5	Homo sapiens	32-38
11836403-8	2002	Because Vpr is packaged via the p6 region of Gag, this approach bypasses the interaction with CA and allows CypA incorporation even in the presence of CsA.	Glycosaminoglycans	45-48	peptidylprolyl isomerase A	Homo sapiens	108-112
11836402-0	2002	Interaction of the CC-chemokine RANTES with glycosaminoglycans activates a p44/p42 mitogen-activated protein kinase-dependent signaling pathway and enhances human immunodeficiency virus type 1 infectivity.	Glycosaminoglycans	44-62	interferon induced protein 44	Homo sapiens	75-78
11836402-0	2002	Interaction of the CC-chemokine RANTES with glycosaminoglycans activates a p44/p42 mitogen-activated protein kinase-dependent signaling pathway and enhances human immunodeficiency virus type 1 infectivity.	Glycosaminoglycans	44-62	cyclin dependent kinase 20	Homo sapiens	79-82
11836402-5	2002	Instead, activation of the PTK signaling pathway is dependent on the expression of glycosaminoglycans (GAGs) on the cell surface, in that it could not be activated by RANTES in GAG-deficient cells.	Glycosaminoglycans	83-101	protein tyrosine kinase 2 beta	Homo sapiens	27-30
11836402-5	2002	Instead, activation of the PTK signaling pathway is dependent on the expression of glycosaminoglycans (GAGs) on the cell surface, in that it could not be activated by RANTES in GAG-deficient cells.	Glycosaminoglycans	103-107	protein tyrosine kinase 2 beta	Homo sapiens	27-30
11836402-7	2002	Here we show that activation of both PTK and MAPK is involved in the enhancement of HIV-1 infectivity caused by RANTES in cells that lack GPCRs for RANTES but which express GAGs.	Glycosaminoglycans	173-177	protein tyrosine kinase 2 beta	Homo sapiens	37-40
11836402-7	2002	Here we show that activation of both PTK and MAPK is involved in the enhancement of HIV-1 infectivity caused by RANTES in cells that lack GPCRs for RANTES but which express GAGs.	Glycosaminoglycans	173-177	C-C motif chemokine ligand 5	Homo sapiens	112-118
11836403-2	2002	CypA is packaged by binding to the capsid (CA) region of Gag.	Glycosaminoglycans	57-60	peptidylprolyl isomerase A	Homo sapiens	0-4
11733538-3	2002	Ym1 was shown to be a neutrophil granule protein and to have weak beta-N-acetylglucosaminidase activity, indicating that it might contribute to the digestion of glycosaminoglycans.	Glycosaminoglycans	161-179	chitinase-like 3	Mus musculus	0-3
11921121-1	2002	When primary torsion dystonia is caused by a GAG deletion in the TOR1A gene (DYT1 dystonia), it typically presents with an early-onset dystonia involving distal limbs, subsequently spreading to a generalized dystonia.	Glycosaminoglycans	45-48	torsin family 1 member A	Homo sapiens	65-70
11921121-1	2002	When primary torsion dystonia is caused by a GAG deletion in the TOR1A gene (DYT1 dystonia), it typically presents with an early-onset dystonia involving distal limbs, subsequently spreading to a generalized dystonia.	Glycosaminoglycans	45-48	torsin family 1 member A	Homo sapiens	77-81
11834942-0	2002	Important contribution of p15 Gag-specific responses to the total Gag-specific CTL responses.	Glycosaminoglycans	30-33	cyclin dependent kinase inhibitor 2B	Homo sapiens	26-29
11834942-0	2002	Important contribution of p15 Gag-specific responses to the total Gag-specific CTL responses.	Glycosaminoglycans	66-69	cyclin dependent kinase inhibitor 2B	Homo sapiens	26-29
11834942-2	2002	However, the extent to which p15 Gag is targeted by the host immune system in natural infection as well as precise cytotoxic T lymphocyte (CTL) epitopes within this protein remains to be defined.	Glycosaminoglycans	33-36	cyclin dependent kinase inhibitor 2B	Homo sapiens	29-32
11834942-5	2002	RESULTS: CD8 T lymphocytes specific to p15 Gag were found in 46% (26/57) of HIV-1 infected individuals studied and contributed on average 17% (range, 0-100%) to the total Gag-specific T-cell responses.	Glycosaminoglycans	43-46	Vpr	Human immunodeficiency virus 1	39-42
11834942-5	2002	RESULTS: CD8 T lymphocytes specific to p15 Gag were found in 46% (26/57) of HIV-1 infected individuals studied and contributed on average 17% (range, 0-100%) to the total Gag-specific T-cell responses.	Glycosaminoglycans	171-174	Vpr	Human immunodeficiency virus 1	39-42
11834942-6	2002	Responses were clustered within three immunodominant regions of p15 Gag, mapping to important functional sites.	Glycosaminoglycans	68-71	Vpr	Human immunodeficiency virus 1	64-67
11834942-7	2002	These studies also include the description of the first three optimally defined CTL epitopes within p15 Gag.	Glycosaminoglycans	104-107	Vpr	Human immunodeficiency virus 1	100-103
11834942-8	2002	CONCLUSIONS: These results indicate that p15 Gag is frequently recognized by HIV-1-specific CD8 T cells in HIV-1 infection and will be important in the comprehensive assessments of CTL responses in infected persons, as well as the design and testing of future HIV-1 vaccines and immunotherapeutic interventions.	Glycosaminoglycans	45-48	Vpr	Human immunodeficiency virus 1	41-44
11895481-11	2002	Localization of the RsulfFP1 protein in the Golgi apparatus and on the cell surface, however, suggests that it may play a role in regulating proteoglycan-mediated signalling by the desulphation of GAGs during biosynthesis or after GAGs are presented in the extracellular space.	Glycosaminoglycans	197-201	sulfatase 1	Rattus norvegicus	20-28
11861391-6	2002	Indeed, we found loss of gag(85-93) in RMA, MBL-2, and EL-4G+ lymphoma cells, which share gag(85-93) as an immunodominant CTL epitope, induced to apoptosis by UV irradiation, mitomycin C, doxorubicin, or daunorubicin.	Glycosaminoglycans	25-28	mannose-binding lectin (protein C) 2	Mus musculus	44-49
11856642-1	2002	Mucopolysaccharidosis type VII (MPS VII) is a heritable lysosomal storage disease caused by a deficiency in beta-glucuronidase (GUSB) activity, leading to progressive accumulation of undegraded glycosaminoglycans in many tissues.	Glycosaminoglycans	194-212	glucuronidase, beta	Mus musculus	108-126
11856642-1	2002	Mucopolysaccharidosis type VII (MPS VII) is a heritable lysosomal storage disease caused by a deficiency in beta-glucuronidase (GUSB) activity, leading to progressive accumulation of undegraded glycosaminoglycans in many tissues.	Glycosaminoglycans	194-212	glucuronidase, beta	Mus musculus	128-132
11843134-8	2002	Highest concentration of IGF-1 (25 microg/ml) significantly increased total DNA content, glycosaminoglycan (GAG) content, GAG synthesis, and size of proteoglycan monomers produced, compared with cultures supplemented with 12.5 microg of IGF-1/ml or untreated cultures.	Glycosaminoglycans	89-106	insulin like growth factor 1	Equus caballus	25-30
11843134-8	2002	Highest concentration of IGF-1 (25 microg/ml) significantly increased total DNA content, glycosaminoglycan (GAG) content, GAG synthesis, and size of proteoglycan monomers produced, compared with cultures supplemented with 12.5 microg of IGF-1/ml or untreated cultures.	Glycosaminoglycans	108-111	insulin like growth factor 1	Equus caballus	25-30
11843134-8	2002	Highest concentration of IGF-1 (25 microg/ml) significantly increased total DNA content, glycosaminoglycan (GAG) content, GAG synthesis, and size of proteoglycan monomers produced, compared with cultures supplemented with 12.5 microg of IGF-1/ml or untreated cultures.	Glycosaminoglycans	122-125	insulin like growth factor 1	Equus caballus	25-30
11847516-0	2002	Proteinase activity regulation by glycosaminoglycans.	Glycosaminoglycans	34-52	endogenous retrovirus group K member 25	Homo sapiens	0-10
11895481-11	2002	Localization of the RsulfFP1 protein in the Golgi apparatus and on the cell surface, however, suggests that it may play a role in regulating proteoglycan-mediated signalling by the desulphation of GAGs during biosynthesis or after GAGs are presented in the extracellular space.	Glycosaminoglycans	231-235	sulfatase 1	Rattus norvegicus	20-28
11707436-7	2002	In vitro, recombinant Hex S was highly active on water-soluble and amphiphilic glycoconjugates including artificial substrates, sulfated GAG fragments, and the sulfated glycosphingolipid SM2.	Glycosaminoglycans	137-140	hematopoietically expressed homeobox	Mus musculus	22-25
11809731-2	2002	HIT is mediated by antibodies directed mostly to epitope(s) formed by complexes between heparin or other anionic mucopolysaccharides and platelet factor 4 (PF4).	Glycosaminoglycans	113-132	platelet factor 4	Homo sapiens	156-159
11829484-2	2002	The deficiency of SGSH results in the lysosomal accumulation and urinary excretion of the glycosaminoglycan heparan sulfate.	Glycosaminoglycans	90-107	N-sulfoglucosamine sulfohydrolase	Canis lupus familiaris	18-22
11842287-1	2002	Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells.	Glycosaminoglycans	236-255	kininogen 1	Homo sapiens	0-10
11886656-4	2002	IGF-I (10-300 ng/mL) maintained wet weight fractions of GAG in constructs seeded at high cell density and increased by up to fivefold GAG fractions in constructs seeded at lower cell density.	Glycosaminoglycans	56-59	IGFI	Bos taurus	0-5
11886656-4	2002	IGF-I (10-300 ng/mL) maintained wet weight fractions of GAG in constructs seeded at high cell density and increased by up to fivefold GAG fractions in constructs seeded at lower cell density.	Glycosaminoglycans	134-137	IGFI	Bos taurus	0-5
11886656-6	2002	IL-4 (1-100 ng/mL) minimized the thickness of the GAG-depleted region at the construct surfaces.	Glycosaminoglycans	50-53	interleukin 4	Bos taurus	0-4
11853965-8	2002	Dermatan sulfate (DS) was the predominant glycosaminoglycan (GAG) present on biglycan and decorin in both tissues.	Glycosaminoglycans	42-59	biglycan	Homo sapiens	77-85
11807313-3	2002	Gag sequences with a discrepant subtype between p17 and p24 were analysed further to indicate approximate sites of recombination.	Glycosaminoglycans	0-3	family with sequence similarity 72 member B	Homo sapiens	48-51
11805336-3	2002	Recently, it was demonstrated that the product of tumor susceptibility gene 101 (TSG101), which contains at its N terminus a domain highly related to ubiquitin-conjugating (E2) enzymes, binds HIV-1 Gag in a p6-dependent fashion.	Glycosaminoglycans	198-201	tumor susceptibility 101	Homo sapiens	81-87
11853965-8	2002	Dermatan sulfate (DS) was the predominant glycosaminoglycan (GAG) present on biglycan and decorin in both tissues.	Glycosaminoglycans	61-64	biglycan	Homo sapiens	77-85
11668175-11	2002	Betaglycan in LLC-PK1 cells exhibits higher molecular weight glycosaminoglycan (GAG) chains than in L6 cells, and a GAG- betaglycan mutant does not inhibit TGF-beta signaling or type I/type II receptor association in LLC-PK1 cells.	Glycosaminoglycans	61-78	transforming growth factor beta receptor 3	Sus scrofa	0-10
12097842-4	2002	Western blot analysis showed that decorin already existed in skeletal muscle by 2.5 months of fetal development, and that decorin had a longer glycosaminoglycan chain in the early fetal stages than in later development, but its core protein was of the same size.	Glycosaminoglycans	143-160	decorin	Bos taurus	122-129
12572850-1	2002	Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked disease caused by a deficiency of the enzyme iduronate-2-sulphatase (IDS), which results in the lysosomal accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	193-211	iduronate 2-sulfatase	Homo sapiens	116-138
12572850-1	2002	Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked disease caused by a deficiency of the enzyme iduronate-2-sulphatase (IDS), which results in the lysosomal accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	193-211	iduronate 2-sulfatase	Homo sapiens	140-143
12572850-1	2002	Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked disease caused by a deficiency of the enzyme iduronate-2-sulphatase (IDS), which results in the lysosomal accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	213-216	iduronate 2-sulfatase	Homo sapiens	116-138
12572850-1	2002	Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked disease caused by a deficiency of the enzyme iduronate-2-sulphatase (IDS), which results in the lysosomal accumulation of glycosaminoglycans (GAG).	Glycosaminoglycans	213-216	iduronate 2-sulfatase	Homo sapiens	140-143
12572850-3	2002	Therapy with IDS results in a marked decrease in urinary GAGs, as well as reduced GAG accumulation in several tissues.	Glycosaminoglycans	57-60	iduronate 2-sulfatase	Homo sapiens	13-16
11993591-1	2002	BACKGROUND: Early, limb-onset primary torsion dystonia (PTD) is commonly due to a trinucleotide GAG deletion in the TOR1A (DYT1) gene on chromosome 9q34.	Glycosaminoglycans	96-99	torsin family 1 member A	Homo sapiens	116-121
11782319-3	2002	Left-right development is dependent on a distinct subset of glycosaminoglycan attachment sites on syndecan-2.	Glycosaminoglycans	60-77	syndecan 2 L homeolog	Xenopus laevis	98-108
12566710-4	2002	Mice vaccinated by syngag but not wt gag developed substantial and highly consistent Gag-specific antibody titers showing a clear T helper 1 polarization even with low doses of DNA.	Glycosaminoglycans	85-88	melanoma antigen	Mus musculus	22-25
11788461-5	2002	The increase in proteoglycan-LDL binding caused by TGF-beta1 could be attributed primarily to the glycosaminoglycan portion of the proteoglycans, since the glycosaminoglycan chains liberated from the core proteins of these proteoglycans synthesized in the presence of TGF-beta1 exhibited increased LDL binding as well.	Glycosaminoglycans	98-115	transforming growth factor beta 1	Homo sapiens	51-60
11788461-5	2002	The increase in proteoglycan-LDL binding caused by TGF-beta1 could be attributed primarily to the glycosaminoglycan portion of the proteoglycans, since the glycosaminoglycan chains liberated from the core proteins of these proteoglycans synthesized in the presence of TGF-beta1 exhibited increased LDL binding as well.	Glycosaminoglycans	156-173	transforming growth factor beta 1	Homo sapiens	51-60
11788461-6	2002	Furthermore, glycosaminoglycan chains initiated on xyloside (an initiator of glycosaminoglycan synthesis) in the presence of TGF-beta1 were longer and displayed enhanced binding to LDL compared with the LDL binding of xyloside-initiated glycosaminoglycan chains from control cultures.	Glycosaminoglycans	13-30	transforming growth factor beta 1	Homo sapiens	125-134
11788461-6	2002	Furthermore, glycosaminoglycan chains initiated on xyloside (an initiator of glycosaminoglycan synthesis) in the presence of TGF-beta1 were longer and displayed enhanced binding to LDL compared with the LDL binding of xyloside-initiated glycosaminoglycan chains from control cultures.	Glycosaminoglycans	77-94	transforming growth factor beta 1	Homo sapiens	125-134
11788461-7	2002	These results indicate that TGF-beta1 promotes LDL-proteoglycan interaction primarily by its effects on the glycosaminoglycan synthetic machinery of the ASMCs.	Glycosaminoglycans	108-125	transforming growth factor beta 1	Homo sapiens	28-37
11993591-1	2002	BACKGROUND: Early, limb-onset primary torsion dystonia (PTD) is commonly due to a trinucleotide GAG deletion in the TOR1A (DYT1) gene on chromosome 9q34.	Glycosaminoglycans	96-99	torsin family 1 member A	Homo sapiens	123-127
11993591-7	2002	CONCLUSION: The authors describe the clinical features of PTD due to the TOR1A GAG deletion in an Irish family illustrating the presence of intrafamilial phenotypic variability.	Glycosaminoglycans	79-82	torsin family 1 member A	Homo sapiens	73-78
11739667-5	2002	The percentage of Gag-specific, tetramer-positive T cells was as high as 13 to 14% of the CD3+ CD8+ T-cell population in the vaginal and cervical laminae propriae of both SIVmac251 and SHIV(KU2) chronically infected macaques.	Glycosaminoglycans	18-21	CD8a molecule	Homo sapiens	95-98
11755208-4	2001	These degradation products which were free heparan sulfate chains with little or no protein covalently attached, were approximately half the size of the original glycosaminoglycan chains and were the only degradation intermediate found in the course of HSPG catabolism in these cells.	Glycosaminoglycans	162-179	syndecan 2	Rattus norvegicus	253-257
11752176-11	2002	After the acute phase, however, this pattern of reactivity changed, and the Mamu-A*01-restricted response against the Gag(181-189)CM9 epitope became dominant.	Glycosaminoglycans	118-121	major histocompatibility complex, class I, A	Macaca mulatta	76-82
11551958-0	2001	Biosynthesis of the linkage region of glycosaminoglycans: cloning and activity of galactosyltransferase II, the sixth member of the beta 1,3-galactosyltransferase family (beta 3GalT6).	Glycosaminoglycans	38-56	beta-1,3-galactosyltransferase 6	Homo sapiens	82-106
11551958-0	2001	Biosynthesis of the linkage region of glycosaminoglycans: cloning and activity of galactosyltransferase II, the sixth member of the beta 1,3-galactosyltransferase family (beta 3GalT6).	Glycosaminoglycans	38-56	beta-1,3-galactosyltransferase 6	Homo sapiens	171-182
11551958-2	2001	We now report a new member of the family (beta3GalT6), involved in glycosaminoglycan biosynthesis.	Glycosaminoglycans	67-84	beta-1,3-galactosyltransferase 6	Homo sapiens	42-52
11551958-7	2001	This product, Galbeta1,3Galbeta is found in the linkage region of heparan sulfate and chondroitin sulfate (GlcAbeta1,3Galbeta1,3Galbeta1,4Xylbeta-O-Ser), indicating that beta3GalT6 is the so-called galactosyltransferase II involved in glycosaminoglycan biosynthesis.	Glycosaminoglycans	235-252	beta-1,3-galactosyltransferase 6	Homo sapiens	170-180
11551958-7	2001	This product, Galbeta1,3Galbeta is found in the linkage region of heparan sulfate and chondroitin sulfate (GlcAbeta1,3Galbeta1,3Galbeta1,4Xylbeta-O-Ser), indicating that beta3GalT6 is the so-called galactosyltransferase II involved in glycosaminoglycan biosynthesis.	Glycosaminoglycans	235-252	beta-1,3-galactosyltransferase 6	Homo sapiens	198-222
11590178-10	2001	The glycosaminoglycan component of endocan consists of a single DS chain covalently attached to serine 137.	Glycosaminoglycans	4-21	endothelial cell specific molecule 1	Homo sapiens	35-42
11786226-0	2001	The binding of lactoferrin to glycosaminoglycans on enterocyte-like HT29-18-C1 cells is mediated through basic residues located in the N-terminus.	Glycosaminoglycans	30-48	lactotransferrin	Mus musculus	15-26
11786226-6	2001	We conclude that the presence of the sequence A(1)PRK(4) in bLf and K(1)ATT(4) in mLf provides an insight into why the interaction of bLf with cell membrane-associated glycosaminoglycans is similar to that of hLf and why binding of these lactoferrin species differs from that of murine Lf.	Glycosaminoglycans	168-186	HLF transcription factor, PAR bZIP family member	Homo sapiens	61-63
11791576-1	2001	Chondroitin sulfate (CS) is a glycosaminoglycan consisting of repeating uronic acid, N-acetylgalactosamine sulfate disaccharide units [-UroA(beta1,3)-GalNAcS(beta1,4)]n. Chondroitin sulfate type A (CSA) contains glucuronic acid, and 90% of the GalNAc residues are sulfated at the 4-position with 10% at the 6-position.	Glycosaminoglycans	30-47	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	141-148
11742862-2	2001	Oxidation may lead to modification of the lysine residues of apolipoprotein B-100 of LDL, which normally mediate the binding of LDL to glycosaminoglycans.	Glycosaminoglycans	135-153	apolipoprotein B	Homo sapiens	61-81
11746443-0	2001	Glycosaminoglycan-promoted muscle reinnervation and insulin-like growth factor-I levels are affected by anti-growth hormone-releasing hormone exposure.	Glycosaminoglycans	0-17	growth hormone releasing hormone	Rattus norvegicus	109-141
11746443-1	2001	The present study shows that exposure to antibodies to growth hormone-releasing hormone (GHRH) partially counteracted the promoting effects of treatment with glycosaminoglycans (GAGs) on muscle reinnervation.	Glycosaminoglycans	158-176	growth hormone releasing hormone	Rattus norvegicus	55-87
11746443-4	2001	In addition, treatment with glycosaminoglycans increased markedly insulin-like growth factor-I (IGF-I) levels in denervated muscles.	Glycosaminoglycans	28-46	insulin-like growth factor 1	Rattus norvegicus	66-94
11746443-4	2001	In addition, treatment with glycosaminoglycans increased markedly insulin-like growth factor-I (IGF-I) levels in denervated muscles.	Glycosaminoglycans	28-46	insulin-like growth factor 1	Rattus norvegicus	96-101
11761721-3	2001	We have now analyzed the expression of the heparan sulfate proteoglycan (HSPG) subtypes agrin, perlecan, glypican-1, syndecans 1-3 and HS glycosaminoglycan (GAG) side chains in CAA in brains of patients with AD and HCHWA-D. Hereto, specific well-characterized antibodies directed against the core protein of these HSPGs and against the GAG side chains were used for immunostaining.	Glycosaminoglycans	336-339	CD44 molecule (Indian blood group)	Homo sapiens	73-77
11761721-3	2001	We have now analyzed the expression of the heparan sulfate proteoglycan (HSPG) subtypes agrin, perlecan, glypican-1, syndecans 1-3 and HS glycosaminoglycan (GAG) side chains in CAA in brains of patients with AD and HCHWA-D. Hereto, specific well-characterized antibodies directed against the core protein of these HSPGs and against the GAG side chains were used for immunostaining.	Glycosaminoglycans	157-160	CD44 molecule (Indian blood group)	Homo sapiens	73-77
11761721-3	2001	We have now analyzed the expression of the heparan sulfate proteoglycan (HSPG) subtypes agrin, perlecan, glypican-1, syndecans 1-3 and HS glycosaminoglycan (GAG) side chains in CAA in brains of patients with AD and HCHWA-D. Hereto, specific well-characterized antibodies directed against the core protein of these HSPGs and against the GAG side chains were used for immunostaining.	Glycosaminoglycans	336-339	CD44 molecule (Indian blood group)	Homo sapiens	43-71
11810193-2	2001	In this study, we developed a sensitive histochemical detection of PrP(sc) deposits in a Gertsmann-Straussler-Scheinker disease (GSS) patient using toluidine blue-O staining, a specific reagent to stain mucins and mucopolysaccharides.	Glycosaminoglycans	214-233	prion protein	Homo sapiens	67-70
11714827-5	2001	Although IP-10/CXCL10 binds to cell surface heparan sulfate glycosaminoglycan (GAG), the receptor expressed by these cells is not GAG, since the affinity of IP-10/CXCL10 for this receptor is much higher than it is for GAG, its binding is not competed by platelet factor 4/CXCL4, and it is present on cells that are genetically incapable of synthesizing GAG.	Glycosaminoglycans	79-82	C-X-C motif chemokine ligand 10	Homo sapiens	9-14
11748259-3	2001	Purified MPO and MPO released by intraluminal degranulation of activated human PMNs avidly bound to aortic endothelial cell glycosaminoglycans in both cell monolayer and isolated vessel models.	Glycosaminoglycans	124-142	myeloperoxidase	Homo sapiens	9-12
11748259-3	2001	Purified MPO and MPO released by intraluminal degranulation of activated human PMNs avidly bound to aortic endothelial cell glycosaminoglycans in both cell monolayer and isolated vessel models.	Glycosaminoglycans	124-142	myeloperoxidase	Homo sapiens	17-20
11709791-7	2001	Two heterozygotes for a 32-bp deletion in CCR5 had the lowest set points (P=.0220) and highest Gag precursor CTL frequencies (P=.0128).	Glycosaminoglycans	95-98	C-C motif chemokine receptor 5	Homo sapiens	42-46
11714827-5	2001	Although IP-10/CXCL10 binds to cell surface heparan sulfate glycosaminoglycan (GAG), the receptor expressed by these cells is not GAG, since the affinity of IP-10/CXCL10 for this receptor is much higher than it is for GAG, its binding is not competed by platelet factor 4/CXCL4, and it is present on cells that are genetically incapable of synthesizing GAG.	Glycosaminoglycans	79-82	C-X-C motif chemokine ligand 10	Homo sapiens	15-21
11779356-2	2001	There was a low degree of heterogeneity of gag p17 matrix sequences in nontransmitting mothers compared with our previously analyzed mother-infant pairs" sequences.	Glycosaminoglycans	43-46	family with sequence similarity 72 member B	Homo sapiens	47-50
11779349-4	2001	When the ability of the Env mutants to associate with SIV Gag particles was examined, we found that deletion of 20 to 80 residues from the carboxyl terminus of the SIV TM cytoplasmic tail abrogated the incorporation of the Env glycoprotein into particles.	Glycosaminoglycans	58-61	endogenous retrovirus group K member 20	Homo sapiens	24-27
11779349-5	2001	By contrast, further truncation of the SIV TM protein by 100 to 140 amino acids restored the ability of the Env protein to associate with Gag particles.	Glycosaminoglycans	138-141	endogenous retrovirus group K member 20	Homo sapiens	108-111
11910525-11	2001	However, controlled expression of GUSB was essential for the metabolism of stored GAGs to achieve normal levels.	Glycosaminoglycans	82-86	glucuronidase beta	Homo sapiens	34-38
11559927-6	2001	HS is the major GAG in the cell membrane of THP-1.	Glycosaminoglycans	16-19	GLI family zinc finger 2	Homo sapiens	44-49
11684667-8	2001	The activity of the Erk MAP kinase pathway is dependent on at least two known regulators of ureteric bud branching; the GDNF-Ret signalling system and sulphated glycosaminoglycans.	Glycosaminoglycans	161-179	mitogen-activated protein kinase 1	Mus musculus	20-23
11757956-2	2001	A GAG deletion at position 946 in the DYT1 gene is responsible for most cases of autosomal dominant early-onset PTD.	Glycosaminoglycans	2-5	torsin family 1 member A	Homo sapiens	38-42
11757956-4	2001	Only three apparently sporadic patients among the 50 individuals tested were positive for the GAG deletion in the DYT1 gene: one with typical, generalized, one with long-lasting, non-progressive segmental, and one with multifocal dystonia.	Glycosaminoglycans	94-97	torsin family 1 member A	Homo sapiens	114-118
11781011-6	2001	Statistically significant changes in glycosaminoglycan (GAG) production compared to control gels either without microspheres or with blank spheres were observed after a 14 day incubation with IGF-I and IGF-I/TGF-beta microspheres combined, with a maximum density of 8.41+/-2.5% wet weight GAG.	Glycosaminoglycans	37-54	IGFI	Bos taurus	192-197
11781011-6	2001	Statistically significant changes in glycosaminoglycan (GAG) production compared to control gels either without microspheres or with blank spheres were observed after a 14 day incubation with IGF-I and IGF-I/TGF-beta microspheres combined, with a maximum density of 8.41+/-2.5% wet weight GAG.	Glycosaminoglycans	37-54	IGFI	Bos taurus	202-207
11781011-6	2001	Statistically significant changes in glycosaminoglycan (GAG) production compared to control gels either without microspheres or with blank spheres were observed after a 14 day incubation with IGF-I and IGF-I/TGF-beta microspheres combined, with a maximum density of 8.41+/-2.5% wet weight GAG.	Glycosaminoglycans	56-59	IGFI	Bos taurus	192-197
11781011-6	2001	Statistically significant changes in glycosaminoglycan (GAG) production compared to control gels either without microspheres or with blank spheres were observed after a 14 day incubation with IGF-I and IGF-I/TGF-beta microspheres combined, with a maximum density of 8.41+/-2.5% wet weight GAG.	Glycosaminoglycans	56-59	IGFI	Bos taurus	202-207
11781011-6	2001	Statistically significant changes in glycosaminoglycan (GAG) production compared to control gels either without microspheres or with blank spheres were observed after a 14 day incubation with IGF-I and IGF-I/TGF-beta microspheres combined, with a maximum density of 8.41+/-2.5% wet weight GAG.	Glycosaminoglycans	289-292	IGFI	Bos taurus	192-197
11781011-6	2001	Statistically significant changes in glycosaminoglycan (GAG) production compared to control gels either without microspheres or with blank spheres were observed after a 14 day incubation with IGF-I and IGF-I/TGF-beta microspheres combined, with a maximum density of 8.41+/-2.5% wet weight GAG.	Glycosaminoglycans	289-292	IGFI	Bos taurus	202-207
11597124-2	2001	The objective of the present study was to evaluate the effects of two growth factors, transforming growth factor (TGF)-beta1 and platelet-derived growth factor (PDGF)-BB, on the SMA content of these cells and their contraction of a collagen-glycosaminoglycan (GAG) analog of extracellular matrix in vitro.	Glycosaminoglycans	241-258	transforming growth factor beta 1	Homo sapiens	86-124
11597124-2	2001	The objective of the present study was to evaluate the effects of two growth factors, transforming growth factor (TGF)-beta1 and platelet-derived growth factor (PDGF)-BB, on the SMA content of these cells and their contraction of a collagen-glycosaminoglycan (GAG) analog of extracellular matrix in vitro.	Glycosaminoglycans	260-263	transforming growth factor beta 1	Homo sapiens	86-124
11597124-4	2001	A notable finding was the increased contraction of the collagen-GAG matrix induced by TGF-beta1 and the decrease in contraction resulting from PDGF-BB treatment, indicating a causal relationship between expression of SMA and the contractility of the cells.	Glycosaminoglycans	64-67	transforming growth factor beta 1	Homo sapiens	86-95
11595301-6	2001	Although similar frequencies of Gag peptide-specific CD8(+) T cells were found in LTNP and progressors by either intracellular IFN-gamma or MHC class I tetramer staining, the breadth of these responses was greater in patients with progressive HIV infection compared with the LTNP group.	Glycosaminoglycans	32-35	CD8a molecule	Homo sapiens	53-56
11602818-4	2001	Ang II (1 microM ) enhanced DNA synthesis and secretion of PAI-1 and glycosaminoglycans and decreased secretion of MMP-2 activity and tPA, whereas it had no effect on secretion of TIMPs and glycosaminoglycans associated with cell layers.	Glycosaminoglycans	69-87	angiotensinogen	Homo sapiens	0-6
11595185-3	2001	The UEV domain of Tsg101 binds to an essential tetrapeptide (PTAP) motif within the p6 domain of the structural Gag protein and also to ubiquitin.	Glycosaminoglycans	112-115	tumor susceptibility 101	Homo sapiens	18-24
11668612-2	2001	Mutations in the 4S gene are responsible for 4S deficiency, which leads to the intralysosomal storage of partially degraded glycosaminoglycans, dermatan sulfate, and chondroitin 4-sulfate.	Glycosaminoglycans	124-142	arylsulfatase B	Homo sapiens	17-19
11593356-7	2001	Transplantation of articular chondrocytes that overexpress human IGF-I also increased DNA synthesis and the synthesis of glycosaminoglycans by the underlying explant cartilage chondrocytes.	Glycosaminoglycans	121-139	insulin like growth factor 1	Homo sapiens	65-70
11668612-2	2001	Mutations in the 4S gene are responsible for 4S deficiency, which leads to the intralysosomal storage of partially degraded glycosaminoglycans, dermatan sulfate, and chondroitin 4-sulfate.	Glycosaminoglycans	124-142	arylsulfatase B	Homo sapiens	45-47
11585631-3	2001	A significantly higher frequency for CSF complete anti-gag profile (p&lt;0.001), and for HIV-specific oligoclonal patterns ("mixed" pattern=p&lt;0.01) was observed in HAND as compared to patterns from the other clinical groups.	Glycosaminoglycans	55-58	colony stimulating factor 2	Homo sapiens	37-40
11585631-4	2001	A decrease in complete anti-env, anti-pol and anti-gag reactivity was present in CSF of patients with CD4+&lt;50 as compared to those with CD4+&gt;50.	Glycosaminoglycans	51-54	colony stimulating factor 2	Homo sapiens	81-84
11579233-2	2001	Blair describes how sulfated glycosaminoglycans affect several developmentally important signaling pathways, including Wnt-Wingless, Fibroblast growth factor, Hedgehog, and Bone morphogenetic protein-4 signaling.	Glycosaminoglycans	29-47	bone morphogenetic protein 4	Homo sapiens	173-201
11718104-1	2001	Addition of human recombinant interleukin 6 (IL-6) to culture medium (supplemented MEM without or with 10% fetal calf serum (FCS)) of human skin fibroblasts exerted a stimulating effect in a dose-dependent manner on glycosaminoglycan (GAG) synthesis, including hyaluronic acid (hyaluronan) synthesis, of young (phase-II) skin fibroblasts in concentrations of 1 ng/ml and 10 ng/ml.	Glycosaminoglycans	216-233	interleukin 6	Homo sapiens	30-43
11718104-1	2001	Addition of human recombinant interleukin 6 (IL-6) to culture medium (supplemented MEM without or with 10% fetal calf serum (FCS)) of human skin fibroblasts exerted a stimulating effect in a dose-dependent manner on glycosaminoglycan (GAG) synthesis, including hyaluronic acid (hyaluronan) synthesis, of young (phase-II) skin fibroblasts in concentrations of 1 ng/ml and 10 ng/ml.	Glycosaminoglycans	216-233	interleukin 6	Homo sapiens	45-49
11718104-1	2001	Addition of human recombinant interleukin 6 (IL-6) to culture medium (supplemented MEM without or with 10% fetal calf serum (FCS)) of human skin fibroblasts exerted a stimulating effect in a dose-dependent manner on glycosaminoglycan (GAG) synthesis, including hyaluronic acid (hyaluronan) synthesis, of young (phase-II) skin fibroblasts in concentrations of 1 ng/ml and 10 ng/ml.	Glycosaminoglycans	235-238	interleukin 6	Homo sapiens	30-43
11718104-1	2001	Addition of human recombinant interleukin 6 (IL-6) to culture medium (supplemented MEM without or with 10% fetal calf serum (FCS)) of human skin fibroblasts exerted a stimulating effect in a dose-dependent manner on glycosaminoglycan (GAG) synthesis, including hyaluronic acid (hyaluronan) synthesis, of young (phase-II) skin fibroblasts in concentrations of 1 ng/ml and 10 ng/ml.	Glycosaminoglycans	235-238	interleukin 6	Homo sapiens	45-49
11579233-3	2001	A new secreted sulfatase, Qsulf1, regulates the sensitivity of vertebrate cells to Wnts, possibly by modifying the sulfation of glycosaminoglycans.	Glycosaminoglycans	128-146	arylsulfatase family member H	Homo sapiens	15-24
11522680-5	2001	The glycosaminoglycans (GAGs) of the secreted PGs from insulin-treated HepG2 cells were enriched in chondroitin sulfate (CS) PGs.	Glycosaminoglycans	4-22	insulin	Homo sapiens	55-62
11461921-2	2001	Here we identify, characterize, and localize heparin/heparan sulfate-binding sites in fibrillin-1 and report on the role of such glycosaminoglycans in the assembly of fibrillin-1.	Glycosaminoglycans	129-147	fibrillin 1	Homo sapiens	86-97
11461921-2	2001	Here we identify, characterize, and localize heparin/heparan sulfate-binding sites in fibrillin-1 and report on the role of such glycosaminoglycans in the assembly of fibrillin-1.	Glycosaminoglycans	129-147	fibrillin 1	Homo sapiens	167-178
11461921-8	2001	Inhibition of the attachment of glycosaminoglycans to core proteins of proteoglycans by beta-d-xylosides resulted in a significant reduction of the fibrillin-1 network.	Glycosaminoglycans	32-50	fibrillin 1	Homo sapiens	148-159
11518760-7	2001	Collectively, this suggests that glycosaminoglycan-bound apoE can occlude binding sites for apoE-containing lipoproteins on glycosaminoglycans.	Glycosaminoglycans	124-142	apolipoprotein E	Homo sapiens	57-61
11514732-4	2001	Vaccination of another two macaques, expressing Mamu A*01 MHC class I, with MVA constructs containing nef and gag-pol under the control of the moderate strength natural vaccinia virus early/late promoter P7.5, again induced an early Nef-specific response, whereas responses to Gag remained undetectable.	Glycosaminoglycans	277-280	Gag-Pol;gag protein	Simian immunodeficiency virus	110-117
11518760-7	2001	Collectively, this suggests that glycosaminoglycan-bound apoE can occlude binding sites for apoE-containing lipoproteins on glycosaminoglycans.	Glycosaminoglycans	124-142	apolipoprotein E	Homo sapiens	92-96
11483744-0	2001	Specific interaction of a novel foamy virus Env leader protein with the N-terminal Gag domain.	Glycosaminoglycans	83-86	endogenous retrovirus group K member 20	Homo sapiens	44-47
11550977-4	2001	RESULTS: GM-CSF (6-100 U/ml) inhibited (30%) [3H]-thymidine incorporation into DNA, and, in contrast, stimulated up to 3.6- and 2-fold [35S]SO4 and [3H]-proline incorporation into glycosaminoglycan side chains and collagen molecules, respectively.	Glycosaminoglycans	180-197	colony stimulating factor 2	Rattus norvegicus	9-15
11483744-9	2001	The purified N-terminal domain of FFV Gag specifically interacted with synthetic peptides and a defined protein domain derived from the N-terminal Env leader protein.	Glycosaminoglycans	38-41	endogenous retrovirus group K member 20	Homo sapiens	147-150
11483744-11	2001	The interaction with Gag required residues within the novel virion-associated FFV Env leader protein of about 16.5 kDa.	Glycosaminoglycans	21-24	endogenous retrovirus group K member 20	Homo sapiens	82-85
11387326-12	2001	Cloning and characterization of heparanase, the first and single functional vertebrate HS-degrading enzyme, may lead to identification of other glycosaminoglycan degrading enzymes, toward elucidation of their significance in normal and pathological processes.	Glycosaminoglycans	144-161	heparanase	Gallus gallus	32-42
11522857-9	2001	ET-1 production was only inhibited by HS-GAG with a high degree of sulphation.	Glycosaminoglycans	41-44	endothelin 1	Homo sapiens	0-4
11522857-12	2001	Inhibition of sulphation of cell surface HS-GAG resulted in the inhibition of ET-1 but not TGF-beta1 production.	Glycosaminoglycans	44-47	endothelin 1	Homo sapiens	78-82
11558154-0	2001	[Effects of glycosaminoglycans on the in vitro colony formation of CD34+ megakaryocytic progenitor cells in human placental/umbilical cord blood].	Glycosaminoglycans	12-30	CD34 molecule	Homo sapiens	67-71
11558154-1	2001	The in vitro effect of various glycosaminoglycans (GAGs) on the clonal growth of CD34+ megakaryocytic progenitor cells (CFU-Megs) isolated from human placental/umbilical cord blood (CB) was evaluated in human plasma containing semisolid culture stimulated by recombinant human thrombopoietin (TPO).	Glycosaminoglycans	31-49	CD34 molecule	Homo sapiens	81-85
11558154-1	2001	The in vitro effect of various glycosaminoglycans (GAGs) on the clonal growth of CD34+ megakaryocytic progenitor cells (CFU-Megs) isolated from human placental/umbilical cord blood (CB) was evaluated in human plasma containing semisolid culture stimulated by recombinant human thrombopoietin (TPO).	Glycosaminoglycans	51-55	CD34 molecule	Homo sapiens	81-85
11476578-10	2001	Furthermore, we show that induced changes of the composition of PG/GAG in the tooth alter SHH signaling.	Glycosaminoglycans	67-70	sonic hedgehog	Mus musculus	90-93
11384972-2	2001	Syndecan-1, present on the surfaces of normal murine mammary gland epithelial cells, is a transmembrane hybrid proteoglycan, which bears glycosaminoglycan (GAG) side chains of heparan sulfate (HS) and chondroitin sulfate (CS).	Glycosaminoglycans	137-154	syndecan 1	Mus musculus	0-10
11384972-2	2001	Syndecan-1, present on the surfaces of normal murine mammary gland epithelial cells, is a transmembrane hybrid proteoglycan, which bears glycosaminoglycan (GAG) side chains of heparan sulfate (HS) and chondroitin sulfate (CS).	Glycosaminoglycans	156-159	syndecan 1	Mus musculus	0-10
11419941-5	2001	Lacritin displays partial similarity to the glycosaminoglycan-binding region of brain-specific neuroglycan C (32 % identity over 102 amino acid residues) and to the possibly mucin-like amino globular region of fibulin-2 (30 % identity over 81 amino acid residues), and localizes primarily to secretory granules and secretory fluid.	Glycosaminoglycans	44-61	lacritin	Homo sapiens	0-8
11435560-3	2001	Sequences that are critical for the expression of both Gag and Pol include not only the 5" splice site positioned at +51 in the R region, which is used to generate the spliced pol mRNA, but also intronic R sequences located well 3" to this splice site.	Glycosaminoglycans	55-58	endogenous retrovirus group W member 4	Homo sapiens	176-179
11435565-5	2001	In addition, the strict requirement of Env expression for capsid budding can be bypassed by addition of a PM-targeting signal to Gag.	Glycosaminoglycans	129-132	endogenous retrovirus group K member 20	Homo sapiens	39-42
11435565-7	2001	The necessity of Env expression for particle egress is most probably due to the lack of a membrane-targeting signal within FV Gag to direct capsids to the PM for release and indicates that Gag-Env interactions are essential to drive particle budding.	Glycosaminoglycans	189-192	endogenous retrovirus group K member 20	Homo sapiens	17-20
11435565-7	2001	The necessity of Env expression for particle egress is most probably due to the lack of a membrane-targeting signal within FV Gag to direct capsids to the PM for release and indicates that Gag-Env interactions are essential to drive particle budding.	Glycosaminoglycans	189-192	endogenous retrovirus group K member 20	Homo sapiens	193-196
11519352-4	2001	IL-1 has been considered as the inductor of several ovulation-associated events such as prostaglandin and progesterone biosynthesis, plasminogen activator production, glycosaminoglycan generation, and enhancement of vascular permeability.	Glycosaminoglycans	167-184	interleukin 1 alpha	Homo sapiens	0-4
11547896-5	2001	Regulatory proteins of the mammary gland that bind GAG include many growth factors and morphogens (fibroblast growth factors, hepatocyte growth factor/scatter factor, members of the midkine family, wnts), matrix proteins (collagen, fibronectin, and laminin), enzymes (lipoprotein lipase) and microbial surface proteins.	Glycosaminoglycans	51-54	fibronectin 1	Homo sapiens	232-243
11547896-5	2001	Regulatory proteins of the mammary gland that bind GAG include many growth factors and morphogens (fibroblast growth factors, hepatocyte growth factor/scatter factor, members of the midkine family, wnts), matrix proteins (collagen, fibronectin, and laminin), enzymes (lipoprotein lipase) and microbial surface proteins.	Glycosaminoglycans	51-54	lipoprotein lipase	Homo sapiens	268-286
11292822-2	2001	In the case of fibroblast growth factor-2 (FGF2) signaling, heparin/heparan sulfate-like glycosaminoglycans (HLGAGs) are involved through interaction with both FGF2 and its receptors (FGFRs) in assembling a tertiary complex and modulating FGF2 activity.	Glycosaminoglycans	89-107	fibroblast growth factor 2	Homo sapiens	160-164
11461996-3	2001	To study whether the MP2 and MNC point mutations exert their compensatory effects in a cis manner, production of Gag proteins was blocked by insertion of stop codons into LD3, LD3-MP2-MNC, and wild-type BH10 such that the constructs generated, i.e., LD3-DG, LD3-MP2-MNC-DG, and BH-DG, only provided RNA transcripts for packaging.	Glycosaminoglycans	113-116	tryptase pseudogene 1	Homo sapiens	180-183
11461996-3	2001	To study whether the MP2 and MNC point mutations exert their compensatory effects in a cis manner, production of Gag proteins was blocked by insertion of stop codons into LD3, LD3-MP2-MNC, and wild-type BH10 such that the constructs generated, i.e., LD3-DG, LD3-MP2-MNC-DG, and BH-DG, only provided RNA transcripts for packaging.	Glycosaminoglycans	113-116	tryptase pseudogene 1	Homo sapiens	180-183
11509017-4	2001	Polymerase chain reaction (PCR)-based DNA sequence analysis of the LDH-B subunit gene revealed a heterozygous nucleotide change: a guanine to adenine substitution in codon 69 (GGG --&gt; GAG) at the third exon of the LDH-B subunit gene that resulted in a glycine to glutamic acid substitution (G69E).	Glycosaminoglycans	187-190	lactate dehydrogenase B	Homo sapiens	67-72
11427703-2	2001	Free ubiquitin (Ub), as well as Ub covalently bound to a small fraction of p6 Gag, is detected in mature HIV particles.	Glycosaminoglycans	78-81	ubiquitin	Oryctolagus cuniculus	32-34
11427703-4	2001	Tsg101 was found to interact with Gag in (i) a yeast two-hybrid assay, (ii) in vitro coimmunoprecipitation by using purified Pr55(Gag) and rabbit reticulocyte lysate-synthesized Tsg101, and (iii) in vivo in the cytoplasm of COS cells transfected with gag.	Glycosaminoglycans	34-37	tumor susceptibility gene 101 protein	Oryctolagus cuniculus	0-6
11427703-4	2001	Tsg101 was found to interact with Gag in (i) a yeast two-hybrid assay, (ii) in vitro coimmunoprecipitation by using purified Pr55(Gag) and rabbit reticulocyte lysate-synthesized Tsg101, and (iii) in vivo in the cytoplasm of COS cells transfected with gag.	Glycosaminoglycans	34-37	tumor susceptibility gene 101 protein	Oryctolagus cuniculus	178-184
11427703-4	2001	Tsg101 was found to interact with Gag in (i) a yeast two-hybrid assay, (ii) in vitro coimmunoprecipitation by using purified Pr55(Gag) and rabbit reticulocyte lysate-synthesized Tsg101, and (iii) in vivo in the cytoplasm of COS cells transfected with gag.	Glycosaminoglycans	251-254	tumor susceptibility gene 101 protein	Oryctolagus cuniculus	0-6
11523564-7	2001	This 18-bp deletion is the first additional mutation, beyond the GAG-deletion (Glu302/303del), to be found in the TOR1A gene, and is associated with a distinct type of early onset dystonia.	Glycosaminoglycans	65-68	torsin family 1 member A	Homo sapiens	114-119
11292822-2	2001	In the case of fibroblast growth factor-2 (FGF2) signaling, heparin/heparan sulfate-like glycosaminoglycans (HLGAGs) are involved through interaction with both FGF2 and its receptors (FGFRs) in assembling a tertiary complex and modulating FGF2 activity.	Glycosaminoglycans	89-107	fibroblast growth factor 2	Homo sapiens	15-41
11292822-2	2001	In the case of fibroblast growth factor-2 (FGF2) signaling, heparin/heparan sulfate-like glycosaminoglycans (HLGAGs) are involved through interaction with both FGF2 and its receptors (FGFRs) in assembling a tertiary complex and modulating FGF2 activity.	Glycosaminoglycans	89-107	fibroblast growth factor 2	Homo sapiens	43-47
11292822-2	2001	In the case of fibroblast growth factor-2 (FGF2) signaling, heparin/heparan sulfate-like glycosaminoglycans (HLGAGs) are involved through interaction with both FGF2 and its receptors (FGFRs) in assembling a tertiary complex and modulating FGF2 activity.	Glycosaminoglycans	89-107	fibroblast growth factor 2	Homo sapiens	160-164
11353333-4	2001	ApoC-III also interferes with lipoprotein particle clearance, but its principal role is as an inhibitor of lipolysis, both through the biochemical inhibition of lipoprotein lipase and by interfering with lipoprotein binding to the cell-surface glycosaminoglycan matrix where lipolytic enzymes and lipoprotein receptors reside.	Glycosaminoglycans	244-261	apolipoprotein C3	Homo sapiens	0-8
11304538-0	2001	Cell type-specific differences in glycosaminoglycans modulate the biological activity of a heparin-binding peptide (RKRLQVQLSIRT) from the G domain of the laminin alpha1 chain.	Glycosaminoglycans	34-52	laminin subunit alpha 1	Homo sapiens	155-169
11460008-7	2001	The low second-order rate constant and the lack of a significant interaction in plasma suggest that the inhibition of thrombin by C1-INH has a minor role in circulating blood; however, its role might be important at the endothelial surface, where high concentrations of glycosaminoglycans occur.	Glycosaminoglycans	270-288	coagulation factor II, thrombin	Homo sapiens	118-126
11460008-7	2001	The low second-order rate constant and the lack of a significant interaction in plasma suggest that the inhibition of thrombin by C1-INH has a minor role in circulating blood; however, its role might be important at the endothelial surface, where high concentrations of glycosaminoglycans occur.	Glycosaminoglycans	270-288	serpin family G member 1	Homo sapiens	130-136
11500960-4	2001	Chondrocytes expanded with FGF-2 and cultured on PGA scaffolds in the presence of BMP-2 for 6 weeks yielded engineered cartilage with similar cellularity and size, 1.5-fold higher wet weight GAG fraction, and more homogenous GAG distribution than the corresponding engineered cartilage cultured without BMP-2.	Glycosaminoglycans	191-194	bone morphogenetic protein 2	Bos taurus	82-87
11500960-4	2001	Chondrocytes expanded with FGF-2 and cultured on PGA scaffolds in the presence of BMP-2 for 6 weeks yielded engineered cartilage with similar cellularity and size, 1.5-fold higher wet weight GAG fraction, and more homogenous GAG distribution than the corresponding engineered cartilage cultured without BMP-2.	Glycosaminoglycans	225-228	bone morphogenetic protein 2	Bos taurus	82-87
11333909-4	2001	It appears that the NTD is the major partner of indirect or direct Gag-Gag interactions.	Glycosaminoglycans	67-70	fuzzy planar cell polarity protein	Homo sapiens	20-23
11380810-11	2001	The addition of conditioned medium, containing HS-GAG fragments, restored the proliferative response to FGF-2, confirming the specificity of the interaction.	Glycosaminoglycans	50-53	fibroblast growth factor 2	Homo sapiens	104-109
11333909-4	2001	It appears that the NTD is the major partner of indirect or direct Gag-Gag interactions.	Glycosaminoglycans	71-74	fuzzy planar cell polarity protein	Homo sapiens	20-23
11356980-9	2001	This conservation of positively charged residues indicates that HVR1 is involved in interactions with negatively charged molecules such as lipids, proteins, or glycosaminoglycans (GAGs).	Glycosaminoglycans	160-178	vasoactive intestinal peptide receptor 1	Homo sapiens	64-68
11353130-3	2001	We have previously identified a polymorphic GAG/CTC trinucleotide repeat within the 5" untranslated region of GLCLC.	Glycosaminoglycans	44-47	glutamate-cysteine ligase catalytic subunit	Homo sapiens	110-115
12604021-8	2001	However, the residual inhibiting activity of C-lobe and the similar efficacy shown by negatively or positively charged peptides strongly support the idea that the antiviral activity of bovine lactoferrin cannot be fully explained simply on the basis of competition between the protein and viral recognition sites for binding to glycosaminoglycans.	Glycosaminoglycans	328-346	lactotransferrin	Bos taurus	192-203
11337044-5	2001	Gag-nested PCR-restriction fragment length polymorphism analysis distinguished two different subtypes of gag gene, A and B. Subtype A was found to be the most prevalent among the infected horses that were tested.	Glycosaminoglycans	0-3	gag protein	Equine infectious anemia virus	105-108
11416984-5	2001	This occurs by the interaction of specific positive segments of the apoB-100 with negative glycosaminoglycan chains of the proteoglycans of the intima extracellular matrix.	Glycosaminoglycans	91-108	apolipoprotein B	Homo sapiens	68-76
11312344-5	2001	Here, we show that while CyP A binds both Gag and mature CA proteins, the two binding interactions are actually different.	Glycosaminoglycans	42-45	peptidylprolyl isomerase A	Homo sapiens	25-30
11312344-8	2001	A structural consequence of Gag binding to CyP A was to block this maturational refolding, resulting in a 24-kDa CA protein retaining the immature Pro-rich loop conformation.	Glycosaminoglycans	28-31	peptidylprolyl isomerase A	Homo sapiens	43-48
11281711-2	2001	DNA sequences encoding p17 of B- and C-subtype were cloned from respective gag sequences.	Glycosaminoglycans	75-78	family with sequence similarity 72 member B	Homo sapiens	23-26
11405632-4	2001	It contains two ORFs: the 5" ORF is related to the retroviral gag gene and encodes a protein with cysteine-rich motifs that are thought to form a "zinc-knuckle" in a nucleic-acid binding protein; the 3" ORF encodes a putative reverse transcriptase that includes the conserved domains found in reverse transcriptases from other LINEs and retroviruses.	Glycosaminoglycans	62-65	Adh-related	Drosophila melanogaster	200-206
11428164-8	2001	These findings suggest that KCl mainly removed fiber associated components probably GAG-s, which hindered the immune recognition of fiber-bound fibronectin.	Glycosaminoglycans	84-89	fibronectin 1	Bos taurus	144-155
11428164-9	2001	The strong association of fibronectin with vitreous collagen suggested a modified model for vitreous structure taking in account the binding of fibronectin both by collagen and GAG-s.	Glycosaminoglycans	177-182	fibronectin 1	Bos taurus	26-37
11428164-9	2001	The strong association of fibronectin with vitreous collagen suggested a modified model for vitreous structure taking in account the binding of fibronectin both by collagen and GAG-s.	Glycosaminoglycans	177-182	fibronectin 1	Bos taurus	144-155
11478381-8	2001	The plasmalogen-selective phospholipase A2 differs from other intracellular phospholipases A2 in molecular mass, kinetic properties, substrate specificity, and response to glycosaminoglycans, gangliosides, and sialoglycoproteins.	Glycosaminoglycans	172-190	phospholipase A2, group IB, pancreas	Mus musculus	26-42
11294894-6	2001	Microtiter plate-binding assays, coprecipitation experiments, and staining of sections predigested with different glycosaminoglycan-degrading enzymes and cell adhesion assays all revealed that layilin binds specifically to hyaluronan but not to other tested glycosaminoglycans.	Glycosaminoglycans	114-131	layilin	Homo sapiens	193-200
11294894-6	2001	Microtiter plate-binding assays, coprecipitation experiments, and staining of sections predigested with different glycosaminoglycan-degrading enzymes and cell adhesion assays all revealed that layilin binds specifically to hyaluronan but not to other tested glycosaminoglycans.	Glycosaminoglycans	258-276	layilin	Homo sapiens	193-200
11323006-1	2001	In the presence of glycosaminoglycans, thrombin is rapidly inactivated by two natural inhibitors secreted from liver: antithrombin (AT) is presumed to be the principal thrombin inhibitor in circulating blood, while for heparin cofactor II (HCII), a role outside circulation has been proposed.	Glycosaminoglycans	19-37	coagulation factor II, thrombin	Homo sapiens	39-47
11277585-1	2001	A GAG deletion at position 946 in the DYT1 gene has been identified as one of the gene mutations responsible for autosomal dominant primary torsion dystonia.	Glycosaminoglycans	2-5	torsin family 1 member A	Homo sapiens	38-42
11278162-0	2001	Apolipoprotein E4 stimulates sulfation of glycosaminoglycans in neural cells.	Glycosaminoglycans	42-60	apolipoprotein E	Homo sapiens	0-17
11278162-1	2001	Apolipoprotein E externally added to neuroblastoma cells in culture stimulates [35S]sulfate incorporation on cell and extracellular matrix glycosaminoglycans (sGAG).	Glycosaminoglycans	139-157	apolipoprotein E	Homo sapiens	0-16
11257118-7	2001	The underlying molecular mechanism depends on glycosaminoglycan (GAG) modification of the syndecan-1 core protein at residues S45 or S47 for cell membrane spreading and on the VC2 region of the cytoplasmic domain for spreading and fascin spike formation.	Glycosaminoglycans	46-63	syndecan 1	Mus musculus	90-100
11257118-7	2001	The underlying molecular mechanism depends on glycosaminoglycan (GAG) modification of the syndecan-1 core protein at residues S45 or S47 for cell membrane spreading and on the VC2 region of the cytoplasmic domain for spreading and fascin spike formation.	Glycosaminoglycans	65-68	syndecan 1	Mus musculus	90-100
11257118-8	2001	Expression of the VC2 deletion mutant or GAG-negative syndecan-1 showed that syndecan-1 is necessary in spreading and fascin spike formation by C2C12 cells on TSP-1.	Glycosaminoglycans	41-44	syndecan 1	Mus musculus	77-87
11323006-1	2001	In the presence of glycosaminoglycans, thrombin is rapidly inactivated by two natural inhibitors secreted from liver: antithrombin (AT) is presumed to be the principal thrombin inhibitor in circulating blood, while for heparin cofactor II (HCII), a role outside circulation has been proposed.	Glycosaminoglycans	19-37	serpin family C member 1	Homo sapiens	118-130
11323006-1	2001	In the presence of glycosaminoglycans, thrombin is rapidly inactivated by two natural inhibitors secreted from liver: antithrombin (AT) is presumed to be the principal thrombin inhibitor in circulating blood, while for heparin cofactor II (HCII), a role outside circulation has been proposed.	Glycosaminoglycans	19-37	coagulation factor II, thrombin	Homo sapiens	122-130
11323006-1	2001	In the presence of glycosaminoglycans, thrombin is rapidly inactivated by two natural inhibitors secreted from liver: antithrombin (AT) is presumed to be the principal thrombin inhibitor in circulating blood, while for heparin cofactor II (HCII), a role outside circulation has been proposed.	Glycosaminoglycans	19-37	serpin family D member 1	Homo sapiens	219-238
11323006-1	2001	In the presence of glycosaminoglycans, thrombin is rapidly inactivated by two natural inhibitors secreted from liver: antithrombin (AT) is presumed to be the principal thrombin inhibitor in circulating blood, while for heparin cofactor II (HCII), a role outside circulation has been proposed.	Glycosaminoglycans	19-37	serpin family D member 1	Homo sapiens	240-244
11242522-5	2001	Similar analysis of the gag(p24) region revealed that the majority of infections were subtype A; however, one-third of the specimens were subtype G. Parallel analysis of gag(p24) and env regions revealed discordant subtypes in many specimens that may reflect possible dual and/or recombinant viruses.	Glycosaminoglycans	24-27	transmembrane p24 trafficking protein 2	Homo sapiens	28-31
11106655-4	2001	Mutational analysis shows that sequences at least 70 amino acids away from the glypican-1 GAG attachment site are required for preferential HS assembly, although more nearby sequences also play a role.	Glycosaminoglycans	90-93	glypican 1	Rattus norvegicus	79-89
11106655-5	2001	The effects of the glypican-1 globular domain on HS assembly could also be demonstrated by fusing this domain to sequences representing the GAG attachment sites of other proteoglycans or, surprisingly, simply by expressing the isolated globular domain in cells and analyzing effects either on an exogenously expressed glypican-1 GAG attachment domain or on endogenous proteoglycans.	Glycosaminoglycans	140-143	glypican 1	Rattus norvegicus	19-29
11106655-5	2001	The effects of the glypican-1 globular domain on HS assembly could also be demonstrated by fusing this domain to sequences representing the GAG attachment sites of other proteoglycans or, surprisingly, simply by expressing the isolated globular domain in cells and analyzing effects either on an exogenously expressed glypican-1 GAG attachment domain or on endogenous proteoglycans.	Glycosaminoglycans	329-332	glypican 1	Rattus norvegicus	19-29
11106655-7	2001	These data identify the glypican-1 globular domain as a structural motif that potently influences GAG class determination and suggest that an important role of glypican globular domains is to ensure a high level of HS substitution of these proteoglycans.	Glycosaminoglycans	98-101	glypican 1	Rattus norvegicus	24-34
11242522-5	2001	Similar analysis of the gag(p24) region revealed that the majority of infections were subtype A; however, one-third of the specimens were subtype G. Parallel analysis of gag(p24) and env regions revealed discordant subtypes in many specimens that may reflect possible dual and/or recombinant viruses.	Glycosaminoglycans	170-173	transmembrane p24 trafficking protein 2	Homo sapiens	174-177
11217091-1	2001	Extracellular-superoxide dismutase (EC-SOD) is one of the three SOD isozymes in humans and has affinity for heparin-like sulfated glycosaminoglycans in the extracellular matrix.	Glycosaminoglycans	130-148	superoxide dismutase 3	Homo sapiens	0-34
11230396-3	2001	In addition, sequences of gag-encoded p24 (gag p24), pol-encoded integrase, and env-encoded gp41 were analyzed to assign group and subtype and to assess nucleotide mismatches at primer and probe binding sites.	Glycosaminoglycans	26-29	transmembrane p24 trafficking protein 2	Homo sapiens	38-41
11085980-4	2001	Transfection of human urokinase plasminogen activator receptor in normal Chinese hamster ovary fibroblasts and in Chinese hamster ovary cells defective for the synthesis of sulfated glycosaminoglycans results in specific urokinase/receptor interaction only in nondefective cells.	Glycosaminoglycans	182-200	plasminogen activator, urokinase receptor	Homo sapiens	22-62
11087729-1	2001	Human UDP-d-xylose:proteoglycan core protein beta-d-xylosyltransferase (EC, XT) initiates the biosynthesis of glycosaminoglycan lateral chains in proteoglycans by transfer of xylose from UDP-xylose to specific serine residues of the core protein.	Glycosaminoglycans	110-127	xylosyltransferase 2	Homo sapiens	6-70
11222399-8	2001	Significant reduction of lysosomal glycosaminoglycan storage corresponded directly with GUS enzyme activity and percentage of histochemically GUS(+) cells in visceral organs and hematopoietic tissues such as thymus, spleen, peripheral blood, and bone marrow.	Glycosaminoglycans	35-52	glucuronidase, beta	Mus musculus	88-91
11222399-8	2001	Significant reduction of lysosomal glycosaminoglycan storage corresponded directly with GUS enzyme activity and percentage of histochemically GUS(+) cells in visceral organs and hematopoietic tissues such as thymus, spleen, peripheral blood, and bone marrow.	Glycosaminoglycans	35-52	glucuronidase, beta	Mus musculus	142-145
11342172-1	2001	We show that cell surface glycans, sialic acid and mannose-containing species, are involved beside glycosaminoglycans (GAGs), heparan sulfate and chondroitin sulfate in the binding of full length (1--68) RANTES not only to CCR5 positive human primary lymphocytes or macrophages but also to CCR5 negative monocytic U937 cells.	Glycosaminoglycans	99-117	C-C motif chemokine receptor 5	Homo sapiens	223-227
11342172-1	2001	We show that cell surface glycans, sialic acid and mannose-containing species, are involved beside glycosaminoglycans (GAGs), heparan sulfate and chondroitin sulfate in the binding of full length (1--68) RANTES not only to CCR5 positive human primary lymphocytes or macrophages but also to CCR5 negative monocytic U937 cells.	Glycosaminoglycans	99-117	C-C motif chemokine receptor 5	Homo sapiens	290-294
11342172-1	2001	We show that cell surface glycans, sialic acid and mannose-containing species, are involved beside glycosaminoglycans (GAGs), heparan sulfate and chondroitin sulfate in the binding of full length (1--68) RANTES not only to CCR5 positive human primary lymphocytes or macrophages but also to CCR5 negative monocytic U937 cells.	Glycosaminoglycans	119-123	C-C motif chemokine receptor 5	Homo sapiens	223-227
11342172-1	2001	We show that cell surface glycans, sialic acid and mannose-containing species, are involved beside glycosaminoglycans (GAGs), heparan sulfate and chondroitin sulfate in the binding of full length (1--68) RANTES not only to CCR5 positive human primary lymphocytes or macrophages but also to CCR5 negative monocytic U937 cells.	Glycosaminoglycans	119-123	C-C motif chemokine receptor 5	Homo sapiens	290-294
11229466-11	2001	CONCLUSION: The results of this study suggest that the deleterious effect of IL-1beta on the anabolism of proteoglycan could involve the repression of GlcAT-I, a key enzyme in the biosynthesis of glycosaminoglycan.	Glycosaminoglycans	196-213	interleukin 1 beta	Rattus norvegicus	77-85
11217091-1	2001	Extracellular-superoxide dismutase (EC-SOD) is one of the three SOD isozymes in humans and has affinity for heparin-like sulfated glycosaminoglycans in the extracellular matrix.	Glycosaminoglycans	130-148	superoxide dismutase 3	Homo sapiens	36-42
11217091-1	2001	Extracellular-superoxide dismutase (EC-SOD) is one of the three SOD isozymes in humans and has affinity for heparin-like sulfated glycosaminoglycans in the extracellular matrix.	Glycosaminoglycans	130-148	superoxide dismutase 3	Homo sapiens	39-42
11016923-6	2001	In the present work, a combination of circular dichroism analysis, affinity chromatography, cathepsin B mutants, and fluorogenic substrate assays were used to characterize the interaction of human cathepsin B with glycosaminoglycans.	Glycosaminoglycans	214-232	cathepsin B	Homo sapiens	92-103
11239517-2	2001	There are two known polymorphisms in exon 11 of the DBP gene resulting in amino acid variants: codons 416 GAT --&gt; GAG (Asp --&gt; Glu) and 420 ACG --&gt; AAG (Thr --&gt; Lys).	Glycosaminoglycans	117-120	D-box binding PAR bZIP transcription factor	Homo sapiens	52-55
11159948-1	2001	Hurler syndrome is the most severe form of a lysosomal storage disease caused by loss of the enzyme alpha-L-iduronidase (encoded by the IDUA gene), which participates in the degradation of glycosaminoglycans (GAGs) within the lysosome.	Glycosaminoglycans	189-207	alpha-L-iduronidase	Homo sapiens	136-140
11016923-6	2001	In the present work, a combination of circular dichroism analysis, affinity chromatography, cathepsin B mutants, and fluorogenic substrate assays were used to characterize the interaction of human cathepsin B with glycosaminoglycans.	Glycosaminoglycans	214-232	cathepsin B	Homo sapiens	197-208
11016923-7	2001	The nature of the cathepsin B-glycosaminoglycans interaction was sensitive to the charge and type of polysaccharide.	Glycosaminoglycans	30-48	cathepsin B	Homo sapiens	18-29
11161477-4	2001	The mutant NPCs contained elevated levels of undegraded glycosaminoglycans (GAGs), the substrate for GUSB.	Glycosaminoglycans	56-74	glucuronidase, beta	Mus musculus	101-105
11310563-1	2001	We report that ATP enhances the activity of galactosyltransferase-I, which synthesizes the linkage region between glycosaminoglycan chains and the core proteins of proteoglycans.	Glycosaminoglycans	114-131	beta-1,4-galactosyltransferase 7	Homo sapiens	44-67
11145607-8	2001	A stimulatory effect on cartilage matrix synthesis, assessed by (35)SO(4) incorporation into glycosaminoglycans, was produced only by the highest concentration of BMP-2.	Glycosaminoglycans	93-111	bone morphogenetic protein 2	Homo sapiens	163-168
11822816-6	2001	Exogenous insulin (0.05-50 microg/ml) increased the growth rate and the glycosaminoglycan fraction of tissue-engineered cartilage, decreased the cell number in the tissue constructs, and improved the morphological appearance, with 2.5 microg/ml being the most favorable concentration.	Glycosaminoglycans	72-89	insulin	Bos taurus	10-17
11684881-4	2001	Binary IGF-IGFBP complexes have high affinities and slow dissociation rates, which may be accelerated by partial IGFBP proteolysis and interaction with glycosaminoglycans.	Glycosaminoglycans	152-170	insulin like growth factor binding protein 3	Homo sapiens	11-16
11134271-2	2001	Three human immunodeficiency virus protease cleavage sites within gag (p2/NC, NC/p1, and NC/TFP) showed considerable in vivo evolution before and after therapy with indinavir, ritonavir, and/or saquinavir.	Glycosaminoglycans	66-69	inhibitor of carbonic anhydrase pseudogene	Homo sapiens	92-95
11374439-7	2000	Glycosaminoglycans purified from stromas had distinct effect on the GM-CSF-mediated proliferation of FDC-P1 cells: those purified from S17 and GR cells were stimulatory, whereas those obtained from SF cells were slightly stimulatory at low concentration, but inhibitory at the higher ones.	Glycosaminoglycans	0-18	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	68-74
11281322-0	2001	Sup35p yeast prion-like protein as an adapter for production of the Gag-p55 antigen of HIV-1 and the L-chain of botulinum neurotoxin in Saccharomyces cerevisiae.	Glycosaminoglycans	68-71	translation termination factor GTPase eRF3	Saccharomyces cerevisiae S288C	0-6
11095655-0	2000	Glycosaminoglycan therapy prevents TGF-beta1 overexpression and pathologic changes in renal tissue of long-term diabetic rats.	Glycosaminoglycans	0-17	transforming growth factor, beta 1	Rattus norvegicus	35-44
11074061-6	2000	Since IGF-I is known as a stimulator of collagen and sulfated glycosaminoglycan biosynthesis, the high concentration of this growth factor in the umbilical cord plasma may be an agent responsible for preeclampsia-associated remodelling of the umbilical cord, which results in dysfunction in fetal circulation.	Glycosaminoglycans	62-79	insulin like growth factor 1	Homo sapiens	6-11
10978312-11	2000	These findings indicate that CS chains containing the E unit as well as heparin-like glycosaminoglycans may be involved in the expression and/or modulation of the multiple neuroregulatory functions of MK such as neuronal adhesion and migration and promotion of neurite outgrowth.	Glycosaminoglycans	85-103	midkine	Rattus norvegicus	201-203
10978312-9	2000	Direct interactions of MK with various glycosaminoglycans were then evaluated using surface plasmon resonance, showing that CS-E bound MK as strongly as heparin, followed by other over-sulfated CS isoforms, CS-H and CS-K.	Glycosaminoglycans	39-57	midkine	Rattus norvegicus	23-25
11095655-8	2000	These results suggest that GAG inhibit TGF-beta1 overexpression at the transcriptional level, possibly via inhibition of high glucose-activated PKC.	Glycosaminoglycans	27-30	transforming growth factor, beta 1	Rattus norvegicus	39-48
11095655-2	2000	In a rat model of diabetes mellitus-induced glomerulosclerosis, daily administration of a modified heparin (mH) glycosaminoglycan (GAG) preparation with low anticoagulant activity prevented glomerular and tubular matrix accumulation, as well as overexpression of TGF-beta1 mRNA and albuminuria, without obvious side effects.	Glycosaminoglycans	112-129	transforming growth factor, beta 1	Rattus norvegicus	263-272
11095655-9	2000	The findings indicate the potential of GAG therapy for the prevention of diabetic glomerulosclerosis by the inhibition of chronic disease-induced TGF-beta1 mRNA overexpression.	Glycosaminoglycans	39-42	transforming growth factor, beta 1	Rattus norvegicus	146-155
11095655-2	2000	In a rat model of diabetes mellitus-induced glomerulosclerosis, daily administration of a modified heparin (mH) glycosaminoglycan (GAG) preparation with low anticoagulant activity prevented glomerular and tubular matrix accumulation, as well as overexpression of TGF-beta1 mRNA and albuminuria, without obvious side effects.	Glycosaminoglycans	131-134	transforming growth factor, beta 1	Rattus norvegicus	263-272
11067924-10	2000	This interaction will tend to retain IL-6 close to its sites of secretion in the tissues by binding to heparin-like glycosaminoglycans, thus favoring a paracrine mode of activity.	Glycosaminoglycans	116-134	interleukin 6	Homo sapiens	37-41
11118069-3	2000	In the present study, we determined env (C2/V3) and gag (p17) subtypes of 25 specimens from central Myanmar (Mandalay).	Glycosaminoglycans	52-55	family with sequence similarity 72 member B	Homo sapiens	57-60
11068038-3	2000	Thrombin inhibition by HCII without glycosaminoglycan was decreased approximately two-fold by the aptamer.	Glycosaminoglycans	36-53	coagulation factor II, thrombin	Homo sapiens	0-8
10950950-7	2000	Consistent with these results, structural analysis showed that versican is modified with at least CS B and CS C. Thus, proteoglycans sufficiently modified with the appropriate glycosaminoglycans should be able to bind L-selectin, P-selectin, and/or CD44.	Glycosaminoglycans	176-194	versican	Homo sapiens	63-71
10950950-3	2000	The binding of versican to L- and P-selectin was inhibited by CS B, CS E, and heparan sulfate (HS) but not by any other glycosaminoglycans tested.	Glycosaminoglycans	120-138	versican	Homo sapiens	15-23
11087801-0	2000	The GAG deletion of the DYT1 gene is infrequent in musicians with focal dystonia.	Glycosaminoglycans	4-7	torsin family 1 member A	Homo sapiens	24-28
11029577-5	2000	To understand the molecular recognition of glycosaminoglycans by Abeta, we have examined a series of synthetic peptides with systematic alanine substitutions.	Glycosaminoglycans	43-61	amyloid beta precursor protein	Homo sapiens	65-70
11029577-9	2000	Interaction of the substituted peptides with heparin and chondroitin sulfate glycosaminoglycans demonstrate that although electrostatic interactions contribute to binding, nonionic interactions such as hydrogen bonding and van der Waals packing play a role in glycosaminoglycan-induced Abeta folding and aggregation.	Glycosaminoglycans	77-94	amyloid beta precursor protein	Homo sapiens	286-291
11104212-3	2000	To determine the frequency of this mutation in a larger series of patients, we examined 44 index patients with sporadic or familial (seven patients) writer"s cramp for the presence of the DYT1 GAG deletion, including eight patients with segmental dystonia involving at least one upper limb.	Glycosaminoglycans	193-196	torsin family 1 member A	Homo sapiens	188-192
11090695-0	2000	Flt3 ligand enhances the immunogenicity of a gag-based HIV-1 vaccine.	Glycosaminoglycans	45-48	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
10951362-4	2000	When cultured for 21 days in vitro in a defined medium supplemented with 10 ng/mL of TGF-beta 3, hMSC/Gelfoam constructs produced a cartilage-like extracellular matrix containing sulfated glycosaminoglycans (s-GAGs) and type-II collagen, as evident upon histologic evaluation.	Glycosaminoglycans	188-206	musculin	Homo sapiens	97-101
10900194-0	2000	TIMP-3 binds to sulfated glycosaminoglycans of the extracellular matrix.	Glycosaminoglycans	25-43	TIMP metallopeptidase inhibitor 3	Homo sapiens	0-6
11054265-0	2000	Calmodulin and HIV type 1: interactions with Gag and Gag products.	Glycosaminoglycans	45-48	calmodulin 1	Homo sapiens	0-10
11054265-0	2000	Calmodulin and HIV type 1: interactions with Gag and Gag products.	Glycosaminoglycans	53-56	calmodulin 1	Homo sapiens	0-10
11038180-4	2000	Additionally, each of the gag mutations prevented mitochondrial fragmentation caused by loss of the mitochondrial fusion factor, Fzo1p, or by treatment of cells with sodium azide.	Glycosaminoglycans	26-29	mitofusin	Saccharomyces cerevisiae S288C	129-134
10922378-3	2000	Proposed cellular binding sites for TFPI include nonspecific association with cell surface glycosaminoglycans and binding to glycosyl phosphatidylinositol-anchored proteins.	Glycosaminoglycans	91-109	tissue factor pathway inhibitor	Homo sapiens	36-40
10900194-2	2000	The present results show that glycosaminoglycans such as heparin, heparan sulfate, chondroitin sulfates A, B, and C, and sulfated compounds such as suramin and pentosan efficiently extract TIMP-3 from the postpartum rat uterus.	Glycosaminoglycans	30-48	TIMP metallopeptidase inhibitor 3	Rattus norvegicus	189-195
11005858-0	2000	sqv-3, -7, and -8, a set of genes affecting morphogenesis in Caenorhabditis elegans, encode enzymes required for glycosaminoglycan biosynthesis.	Glycosaminoglycans	113-130	Xylosylprotein 4-beta-galactosyltransferase	Caenorhabditis elegans	0-17
10995555-11	2000	The presence of consensus sites for glycosaminoglycan attachment in the deduced sequence of mouse SPACR and the absence of these sites in human SPACR provide molecular verification of our biochemical results, suggesting that differences in post-translational modifications of SPACR may be important in SPACR function in foveate and non-foveate retinas.	Glycosaminoglycans	36-53	interphotoreceptor matrix proteoglycan 1	Mus musculus	98-103
11005858-3	2000	Using a combination of in vitro analysis of SQV enzymatic activities, sqv(+)-mediated rescue of vertebrate cell lines, and biochemical characterization of sqv mutants, we show that sqv-3, -7, and -8 all affect the biosynthesis of glycosaminoglycans and therefore compromise the function of one specific class of glycoconjugates, proteoglycans.	Glycosaminoglycans	230-248	Xylosylprotein 4-beta-galactosyltransferase	Caenorhabditis elegans	181-198
10842173-2	2000	Galbeta1,3-glucuronosyltransferase (GlcAT-I) that catalyzes the transfer of a glucuronic acid residue onto the trisaccharide primer of the glycosaminoglycan-protein linkage region plays an essential role in the early steps of the biosynthesis of glycosaminoglycans.	Glycosaminoglycans	246-264	beta-1,3-glucuronyltransferase 3	Homo sapiens	36-43
11006120-4	2000	The 3-OST-1 enzyme is involved in heparan sulfate biosynthesis and introduces a critical 3-O-sulfo group into this glycosaminoglycan affording the appropriate pentasaccharide sequence capable of high affinity binding to ATIII.	Glycosaminoglycans	115-132	heparan sulfate-glucosamine 3-sulfotransferase 1	Homo sapiens	4-11
11006120-4	2000	The 3-OST-1 enzyme is involved in heparan sulfate biosynthesis and introduces a critical 3-O-sulfo group into this glycosaminoglycan affording the appropriate pentasaccharide sequence capable of high affinity binding to ATIII.	Glycosaminoglycans	115-132	serpin family C member 1	Homo sapiens	220-225
10961890-1	2000	Glycosaminoglycans (GAG) are a group of negatively charged molecules that have been shown to bind and directly regulate the bioactivity of growth factors and cytokines such as basic fibroblast growth factor, transforming growth factor-beta, IL-7, and interferon-gamma.	Glycosaminoglycans	0-18	interleukin 7	Homo sapiens	241-245
10957718-0	2000	Polymorphism of HIV type 1 gag p7/p1 and p1/p6 cleavage sites: clinical significance and implications for resistance to protease inhibitors.	Glycosaminoglycans	27-30	crystallin gamma F, pseudogene	Homo sapiens	31-36
10961890-1	2000	Glycosaminoglycans (GAG) are a group of negatively charged molecules that have been shown to bind and directly regulate the bioactivity of growth factors and cytokines such as basic fibroblast growth factor, transforming growth factor-beta, IL-7, and interferon-gamma.	Glycosaminoglycans	0-18	interferon gamma	Homo sapiens	251-267
10961890-1	2000	Glycosaminoglycans (GAG) are a group of negatively charged molecules that have been shown to bind and directly regulate the bioactivity of growth factors and cytokines such as basic fibroblast growth factor, transforming growth factor-beta, IL-7, and interferon-gamma.	Glycosaminoglycans	20-23	interleukin 7	Homo sapiens	241-245
10961890-1	2000	Glycosaminoglycans (GAG) are a group of negatively charged molecules that have been shown to bind and directly regulate the bioactivity of growth factors and cytokines such as basic fibroblast growth factor, transforming growth factor-beta, IL-7, and interferon-gamma.	Glycosaminoglycans	20-23	interferon gamma	Homo sapiens	251-267
10961890-2	2000	The ability of GAG to interact with human IL-10 (hIL-10) and the effect of these interactions on its biologic activity were analyzed.	Glycosaminoglycans	15-18	interleukin 10	Homo sapiens	42-47
10961890-2	2000	The ability of GAG to interact with human IL-10 (hIL-10) and the effect of these interactions on its biologic activity were analyzed.	Glycosaminoglycans	15-18	interleukin 10	Homo sapiens	49-55
10961890-11	2000	Taken together, these findings support the hypothesis that soluble and cell-surface GAG and, in particular, their sulfate groups are important in binding and modulation of hIL-10 activity.	Glycosaminoglycans	84-87	interleukin 10	Homo sapiens	172-178
11054083-2	2000	One allele contained a novel four base-pair deletion (TGAG) that eliminated the last base of the codon for Ser39 (AGT) and the entire codon for Glu40 (GAG), causing a reading frame shift that yielded a stretch of 51 amino acids before a premature stop codon.	Glycosaminoglycans	55-58	angiotensinogen	Homo sapiens	114-117
10951195-0	2000	O-glycosylation of insulin-like growth factor (IGF) binding protein-6 maintains high IGF-II binding affinity by decreasing binding to glycosaminoglycans and susceptibility to proteolysis.	Glycosaminoglycans	134-152	insulin like growth factor binding protein 6	Homo sapiens	19-69
10984667-1	2000	Early onset torsion dystonia (DYT1) is a dominantly inherited dystonia caused by a deletion of three bases, GAG, coding glutamic acid, in chromosome 9q34.	Glycosaminoglycans	108-111	torsin family 1 member A	Homo sapiens	30-34
10951195-0	2000	O-glycosylation of insulin-like growth factor (IGF) binding protein-6 maintains high IGF-II binding affinity by decreasing binding to glycosaminoglycans and susceptibility to proteolysis.	Glycosaminoglycans	134-152	insulin like growth factor 2	Homo sapiens	85-91
10954568-5	2000	In addition, we show that Gag and Env colocalize at the plasma membrane and that mistargeting of a mutant Gag to the Golgi apparatus alters the pattern of surface expression of Env.	Glycosaminoglycans	26-29	endogenous retrovirus group W member 1, envelope	Homo sapiens	177-180
10951195-3	2000	Binding of recombinant human nonglycosylated (n-g) IGFBP-6 to a range of glycosaminoglycans in vitro was approximately threefold greater than that of glycosylated (g) IGFBP-6.	Glycosaminoglycans	73-91	insulin like growth factor binding protein 6	Homo sapiens	51-58
10951195-4	2000	When bound to glycosaminoglycans, IGFBP-6 had approximately 10-fold reduced binding affinity for IGF-II.	Glycosaminoglycans	14-32	insulin like growth factor binding protein 6	Homo sapiens	34-41
10951195-4	2000	When bound to glycosaminoglycans, IGFBP-6 had approximately 10-fold reduced binding affinity for IGF-II.	Glycosaminoglycans	14-32	insulin like growth factor 2	Homo sapiens	97-103
10954568-5	2000	In addition, we show that Gag and Env colocalize at the plasma membrane and that mistargeting of a mutant Gag to the Golgi apparatus alters the pattern of surface expression of Env.	Glycosaminoglycans	106-109	endogenous retrovirus group W member 1, envelope	Homo sapiens	177-180
11009204-8	2000	The GAG deletion in the DYT1 gene was excluded in the index case.	Glycosaminoglycans	4-7	torsin family 1 member A	Homo sapiens	24-28
10827174-7	2000	Here we demonstrate that the thrombospondin type-1 (TSP-1) motif located within the C terminus of aggrecanase-1 binds to the glycosaminoglycans of aggrecan.	Glycosaminoglycans	125-143	thrombospondin 1	Homo sapiens	29-50
10827174-7	2000	Here we demonstrate that the thrombospondin type-1 (TSP-1) motif located within the C terminus of aggrecanase-1 binds to the glycosaminoglycans of aggrecan.	Glycosaminoglycans	125-143	thrombospondin 1	Homo sapiens	52-57
10827174-7	2000	Here we demonstrate that the thrombospondin type-1 (TSP-1) motif located within the C terminus of aggrecanase-1 binds to the glycosaminoglycans of aggrecan.	Glycosaminoglycans	125-143	ADAM metallopeptidase with thrombospondin type 1 motif 4	Homo sapiens	98-111
10917892-6	2000	Specific inhibitors of RANTES-induced activation, such as soluble glycosaminoglycans, MIP-1alpha and MIP-1beta, acted by preventing the binding of RANTES on the cell surface.	Glycosaminoglycans	66-84	C-C motif chemokine ligand 5	Homo sapiens	23-29
11776053-3	2000	The antithrombin mechanism of GAG was checked by assaying its effects on the thrombin activity in normal human pooled plasma, purified human heparin cofactor II system and antithrombin III system.	Glycosaminoglycans	30-33	serpin family C member 1	Homo sapiens	4-16
11776053-3	2000	The antithrombin mechanism of GAG was checked by assaying its effects on the thrombin activity in normal human pooled plasma, purified human heparin cofactor II system and antithrombin III system.	Glycosaminoglycans	30-33	coagulation factor II, thrombin	Homo sapiens	8-16
11776053-3	2000	The antithrombin mechanism of GAG was checked by assaying its effects on the thrombin activity in normal human pooled plasma, purified human heparin cofactor II system and antithrombin III system.	Glycosaminoglycans	30-33	serpin family C member 1	Homo sapiens	172-184
11776053-5	2000	We studied the effect of GAG on the expression and transcription of tissue factor (TF) and thrombomodulin (TM) in LPS (lipopolysaccharide)-stimulated human umbilical vein endothelial cells (HUVECs), and used heparin as a control.	Glycosaminoglycans	25-28	coagulation factor III, tissue factor	Homo sapiens	68-81
11776053-5	2000	We studied the effect of GAG on the expression and transcription of tissue factor (TF) and thrombomodulin (TM) in LPS (lipopolysaccharide)-stimulated human umbilical vein endothelial cells (HUVECs), and used heparin as a control.	Glycosaminoglycans	25-28	coagulation factor III, tissue factor	Homo sapiens	83-85
11776053-5	2000	We studied the effect of GAG on the expression and transcription of tissue factor (TF) and thrombomodulin (TM) in LPS (lipopolysaccharide)-stimulated human umbilical vein endothelial cells (HUVECs), and used heparin as a control.	Glycosaminoglycans	25-28	thrombomodulin	Homo sapiens	91-105
11776053-10	2000	GAG inhibited thrombin activity in the presence of HCII with a second order rate constant of 1.14 x 10(7) m-1.min-1, which was 4.6 times higher than that of ATIII.	Glycosaminoglycans	0-3	coagulation factor II, thrombin	Homo sapiens	14-22
11776053-10	2000	GAG inhibited thrombin activity in the presence of HCII with a second order rate constant of 1.14 x 10(7) m-1.min-1, which was 4.6 times higher than that of ATIII.	Glycosaminoglycans	0-3	serpin family D member 1	Homo sapiens	51-55
11776053-11	2000	GAG significantly inhibited the polymerization of fibrin monomer and enhanced the activity of plasmin in a concentration dependent manner.	Glycosaminoglycans	0-3	plasminogen	Homo sapiens	94-101
11776053-12	2000	GAG could impair TF mRNA expression and up-regulate TM mRNA expression.	Glycosaminoglycans	0-3	coagulation factor III, tissue factor	Homo sapiens	17-19
11776053-16	2000	GAG was similar to dermatan sulfate both in the efficiency and in the mechanism of antithrombin.	Glycosaminoglycans	0-3	serpin family C member 1	Homo sapiens	83-95
11776053-17	2000	The acceleration of colt lysis by GAG depended on its ability to increase the activity of plasmin, to inhibit the polymerizing of fibrin monomer, and consequently, to alter the architecture of the fibrin net work.	Glycosaminoglycans	34-37	plasminogen	Homo sapiens	90-97
10917892-6	2000	Specific inhibitors of RANTES-induced activation, such as soluble glycosaminoglycans, MIP-1alpha and MIP-1beta, acted by preventing the binding of RANTES on the cell surface.	Glycosaminoglycans	66-84	C-C motif chemokine ligand 5	Homo sapiens	147-153
10895897-7	2000	Chondrocytes exposed to IL-1beta had loss of GAG, increased PGE2 and MMP-3 concentrations, and lack of collagen type-II synthesis.	Glycosaminoglycans	45-48	interleukin 1 beta	Canis lupus familiaris	24-32
10951557-1	2000	Our preliminary studies suggested that the novel gag-truncated mos (tmos) open reading frame (ORF) of R7, a spontaneous deletion mutant of Moloney murine sarcoma virus 124 (MoMuSV124), may be responsible for R7"s unique ability to induce brain lesions in all R7-injected mice.	Glycosaminoglycans	49-52	Moloney sarcoma oncogene	Mus musculus	63-66
10951557-2	2000	However, when we replaced the gag-tmos ORF with either the MoMuSV124 or the homologous myeloproliferative sarcoma virus env-mos gene, we found that both recombinant viruses also induced brain lesions in all injected mice.	Glycosaminoglycans	30-33	Moloney sarcoma oncogene	Mus musculus	35-38
10884430-5	2000	Constructs encoding gag p24 and nef stimulate gag-specific CD4 proliferation and a secondary cytotoxic T lymphocyte response in HIV-infected donor peripheral blood mononuclear cells in vitro.	Glycosaminoglycans	20-23	transmembrane p24 trafficking protein 2	Homo sapiens	24-27
10884430-5	2000	Constructs encoding gag p24 and nef stimulate gag-specific CD4 proliferation and a secondary cytotoxic T lymphocyte response in HIV-infected donor peripheral blood mononuclear cells in vitro.	Glycosaminoglycans	20-23	CD4 molecule	Homo sapiens	59-62
10884430-5	2000	Constructs encoding gag p24 and nef stimulate gag-specific CD4 proliferation and a secondary cytotoxic T lymphocyte response in HIV-infected donor peripheral blood mononuclear cells in vitro.	Glycosaminoglycans	46-49	transmembrane p24 trafficking protein 2	Homo sapiens	24-27
10884430-5	2000	Constructs encoding gag p24 and nef stimulate gag-specific CD4 proliferation and a secondary cytotoxic T lymphocyte response in HIV-infected donor peripheral blood mononuclear cells in vitro.	Glycosaminoglycans	46-49	S100 calcium binding protein B	Homo sapiens	32-35
10884430-5	2000	Constructs encoding gag p24 and nef stimulate gag-specific CD4 proliferation and a secondary cytotoxic T lymphocyte response in HIV-infected donor peripheral blood mononuclear cells in vitro.	Glycosaminoglycans	46-49	CD4 molecule	Homo sapiens	59-62
10992429-6	2000	When serum was replaced however by insulin-like growth factor-1 (IGF-1) (10 ng/mL) plus transforming growth factor-beta2 (TGF-beta2) (10 ng/mL) an increased glycosaminoglycan production and induction of collagen type II was found, especially in cells isolated from perichondrium of the ear.	Glycosaminoglycans	157-174	insulin-like growth factor I	Oryctolagus cuniculus	35-63
10992429-6	2000	When serum was replaced however by insulin-like growth factor-1 (IGF-1) (10 ng/mL) plus transforming growth factor-beta2 (TGF-beta2) (10 ng/mL) an increased glycosaminoglycan production and induction of collagen type II was found, especially in cells isolated from perichondrium of the ear.	Glycosaminoglycans	157-174	insulin-like growth factor I	Oryctolagus cuniculus	65-70
10992429-6	2000	When serum was replaced however by insulin-like growth factor-1 (IGF-1) (10 ng/mL) plus transforming growth factor-beta2 (TGF-beta2) (10 ng/mL) an increased glycosaminoglycan production and induction of collagen type II was found, especially in cells isolated from perichondrium of the ear.	Glycosaminoglycans	157-174	transforming growth factor beta-2 proprotein	Oryctolagus cuniculus	88-120
10992429-6	2000	When serum was replaced however by insulin-like growth factor-1 (IGF-1) (10 ng/mL) plus transforming growth factor-beta2 (TGF-beta2) (10 ng/mL) an increased glycosaminoglycan production and induction of collagen type II was found, especially in cells isolated from perichondrium of the ear.	Glycosaminoglycans	157-174	transforming growth factor beta-2 proprotein	Oryctolagus cuniculus	122-131
10806213-3	2000	Three genes recently demonstrated to affect signaling by members of the Wnt, transforming growth factor-beta, Hedgehog, and fibroblast growth factor families in Drosophila encode proteins with homology to vertebrate enzymes involved in glycosaminoglycan synthesis.	Glycosaminoglycans	236-253	hedgehog	Drosophila melanogaster	110-118
10809899-3	2000	IGF-I is known as a stimulator of collagen and sulphated glycosaminoglycans (GAGs) biosynthesis.	Glycosaminoglycans	57-75	insulin like growth factor 1	Homo sapiens	0-5
11028764-3	2000	IGF-1 is a stimulator of biosynthetics of collagen and sulphated glycosaminoglycans.	Glycosaminoglycans	65-83	insulin like growth factor 1	Homo sapiens	0-5
11028764-14	2000	This may be a factor, which prevents the binding of IGF-1 by BPs and facilitates the binding of IGF-1 to cells, stimulating them to produce sulphated glycosaminoglycans in Wharton"s jelly.	Glycosaminoglycans	150-168	insulin like growth factor 1	Homo sapiens	52-57
11028764-14	2000	This may be a factor, which prevents the binding of IGF-1 by BPs and facilitates the binding of IGF-1 to cells, stimulating them to produce sulphated glycosaminoglycans in Wharton"s jelly.	Glycosaminoglycans	150-168	insulin like growth factor 1	Homo sapiens	96-101
10749870-8	2000	In conclusion, both biglycan and decorin from atherosclerotic plaque possessed reduced activity with HCII, but only biglycan demonstrated a correlation between activity and specific glycosaminoglycan structural features.	Glycosaminoglycans	182-199	biglycan	Homo sapiens	116-124
10907641-9	2000	Serum p24 gag was detected at 2 weeks after inoculation, after which total CD4-positive cell numbers declined, as seen clinically in patients infected with HIV.	Glycosaminoglycans	10-13	transmembrane p24 trafficking protein 2	Homo sapiens	6-9
10907641-9	2000	Serum p24 gag was detected at 2 weeks after inoculation, after which total CD4-positive cell numbers declined, as seen clinically in patients infected with HIV.	Glycosaminoglycans	10-13	CD4 molecule	Homo sapiens	75-78
10817918-0	2000	Glycosaminoglycans co-administration enhance insulin-like growth factor-I neuroprotective and neuroregenerative activity in traumatic and genetic models of motor neuron disease: a review.	Glycosaminoglycans	0-18	insulin-like growth factor 1	Rattus norvegicus	45-73
10817918-6	2000	In saline-treated rats, reinnervation was only partial and there was a marked muscle fibre atrophy, whereas, glycosaminoglycan treatment of lesioned rats increased IGF-I mRNA and protein in the reinnervated muscle, and IGF-I and insulin-like growth factor binding protein-3 plasma levels.	Glycosaminoglycans	109-126	insulin-like growth factor 1	Rattus norvegicus	164-169
10817918-6	2000	In saline-treated rats, reinnervation was only partial and there was a marked muscle fibre atrophy, whereas, glycosaminoglycan treatment of lesioned rats increased IGF-I mRNA and protein in the reinnervated muscle, and IGF-I and insulin-like growth factor binding protein-3 plasma levels.	Glycosaminoglycans	109-126	insulin-like growth factor 1	Rattus norvegicus	219-273
10751422-2	2000	To this end, we examined the in vitro binding of apoE complexed with dimyristoylphosphatidylcholine (DMPC) to human aortic Bg before and after glycosaminoglycan (GAG) depletion.	Glycosaminoglycans	143-160	apolipoprotein E	Homo sapiens	49-53
10823874-4	2000	In addition, this study shows that VCP-through its ability to bind to glycosaminoglycans (heparin-like molecules) on the surface of human endothelial cells-is able to block antibody binding to surface major histocompatibility complex class I molecules.	Glycosaminoglycans	70-88	valosin containing protein	Homo sapiens	35-38
10823876-6	2000	The results show that 3 out of 46 peptides spanning p17(Gag) and p24(Gag) sequences tested contain two-thirds of the dominant Gag-specific epitopes, irrespective of the clade, ethnicity, or age group studied.	Glycosaminoglycans	56-59	family with sequence similarity 72 member B	Homo sapiens	52-55
10823876-6	2000	The results show that 3 out of 46 peptides spanning p17(Gag) and p24(Gag) sequences tested contain two-thirds of the dominant Gag-specific epitopes, irrespective of the clade, ethnicity, or age group studied.	Glycosaminoglycans	69-72	transmembrane p24 trafficking protein 2	Homo sapiens	65-68
10823876-6	2000	The results show that 3 out of 46 peptides spanning p17(Gag) and p24(Gag) sequences tested contain two-thirds of the dominant Gag-specific epitopes, irrespective of the clade, ethnicity, or age group studied.	Glycosaminoglycans	69-72	transmembrane p24 trafficking protein 2	Homo sapiens	65-68
10823876-8	2000	Dominant responses in Caucasoids were more often within p17(Gag) peptide residues 16 to 30 (38 versus 12%; P &lt; 0.01), while p24(Gag) peptide residues 41 to 60 contained the dominant Gag epitope more often in the African subjects tested (39 versus 4%; P &lt; 0.005).	Glycosaminoglycans	131-134	transmembrane p24 trafficking protein 2	Homo sapiens	127-130
10823876-8	2000	Dominant responses in Caucasoids were more often within p17(Gag) peptide residues 16 to 30 (38 versus 12%; P &lt; 0.01), while p24(Gag) peptide residues 41 to 60 contained the dominant Gag epitope more often in the African subjects tested (39 versus 4%; P &lt; 0.005).	Glycosaminoglycans	131-134	transmembrane p24 trafficking protein 2	Homo sapiens	127-130
10823876-9	2000	Within this 20-mer p24(Gag), an epitope presented by both B42 and B81 is defined which represents the dominant Gag response in &gt;30% of the total infected population in Durban.	Glycosaminoglycans	23-26	transmembrane p24 trafficking protein 2	Homo sapiens	19-22
10823876-9	2000	Within this 20-mer p24(Gag), an epitope presented by both B42 and B81 is defined which represents the dominant Gag response in &gt;30% of the total infected population in Durban.	Glycosaminoglycans	23-26	proline rich nuclear receptor coactivator 1	Homo sapiens	58-61
10823876-9	2000	Within this 20-mer p24(Gag), an epitope presented by both B42 and B81 is defined which represents the dominant Gag response in &gt;30% of the total infected population in Durban.	Glycosaminoglycans	111-114	transmembrane p24 trafficking protein 2	Homo sapiens	19-22
10823876-9	2000	Within this 20-mer p24(Gag), an epitope presented by both B42 and B81 is defined which represents the dominant Gag response in &gt;30% of the total infected population in Durban.	Glycosaminoglycans	111-114	proline rich nuclear receptor coactivator 1	Homo sapiens	58-61
10802779-1	2000	OBJECTIVE: To develop diagnostic testing guidelines for the DYT1 GAG deletion in the Ashkenazi Jewish (AJ) and non-Jewish (NJ) primary torsion dystonia (PTD) populations and to determine the range of dystonic features in affected DYT1 deletion carriers.	Glycosaminoglycans	65-68	torsin family 1 member A	Homo sapiens	60-64
10857760-0	2000	Glycosaminoglycans alter the conformation of interferon-gamma.	Glycosaminoglycans	0-18	interferon gamma	Homo sapiens	45-61
10773191-2	2000	Here we provide evidence that TN-R derived from adult mouse brain expresses chondroitin sulfate (CS) glycosaminoglycans (GAGs), i.e. C-6S and C-4S, that are recognized by the CS/dermatan sulfate-specific monoclonal antibodies 473 HD and CS-56.	Glycosaminoglycans	101-119	tenascin R	Mus musculus	30-34
10806049-6	2000	TNFalpha at 5, 1, 0.5 and 0.25 ng/ml (but not 0.1 ng/ml) significantly increased glycosaminoglycans (GAG) release from cartilage explants in a dose-dependent manner.	Glycosaminoglycans	81-99	tumor necrosis factor	Homo sapiens	0-8
10806049-6	2000	TNFalpha at 5, 1, 0.5 and 0.25 ng/ml (but not 0.1 ng/ml) significantly increased glycosaminoglycans (GAG) release from cartilage explants in a dose-dependent manner.	Glycosaminoglycans	101-104	tumor necrosis factor	Homo sapiens	0-8
10894267-11	2000	Glycosaminoglycan (GAG) synthesis from cartilage shavings from treated joints suggests that Ad.FasL does not induce significant apoptosis in resident articular chondrocytes.	Glycosaminoglycans	0-17	Fas ligand	Homo sapiens	95-99
10849326-7	2000	A silent base substitution (GAG to GAA) at codon 131 was also identified in six rat tumors as well as in one human gastric cancer.	Glycosaminoglycans	28-31	alpha glucosidase	Rattus norvegicus	35-38
10773191-2	2000	Here we provide evidence that TN-R derived from adult mouse brain expresses chondroitin sulfate (CS) glycosaminoglycans (GAGs), i.e. C-6S and C-4S, that are recognized by the CS/dermatan sulfate-specific monoclonal antibodies 473 HD and CS-56.	Glycosaminoglycans	121-125	tenascin R	Mus musculus	30-34
10773191-4	2000	Our findings suggest the functional implication of TN-R-linked CS GAGs in matrix interactions with fibronectin and TN-C that are likely to contribute to a modulation of cellular behavior and the macromolecular organization of matrix components in the developing or injured adult CNS.	Glycosaminoglycans	66-70	tenascin R	Mus musculus	51-55
10759543-6	2000	The monkeys that received IL-2/Ig plasmid generated 30-fold higher Env-specific antibody titers and 5-fold higher Gag-specific, tetramer-positive CD8+ T cell levels than the monkeys receiving the DNA vaccines alone.	Glycosaminoglycans	114-117	interleukin 2	Homo sapiens	26-30
10717345-3	2000	FPV gag/pol-IFNgamma vaccinations were safe and enhanced T cell proliferative responses to Gag antigens (but not control tetanus antigens).	Glycosaminoglycans	91-94	interferon gamma	Homo sapiens	12-20
10766793-0	2000	Examination of the function of RANTES, MIP-1alpha, and MIP-1beta following interaction with heparin-like glycosaminoglycans.	Glycosaminoglycans	105-123	C-C motif chemokine ligand 5	Homo sapiens	31-37
10766793-7	2000	Radioligand binding experiments demonstrated that specific chemokine receptors expressed by wild-type cells had a significantly greater affinity for MIP-1alpha than similar receptors expressed by GAG-deficient mutants.	Glycosaminoglycans	196-199	C-C motif chemokine ligand 3	Homo sapiens	149-159
10766996-4	2000	The DNA sequencing demonstrated novel mutations in exon 3A of AT3: a G to T substitution at nucleotide position 5333 in codon GAG for Glu 113, causing a stop codon (E113X), and an A to T substitution at position 5338 in codon AAA for Lys 114, forming Asn (K114N).	Glycosaminoglycans	126-129	serpin family C member 1	Homo sapiens	62-65
10760480-0	2000	Endogenously produced glycosaminoglycans affecting the release of lipoprotein lipase from macrophages and the interaction with lipoproteins.	Glycosaminoglycans	22-40	lipoprotein lipase	Homo sapiens	66-84
10772110-5	2000	RESULTS: Human recombinant IL-1alpha (40 ng/ml) increased the amount of labeled GAG released and decreased labeled and total GAG remaining in explants, and IL-1alpha decreased mitogenic response.	Glycosaminoglycans	80-83	interleukin 1 alpha	Homo sapiens	27-36
10772110-5	2000	RESULTS: Human recombinant IL-1alpha (40 ng/ml) increased the amount of labeled GAG released and decreased labeled and total GAG remaining in explants, and IL-1alpha decreased mitogenic response.	Glycosaminoglycans	125-128	interleukin 1 alpha	Homo sapiens	27-36
10772110-7	2000	In general, IGF-1 decreased total and labeled GAG released into the medium, compared with IL-1alpha-treated explants (positive-control sample).	Glycosaminoglycans	46-49	insulin like growth factor 1	Equus caballus	12-17
10772110-9	2000	A significant increase in total and newly synthesized GAG in the explants at termination of the experiment was observed with 500 ng of IGF-1/ml.	Glycosaminoglycans	54-57	insulin like growth factor 1	Equus caballus	135-140
10772110-10	2000	Labeled GAG remaining in explants was greater with treatment at 50 ng of IGF-1/ml, compared with treatment with IL-1alpha alone.	Glycosaminoglycans	8-11	insulin like growth factor 1	Equus caballus	73-78
10772110-10	2000	Labeled GAG remaining in explants was greater with treatment at 50 ng of IGF-1/ml, compared with treatment with IL-1alpha alone.	Glycosaminoglycans	8-11	interleukin 1 alpha	Equus caballus	112-121
10722749-5	2000	In addition, endoglycan contains several potential glycosaminoglycan attachment sites and is modified with chondroitin sulfate.	Glycosaminoglycans	51-68	podocalyxin like 2	Homo sapiens	13-23
10723065-4	2000	Here we provide first evidence that TN-R derived from whole rat brain or cultured oligodendrocytes expresses chondroitin sulfate (CS) glycosaminoglycans (GAGs), i.e., C-4S and C-6S, that are recognized by CS-56, a CS/dermatan sulfate-specific monoclonal antibody.	Glycosaminoglycans	134-152	tenascin R	Rattus norvegicus	36-40
10729129-5	2000	Through the analysis of viral revertants, we demonstrate that a single amino acid change (34VI) in the matrix domain of Gag reverses the Env incorporation and infectivity defect imposed by a small deletion near the C terminus of alpha-helix 2.	Glycosaminoglycans	120-123	endogenous retrovirus group W member 1, envelope	Homo sapiens	137-140
10729160-7	2000	A small amount of p24(gag) was released and was in the form of fully infectious virus.	Glycosaminoglycans	22-25	transmembrane p24 trafficking protein 2	Homo sapiens	18-21
10775070-1	2000	We have previously shown that the in vivo infusion of interleukin-8 (IL8) in rats causes albuminuria and an increased catabolism of the heparan sulfate (HS) glycosaminoglycans (GAG).	Glycosaminoglycans	177-180	C-X-C motif chemokine ligand 8	Homo sapiens	69-72
11876983-4	2000	RESULTS: GAG could down-regulate the expression of TF antigen and mRNA, up-regulate the expression of TM antigen and mRNA, down-regulate the PCA of stimulated endothelial cells.	Glycosaminoglycans	9-12	coagulation factor III, tissue factor	Homo sapiens	51-53
11876983-4	2000	RESULTS: GAG could down-regulate the expression of TF antigen and mRNA, up-regulate the expression of TM antigen and mRNA, down-regulate the PCA of stimulated endothelial cells.	Glycosaminoglycans	9-12	thrombomodulin	Homo sapiens	102-104
11876983-5	2000	CONCLUSION: Down-regulating TF expression and up-regulating TM expression of stimulated endothelial cells may be one of the mechanisms of GAG antithrombosis.	Glycosaminoglycans	138-141	coagulation factor III, tissue factor	Homo sapiens	28-30
11876983-5	2000	CONCLUSION: Down-regulating TF expression and up-regulating TM expression of stimulated endothelial cells may be one of the mechanisms of GAG antithrombosis.	Glycosaminoglycans	138-141	thrombomodulin	Homo sapiens	60-62
10772536-2	2000	Phylogenetic sequence analysis of a fragment of 729 base pairs (bp) covering the Gag-coding region for half of p24 and all of p17 revealed the gag subtype of all 60 viruses included in the study: A (n = 20), B (n = 12), C (n = 7), D (n = 10), E (n = 3), F (n = 4), G (n = 3), and H (n = 1).	Glycosaminoglycans	81-84	transmembrane p24 trafficking protein 2	Homo sapiens	111-114
10772536-2	2000	Phylogenetic sequence analysis of a fragment of 729 base pairs (bp) covering the Gag-coding region for half of p24 and all of p17 revealed the gag subtype of all 60 viruses included in the study: A (n = 20), B (n = 12), C (n = 7), D (n = 10), E (n = 3), F (n = 4), G (n = 3), and H (n = 1).	Glycosaminoglycans	143-146	transmembrane p24 trafficking protein 2	Homo sapiens	111-114
10772536-2	2000	Phylogenetic sequence analysis of a fragment of 729 base pairs (bp) covering the Gag-coding region for half of p24 and all of p17 revealed the gag subtype of all 60 viruses included in the study: A (n = 20), B (n = 12), C (n = 7), D (n = 10), E (n = 3), F (n = 4), G (n = 3), and H (n = 1).	Glycosaminoglycans	143-146	family with sequence similarity 72 member B	Homo sapiens	126-129
10714658-2	2000	A GAG deletion at position 946 of the DYT1 gene was the first mutation found, in early-onset dystonia, with an autosomal dominant transmission and reduced penetrance.	Glycosaminoglycans	2-5	torsin family 1 member A	Homo sapiens	38-42
10704346-4	2000	The HS-GAG analog heparin decreased Ad5- and Ad2-mediated infection and binding starting from the concentration of 0.1 microgram/ml, up to a maximum of 50%.	Glycosaminoglycans	7-10	Alzheimer disease, familial, type 5	Homo sapiens	36-39
10737389-7	2000	Similarly, SK-mel-29 melanoma cells were also efficiently lysed by HLA-A2/gag-specific CTL when HLA-A2/gag complexes were linked to their surface via the HMW-MAA specific anti-melanoma antibody 225.28s.	Glycosaminoglycans	74-77	chondroitin sulfate proteoglycan 4	Homo sapiens	154-161
10688805-6	2000	KKO also bound to hPF4 in association with other glycosaminoglycans.	Glycosaminoglycans	49-67	platelet factor 4	Homo sapiens	18-22
10782998-1	2000	The binding of selenoprotein P to glycosaminoglycans using heparin as a model compound was studied by surface plasmon resonance.	Glycosaminoglycans	34-52	selenoprotein P	Homo sapiens	15-30
10683465-6	2000	Rabbits failed to be infected, but anti- p55 gag-specific antibodies could be demonstrated by Western blot.	Glycosaminoglycans	45-48	protein disulfide-isomerase	Oryctolagus cuniculus	41-44
10737389-7	2000	Similarly, SK-mel-29 melanoma cells were also efficiently lysed by HLA-A2/gag-specific CTL when HLA-A2/gag complexes were linked to their surface via the HMW-MAA specific anti-melanoma antibody 225.28s.	Glycosaminoglycans	103-106	chondroitin sulfate proteoglycan 4	Homo sapiens	154-161
10839203-2	2000	IGF-I is expressed in most fetal tissues and it is involved in anabolic effects on protein and sulphated glycosaminoglycans biosynthesis, cell proliferation and differentiation.	Glycosaminoglycans	105-123	insulin like growth factor 1	Homo sapiens	0-5
10770600-6	2000	Concentration of GAG was significantly increased in the media of pellets stimulated by both IGF-Ialpha and IL-1alpha.	Glycosaminoglycans	17-20	interleukin 1 alpha	Equus caballus	107-116
10770600-8	2000	A high correlation between GAG and antigenic KS concentrations was found in the media of pellets stimulated by IL-1alpha (r=0.87), but not in those stimulated by IGF-Ialpha (r=0.43).	Glycosaminoglycans	27-30	interleukin 1 alpha	Equus caballus	111-120
10803109-6	2000	The concentration of GAG was significantly increased both in the media of pellets stimulated by IGF-I alpha and in those stimulated by IL-1 alpha.	Glycosaminoglycans	21-24	interleukin 1 alpha	Equus caballus	135-145
10803109-8	2000	A high correlation between GAG and KS concentrations was found in the media of pellets stimulated by IL-1 alpha (r = 0.84), but not in those stimulated by IGF-I alpha (r = 0.59).	Glycosaminoglycans	27-30	interleukin 1 alpha	Equus caballus	101-111
10681554-5	2000	This increase depended on strong interactions between LPL that was bound to the glycosaminoglycan chains of the collagen-bound decorin and native and oxidized LDL (kDa 12 and 5.9 nM, respectively).	Glycosaminoglycans	80-97	lipoprotein lipase	Homo sapiens	54-57
10640397-5	2000	We now report that the glycosaminoglycan chains of syndecan-4 bind recombinant HepII and it is incorporated into forming focal adhesions.	Glycosaminoglycans	23-40	syndecan 4	Homo sapiens	51-61
10710214-3	2000	From the latter experiments, we conclude that Gag proteins that include p17, and perhaps also p7, sequences flanking the central p24 capsid protein, are better stimulants than proteins that comprise only p24 sequences.	Glycosaminoglycans	46-49	family with sequence similarity 72 member B	Homo sapiens	72-75
10710214-3	2000	From the latter experiments, we conclude that Gag proteins that include p17, and perhaps also p7, sequences flanking the central p24 capsid protein, are better stimulants than proteins that comprise only p24 sequences.	Glycosaminoglycans	46-49	transmembrane p24 trafficking protein 2	Homo sapiens	129-132
10710214-3	2000	From the latter experiments, we conclude that Gag proteins that include p17, and perhaps also p7, sequences flanking the central p24 capsid protein, are better stimulants than proteins that comprise only p24 sequences.	Glycosaminoglycans	46-49	transmembrane p24 trafficking protein 2	Homo sapiens	204-207
10652303-10	2000	Studies with CHO-K1 cell mutants show that binding of sPLA2s to glycosaminoglycans is not the basis for poor plasma membrane hydrolysis by group IB, IIA, and V sPLA2s.	Glycosaminoglycans	64-82	phospholipase A2 group IID	Homo sapiens	54-60
10739388-8	2000	Furthermore, CHO cells genetically deficient in glycosaminoglycans efficiently degraded t-PA/PAI-1.	Glycosaminoglycans	48-66	plasminogen activator, tissue type	Homo sapiens	88-92
10674345-5	2000	Third, CNP stimulates cartilage matrix production as assessed by incorporation of 35SO4 into glycosaminoglycans.	Glycosaminoglycans	93-111	natriuretic peptide C	Rattus norvegicus	7-10
10674345-8	2000	Consistent with this hypothesis, we found that 8-Br-cGMP, like CNP, stimulates longitudinal growth and glycosaminoglycan synthesis.	Glycosaminoglycans	103-120	natriuretic peptide C	Rattus norvegicus	63-66
10652016-8	2000	The two other novel mutations were the GAG to AAG transition, leading to a Glu447Lys and the GAC to GTC transition, predicting an Asp819Val substitution in the nephrin protein.	Glycosaminoglycans	39-42	N-methylpurine DNA glycosylase	Homo sapiens	46-49
10652016-8	2000	The two other novel mutations were the GAG to AAG transition, leading to a Glu447Lys and the GAC to GTC transition, predicting an Asp819Val substitution in the nephrin protein.	Glycosaminoglycans	39-42	NPHS1 adhesion molecule, nephrin	Homo sapiens	160-167
10821421-6	2000	We considered insulin-like growth factor-I (IGF-I) as a potential candidate involved in regulation of GAG biosynthesis in both experimental models of animals.	Glycosaminoglycans	102-105	insulin-like growth factor 1	Rattus norvegicus	14-42
10821421-6	2000	We considered insulin-like growth factor-I (IGF-I) as a potential candidate involved in regulation of GAG biosynthesis in both experimental models of animals.	Glycosaminoglycans	102-105	insulin-like growth factor 1	Rattus norvegicus	44-49
10739388-6	2000	As glycosaminoglycans can bind t-PA and PAI-1 we investigated whether they are involved in t-PA/PAI-1 degradation.	Glycosaminoglycans	3-21	plasminogen activator, tissue type	Homo sapiens	31-35
10739388-6	2000	As glycosaminoglycans can bind t-PA and PAI-1 we investigated whether they are involved in t-PA/PAI-1 degradation.	Glycosaminoglycans	3-21	serpin family E member 1	Homo sapiens	40-45
10739388-6	2000	As glycosaminoglycans can bind t-PA and PAI-1 we investigated whether they are involved in t-PA/PAI-1 degradation.	Glycosaminoglycans	3-21	plasminogen activator, tissue type	Homo sapiens	91-95
10739388-6	2000	As glycosaminoglycans can bind t-PA and PAI-1 we investigated whether they are involved in t-PA/PAI-1 degradation.	Glycosaminoglycans	3-21	serpin family E member 1	Homo sapiens	96-101
10739388-8	2000	Furthermore, CHO cells genetically deficient in glycosaminoglycans efficiently degraded t-PA/PAI-1.	Glycosaminoglycans	48-66	serpin family E member 1	Homo sapiens	93-98
10618286-3	2000	Denatured Env-Gag did not cause any effect on the NK cell activity of LGL.	Glycosaminoglycans	14-17	endogenous retrovirus group K member 20	Homo sapiens	10-13
10623797-8	2000	This study demonstrates for the first time that mast cells can present IFN-gamma to other cells via glycosaminoglycans.	Glycosaminoglycans	100-118	interferon gamma	Mus musculus	71-80
10625699-9	2000	Moreover, only in the dense cell cultures did TGF-beta(1) cause CS/DSPG hydrodynamic size to increase, which was due to the synthesis of CS/DSPGs with longer glycosaminoglycan chains.	Glycosaminoglycans	158-175	transforming growth factor beta 1	Bos taurus	46-57
10625699-12	2000	Furthermore, glycosaminoglycan chains are elongated only in biglycan synthesized by the cells at a high cell density.	Glycosaminoglycans	13-30	biglycan	Bos taurus	60-68
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
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
10570220-9	2000	We have previously shown that gp120 of X4 strain HIV-1LAI presents specific carbohydrate-binding properties for mannosylated derivatives, including mannan, and for GAGs including heparin.	Glycosaminoglycans	164-168	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	30-35
10570220-10	2000	The present data therefore indicate that, in the same manner as HIV-1 Env, SDF-1alpha can interact with GAGs and glycans at the cell surface.	Glycosaminoglycans	104-108	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	70-73
10714610-8	2000	Furthermore, glycosaminoglycans with a sulfate residue, chondroitin sulfate B and C (each 10 microg/mL) also inhibited the binding of 125I-bFGF The in vivo transcytosis of 125I-bFGF from the luminal side to the brain was also inhibited by the presence of heparin (10 microg/mL) and poly-L-lysine (300 microM), whereas neither hyaruronic acid (10 microg/mL) nor insulin (10 microM) had any effect.	Glycosaminoglycans	13-31	fibroblast growth factor 2	Bos taurus	139-143
10617123-4	2000	Compounds such as glycosaminoglycans and Congo red (CR) have been shown to interfere with both in vitro and in vivo PrP(Sc) formation.	Glycosaminoglycans	18-36	prion protein	Mus musculus	116-119
10714610-8	2000	Furthermore, glycosaminoglycans with a sulfate residue, chondroitin sulfate B and C (each 10 microg/mL) also inhibited the binding of 125I-bFGF The in vivo transcytosis of 125I-bFGF from the luminal side to the brain was also inhibited by the presence of heparin (10 microg/mL) and poly-L-lysine (300 microM), whereas neither hyaruronic acid (10 microg/mL) nor insulin (10 microM) had any effect.	Glycosaminoglycans	13-31	fibroblast growth factor 2	Bos taurus	177-181
10600521-0	1999	Glycosaminoglycans promote HARP/PTN dimerization.	Glycosaminoglycans	0-18	pleiotrophin	Homo sapiens	27-31
10593925-3	1999	Feline N-acetylgalactosamine-4-sulfatase was effective in reducing urinary glycosaminoglycan levels and lysosomal storage in all cell types examined except for corneal keratocytes and cartilage chondrocytes.	Glycosaminoglycans	75-92	arylsulfatase B	Felis catus	7-40
10600521-0	1999	Glycosaminoglycans promote HARP/PTN dimerization.	Glycosaminoglycans	0-18	pleiotrophin	Homo sapiens	32-35
10600606-7	1999	These data demonstrate that glycans and glycosaminoglycans are directly or indirectly involved in the interactions of HIV-1 gp120(LAI) and of SDF-1alpha with membrane ligands of CD4(+) CXCR4(+) cells and thus could play a role both in HIV-1 infection and in the physiology of SDF-1alpha.	Glycosaminoglycans	40-58	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	124-129
10600606-7	1999	These data demonstrate that glycans and glycosaminoglycans are directly or indirectly involved in the interactions of HIV-1 gp120(LAI) and of SDF-1alpha with membrane ligands of CD4(+) CXCR4(+) cells and thus could play a role both in HIV-1 infection and in the physiology of SDF-1alpha.	Glycosaminoglycans	40-58	CD4 molecule	Homo sapiens	178-181
10600606-7	1999	These data demonstrate that glycans and glycosaminoglycans are directly or indirectly involved in the interactions of HIV-1 gp120(LAI) and of SDF-1alpha with membrane ligands of CD4(+) CXCR4(+) cells and thus could play a role both in HIV-1 infection and in the physiology of SDF-1alpha.	Glycosaminoglycans	40-58	C-X-C motif chemokine receptor 4	Homo sapiens	185-190
10600521-5	1999	In vitro, different glycosaminoglycans, such as dermatan sulfate and chondroitin sulfate-C, also induce a dimer assembly of HARP.	Glycosaminoglycans	20-38	pleiotrophin	Homo sapiens	124-128
10595940-7	1999	Our results suggest that glycosaminoglycan side chains of the HSPGs agrin, syndecan, and glypican, but not perlecan, may play an important role in the formation of both senile plaques and neurofibrillary tangles.	Glycosaminoglycans	25-42	agrin	Homo sapiens	68-73
10588734-5	1999	To further investigate this dependence, we examined whether soluble GAG could reconstitute the biological activities of RANTES on glycanase-treated cells.	Glycosaminoglycans	68-71	C-C motif chemokine ligand 5	Homo sapiens	120-126
10574918-1	1999	Heparin cofactor II (HCII) is a serpin whose thrombin inhibition activity is accelerated by glycosaminoglycans.	Glycosaminoglycans	92-110	serpin family D member 1	Homo sapiens	0-19
10574918-1	1999	Heparin cofactor II (HCII) is a serpin whose thrombin inhibition activity is accelerated by glycosaminoglycans.	Glycosaminoglycans	92-110	serpin family D member 1	Homo sapiens	21-25
10574918-1	1999	Heparin cofactor II (HCII) is a serpin whose thrombin inhibition activity is accelerated by glycosaminoglycans.	Glycosaminoglycans	92-110	coagulation factor II, thrombin	Homo sapiens	45-53
10574918-12	1999	In a plasma-based assay, the glycosaminoglycan-dependent inhibition of thrombin by rHCII-CHis(6) was significantly greater compared with wt-rHCII.	Glycosaminoglycans	29-46	coagulation factor II, thrombin	Homo sapiens	71-79
10595940-7	1999	Our results suggest that glycosaminoglycan side chains of the HSPGs agrin, syndecan, and glypican, but not perlecan, may play an important role in the formation of both senile plaques and neurofibrillary tangles.	Glycosaminoglycans	25-42	syndecan 1	Homo sapiens	75-83
10595940-7	1999	Our results suggest that glycosaminoglycan side chains of the HSPGs agrin, syndecan, and glypican, but not perlecan, may play an important role in the formation of both senile plaques and neurofibrillary tangles.	Glycosaminoglycans	25-42	glypican 1	Homo sapiens	89-97
10545594-6	1999	Indirect evidence suggests that EXT proteins are involved in glycosaminoglycan synthesis, act as tumor suppressors and affect hedgehog signaling.	Glycosaminoglycans	61-78	exostosin glycosyltransferase 1	Homo sapiens	32-35
10569980-7	1999	Addition of a glycosaminoglycan antagonist, hexadimethrine bromide, to FGF-2-treated cultures inhibited DNA synthesis due to FGF-2, although not completely.	Glycosaminoglycans	14-31	fibroblast growth factor 2	Gallus gallus	71-76
10569980-7	1999	Addition of a glycosaminoglycan antagonist, hexadimethrine bromide, to FGF-2-treated cultures inhibited DNA synthesis due to FGF-2, although not completely.	Glycosaminoglycans	14-31	fibroblast growth factor 2	Gallus gallus	125-130
10607916-6	1999	Capillary electrophoresis of chondroitinase ABC-digested proteoglycans isolated from mature chondrocytes showed 2-4-fold increases in the amounts of the 4S- and 6S-substituted GAG chains for the PTN-treated chondrocytes.	Glycosaminoglycans	176-179	pleiotrophin	Bos taurus	195-198
10611943-2	1999	In vitro, glycosaminoglycans have been shown to inhibit the proteolysis of A beta fibrils, accelerate formation and maintain their stability.	Glycosaminoglycans	10-28	amyloid beta precursor protein	Rattus norvegicus	75-81
10616001-10	1999	Fluoxetine and amitriptyline (1 microg/ml) partially reversed IL-1beta-induced inhibition of 35S-GAG synthesis by human cartilage cultures (P&lt;0.05).	Glycosaminoglycans	97-100	interleukin 1 beta	Homo sapiens	62-70
10667847-0	1999	Granulocyte-colony stimulating factor decreases glycosaminoglycan concentration and increases nitric oxide production in rat articular cartilage.	Glycosaminoglycans	48-65	colony stimulating factor 3	Rattus norvegicus	0-37
10536375-11	1999	Overall, these results show that the inhibitory action of DCN is dependent of substratum binding, is differentially mediated by its glycosaminoglycan side chains (chondroitin-sulfate vs. dermatan-sulfate chains), and is independent of a steric hindrance effect exerted by its glycosaminoglycan side chains.	Glycosaminoglycans	132-149	decorin	Homo sapiens	58-61
10536375-11	1999	Overall, these results show that the inhibitory action of DCN is dependent of substratum binding, is differentially mediated by its glycosaminoglycan side chains (chondroitin-sulfate vs. dermatan-sulfate chains), and is independent of a steric hindrance effect exerted by its glycosaminoglycan side chains.	Glycosaminoglycans	276-293	decorin	Homo sapiens	58-61
10576765-2	1999	There are two known polymorphisms in exon 11 of the DBP gene that result in amino acid variants: at codons 416 GAT--&gt;GAG (Asp--&gt;Glu) and 420 ACG--&gt;AAG (Thr--&gt;Lys).	Glycosaminoglycans	120-123	D-box binding PAR bZIP transcription factor	Homo sapiens	52-55
10545594-10	1999	The EXT2-GalNAc-T5 interaction provides the first direct physical link between EXT proteins and known components of glycosamino-glycan synthesis.	Glycosaminoglycans	116-134	exostosin glycosyltransferase 2	Homo sapiens	4-8
10545594-10	1999	The EXT2-GalNAc-T5 interaction provides the first direct physical link between EXT proteins and known components of glycosamino-glycan synthesis.	Glycosaminoglycans	116-134	exostosin glycosyltransferase 1	Homo sapiens	4-7
10665061-4	1999	However, during Vpr and Gag co-expression in the baculovirus expression system, Vpr content in the nuclei is decreased, since this protein incorporates effectively into virus-like particles and forms stable complexes with Gag polyprotein.	Glycosaminoglycans	24-27	Vpr	Human immunodeficiency virus 1	80-83
10545953-8	1999	Hspg2-/- cartilage matrix contained reduced and disorganized collagen fibrils and glycosaminoglycans, suggesting that perlecan has an important role in matrix structure.	Glycosaminoglycans	82-100	perlecan (heparan sulfate proteoglycan 2)	Mus musculus	0-5
10665061-5	1999	Presumably, the Vpr-Gag post-translational interactions are needed for the Vpr incorporation into virions and suppress the nuclear import of this protein.	Glycosaminoglycans	20-23	Vpr	Human immunodeficiency virus 1	16-19
10665061-5	1999	Presumably, the Vpr-Gag post-translational interactions are needed for the Vpr incorporation into virions and suppress the nuclear import of this protein.	Glycosaminoglycans	20-23	Vpr	Human immunodeficiency virus 1	75-78
10512728-1	1999	Fibroblast growth factor-4 (FGF4), like other FGFs, shares a high affinity for the anionic glycosaminoglycans heparin and heparan sulfate (HS), which in turn enhance FGF-receptor (FGFR) binding and activation.	Glycosaminoglycans	91-109	fibroblast growth factor 4	Homo sapiens	0-26
10531349-0	1999	Acidic pH modulates the interaction between human granulocyte-macrophage colony-stimulating factor and glycosaminoglycans.	Glycosaminoglycans	103-121	colony stimulating factor 2	Homo sapiens	50-98
10531349-3	1999	In this work, we have performed in vitro studies of the interaction between GM-CSF and glycosaminoglycans.	Glycosaminoglycans	87-105	colony stimulating factor 2	Homo sapiens	76-82
10531349-6	1999	The dependence on acidic pH, together with a strict dependence on glycosaminoglycan sulfation and the fact that high ionic strength destabilized the interaction, indicates that the association between GM-CSF and glycosaminoglycans is mediated by electrostatic interactions.	Glycosaminoglycans	66-83	colony stimulating factor 2	Homo sapiens	201-207
10531349-6	1999	The dependence on acidic pH, together with a strict dependence on glycosaminoglycan sulfation and the fact that high ionic strength destabilized the interaction, indicates that the association between GM-CSF and glycosaminoglycans is mediated by electrostatic interactions.	Glycosaminoglycans	212-230	colony stimulating factor 2	Homo sapiens	201-207
10531349-7	1999	These interactions probably involve sulfate groups in the glycosaminoglycans and positively charged histidine residues in GM-CSF.	Glycosaminoglycans	58-76	colony stimulating factor 2	Homo sapiens	122-128
10512728-1	1999	Fibroblast growth factor-4 (FGF4), like other FGFs, shares a high affinity for the anionic glycosaminoglycans heparin and heparan sulfate (HS), which in turn enhance FGF-receptor (FGFR) binding and activation.	Glycosaminoglycans	91-109	fibroblast growth factor 4	Homo sapiens	28-32
10564347-0	1999	Long-term neuroprotective effects of glycosaminoglycans-IGF-I cotreatment in the motor neuron degeneration (mnd) mutant mouse.	Glycosaminoglycans	37-55	insulin-like growth factor 1	Mus musculus	56-61
10658113-5	1999	TGFbeta1 stimulated glycosaminoglycan (GAG) synthesis throughout all developmental stages approximately 1.8-2.6 fold.	Glycosaminoglycans	20-37	transforming growth factor, beta 1	Mus musculus	0-8
10658113-5	1999	TGFbeta1 stimulated glycosaminoglycan (GAG) synthesis throughout all developmental stages approximately 1.8-2.6 fold.	Glycosaminoglycans	39-42	transforming growth factor, beta 1	Mus musculus	0-8
10504408-0	1999	Inhibition of phosphodiesterase/pyrophosphatase activity of PC-1 by its association with glycosaminoglycans.	Glycosaminoglycans	89-107	ectonucleotide pyrophosphatase/phosphodiesterase 1	Homo sapiens	60-64
10504408-6	1999	The phosphodiesterase/pyrophosphatase activity of PC-1 was competitively inhibited by glycosaminoglycans, such as heparin and heparan sulfate, which are the major components of the extracellular matrix.	Glycosaminoglycans	86-104	ectonucleotide pyrophosphatase/phosphodiesterase 1	Homo sapiens	50-54
10504408-9	1999	These results suggest that PC-1 might function as an adhesion molecule independent of its enzyme activity to associate with glycosaminoglycans in the extracellular matrix.	Glycosaminoglycans	124-142	ectonucleotide pyrophosphatase/phosphodiesterase 1	Homo sapiens	27-31
10496984-6	1999	Interaction of these two glycosaminoglycans (GAGs) with TFPI-2/MSPI involved one or more common protein domains, as evidenced by cross-competition experiments.	Glycosaminoglycans	25-43	tissue factor pathway inhibitor 2	Homo sapiens	56-62
10496984-6	1999	Interaction of these two glycosaminoglycans (GAGs) with TFPI-2/MSPI involved one or more common protein domains, as evidenced by cross-competition experiments.	Glycosaminoglycans	45-49	tissue factor pathway inhibitor 2	Homo sapiens	56-62
10496984-8	1999	Binding of TFPI-2/MSPI to GAGs was inhibited by NaCl or arginine but not by glucose, mannose, galactose, 6-aminohexanoic acid, or urea, suggesting that arginine-mediated ionic interactions participate in the GAG binding of TFPI-2/MSPI.	Glycosaminoglycans	26-30	tissue factor pathway inhibitor 2	Homo sapiens	11-17
10496984-8	1999	Binding of TFPI-2/MSPI to GAGs was inhibited by NaCl or arginine but not by glucose, mannose, galactose, 6-aminohexanoic acid, or urea, suggesting that arginine-mediated ionic interactions participate in the GAG binding of TFPI-2/MSPI.	Glycosaminoglycans	26-30	tissue factor pathway inhibitor 2	Homo sapiens	223-229
10496984-8	1999	Binding of TFPI-2/MSPI to GAGs was inhibited by NaCl or arginine but not by glucose, mannose, galactose, 6-aminohexanoic acid, or urea, suggesting that arginine-mediated ionic interactions participate in the GAG binding of TFPI-2/MSPI.	Glycosaminoglycans	26-29	tissue factor pathway inhibitor 2	Homo sapiens	11-17
10496984-8	1999	Binding of TFPI-2/MSPI to GAGs was inhibited by NaCl or arginine but not by glucose, mannose, galactose, 6-aminohexanoic acid, or urea, suggesting that arginine-mediated ionic interactions participate in the GAG binding of TFPI-2/MSPI.	Glycosaminoglycans	26-29	tissue factor pathway inhibitor 2	Homo sapiens	223-229
10890144-4	1999	Histopathological analysis in patients with a COCH mutation revealed the presence of an acidophylic mucopolysaccharide deposit in the inner ear.	Glycosaminoglycans	100-118	cochlin	Homo sapiens	46-50
10564347-0	1999	Long-term neuroprotective effects of glycosaminoglycans-IGF-I cotreatment in the motor neuron degeneration (mnd) mutant mouse.	Glycosaminoglycans	37-55	CLN8 transmembrane ER and ERGIC protein	Mus musculus	81-106
10504292-1	1999	The formation of focal adhesions and actin stress fibers on fibronectin is dependent on signaling through (&amp;bgr;)1 integrins and the heparan sulfate proteoglycan syndecan-4, and we have analyzed the requirement of the glycosaminoglycan chains of syndecan-4 during these events.	Glycosaminoglycans	222-239	fibronectin 1	Gallus gallus	60-71
10506571-0	1999	FGF-2/fibroblast growth factor receptor/heparin-like glycosaminoglycan interactions: a compensation model for FGF-2 signaling.	Glycosaminoglycans	53-70	fibroblast growth factor 2	Homo sapiens	0-5
10506571-0	1999	FGF-2/fibroblast growth factor receptor/heparin-like glycosaminoglycan interactions: a compensation model for FGF-2 signaling.	Glycosaminoglycans	53-70	fibroblast growth factor 2	Homo sapiens	110-115
10506571-1	1999	Heparin-like glycosaminoglycans (HLGAGs) play a central role in the biological activity and signaling behavior of basic fibroblast growth factor (FGF-2).	Glycosaminoglycans	13-31	fibroblast growth factor 2	Homo sapiens	146-151
10484981-7	1999	In the analyses of tumor tissues from the propositus and his daughter, a P16INK4A codon 94 missense point mutation (GCG-->GAG; Ala-->Glu) was observed with the hereditary TP53 mutation.	Glycosaminoglycans	122-125	cyclin dependent kinase inhibitor 2A	Homo sapiens	73-81
10490614-4	1999	The acidic box and the glycosaminoglycan modification site are encoded by an alternative exon of the FGFR2 gene.	Glycosaminoglycans	23-40	fibroblast growth factor receptor 2	Homo sapiens	101-106
10504268-3	1999	Chemokines bind to glycosaminoglycans on human umbilical vein endothelial cells (HUVECs) with affinities in the micromolar range: RANTES &gt; MCP-1 &gt; IL-8 &gt; MIP-1alpha.	Glycosaminoglycans	19-37	C-C motif chemokine ligand 5	Homo sapiens	130-136
10504268-3	1999	Chemokines bind to glycosaminoglycans on human umbilical vein endothelial cells (HUVECs) with affinities in the micromolar range: RANTES &gt; MCP-1 &gt; IL-8 &gt; MIP-1alpha.	Glycosaminoglycans	19-37	C-C motif chemokine ligand 2	Homo sapiens	142-147
10504268-3	1999	Chemokines bind to glycosaminoglycans on human umbilical vein endothelial cells (HUVECs) with affinities in the micromolar range: RANTES &gt; MCP-1 &gt; IL-8 &gt; MIP-1alpha.	Glycosaminoglycans	19-37	C-X-C motif chemokine ligand 8	Homo sapiens	153-157
10504268-3	1999	Chemokines bind to glycosaminoglycans on human umbilical vein endothelial cells (HUVECs) with affinities in the micromolar range: RANTES &gt; MCP-1 &gt; IL-8 &gt; MIP-1alpha.	Glycosaminoglycans	19-37	C-C motif chemokine ligand 3	Homo sapiens	163-173
10504268-5	1999	RANTES binding showed the widest discrimination between glycosaminoglycans (700-fold), whereas MIP-1alpha was the least selective.	Glycosaminoglycans	56-74	C-C motif chemokine ligand 5	Homo sapiens	0-6
10464301-7	1999	Overlay blots with biotinylated actin and in vitro translated, [(35)S]methionine-labeled p58(gag), respectively, showed specific interactions of actin with gp55 and gp120 and of p58(gag) with gp65 and gp55.	Glycosaminoglycans	93-96	protein disulfide isomerase family A, member 3	Rattus norvegicus	89-92
10464301-7	1999	Overlay blots with biotinylated actin and in vitro translated, [(35)S]methionine-labeled p58(gag), respectively, showed specific interactions of actin with gp55 and gp120 and of p58(gag) with gp65 and gp55.	Glycosaminoglycans	93-96	protein disulfide isomerase family A, member 3	Rattus norvegicus	178-181
10464301-7	1999	Overlay blots with biotinylated actin and in vitro translated, [(35)S]methionine-labeled p58(gag), respectively, showed specific interactions of actin with gp55 and gp120 and of p58(gag) with gp65 and gp55.	Glycosaminoglycans	93-96	neurotrimin	Rattus norvegicus	192-196
10464301-7	1999	Overlay blots with biotinylated actin and in vitro translated, [(35)S]methionine-labeled p58(gag), respectively, showed specific interactions of actin with gp55 and gp120 and of p58(gag) with gp65 and gp55.	Glycosaminoglycans	182-185	protein disulfide isomerase family A, member 3	Rattus norvegicus	89-92
10464301-7	1999	Overlay blots with biotinylated actin and in vitro translated, [(35)S]methionine-labeled p58(gag), respectively, showed specific interactions of actin with gp55 and gp120 and of p58(gag) with gp65 and gp55.	Glycosaminoglycans	182-185	protein disulfide isomerase family A, member 3	Rattus norvegicus	178-181
10456986-5	1999	In the present study, a novel monoclonal antibody (TC2) that recognizes a native epitope on glycosaminoglycans enriched in chondroitin-4-sulfate revealed a transient and restricted expression in the developing gerbil TM.	Glycosaminoglycans	92-110	transcobalamin 2	Homo sapiens	51-54
10484981-7	1999	In the analyses of tumor tissues from the propositus and his daughter, a P16INK4A codon 94 missense point mutation (GCG-->GAG; Ala-->Glu) was observed with the hereditary TP53 mutation.	Glycosaminoglycans	122-125	glucagon	Homo sapiens	116-119
10484981-7	1999	In the analyses of tumor tissues from the propositus and his daughter, a P16INK4A codon 94 missense point mutation (GCG-->GAG; Ala-->Glu) was observed with the hereditary TP53 mutation.	Glycosaminoglycans	122-125	tumor protein p53	Homo sapiens	171-175
10438523-2	1999	Human beta-glucuronidase (hGUSB) is a member of family 2 glycosylhydrolases that cleaves beta-D-glucuronic acid residues from the nonreducing termini of glycosaminoglycans.	Glycosaminoglycans	153-171	glucuronidase beta	Homo sapiens	6-24
10534143-7	1999	When plasma viral load was analyzed as a continuous variable, there was a strong correlation between higher CTL activity and lower viral load for nef (r2 = .77; p &lt; .001), pol (r2 = .63; p &lt; .001) and gag (r2 = 0.75; p &lt; .001) targets by the AUC, but not for the LU20 analysis.	Glycosaminoglycans	207-210	S100 calcium binding protein B	Homo sapiens	146-149
10469649-3	1999	Complete deletion of p12 and mutations affecting the PPPY motif caused substantial reduction in the yield of virions and a modest reduction in Gag processing.	Glycosaminoglycans	143-146	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	21-24
10456887-3	1999	The mechanism involves specific bacterial recruitment of heparin, glycosaminoglycans, or related sulfated polysaccharides, which in turn serve as universal binding sites for a diverse array of mammalian heparin binding proteins, including adhesive glycoproteins (vitronectin and fibronectin), inflammatory (MCP-3, PF-4, and MIP-1alpha) and immunomodulatory (gamma interferon) intermediates, and fibroblast growth factor.	Glycosaminoglycans	66-84	vitronectin	Homo sapiens	263-274
10456887-3	1999	The mechanism involves specific bacterial recruitment of heparin, glycosaminoglycans, or related sulfated polysaccharides, which in turn serve as universal binding sites for a diverse array of mammalian heparin binding proteins, including adhesive glycoproteins (vitronectin and fibronectin), inflammatory (MCP-3, PF-4, and MIP-1alpha) and immunomodulatory (gamma interferon) intermediates, and fibroblast growth factor.	Glycosaminoglycans	66-84	fibronectin 1	Homo sapiens	279-290
10456887-3	1999	The mechanism involves specific bacterial recruitment of heparin, glycosaminoglycans, or related sulfated polysaccharides, which in turn serve as universal binding sites for a diverse array of mammalian heparin binding proteins, including adhesive glycoproteins (vitronectin and fibronectin), inflammatory (MCP-3, PF-4, and MIP-1alpha) and immunomodulatory (gamma interferon) intermediates, and fibroblast growth factor.	Glycosaminoglycans	66-84	C-C motif chemokine ligand 7	Homo sapiens	307-312
10456887-3	1999	The mechanism involves specific bacterial recruitment of heparin, glycosaminoglycans, or related sulfated polysaccharides, which in turn serve as universal binding sites for a diverse array of mammalian heparin binding proteins, including adhesive glycoproteins (vitronectin and fibronectin), inflammatory (MCP-3, PF-4, and MIP-1alpha) and immunomodulatory (gamma interferon) intermediates, and fibroblast growth factor.	Glycosaminoglycans	66-84	platelet factor 4	Homo sapiens	314-318
10456887-3	1999	The mechanism involves specific bacterial recruitment of heparin, glycosaminoglycans, or related sulfated polysaccharides, which in turn serve as universal binding sites for a diverse array of mammalian heparin binding proteins, including adhesive glycoproteins (vitronectin and fibronectin), inflammatory (MCP-3, PF-4, and MIP-1alpha) and immunomodulatory (gamma interferon) intermediates, and fibroblast growth factor.	Glycosaminoglycans	66-84	C-C motif chemokine ligand 3	Homo sapiens	324-334
10449567-1	1999	A GAG deletion in the DYT1 gene accounts for most early, limb onset primary torsion dystonia (PTD).	Glycosaminoglycans	2-5	torsin family 1 member A	Homo sapiens	22-26
10495044-11	1999	The GAG deletion in the DYT1 gene was excluded in the proband and in the family member affected by writer"s cramp.	Glycosaminoglycans	4-7	torsin family 1 member A	Homo sapiens	24-28
10438523-2	1999	Human beta-glucuronidase (hGUSB) is a member of family 2 glycosylhydrolases that cleaves beta-D-glucuronic acid residues from the nonreducing termini of glycosaminoglycans.	Glycosaminoglycans	153-171	glucuronidase beta	Homo sapiens	26-31
10419889-2	1999	The first ones, referred to as type I, involve interactions with the conserved domain of CyPB and promote the endocytosis of surface-bound ligand, while the second type of binding sites, termed type II, are represented by glycosaminoglycans (GAG).	Glycosaminoglycans	222-240	peptidylprolyl isomerase B	Homo sapiens	89-93
10419484-7	1999	A testable model for elastin-glycosaminoglycan interactions is proposed, where tropoelastin deposition during elastogenesis is encouraged by local exposure to matrix glycosaminoglycans.	Glycosaminoglycans	29-46	elastin	Homo sapiens	21-28
10542133-4	1999	The deduced IPM 200 core protein contains a putative transmembrane domain, two EGF-like repeats, numerous N- and O-linked glycosylation consensus sequences and one consensus sequence for glycosaminoglycan attachment.	Glycosaminoglycans	187-204	interphotoreceptor matrix proteoglycan 2	Homo sapiens	12-19
10593481-5	1999	Late passage animals (P3 and P4) had a two-log increase in the level of plasma p27(gag) antigen.	Glycosaminoglycans	83-86	interferon alpha inducible protein 27	Homo sapiens	79-82
10445316-5	1999	Furthermore, the displacement of the bacteria from immobilized mucin by highly sulphated glycosaminoglycans was observed.	Glycosaminoglycans	89-107	LOC100508689	Homo sapiens	63-68
10419484-7	1999	A testable model for elastin-glycosaminoglycan interactions is proposed, where tropoelastin deposition during elastogenesis is encouraged by local exposure to matrix glycosaminoglycans.	Glycosaminoglycans	29-46	elastin	Homo sapiens	79-91
10419484-7	1999	A testable model for elastin-glycosaminoglycan interactions is proposed, where tropoelastin deposition during elastogenesis is encouraged by local exposure to matrix glycosaminoglycans.	Glycosaminoglycans	166-184	elastin	Homo sapiens	21-28
10419484-7	1999	A testable model for elastin-glycosaminoglycan interactions is proposed, where tropoelastin deposition during elastogenesis is encouraged by local exposure to matrix glycosaminoglycans.	Glycosaminoglycans	166-184	elastin	Homo sapiens	79-91
10419484-9	1999	Following lysyl oxidase modification of tropoelastin lysine residues, they are released from glycosaminoglycan interactions, thereby permitting those residues to contribute to elastin cross-links.	Glycosaminoglycans	93-110	elastin	Homo sapiens	40-52
10419484-9	1999	Following lysyl oxidase modification of tropoelastin lysine residues, they are released from glycosaminoglycan interactions, thereby permitting those residues to contribute to elastin cross-links.	Glycosaminoglycans	93-110	elastin	Homo sapiens	45-52
10375392-0	1999	Oxidative modification of apolipoprotein E in human very-low-density lipoprotein and its inhibition by glycosaminoglycans.	Glycosaminoglycans	103-121	apolipoprotein E	Homo sapiens	26-42
10383394-4	1999	We found that treatment of HASMC with chondroitinase ABC, an enzyme that degrades chondroitin sulfate GAG, reduced IFN-gamma binding by more than 50%.	Glycosaminoglycans	102-105	interferon gamma	Homo sapiens	115-124
10383394-9	1999	The interaction of IFN-gamma with chondroitin sulfate GAG was confirmed by affinity chromatography of isolated cell-associated 35S-, 3H-labeled PG on a column with immobilized IFN-gamma.	Glycosaminoglycans	54-57	interferon gamma	Homo sapiens	19-28
10383394-9	1999	The interaction of IFN-gamma with chondroitin sulfate GAG was confirmed by affinity chromatography of isolated cell-associated 35S-, 3H-labeled PG on a column with immobilized IFN-gamma.	Glycosaminoglycans	54-57	interferon gamma	Homo sapiens	176-185
10375392-1	1999	The mechanism of metal ion-catalyzed oxidative modification of apolipoprotein E (apoE) in human very-low-density lipoprotein (VLDL) and its inhibition by glycosaminoglycan (GAG) was investigated in vitro.	Glycosaminoglycans	154-171	apolipoprotein E	Homo sapiens	63-79
10375392-1	1999	The mechanism of metal ion-catalyzed oxidative modification of apolipoprotein E (apoE) in human very-low-density lipoprotein (VLDL) and its inhibition by glycosaminoglycan (GAG) was investigated in vitro.	Glycosaminoglycans	154-171	apolipoprotein E	Homo sapiens	81-85
10375392-1	1999	The mechanism of metal ion-catalyzed oxidative modification of apolipoprotein E (apoE) in human very-low-density lipoprotein (VLDL) and its inhibition by glycosaminoglycan (GAG) was investigated in vitro.	Glycosaminoglycans	173-176	apolipoprotein E	Homo sapiens	63-79
10375392-1	1999	The mechanism of metal ion-catalyzed oxidative modification of apolipoprotein E (apoE) in human very-low-density lipoprotein (VLDL) and its inhibition by glycosaminoglycan (GAG) was investigated in vitro.	Glycosaminoglycans	173-176	apolipoprotein E	Homo sapiens	81-85
10375392-5	1999	The lipid peroxidation and oxidative modification of apoE in VLDL mediated by Cu2+ and an aqueous radical generator were suppressed by GAG, heparan sulfate, heparin, and chondroitin sulfate A, even though GAGs demonstrated no ability to scavenge alpha,alpha-diphenyl-beta-picrylhydrazyl radical.	Glycosaminoglycans	135-138	apolipoprotein E	Homo sapiens	53-57
10375392-5	1999	The lipid peroxidation and oxidative modification of apoE in VLDL mediated by Cu2+ and an aqueous radical generator were suppressed by GAG, heparan sulfate, heparin, and chondroitin sulfate A, even though GAGs demonstrated no ability to scavenge alpha,alpha-diphenyl-beta-picrylhydrazyl radical.	Glycosaminoglycans	205-209	apolipoprotein E	Homo sapiens	53-57
10375392-8	1999	These studies suggest that GAGs preserve the biological functions of apoE from oxidative stress.	Glycosaminoglycans	27-31	apolipoprotein E	Homo sapiens	69-73
10233961-5	1999	Comparison of the transduction efficiencies of vectors containing different portions of the FIV Gag coding region indicates that at least a functional part of the FIV packaging signal (Psi) is located within an area which includes the 5" LTR and the first 350 bp of gag.	Glycosaminoglycans	266-269	gag protein	Feline immunodeficiency virus	96-99
10435508-0	1999	GAG deletion in the DYT1 gene in early limb-onset idiopathic torsion dystonia in Germany.	Glycosaminoglycans	0-3	torsin family 1 member A	Homo sapiens	20-24
10341217-3	1999	We have investigated the effects of exogenous glycosaminoglycan addition upon hepatocyte growth factor-stimulated motility of Madin-Darby canine kidney cells.	Glycosaminoglycans	46-63	hepatocyte growth factor	Canis lupus familiaris	78-102
10341217-9	1999	These findings suggest that hepatocyte growth factor activity is not only critically dependent upon the presence of glycosaminoglycan, but specifically requires an intact proteoglycan structure located in close apposition to cell surface Met.	Glycosaminoglycans	116-133	hepatocyte growth factor	Canis lupus familiaris	28-52
10404013-9	1999	When MK cDNA was transfected into ATDC5 chondrogenic cells and overexpressed, the majority of transfected cells with strong MK expression showed enhanced chondrogenesis as revealed by increased synthesis of sulfated glycosaminoglycans, aggrecan, and type II collagen.	Glycosaminoglycans	216-234	midkine	Mus musculus	5-7
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
10233982-3	1999	9, that developed in a BALB/c mouse, we have found an insertion of a 1.2-kb sequence, consisting of a 5" long terminal repeat and gag sequences of an intracisternal type A particle (IAP) as well as an extra copy of the Notch4/int3 genomic sequences containing exons 23 and 24, into the intron between exons 24 and 25 of the Notch4/int3 gene.	Glycosaminoglycans	130-133	intracisternal A particle, Eya1 linked	Mus musculus	182-185
10404773-2	1999	In order to go further in the mechanisms, the relationship between the antithrombotic activity, the HCII-mediated anti-IIa activity and the plasma GAG content was investigated.	Glycosaminoglycans	147-150	heparin cofactor 2	Oryctolagus cuniculus	100-104
10404773-3	1999	We showed that the in vitro specific activity on the inhibition of thrombin by HCII of the plasma GAG extract from naroparcil-treated rabbits was increased by a factor of 60 when compared to controls.	Glycosaminoglycans	98-101	prothrombin	Oryctolagus cuniculus	67-75
10404773-4	1999	In addition, the fractionation of the plasma GAG extract by affinity chromatography on immobilized HCII led to a more potent material whereas the low-affinity fraction was shown to be inactive in thrombin inhibition by HCII.	Glycosaminoglycans	45-48	heparin cofactor 2	Oryctolagus cuniculus	99-103
10404773-3	1999	We showed that the in vitro specific activity on the inhibition of thrombin by HCII of the plasma GAG extract from naroparcil-treated rabbits was increased by a factor of 60 when compared to controls.	Glycosaminoglycans	98-101	heparin cofactor 2	Oryctolagus cuniculus	79-83
10404773-6	1999	In vitro experiments using immuno-depleted plasma in antithrombin III (ATIII), HCII or both, indicated that the anti-IIa activity of the plasma GAG extract from naroparcil-treated rabbits was mainly due to HCII potentialisation.	Glycosaminoglycans	144-147	heparin cofactor 2	Oryctolagus cuniculus	79-83
10224052-8	1999	The mutation most likely lies in the structural gene encoding GlcAT-I since transfection of the mutant with a cDNA for GlcAT-I completely restored enzyme activity and glycosaminoglycan synthesis.	Glycosaminoglycans	167-184	galactosylgalactosylxylosylprotein 3-beta-glucuronosyltransferase 3	Cricetulus griseus	62-69
10404773-6	1999	In vitro experiments using immuno-depleted plasma in antithrombin III (ATIII), HCII or both, indicated that the anti-IIa activity of the plasma GAG extract from naroparcil-treated rabbits was mainly due to HCII potentialisation.	Glycosaminoglycans	144-147	heparin cofactor 2	Oryctolagus cuniculus	206-210
10404773-8	1999	These results show that the antithrombotic activity of naroparcil is dependent on modification in the plasma GAG profile which inactivates thrombin via the HCII.	Glycosaminoglycans	109-112	prothrombin	Oryctolagus cuniculus	139-147
10404773-8	1999	These results show that the antithrombotic activity of naroparcil is dependent on modification in the plasma GAG profile which inactivates thrombin via the HCII.	Glycosaminoglycans	109-112	heparin cofactor 2	Oryctolagus cuniculus	156-160
10224052-8	1999	The mutation most likely lies in the structural gene encoding GlcAT-I since transfection of the mutant with a cDNA for GlcAT-I completely restored enzyme activity and glycosaminoglycan synthesis.	Glycosaminoglycans	167-184	galactosylgalactosylxylosylprotein 3-beta-glucuronosyltransferase 3	Cricetulus griseus	119-126
10331444-2	1999	To characterize the HIV-1 subtypes circulating in this area, we have examined a 330-bp fragment of the p17 region of the gag gene of HIV-1 strains obtained from 70 patients (55 mothers, 15 children), of whom 61 were epidemiologically unlinked.	Glycosaminoglycans	121-124	family with sequence similarity 72 member B	Homo sapiens	103-106
10331444-8	1999	This level of gag(p17) gene variation in the DRC is considerably greater than previously appreciated.	Glycosaminoglycans	14-17	family with sequence similarity 72 member B	Homo sapiens	18-21
10212223-5	1999	Midkine and pleiotrophin binding to PTPzeta were equally inhibited by soluble pleiotrophin and also by some specific glycosaminoglycans.	Glycosaminoglycans	117-135	midkine	Homo sapiens	0-7
10427856-5	1999	Finally, based on the double recognition of L-selectin with Lewis type and glycosaminoglycan structures, we tentatively introduced a possible link between the selectin- and the integrin-mediated lymphocyte adhesion systems.	Glycosaminoglycans	75-92	selectin L	Homo sapiens	44-54
10328871-0	1999	Binding of interferon gamma by glycosaminoglycans: a strategy for localization and/or inhibition of its activity.	Glycosaminoglycans	31-49	interferon gamma	Homo sapiens	11-27
10330124-3	1999	In this study, we have determined that the human DSPG3 gene is composed of seven exons: Exon 2 of DSPG3 includes the start codon, exons 4-7 code for the leucine-rich repeats, exons 3 and 7 contain the potential glycosaminoglycan attachment sites, and exon 7 contains the potential N-glycosylation sites and the stop codon.	Glycosaminoglycans	211-228	epiphycan	Homo sapiens	49-54
10448867-3	1999	PECAM-1 mediates homophilic and heterophilic interactions (with glycosaminoglycans and alphaVbeta3), but deletion of exon 14 results in a loss of heterophilic adhesion.	Glycosaminoglycans	64-82	platelet and endothelial cell adhesion molecule 1	Homo sapiens	0-7
10212210-2	1999	PF-4 binding has been shown to be independent of interleukin-8 receptors and could be inhibited by soluble chondroitin sulfate type glycosaminoglycans or by pretreatment of cells with chondroitinase ABC.	Glycosaminoglycans	132-150	platelet factor 4	Bos taurus	0-4
10212210-3	1999	Here we present evidence that surface-expressed neutrophil glycosaminoglycans are of chondroitin sulfate type and that this species binds to the tetrameric form of PF-4.	Glycosaminoglycans	59-77	platelet factor 4	Bos taurus	164-168
10212210-7	1999	The di-O-sulfated disaccharide units in neutrophil glycosaminoglycans clearly promoted the affinity to PF-4, which showed a Kd approximately 0.8 microM, as the affinities of bovine cartilage chondroitin sulfate A, porcine skin dermatan sulfate, or bovine cartilage chondroitin sulfate C, all consisting exclusively of monosulfated disaccharide units, were found to be 3-5-fold lower.	Glycosaminoglycans	51-69	platelet factor 4	Bos taurus	103-107
10323780-4	1999	There is also evidence that both LDL and PLA2 bind to the glycosaminoglycan (GAG) chains of extracellular proteoglycans in the arterial wall.	Glycosaminoglycans	58-75	phospholipase A2 group IB	Homo sapiens	41-45
10323780-5	1999	Here we studied the effect of heparin GAG on the lipolytic modification of LDL by PLA2.	Glycosaminoglycans	38-41	phospholipase A2 group IB	Homo sapiens	82-86
10323780-12	1999	Thus, it is possible that within the GAG meshwork of the arterial intima, PLA2-induced modification of LDL is one source of the lipid droplets during atherogenesis.	Glycosaminoglycans	37-40	phospholipase A2 group IB	Homo sapiens	74-78
10399314-2	1999	It binds glycosaminoglycans, collagen, plasminogen and the urokinase-receptor, and also stabilizes the inhibitory conformation of plasminogen activation inhibitor-1.	Glycosaminoglycans	9-27	protein phosphatase 1 regulatory inhibitor subunit 1A	Homo sapiens	153-164
10408366-6	1999	Factor H is a multifunctional protein and displays functions outside the complement system: it binds to the cellular integrin receptor (CD11b/CD18), interacts with cell surface glycosaminoglycans and also binds to the surface of certain pathogenic microorganisms.	Glycosaminoglycans	177-195	complement factor H	Homo sapiens	0-8
10212223-5	1999	Midkine and pleiotrophin binding to PTPzeta were equally inhibited by soluble pleiotrophin and also by some specific glycosaminoglycans.	Glycosaminoglycans	117-135	pleiotrophin	Homo sapiens	12-24
10212223-5	1999	Midkine and pleiotrophin binding to PTPzeta were equally inhibited by soluble pleiotrophin and also by some specific glycosaminoglycans.	Glycosaminoglycans	117-135	protein tyrosine phosphatase receptor type Z1	Homo sapiens	36-43
10338119-8	1999	These results suggest that the inhibition of an autoregulatory role wielded by protein kinase C on the protein kinase C-alpha and -delta gene expression might represent a possible mechanism by which glycosaminoglycans modulate the cell growth.	Glycosaminoglycans	199-217	protein kinase C alpha	Homo sapiens	103-136
10207021-6	1999	The interaction of biotin-laminin-1 with alphaDG was inhibited by soluble alphaDG contained in the conditioned medium from DG cDNA-transfected BAE cells and by a series of glycosaminoglycans (heparin, dextran sulfate, and fucoidan).	Glycosaminoglycans	172-190	dystroglycan 1	Bos taurus	46-48
10211608-8	1999	IL-1beta dose-dependently increased [3H]glucosamine incorporation into GAG by both cells.	Glycosaminoglycans	71-74	interleukin 1 beta	Homo sapiens	0-8
10408016-8	1999	These results suggest that both, IL-1 beta and IL-1 alpha, stimulate GAG and especially hyaluronic acid synthesis, but not DNA synthesis, in vitro.	Glycosaminoglycans	69-72	interleukin 1 beta	Homo sapiens	33-42
10408016-8	1999	These results suggest that both, IL-1 beta and IL-1 alpha, stimulate GAG and especially hyaluronic acid synthesis, but not DNA synthesis, in vitro.	Glycosaminoglycans	69-72	interleukin 1 alpha	Homo sapiens	47-57
10067859-5	1999	Among IGFBPs, only IGFBP-5 showed weak competition, indicating that IGFBP-3 binding to breast cancer cell surfaces is specific and cannot be attributed to nonspecific interaction with glycosaminoglycans.	Glycosaminoglycans	184-202	insulin like growth factor binding protein 3	Homo sapiens	68-75
10075664-0	1999	Glycosaminoglycans differentially bind HARP and modulate its biological activity.	Glycosaminoglycans	0-18	pleiotrophin	Mus musculus	39-43
10051565-0	1999	Fibroblast growth factors 1 and 2 are distinct in oligomerization in the presence of heparin-like glycosaminoglycans.	Glycosaminoglycans	98-116	fibroblast growth factor 1	Homo sapiens	0-33
10064580-3	1999	The p24 construct used is a variant with an N-terminal extension that mimics to some extent the Gag context of p24.	Glycosaminoglycans	96-99	transmembrane p24 trafficking protein 2	Homo sapiens	4-7
10064580-3	1999	The p24 construct used is a variant with an N-terminal extension that mimics to some extent the Gag context of p24.	Glycosaminoglycans	96-99	transmembrane p24 trafficking protein 2	Homo sapiens	111-114
10914239-1	1999	Danaparoid sodium is an antithrombin composed of 3 glycosaminoglycans: heparan sulfate, dermatan sulfate and chondroitin sulfate.	Glycosaminoglycans	51-69	serpin family C member 1	Homo sapiens	24-36
10071085-1	1999	Lysozyme, a myelomonocytic marker not only exerts bacteriolytic, but also immunomodulatoric properties and was found to bind to the glycosaminoglycan serglycin, an important constituent of the extracellular matrix (ECM).	Glycosaminoglycans	132-149	lysozyme	Homo sapiens	0-8
10211608-3	1999	In the present study, we investigated interleukin (IL)-1beta-induced oxygen free radical production and the role of oxygen free radicals in IL-1beta-induced GAG production in retro-ocular fibroblasts from both normal subjects and patients with GO.	Glycosaminoglycans	157-160	interleukin 1 beta	Homo sapiens	140-148
10211608-10	1999	Scavenging oxygen free radicals by the use of SOD (100 U/mL) and catalase (300 U/mL) partially blocked the IL-1beta-induced GAG production in both cells.	Glycosaminoglycans	124-127	superoxide dismutase 1	Homo sapiens	46-49
10211608-10	1999	Scavenging oxygen free radicals by the use of SOD (100 U/mL) and catalase (300 U/mL) partially blocked the IL-1beta-induced GAG production in both cells.	Glycosaminoglycans	124-127	catalase	Homo sapiens	51-73
10211608-10	1999	Scavenging oxygen free radicals by the use of SOD (100 U/mL) and catalase (300 U/mL) partially blocked the IL-1beta-induced GAG production in both cells.	Glycosaminoglycans	124-127	interleukin 1 beta	Homo sapiens	107-115
10211608-11	1999	These results suggest that stress related oxygen free radicals are present in the retro-ocular tissue in GO and that oxygen free radicals are involved in GAG accumulation induced by cytokine IL-1beta.	Glycosaminoglycans	154-157	interleukin 1 beta	Homo sapiens	191-199
10723059-1	1999	The present study shows that sciatic nerve crush in 2-day-old rats causes extensor digitorum longus (EDL) muscle atrophy and motor neuron loss and that treatment with glycosaminoglycans (GAGs) promotes muscle reinnervation, motor neuron survival, and markedly increases insulin-like growth factor-I (IGF-I) content in the denervated muscles.	Glycosaminoglycans	167-185	insulin-like growth factor 1	Rattus norvegicus	300-305
10723059-1	1999	The present study shows that sciatic nerve crush in 2-day-old rats causes extensor digitorum longus (EDL) muscle atrophy and motor neuron loss and that treatment with glycosaminoglycans (GAGs) promotes muscle reinnervation, motor neuron survival, and markedly increases insulin-like growth factor-I (IGF-I) content in the denervated muscles.	Glycosaminoglycans	187-191	insulin-like growth factor 1	Rattus norvegicus	300-305
10368283-9	1999	In this model, the heparin-binding residues of IL-8 are exposed, thereby allowing presentation of the chemokine from endothelial cell-surface glycosaminoglycans.	Glycosaminoglycans	142-160	C-X-C motif chemokine ligand 8	Homo sapiens	47-51
10723059-7	1999	Treatment with GAGs selectively affects IGF-I content in denervated hindlimb muscles, which is augmented from 7.02 +/- 0.71 ng/mg tissue to 25.72 +/- 0.7 in the EDL and from 3.2 +/- 0.18 to a robust 211 +/- 9.6 in the soleus.	Glycosaminoglycans	15-19	insulin-like growth factor 1	Rattus norvegicus	40-45
9878016-3	1999	Despite good reactivity to recall antigens, at baseline approximately 33% had proliferative responses to gp160, and approximately 42% showed p24 gag responses.	Glycosaminoglycans	145-148	transmembrane p24 trafficking protein 2	Homo sapiens	141-144
10099930-9	1999	Similarly, removal of ZG16p or prevention of its interaction with glycosaminoglycans (GAGs) in the submembranous matrix of ZGM by sodium bicarbonate treatment or chondroitinase digestion of ZGM also inhibits the binding efficiency of secretory proteins to ZGM to about the same extent.	Glycosaminoglycans	66-84	zymogen granule protein 16	Rattus norvegicus	22-27
10022587-4	1999	The administration of recombinant beta-glucuronidase from birth significantly reduces glycosaminoglycan storage in most tissues, increases life span, and improves the animal"s cognitive ability and mobility.	Glycosaminoglycans	86-103	glucuronidase, beta	Mus musculus	34-52
9891023-11	1999	The artificial proteoglycans were also used as a model system to explore the glycosaminoglycan binding properties of basic-fibroblast growth factor and the chemokine RANTES.	Glycosaminoglycans	77-94	C-C motif chemokine ligand 5	Homo sapiens	166-172
9916738-8	1999	Treatment of normal human articular cartilage with IL-18 increased the release of glycosaminoglycans.	Glycosaminoglycans	82-100	interleukin 18	Homo sapiens	51-56
9857078-0	1998	The NH2-terminal region of apolipoprotein B is sufficient for lipoprotein association with glycosaminoglycans.	Glycosaminoglycans	91-109	apolipoprotein B	Homo sapiens	27-43
9872999-1	1999	Mutations in the acid beta-glucuronidase gene lead to systemic accumulation of undegraded glycosaminoglycans in lysosomes and ultimately to clinical manifestations of mucopolysaccharidosis VII (Sly disease).	Glycosaminoglycans	90-108	glucuronidase, beta	Mus musculus	22-40
10027728-1	1999	Syndecan-1 (CD138) is a surface proteoglycan consisting of long unbranched glycosaminoglycan (GAG) chains covalently attached to a protein backbone.	Glycosaminoglycans	75-92	syndecan 1	Homo sapiens	0-10
10027728-1	1999	Syndecan-1 (CD138) is a surface proteoglycan consisting of long unbranched glycosaminoglycan (GAG) chains covalently attached to a protein backbone.	Glycosaminoglycans	75-92	syndecan 1	Homo sapiens	12-17
10027728-1	1999	Syndecan-1 (CD138) is a surface proteoglycan consisting of long unbranched glycosaminoglycan (GAG) chains covalently attached to a protein backbone.	Glycosaminoglycans	94-97	syndecan 1	Homo sapiens	0-10
10027728-1	1999	Syndecan-1 (CD138) is a surface proteoglycan consisting of long unbranched glycosaminoglycan (GAG) chains covalently attached to a protein backbone.	Glycosaminoglycans	94-97	syndecan 1	Homo sapiens	12-17
10050893-1	1999	A GAG deletion at position 946 in DYT1, one of the genes responsible for autosomal dominant idiopathic torsion dystonia (ITD), has recently been identified.	Glycosaminoglycans	2-5	torsin family 1 member A	Homo sapiens	34-38
9847364-0	1999	Interaction with the p6 domain of the gag precursor mediates incorporation into virions of Vpr and Vpx proteins from primate lentiviruses.	Glycosaminoglycans	38-41	vpx protein	Simian immunodeficiency virus	99-102
10229268-3	1999	When a viral suspension of high titer (10(3.93) TCID50 ml(-1) was filtered, efficient reduction (&gt;99%) of gag p24 antigen levels and infectious titer resulted.	Glycosaminoglycans	109-112	transmembrane p24 trafficking protein 2	Homo sapiens	113-116
10465440-0	1999	Glycosaminoglycans boost insulin-like growth factor-I-promoted neuroprotection: blockade of motor neuron death in the wobbler mouse.	Glycosaminoglycans	0-18	insulin-like growth factor 1	Mus musculus	25-53
10738516-0	1999	Detailed haplotype analysis in Ashkenazi Jewish and non-Jewish British dystonic patients carrying the GAG deletion in the DYT1 gene: evidence for a limited number of founder mutations.	Glycosaminoglycans	102-105	torsin family 1 member A	Homo sapiens	122-126
10738516-5	1999	In this study, we analysed the haplotypes surrounding DYT1 in 9 AJ and 15 non-Jewish British patients carrying the GAG deletion in the DYT1 gene.	Glycosaminoglycans	115-118	torsin family 1 member A	Homo sapiens	135-139
10738516-8	1999	This supports the hypothesis that the GAG deletion in the DYT1 gene is not a very frequent mutation, and that it has arisen only a limited number of times throughout the centuries.	Glycosaminoglycans	38-41	torsin family 1 member A	Homo sapiens	58-62
9891886-5	1999	The Wg/Wnt ligands pass through the secretory pathway and associate with extracellular matrix components; recent work shows that sulfated glycosaminoglycans are essential for proper transduction of the signal.	Glycosaminoglycans	138-156	Wnt oncogene analog 5	Drosophila melanogaster	7-10
9934708-5	1999	The relative rates of change for FV structural proteins were Pol &lt; Env &lt; Gag in increasing order, which differs from all other retroviruses.	Glycosaminoglycans	79-82	endogenous retrovirus group K member 20	Homo sapiens	70-73
10447213-0	1999	Specificity of glycosaminoglycan suppression of endothelin-1 production by human umbilical vein endothelial cells.	Glycosaminoglycans	15-32	endothelin 1	Homo sapiens	48-60
10447213-3	1999	By inhibiting thrombin we have previously shown that heparin, a highly negatively-charged glycosaminoglycan (GAG), suppresses the production of ET-1 by cultured human umbilical vein endothelial cells (HUVEC).	Glycosaminoglycans	90-107	coagulation factor II, thrombin	Homo sapiens	14-22
10447213-3	1999	By inhibiting thrombin we have previously shown that heparin, a highly negatively-charged glycosaminoglycan (GAG), suppresses the production of ET-1 by cultured human umbilical vein endothelial cells (HUVEC).	Glycosaminoglycans	90-107	endothelin 1	Homo sapiens	144-148
10447213-4	1999	The purpose of our study is to determine the effect of other GAGs and related compounds on ET-1 production.	Glycosaminoglycans	61-65	endothelin 1	Homo sapiens	91-95
10447213-8	1999	GAGs and related molecules with higher sulfate content, heparin, chondroitin sulfate B, low and high molecular weight dextran sulfates significantly suppressed ET-1 production by HUVEC.	Glycosaminoglycans	0-4	endothelin 1	Homo sapiens	160-164
10463198-0	1999	Glycosaminoglycan prevents hyperglycemia-induced renal TGF-beta 1 gene expression.	Glycosaminoglycans	0-17	transforming growth factor beta 1	Homo sapiens	55-65
10482050-10	1999	Interestingly, we also identified a dually infected individual with viruses belonging to subtypes B and F, as demonstrated by molecular cloning analysis of the env V3 and the gag p17 regions.	Glycosaminoglycans	175-178	family with sequence similarity 72 member B	Homo sapiens	179-182
9852062-1	1998	Human beta-glucuronidase is a member of the Family 2 glycosylhydrolases that cleaves beta-D-glucuronic acid residues from the nonreducing termini of glycosaminoglycans.	Glycosaminoglycans	149-167	glucuronidase beta	Homo sapiens	6-24
9837831-3	1998	To evaluate the role of these loci in focal dystonia, we tested 85 patients from northern Germany who had primary focal dystonia, both for the GAG deletion in the DYT1 gene on chromosome 9q34 and for linkage disequilibrium at the chromosome 18p markers D18S1105, D18S1098, D18S481, and D18S54.	Glycosaminoglycans	143-146	torsin family 1 member A	Homo sapiens	163-167
9841882-5	1998	We first provide evidence that the CyPB binding to heparin-Sepharose is prevented by soluble sulphated glycosaminoglycans (GAG), raising the interesting possibility that such interactions may occur on the T-cell surface.	Glycosaminoglycans	103-121	peptidylprolyl isomerase B	Homo sapiens	35-39
9841882-5	1998	We first provide evidence that the CyPB binding to heparin-Sepharose is prevented by soluble sulphated glycosaminoglycans (GAG), raising the interesting possibility that such interactions may occur on the T-cell surface.	Glycosaminoglycans	123-126	peptidylprolyl isomerase B	Homo sapiens	35-39
9841882-6	1998	We then characterized CyPB binding to T-cell surface GAG and found that these interactions involved the N-terminal extension of CyPB, but not its conserved CsA-binding domain.	Glycosaminoglycans	53-56	peptidylprolyl isomerase B	Homo sapiens	22-26
9841882-9	1998	The conclusion that CyPB binding to the type I site is distinct from the interactions with GAG was based on the findings that it was (1) resistant to NaCl wash and GAG-degrading enzyme treatments, (2) reduced in the presence of CsA or cyclophilin C, and (3) unmodified in the presence of either the N-terminal peptide of CyPB or protamine.	Glycosaminoglycans	164-167	peptidylprolyl isomerase B	Homo sapiens	20-24
9837939-2	1998	Heparin cofactor II is a naturally occurring anticoagulant that acts by specifically inhibiting thrombin and is facilitated by the binding of glycosaminoglycans such as heparin and dermatan sulfate.	Glycosaminoglycans	142-160	heparin cofactor 2	Oryctolagus cuniculus	0-19
9815256-8	1998	Antigenic variation was also detected in the p17 Gag epitope; a dominant viral variant present in the patient was well recognized by a specific CD4(+) T lymphocyte line, whereas several natural mutants were not.	Glycosaminoglycans	49-52	family with sequence similarity 72 member B	Homo sapiens	45-48
9848887-0	1998	Phospholipase A2 type II binds to extracellular matrix biglycan: modulation of its activity on LDL by colocalization in glycosaminoglycan matrixes.	Glycosaminoglycans	120-137	phospholipase A2 group IB	Homo sapiens	0-16
9848887-0	1998	Phospholipase A2 type II binds to extracellular matrix biglycan: modulation of its activity on LDL by colocalization in glycosaminoglycan matrixes.	Glycosaminoglycans	120-137	biglycan	Homo sapiens	55-63
9874484-6	1998	Twenty-two patients were positive for the GAG deletion in the DYT1 gene.	Glycosaminoglycans	42-45	torsin family 1 member A	Homo sapiens	62-66
9813026-1	1998	Site-directed mutagenesis was used to investigate the role of basic residues in the thrombin anion-binding exosite-I during formation of thrombin-antithrombin III (ATIII), thrombin-protease nexin 1 (PN1), and thrombin-heparin cofactor II (HCII) inhibitor complexes, in the absence and presence of glycosaminoglycans.	Glycosaminoglycans	297-315	coagulation factor II, thrombin	Homo sapiens	84-92
9880676-2	1998	The nucleotide sequence of Fv1 bears similarity to the gag of a human endogenous retrovirus, HERV-L, but is more closely related to the gag-coding sequence of a newly described class of HERV-L-related mouse endogenous retroviruses designated MuERV-L.	Glycosaminoglycans	55-58	Friend virus susceptibility 1	Mus musculus	27-30
9880676-2	1998	The nucleotide sequence of Fv1 bears similarity to the gag of a human endogenous retrovirus, HERV-L, but is more closely related to the gag-coding sequence of a newly described class of HERV-L-related mouse endogenous retroviruses designated MuERV-L.	Glycosaminoglycans	136-139	Friend virus susceptibility 1	Mus musculus	27-30
9880676-3	1998	Both observations suggest an origin of Fv1 from endogenous gag sequences.	Glycosaminoglycans	59-62	Friend virus susceptibility 1	Mus musculus	39-42
9815256-8	1998	Antigenic variation was also detected in the p17 Gag epitope; a dominant viral variant present in the patient was well recognized by a specific CD4(+) T lymphocyte line, whereas several natural mutants were not.	Glycosaminoglycans	49-52	CD4 molecule	Homo sapiens	144-147
9815269-0	1998	A new monoclonal antibody, mAb 4A12, identifies a role for the glycosaminoglycan (GAG) binding domain of RANTES in the antiviral effect against HIV-1 and intracellular Ca2+ signaling.	Glycosaminoglycans	63-80	C-C motif chemokine ligand 5	Homo sapiens	105-111
9815269-0	1998	A new monoclonal antibody, mAb 4A12, identifies a role for the glycosaminoglycan (GAG) binding domain of RANTES in the antiviral effect against HIV-1 and intracellular Ca2+ signaling.	Glycosaminoglycans	82-85	C-C motif chemokine ligand 5	Homo sapiens	105-111
9815269-8	1998	Taken together, these studies demonstrate that the COOH-terminal alpha-helical region of RANTES plays a key role in GAG-binding, antiviral activity, and intracellular Ca2+ signaling and support a model in which GAGs play a key role in the biological activities of this chemokine.	Glycosaminoglycans	116-119	C-C motif chemokine ligand 5	Homo sapiens	89-95
9825824-0	1998	Sulfation-dependent down-regulation of interferon-gamma-induced major histocompatibility complex class I and II and intercellular adhesion molecule-1 expression on tubular and endothelial cells by glycosaminoglycans.	Glycosaminoglycans	197-215	interferon gamma	Homo sapiens	39-55
9825824-0	1998	Sulfation-dependent down-regulation of interferon-gamma-induced major histocompatibility complex class I and II and intercellular adhesion molecule-1 expression on tubular and endothelial cells by glycosaminoglycans.	Glycosaminoglycans	197-215	intercellular adhesion molecule 1	Homo sapiens	116-149
9825824-8	1998	Heparin and supersulfated glycosaminoglycans (GAGs) were able to bind to IFN-gamma, whereas N-desulfated N-acetylated GAGs with a low amount of sulfate were not.	Glycosaminoglycans	26-44	interferon gamma	Homo sapiens	73-82
9825824-8	1998	Heparin and supersulfated glycosaminoglycans (GAGs) were able to bind to IFN-gamma, whereas N-desulfated N-acetylated GAGs with a low amount of sulfate were not.	Glycosaminoglycans	46-50	interferon gamma	Homo sapiens	73-82
9825824-12	1998	Supersulfated GAGs with low anti-coagulant activity could be used therapeutically to decrease MHC and ICAM-1 expression on organ grafts.	Glycosaminoglycans	14-18	intercellular adhesion molecule 1	Homo sapiens	102-108
9753677-5	1998	Wnt-4 signaling depends on cell contact and sulphated glycosaminoglycans and is only required for triggering tubulogenesis but not for later events.	Glycosaminoglycans	54-72	Wnt family member 4	Homo sapiens	0-5
9824320-3	1998	High CTLm responses against Gag, but not Pol or Env, soon after seroconversion were associated with a slower loss of CD4+ T cells 1-4 years after seroconversion.	Glycosaminoglycans	28-31	CD4 molecule	Homo sapiens	117-120
9846893-3	1998	However, glycation of tau results in the bundling of the tau filaments formed by glycosaminoglycan-induced polymerisation.	Glycosaminoglycans	81-98	microtubule associated protein tau	Homo sapiens	22-25
9846893-3	1998	However, glycation of tau results in the bundling of the tau filaments formed by glycosaminoglycan-induced polymerisation.	Glycosaminoglycans	81-98	microtubule associated protein tau	Homo sapiens	57-60
9792674-9	1998	Therefore, we conclude that the Lys-58 and His-66 residues in the C-terminal alpha-helix of MCP-1 are essential for glycosaminoglycan binding and probably for the binding to the endothelial surface proteoglycans.	Glycosaminoglycans	116-133	C-C motif chemokine ligand 2	Homo sapiens	92-97
9794421-3	1998	The dominant in vivo activated CTL response was directed against two overlapping Gag CTL epitopes in an area of p17 known to be essential for viral replication.	Glycosaminoglycans	81-84	family with sequence similarity 72 member B	Homo sapiens	112-115
9786878-10	1998	The glycosaminoglycans heparin and heparan sulfate bind to IGFBP-5 through its basic carboxyl-terminal domain.	Glycosaminoglycans	4-22	insulin like growth factor binding protein 5	Homo sapiens	59-66
9765414-4	1998	By using constructed baculovirus vectors and TED Gag-specific antiserum, we show that the principal translation product of gag (Pr55(gag)) is cleaved to produce a single VLP structural protein, p37(gag).	Glycosaminoglycans	49-52	heterogeneous nuclear ribonucleoprotein D	Homo sapiens	194-197
9765414-4	1998	By using constructed baculovirus vectors and TED Gag-specific antiserum, we show that the principal translation product of gag (Pr55(gag)) is cleaved to produce a single VLP structural protein, p37(gag).	Glycosaminoglycans	123-126	NALCN channel auxiliary factor 2	Homo sapiens	45-48
9765414-4	1998	By using constructed baculovirus vectors and TED Gag-specific antiserum, we show that the principal translation product of gag (Pr55(gag)) is cleaved to produce a single VLP structural protein, p37(gag).	Glycosaminoglycans	123-126	heterogeneous nuclear ribonucleoprotein D	Homo sapiens	194-197
9862465-7	1998	Recent data have indicated an effect of UDPGDH on cell surface glycosaminoglycans (GAGs) which modulate the activity of growth factors, and in particular wingless signaling.	Glycosaminoglycans	63-81	sugarless	Drosophila melanogaster	40-46
9786878-11	1998	At high concentrations, these glycosaminoglycans inhibited ALS binding to binary complexed IGF-BP-5.	Glycosaminoglycans	30-48	insulin like growth factor binding protein 5	Homo sapiens	91-99
9780212-5	1998	Reduction of PF-4 binding and PF-4-induced exocytosis in the presence of various glycosaminoglycans or following treatment of cells with chondroitinase ABC (but not other glycosaminoglycan-degrading enzymes) altogether demonstrates that the PF-4 receptor is a proteoglycan of the chondroitin sulfate class.	Glycosaminoglycans	81-99	platelet factor 4	Homo sapiens	13-17
9774430-5	1998	The total glycosaminoglycan mixture present in wound fluid supported the ability of fibroblast growth factor-2 to signal cell proliferation.	Glycosaminoglycans	10-27	fibroblast growth factor 2	Homo sapiens	84-110
9795242-1	1998	Incubation of human articular cartilage explants with interleukin-1alpha (IL-1alpha) inhibited the rate of [35S]sulphate incorporation into glycosaminoglycan (GAG) chains concomitant with an increase in nitric oxide (NO) production.	Glycosaminoglycans	140-157	interleukin 1 alpha	Homo sapiens	54-72
9795242-1	1998	Incubation of human articular cartilage explants with interleukin-1alpha (IL-1alpha) inhibited the rate of [35S]sulphate incorporation into glycosaminoglycan (GAG) chains concomitant with an increase in nitric oxide (NO) production.	Glycosaminoglycans	140-157	interleukin 1 alpha	Homo sapiens	74-83
9795242-1	1998	Incubation of human articular cartilage explants with interleukin-1alpha (IL-1alpha) inhibited the rate of [35S]sulphate incorporation into glycosaminoglycan (GAG) chains concomitant with an increase in nitric oxide (NO) production.	Glycosaminoglycans	159-162	interleukin 1 alpha	Homo sapiens	54-72
9795242-1	1998	Incubation of human articular cartilage explants with interleukin-1alpha (IL-1alpha) inhibited the rate of [35S]sulphate incorporation into glycosaminoglycan (GAG) chains concomitant with an increase in nitric oxide (NO) production.	Glycosaminoglycans	159-162	interleukin 1 alpha	Homo sapiens	74-83
9780219-5	1998	Detailed analysis of two gag-specific clones from one of the individuals demonstrated HLA class I restriction and recognition of the same p24 epitope (EQASQEVKNWMT).	Glycosaminoglycans	25-28	transmembrane p24 trafficking protein 2	Homo sapiens	138-141
9795242-8	1998	Disaccharide analysis of the [35S]GAG chains showed that IL-1alpha preferentially inhibited sulphation of the 6-sulphated isomer and that l-NIO reversed this effect.	Glycosaminoglycans	34-37	interleukin 1 alpha	Homo sapiens	57-66
9795242-9	1998	Thus, IL-1alpha-induced NO mediates the inhibition of sulphate incorporation and alters the sulphation pattern of newly synthesised GAG chains.	Glycosaminoglycans	132-135	interleukin 1 alpha	Homo sapiens	6-15
9780212-5	1998	Reduction of PF-4 binding and PF-4-induced exocytosis in the presence of various glycosaminoglycans or following treatment of cells with chondroitinase ABC (but not other glycosaminoglycan-degrading enzymes) altogether demonstrates that the PF-4 receptor is a proteoglycan of the chondroitin sulfate class.	Glycosaminoglycans	81-99	platelet factor 4	Homo sapiens	30-34
9780212-5	1998	Reduction of PF-4 binding and PF-4-induced exocytosis in the presence of various glycosaminoglycans or following treatment of cells with chondroitinase ABC (but not other glycosaminoglycan-degrading enzymes) altogether demonstrates that the PF-4 receptor is a proteoglycan of the chondroitin sulfate class.	Glycosaminoglycans	81-99	platelet factor 4	Homo sapiens	30-34
9780212-5	1998	Reduction of PF-4 binding and PF-4-induced exocytosis in the presence of various glycosaminoglycans or following treatment of cells with chondroitinase ABC (but not other glycosaminoglycan-degrading enzymes) altogether demonstrates that the PF-4 receptor is a proteoglycan of the chondroitin sulfate class.	Glycosaminoglycans	81-98	platelet factor 4	Homo sapiens	13-17
9780212-5	1998	Reduction of PF-4 binding and PF-4-induced exocytosis in the presence of various glycosaminoglycans or following treatment of cells with chondroitinase ABC (but not other glycosaminoglycan-degrading enzymes) altogether demonstrates that the PF-4 receptor is a proteoglycan of the chondroitin sulfate class.	Glycosaminoglycans	81-98	platelet factor 4	Homo sapiens	30-34
9780212-5	1998	Reduction of PF-4 binding and PF-4-induced exocytosis in the presence of various glycosaminoglycans or following treatment of cells with chondroitinase ABC (but not other glycosaminoglycan-degrading enzymes) altogether demonstrates that the PF-4 receptor is a proteoglycan of the chondroitin sulfate class.	Glycosaminoglycans	81-98	platelet factor 4	Homo sapiens	30-34
9731743-10	1998	Simultaneous treatment with RA and TGF-beta also stimulated gycosaminoglycan (GAG) synthesis to an extent greater than that seen with TGF-beta treatment alone, this despite the ability of RA to inhibit GAG synthesis.	Glycosaminoglycans	78-81	transforming growth factor, beta 1	Mus musculus	35-43
9731743-10	1998	Simultaneous treatment with RA and TGF-beta also stimulated gycosaminoglycan (GAG) synthesis to an extent greater than that seen with TGF-beta treatment alone, this despite the ability of RA to inhibit GAG synthesis.	Glycosaminoglycans	202-205	transforming growth factor, beta 1	Mus musculus	35-43
9731758-0	1998	Glycosaminoglycans bind granulocyte-macrophage colony-stimulating factor and modulate its mitogenic activity and signaling in human osteoblastic cells.	Glycosaminoglycans	0-18	colony stimulating factor 2	Homo sapiens	24-72
9731743-11	1998	These data demonstrate a role for RA and RA-induced TGF-beta in the regulation of palate cell proliferation and GAG synthesis and suggest a role for TGF-beta in retinoid-induced cleft palate.	Glycosaminoglycans	112-115	transforming growth factor, beta 1	Mus musculus	52-60
9731758-3	1998	Using a bioassay in which the mitogenic activity of recombinant human (rh) GM-CSF was measured after incubation in the presence of an hOB cell layer or extracellular matrix (ECM) produced by these cells, we showed that rhGM-CSF binds to GAG components present in the ECM and that the bound rhGM-CSF retains its ability to stimulate hOB cell proliferation.	Glycosaminoglycans	237-240	colony stimulating factor 2	Homo sapiens	75-81
9822202-10	1998	These findings may explain why phenotypic consequences of DTDST mutations are restricted to cartilage, a tissue with high GAG synthesis rate and poor vascular supply, and imply that pharmacological therapy aimed at restoring the intracellular sulfate pool might improve PG sulfation in DTD and related disorders.	Glycosaminoglycans	122-125	solute carrier family 26 member 2	Homo sapiens	58-63
9733888-10	1998	When we investigated whether cell surface GAGs also participate in A27L-dependent fusion, our results indicated that soluble A27L protein blocked cell fusion, whereas D-A27L protein did not.	Glycosaminoglycans	42-46	IMV surface protein	Vaccinia virus	67-71
9733888-10	1998	When we investigated whether cell surface GAGs also participate in A27L-dependent fusion, our results indicated that soluble A27L protein blocked cell fusion, whereas D-A27L protein did not.	Glycosaminoglycans	42-46	IMV surface protein	Vaccinia virus	125-129
9733888-10	1998	When we investigated whether cell surface GAGs also participate in A27L-dependent fusion, our results indicated that soluble A27L protein blocked cell fusion, whereas D-A27L protein did not.	Glycosaminoglycans	42-46	IMV surface protein	Vaccinia virus	125-129
9733888-11	1998	Taken together, the results therefore demonstrated that A27L-mediated cell fusion is triggered by its interaction with cell surface GAGs through the N-terminal domain.	Glycosaminoglycans	132-136	IMV surface protein	Vaccinia virus	56-60
9749609-3	1998	We excluded the GAG deletion in the DYT1 gene and linkage to any of the above-mentioned dystonia loci, thus suggesting an as yet undefined dystonia gene in our family.	Glycosaminoglycans	16-19	torsin family 1 member A	Homo sapiens	36-40
9737970-10	1998	Preliminary expression studies indicated that proinflammatory cytokines, such as interleukin 1beta, can substantially increase the expression of human UGDH in cultured human fibroblasts, suggesting that glycosaminoglycan biosynthesis may be partly regulated by the availability of activated UDP-glucuronate, as determined by relative Udpgdh expression levels.	Glycosaminoglycans	203-220	UDP-glucose 6-dehydrogenase	Homo sapiens	334-340
9726998-7	1998	This binding required Ca2+/Mg2+ ions, was lysine-mediated, and was markedly decreased in the presence of GAG-depleted decorin, suggesting the ionic nature of the interaction likely involving apoB100 and the GAG component of decorin.	Glycosaminoglycans	105-108	apolipoprotein B	Homo sapiens	191-198
9726998-11	1998	In the case of whole Lp(a), the binding to immobilized decorin was mostly GAG-dependent and ionic in nature.	Glycosaminoglycans	74-77	lipoprotein(a)	Homo sapiens	21-26
9737970-1	1998	The enzyme UDP-glucose dehydrogenase (Udpgdh) (EC 1.1.1.22) converts UDP-glucose to UDP-glucuronate, a critical component of the glycosaminoglycans, hyaluronan, chondroitin sulfate, and heparan sulfate.	Glycosaminoglycans	129-147	UDP-glucose 6-dehydrogenase	Homo sapiens	11-36
9737970-1	1998	The enzyme UDP-glucose dehydrogenase (Udpgdh) (EC 1.1.1.22) converts UDP-glucose to UDP-glucuronate, a critical component of the glycosaminoglycans, hyaluronan, chondroitin sulfate, and heparan sulfate.	Glycosaminoglycans	129-147	UDP-glucose 6-dehydrogenase	Homo sapiens	38-44
9737970-10	1998	Preliminary expression studies indicated that proinflammatory cytokines, such as interleukin 1beta, can substantially increase the expression of human UGDH in cultured human fibroblasts, suggesting that glycosaminoglycan biosynthesis may be partly regulated by the availability of activated UDP-glucuronate, as determined by relative Udpgdh expression levels.	Glycosaminoglycans	203-220	UDP-glucose 6-dehydrogenase	Homo sapiens	151-155
9722571-3	1998	In this study, we show that human recombinant CD48 binds to the glycosaminoglycan heparan sulfate on the surface of human epithelial cells.	Glycosaminoglycans	64-81	CD48 molecule	Homo sapiens	46-50
9721154-9	1998	IL-10 also inhibited the increase in collagenase and stromelysin-1 in the explant culture supernatants and the loss of glycosaminoglycans.	Glycosaminoglycans	119-137	interleukin 10	Homo sapiens	0-5
9658109-4	1998	Cloning and sequencing showed that these viruses retained the original 16-nt deletion but possessed two additional point mutations, which were located within the p2 and NC regions of the Gag coding region, respectively, and which were therefore named MP2 and MNC.	Glycosaminoglycans	187-190	tryptase pseudogene 1	Homo sapiens	251-254
9782429-3	1998	Glycosaminoglycan components were determined by enzyme digestion with hyaluronidase or chondroitinase AC and ABC and immunohistochemistry for chondroitin, chondroitin-4-sulfate, chondroitin-6-sulfate, and dermatan sulfate.	Glycosaminoglycans	0-17	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	109-112
10197168-5	1998	RESULTS: IL-1 beta induced a profound GAG release (approximately 80% after 2 days at 20 ng/ml IL-1 beta) that was both time and IL-1 beta concentration dependent.	Glycosaminoglycans	38-41	interleukin 1 beta	Homo sapiens	9-18
10197168-5	1998	RESULTS: IL-1 beta induced a profound GAG release (approximately 80% after 2 days at 20 ng/ml IL-1 beta) that was both time and IL-1 beta concentration dependent.	Glycosaminoglycans	38-41	interleukin 1 beta	Homo sapiens	94-103
10197168-5	1998	RESULTS: IL-1 beta induced a profound GAG release (approximately 80% after 2 days at 20 ng/ml IL-1 beta) that was both time and IL-1 beta concentration dependent.	Glycosaminoglycans	38-41	interleukin 1 beta	Homo sapiens	94-103
10197168-9	1998	In the presence of APMA, GAG release from IL-1 beta treated beads was significantly increased from 24 to 31%.	Glycosaminoglycans	25-28	interleukin 1 beta	Homo sapiens	42-51
9725565-8	1998	It is speculated that BMP-2 might be secreted by tumor cells and play a role in chondroid formation in PA by inducing some tumor cells to produce type II collagen and other chondroid matrical substances, like glycosaminoglycans.	Glycosaminoglycans	209-227	bone morphogenetic protein 2	Homo sapiens	22-27
9692391-8	1998	GAG anti-thrombin activity was completely abolished by heparin lyase III.	Glycosaminoglycans	0-3	coagulation factor II, thrombin	Homo sapiens	9-17
9692954-11	1998	Homology modeling of PEDF based on the X-ray crystal structures of antithrombin III and ovalbumin shows a region at the center of beta-sheet A-strands 2 and 3- and helix F that has a basic electrostatic surface potential and is densely populated with lysines exposed to the surface (K134, K137, K189, K191, H212, and K214) that are available to interact with various glycosaminoglycans/polyanions.	Glycosaminoglycans	367-385	serpin family F member 1	Homo sapiens	21-25
9692954-3	1998	We have used affinity chromatography and ultrafiltration to probe for direct binding of PEDF to glycosaminoglycans/polyanions.	Glycosaminoglycans	96-114	serpin family F member 1	Homo sapiens	88-92
9692954-11	1998	Homology modeling of PEDF based on the X-ray crystal structures of antithrombin III and ovalbumin shows a region at the center of beta-sheet A-strands 2 and 3- and helix F that has a basic electrostatic surface potential and is densely populated with lysines exposed to the surface (K134, K137, K189, K191, H212, and K214) that are available to interact with various glycosaminoglycans/polyanions.	Glycosaminoglycans	367-385	serpin family C member 1	Homo sapiens	67-83
9667600-1	1998	Recently, the mutation causing early-onset generalized torsion dystonia has been identified as a GAG deletion in the gene for an adenosine triphosphate-binding protein named torsinA.	Glycosaminoglycans	97-100	torsin family 1 member A	Homo sapiens	174-181
9634539-3	1998	The molecular diversity of CD44 isoforms is further compounded by differential biosynthetic processes and post-translational modifications [e.g. N-/O-glycosylation or glycosaminoglycan (GAG) addition].	Glycosaminoglycans	167-184	CD44 molecule (Indian blood group)	Homo sapiens	27-31
9634539-3	1998	The molecular diversity of CD44 isoforms is further compounded by differential biosynthetic processes and post-translational modifications [e.g. N-/O-glycosylation or glycosaminoglycan (GAG) addition].	Glycosaminoglycans	186-189	CD44 molecule (Indian blood group)	Homo sapiens	27-31
9713170-1	1998	We investigated the effect of cell surface glycosaminoglycans (GAGs) on the inactivation of factor VIIa-tissue factor activity by antithrombin III (ATIII) on a human bladder carcinoma (J82) cell line and an ovarian carcinoma (OC-2008) cell line, two tumor cell lines which constitutively synthesize and express high levels of cell surface tissue factor.	Glycosaminoglycans	43-61	serpin family C member 1	Homo sapiens	148-153
9618171-1	1998	The DYT1 gene recently has been cloned and shown to contain a three nucleotide (GAG) deletion responsible for most cases of autosomal dominant early-onset torsion dystonia.	Glycosaminoglycans	80-83	torsin family 1 member A	Homo sapiens	4-8
9642104-4	1998	Alternatively spliced versican isoforms containing the alpha domain of the glycosaminoglycan attachment region were present at a relatively low level during the late embryonic and early postnatal period, decreased by approximately 50% between 1 and 2 weeks postnatal, and then increased steadily in concentration to reach a maximum at 100 days that was 7-fold that present at 10 days postnatal.	Glycosaminoglycans	75-92	versican	Rattus norvegicus	22-30
9632647-9	1998	The glycosaminoglycan chains of PG-100/PG-MCSF, but not the core proteins, were responsible for binding to native LDL.	Glycosaminoglycans	4-21	colony stimulating factor 1	Homo sapiens	42-46
9624135-1	1998	Interleukin-8, a member of the CXC chemokine family, has been shown to bind to glycosaminoglycans.	Glycosaminoglycans	79-97	C-X-C motif chemokine ligand 8	Homo sapiens	0-13
9659379-0	1998	Murine betaglycan primary structure, expression and glycosaminoglycan attachment sites.	Glycosaminoglycans	52-69	transforming growth factor, beta receptor III	Mus musculus	7-17
9592153-3	1998	While GAF binding sites are typically composed of 3.5 GA repeats, the Drosophila hsp70 gene contains much smaller elements, some of which are as little as three bases (GAG) in length.	Glycosaminoglycans	168-171	Heat-shock-protein-70Ab	Drosophila melanogaster	81-86
9592153-5	1998	Moreover, a simple synthetic GAG sequence is sufficient to bind GAF in vitro .	Glycosaminoglycans	29-32	Trithorax-like	Drosophila melanogaster	64-67
9637523-6	1998	We have now defined the optimal SIV gag CTL epitope restricted by the rhesus MHC class I molecule Mamu-A*01 and defined a general peptide binding motif for this molecule that is characterized by a dominant position 3 anchor (proline).	Glycosaminoglycans	36-39	major histocompatibility complex, class I, A	Macaca mulatta	98-104
9637523-8	1998	Mamu-A*01 is unique in that it is found at a high frequency in rhesus macaques, and all SIV-infected Mamu-A*01-positive rhesus macaques studied to date develop an immunodominant gag-specific CTL response restricted by this molecule.	Glycosaminoglycans	178-181	major histocompatibility complex, class I, A	Macaca mulatta	0-6
9694594-2	1998	To study its possible interaction with glycosaminoglycans, the NC1 domain of chicken collagen XIV was overproduced in E. coli.	Glycosaminoglycans	39-57	collagen type XIV alpha 1 chain	Gallus gallus	85-97
9634701-3	1998	The binding of VEGF to its two known receptors, KDR and Flt-1, is modulated by cell-surface-associated heparin-like glycosaminoglycans and exogenous heparin or heparan sulfate.	Glycosaminoglycans	116-134	vascular endothelial growth factor A	Homo sapiens	15-19
9634701-3	1998	The binding of VEGF to its two known receptors, KDR and Flt-1, is modulated by cell-surface-associated heparin-like glycosaminoglycans and exogenous heparin or heparan sulfate.	Glycosaminoglycans	116-134	kinase insert domain receptor	Homo sapiens	48-51
9634701-3	1998	The binding of VEGF to its two known receptors, KDR and Flt-1, is modulated by cell-surface-associated heparin-like glycosaminoglycans and exogenous heparin or heparan sulfate.	Glycosaminoglycans	116-134	fms related receptor tyrosine kinase 1	Homo sapiens	56-61
9619373-9	1998	The authors show in addition, that TFG-beta blocks the IL-1 induced inhibitory effect on glycosaminoglycan (GAG) and collagen production, evaluated with [3H]glucosamine and [3H]proline incorporation studies, respectively.	Glycosaminoglycans	89-106	interleukin 1 complex	Mus musculus	55-59
9682679-11	1998	An increase in the length of the dermatan sulphate chain on decorin, a previously reported characteristic of this glycosaminoglycan in hypertrophic scar, was seen in all but two of the strains treated with transforming growth factor-beta 1.	Glycosaminoglycans	114-131	transforming growth factor beta 1	Homo sapiens	206-239
9565561-4	1998	To determine whether PECAM-1 is capable of interacting directly with glycosaminoglycans, we examined the adhesive properties of multiple monovalent and multivalent forms of this adhesion molecule.	Glycosaminoglycans	69-87	platelet and endothelial cell adhesion molecule 1	Homo sapiens	21-28
9565561-7	1998	In addition, an amino acid sequence motif inadvertently created by the juxtaposition of PECAM-1 and IgG sequences within the hinge region of certain PECAM-1/IgG chimeric constructs was found to confer glycosaminoglycan binding properties not normally present within the extracellular domain of the native molecule.	Glycosaminoglycans	201-218	platelet and endothelial cell adhesion molecule 1	Homo sapiens	88-95
9565561-7	1998	In addition, an amino acid sequence motif inadvertently created by the juxtaposition of PECAM-1 and IgG sequences within the hinge region of certain PECAM-1/IgG chimeric constructs was found to confer glycosaminoglycan binding properties not normally present within the extracellular domain of the native molecule.	Glycosaminoglycans	201-218	platelet and endothelial cell adhesion molecule 1	Homo sapiens	149-156
9619373-9	1998	The authors show in addition, that TFG-beta blocks the IL-1 induced inhibitory effect on glycosaminoglycan (GAG) and collagen production, evaluated with [3H]glucosamine and [3H]proline incorporation studies, respectively.	Glycosaminoglycans	108-111	interleukin 1 complex	Mus musculus	55-59
9558116-9	1998	These studies demonstrate that factor H is an adhesion molecule for human neutrophils and suggest that the interaction of factor H with glycosaminoglycans may facilitate the tethering of this protein in tissues allowing factor H to serve as a neutrophil adhesion ligand in vivo.	Glycosaminoglycans	136-154	complement factor H	Homo sapiens	31-39
9558116-9	1998	These studies demonstrate that factor H is an adhesion molecule for human neutrophils and suggest that the interaction of factor H with glycosaminoglycans may facilitate the tethering of this protein in tissues allowing factor H to serve as a neutrophil adhesion ligand in vivo.	Glycosaminoglycans	136-154	complement factor H	Homo sapiens	122-130
9558116-9	1998	These studies demonstrate that factor H is an adhesion molecule for human neutrophils and suggest that the interaction of factor H with glycosaminoglycans may facilitate the tethering of this protein in tissues allowing factor H to serve as a neutrophil adhesion ligand in vivo.	Glycosaminoglycans	136-154	complement factor H	Homo sapiens	122-130
9598980-3	1998	In contrast to B-B4, the B-B2 epitope is close to a potential glycosaminoglycan attachment site.	Glycosaminoglycans	62-79	intercellular adhesion molecule 1	Homo sapiens	25-29
9568695-0	1998	Sulfate content and specific glycosaminoglycan backbone of perlecan are critical for perlecan"s enhancement of islet amyloid polypeptide (amylin) fibril formation.	Glycosaminoglycans	29-46	heparan sulfate proteoglycan 2	Rattus norvegicus	59-67
9586576-4	1998	In vitro, the activity of cleavage of fibrinogen by thrombin or prothrombinase activity was more potently depressed by GAG-UTM than by r-UTM, and the generation of activated protein C by TM-thrombin complex was accelerated by GAG modification.	Glycosaminoglycans	119-122	coagulation factor II	Rattus norvegicus	52-60
9586576-4	1998	In vitro, the activity of cleavage of fibrinogen by thrombin or prothrombinase activity was more potently depressed by GAG-UTM than by r-UTM, and the generation of activated protein C by TM-thrombin complex was accelerated by GAG modification.	Glycosaminoglycans	119-122	coagulation factor II, thrombin	Homo sapiens	67-75
9586576-2	1998	As rabbit TM with glycosaminoglycan (GAG) has a more potent anticoagulant activity than that without GAG, we expressed recombinant GAG-modified urinary thrombomodulin (GAG-UTM) in C-127 cells.	Glycosaminoglycans	37-40	thrombomodulin	Rattus norvegicus	152-166
9586576-2	1998	As rabbit TM with glycosaminoglycan (GAG) has a more potent anticoagulant activity than that without GAG, we expressed recombinant GAG-modified urinary thrombomodulin (GAG-UTM) in C-127 cells.	Glycosaminoglycans	101-104	thrombomodulin	Rattus norvegicus	152-166
9586576-2	1998	As rabbit TM with glycosaminoglycan (GAG) has a more potent anticoagulant activity than that without GAG, we expressed recombinant GAG-modified urinary thrombomodulin (GAG-UTM) in C-127 cells.	Glycosaminoglycans	101-104	thrombomodulin	Rattus norvegicus	152-166
9662467-8	1998	An interaction between antithrombin and heparin-like glycosaminoglycans on the endothelial cell surface appears to be important for this effect.	Glycosaminoglycans	53-71	serpin family C member 1	Homo sapiens	23-35
9662467-9	1998	Heparin inhibits such therapeutic effects of antithrombin by preventing it from interacting with the cell surface heparin-like glycosaminoglycans.	Glycosaminoglycans	127-145	serpin family C member 1	Homo sapiens	45-57
9568695-0	1998	Sulfate content and specific glycosaminoglycan backbone of perlecan are critical for perlecan"s enhancement of islet amyloid polypeptide (amylin) fibril formation.	Glycosaminoglycans	29-46	heparan sulfate proteoglycan 2	Rattus norvegicus	85-93
9568695-0	1998	Sulfate content and specific glycosaminoglycan backbone of perlecan are critical for perlecan"s enhancement of islet amyloid polypeptide (amylin) fibril formation.	Glycosaminoglycans	29-46	islet amyloid polypeptide	Homo sapiens	138-144
9568695-5	1998	The binding of human amylin to perlecan was similarly observed using perlecan heparan sulfate glycosaminoglycans (GAGs), and was completely abolished by 10 micromol/l heparin.	Glycosaminoglycans	114-118	islet amyloid polypeptide	Homo sapiens	21-27
9568695-5	1998	The binding of human amylin to perlecan was similarly observed using perlecan heparan sulfate glycosaminoglycans (GAGs), and was completely abolished by 10 micromol/l heparin.	Glycosaminoglycans	114-118	heparan sulfate proteoglycan 2	Rattus norvegicus	31-39
9568695-6	1998	Using thioflavin T fluorometry, Congo red staining, and electron microscopy methodology, intact perlecan was found to enhance amylin fibril formation in a dosage-dependent manner, with the majority of these effects attributed to the heparan sulfate GAG chains of perlecan.	Glycosaminoglycans	249-252	heparan sulfate proteoglycan 2	Rattus norvegicus	96-104
9568695-7	1998	Other sulfated GAGs and related macromolecules were also effective in the enhancement of amylin fibril formation in the order of heparin &gt; heparan sulfate &gt; chondroitin-4-sulfate = dermatan sulfate = dextran sulfate &gt; pentosan polysulfate, implicating the importance of the specific GAG/carbohydrate backbone.	Glycosaminoglycans	15-19	islet amyloid polypeptide	Homo sapiens	89-95
9568695-7	1998	Other sulfated GAGs and related macromolecules were also effective in the enhancement of amylin fibril formation in the order of heparin &gt; heparan sulfate &gt; chondroitin-4-sulfate = dermatan sulfate = dextran sulfate &gt; pentosan polysulfate, implicating the importance of the specific GAG/carbohydrate backbone.	Glycosaminoglycans	15-18	islet amyloid polypeptide	Homo sapiens	89-95
9568695-9	1998	These studies suggest that the enhancement effects of perlecan on amylin fibril formation are mediated primarily by both specific GAG chain backbone and GAG sulfate content, and implicate perlecan as an important macromolecule that is likely involved in the pathogenesis of islet amyloidosis.	Glycosaminoglycans	130-133	heparan sulfate proteoglycan 2	Rattus norvegicus	54-62
9568695-9	1998	These studies suggest that the enhancement effects of perlecan on amylin fibril formation are mediated primarily by both specific GAG chain backbone and GAG sulfate content, and implicate perlecan as an important macromolecule that is likely involved in the pathogenesis of islet amyloidosis.	Glycosaminoglycans	130-133	islet amyloid polypeptide	Homo sapiens	66-72
9500522-9	1998	IL-5 interacts with iduronic acid containing glycosaminoglycans, and heparan sulfate preparations that have numerous N-sulfated domains per chain are especially efficient at inhibiting heparin binding.	Glycosaminoglycans	45-63	interleukin 5	Homo sapiens	0-4
9525617-7	1998	These results show that ubiquitination of Gag is conserved among these retroviruses and occurs in the p6Gag portion of the Gag polyprotein, a region that is likely to be involved in assembly and budding.	Glycosaminoglycans	42-45	endogenous retrovirus group K member 9	Homo sapiens	123-138
9684349-14	1998	In the doughnut-shaped particles, Gag p17 and p24 proteins exist facing each other against an inner electron-dense ring, suggesting that the inner ring consists of a precursor Gag protein showing a defect at the viral proteinase.	Glycosaminoglycans	34-37	family with sequence similarity 72 member B	Homo sapiens	38-41
9684349-14	1998	In the doughnut-shaped particles, Gag p17 and p24 proteins exist facing each other against an inner electron-dense ring, suggesting that the inner ring consists of a precursor Gag protein showing a defect at the viral proteinase.	Glycosaminoglycans	176-179	family with sequence similarity 72 member B	Homo sapiens	38-41
9684349-14	1998	In the doughnut-shaped particles, Gag p17 and p24 proteins exist facing each other against an inner electron-dense ring, suggesting that the inner ring consists of a precursor Gag protein showing a defect at the viral proteinase.	Glycosaminoglycans	176-179	transmembrane p24 trafficking protein 2	Homo sapiens	46-49
9545645-1	1998	SPOCK, previously identified as testican, is a modular proteoglycan that carries both chondroitin and heparan sulfate glycosaminoglycan side chains.	Glycosaminoglycans	118-135	SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1	Homo sapiens	0-5
9488672-9	1998	Importantly, plasminogen interacted specifically with GAG-bound HPRG.	Glycosaminoglycans	54-57	histidine rich glycoprotein	Homo sapiens	64-68
9631176-7	1998	These results indicate that glycosaminoglycan species present in human cementum include C4-S, DS, C6-S, and novel sulphated CS epitopes.	Glycosaminoglycans	28-45	complement C4A (Rodgers blood group)	Homo sapiens	88-92
9486973-5	1998	Sequencing of the entire Na+/I- symporter (NIS) cDNA revealed a C to G transversion of nucleotide (nt) 1146 in exon 6, resulting in a Gln 267 (CAG) to Glu (GAG) substitution.	Glycosaminoglycans	156-159	solute carrier family 5 member 5	Homo sapiens	25-41
9525516-9	1998	Histologically, the bFGF-treated flaps showed increased cellularity, fibroblasts, and extracellular mucopolysaccharides compared with controls.	Glycosaminoglycans	100-119	fibroblast growth factor 2	Homo sapiens	20-24
9485332-6	1998	Results of measuring the effects of point mutations in the DNA binding site on the affinity of WT1 and EGR1 indicates a significant difference in the optimal binding sites: for EGR1, the highest affinity binding site has the sequence GNG-(T/G)GG-G(T/C)G, while for WT1 the highest affinity binding site has the sequence G(T/C)G-(T/G)GG-GAG-(T/C)G(T/C).	Glycosaminoglycans	336-339	WT1 transcription factor	Homo sapiens	95-98
9487127-2	1998	The basic PRP caused a dose-dependent increase in sulfation of PRPg and also increased the extent to which PRPg polypeptide backbones are modified by a GAG chain.	Glycosaminoglycans	152-155	proline rich protein HaeIII subfamily 1	Mus musculus	10-13
9487127-5	1998	Analysis of the regulated secretion of both the basic PRP and PRPg has indicated that while the presence of the GAG chain improves the storage of PRPg, the presence of PRPg does not increase the storage of basic PRP.	Glycosaminoglycans	112-115	proline rich protein HaeIII subfamily 1	Mus musculus	62-65
9485332-6	1998	Results of measuring the effects of point mutations in the DNA binding site on the affinity of WT1 and EGR1 indicates a significant difference in the optimal binding sites: for EGR1, the highest affinity binding site has the sequence GNG-(T/G)GG-G(T/C)G, while for WT1 the highest affinity binding site has the sequence G(T/C)G-(T/G)GG-GAG-(T/C)G(T/C).	Glycosaminoglycans	336-339	early growth response 1	Homo sapiens	103-107
9485332-6	1998	Results of measuring the effects of point mutations in the DNA binding site on the affinity of WT1 and EGR1 indicates a significant difference in the optimal binding sites: for EGR1, the highest affinity binding site has the sequence GNG-(T/G)GG-G(T/C)G, while for WT1 the highest affinity binding site has the sequence G(T/C)G-(T/G)GG-GAG-(T/C)G(T/C).	Glycosaminoglycans	336-339	early growth response 1	Homo sapiens	177-181
9485332-6	1998	Results of measuring the effects of point mutations in the DNA binding site on the affinity of WT1 and EGR1 indicates a significant difference in the optimal binding sites: for EGR1, the highest affinity binding site has the sequence GNG-(T/G)GG-G(T/C)G, while for WT1 the highest affinity binding site has the sequence G(T/C)G-(T/G)GG-GAG-(T/C)G(T/C).	Glycosaminoglycans	336-339	WT1 transcription factor	Homo sapiens	265-268
9506849-8	1998	These results suggest that inhibition of PKC-mediated ODC gene expression by glycosaminoglycans may represent an important mechanism in the regulation of HEC proliferation.	Glycosaminoglycans	77-95	ornithine decarboxylase 1	Homo sapiens	54-57
9466983-3	1998	L-selectin also recognizes endothelial proteoglycans in a calcium-dependent manner, via heparan sulfate (HS) glycosaminoglycan chains enriched in unsubstituted glucosamine units.	Glycosaminoglycans	109-126	selectin L	Homo sapiens	0-10
9517991-1	1998	OBJECTIVE: To investigate the suitability of HIV sequence analysis, based on the p17 region of the gag gene, to characterize the sexual networks in and around a trading town in south-west Uganda.	Glycosaminoglycans	99-102	family with sequence similarity 72 member B	Homo sapiens	81-84
9477985-6	1998	The absence of the 12-amino acid insert indicated that APLP2 could be modified by the addition of a chondroitin sulfate (CS) glycosaminoglycan chain.	Glycosaminoglycans	125-142	amyloid beta precursor like protein 2	Rattus norvegicus	55-60
9452487-2	1998	CDC37 also binds DNA and glycosaminoglycans in a sequence-specific manner.	Glycosaminoglycans	25-43	cell division cycle 37	Gallus gallus	0-5
9448726-1	1998	Decorin, a small dermatan sulfate proteoglycan, is characterized by a core protein with central leucine-rich repeat structures and a single glycosaminoglycan chain.	Glycosaminoglycans	140-157	decorin	Homo sapiens	0-7
9466427-8	1998	In addition glycosaminoglycan treatment of lesioned rats increased insulin-like growth factor-I messenger RNA and protein in the reinnervated muscle, and insulin-like growth factor-I and insulin-like growth factor binding protein-3 plasma levels.	Glycosaminoglycans	12-29	insulin-like growth factor 1	Rattus norvegicus	67-95
9466427-10	1998	These data suggest that glycosaminoglycans are potent stimulants of muscle reinnervation and that their effects may be mediated by increased levels of insulin-like growth factor-I.	Glycosaminoglycans	24-42	insulin-like growth factor 1	Rattus norvegicus	151-179
9454705-0	1998	Induction of V3-specific cytotoxic T lymphocyte responses by HIV gag particles carrying multiple immunodominant V3 epitopes of gp120.	Glycosaminoglycans	65-68	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	127-132
9461296-1	1997	At ejaculation, PDC-109, the major heparin-binding protein of bull seminal plasma, binds to the phosphorylcholine group of sperm lipids and modulates capacitation promoted by glycosaminoglycans during sperm residence in the female genital tract.	Glycosaminoglycans	175-193	seminal plasma protein PDC-109	Bos taurus	16-23
9597755-1	1998	Thrombomodulin (TM) is an anticoagulant glycoprotein on the surface of endothelial cell that directly inhibits the procoagulant activities of thrombin, and the TM-thrombin complex accelerates thrombin-catalyzed activation of protein C. Soluble TM in urine has no glycosaminoglycan (GAG) chain which accelerates the anticoagulant activities.	Glycosaminoglycans	263-280	thrombomodulin	Homo sapiens	0-14
9597755-1	1998	Thrombomodulin (TM) is an anticoagulant glycoprotein on the surface of endothelial cell that directly inhibits the procoagulant activities of thrombin, and the TM-thrombin complex accelerates thrombin-catalyzed activation of protein C. Soluble TM in urine has no glycosaminoglycan (GAG) chain which accelerates the anticoagulant activities.	Glycosaminoglycans	263-280	coagulation factor II, thrombin	Homo sapiens	163-171
9597755-1	1998	Thrombomodulin (TM) is an anticoagulant glycoprotein on the surface of endothelial cell that directly inhibits the procoagulant activities of thrombin, and the TM-thrombin complex accelerates thrombin-catalyzed activation of protein C. Soluble TM in urine has no glycosaminoglycan (GAG) chain which accelerates the anticoagulant activities.	Glycosaminoglycans	263-280	coagulation factor II, thrombin	Homo sapiens	163-171
9597755-1	1998	Thrombomodulin (TM) is an anticoagulant glycoprotein on the surface of endothelial cell that directly inhibits the procoagulant activities of thrombin, and the TM-thrombin complex accelerates thrombin-catalyzed activation of protein C. Soluble TM in urine has no glycosaminoglycan (GAG) chain which accelerates the anticoagulant activities.	Glycosaminoglycans	282-285	thrombomodulin	Homo sapiens	0-14
9597755-1	1998	Thrombomodulin (TM) is an anticoagulant glycoprotein on the surface of endothelial cell that directly inhibits the procoagulant activities of thrombin, and the TM-thrombin complex accelerates thrombin-catalyzed activation of protein C. Soluble TM in urine has no glycosaminoglycan (GAG) chain which accelerates the anticoagulant activities.	Glycosaminoglycans	282-285	coagulation factor II, thrombin	Homo sapiens	163-171
9597755-1	1998	Thrombomodulin (TM) is an anticoagulant glycoprotein on the surface of endothelial cell that directly inhibits the procoagulant activities of thrombin, and the TM-thrombin complex accelerates thrombin-catalyzed activation of protein C. Soluble TM in urine has no glycosaminoglycan (GAG) chain which accelerates the anticoagulant activities.	Glycosaminoglycans	282-285	coagulation factor II, thrombin	Homo sapiens	163-171
9597755-2	1998	Therefore, we expressed recombinant GAG-modified urinary thrombomodulin (GAG-UTM) in C127 cells.	Glycosaminoglycans	36-39	thrombomodulin	Homo sapiens	57-71
9422374-8	1998	It is interesting that both SAP and proteoglycan binding to A beta fibrils can be inhibited by glycosaminoglycans and Congo red.	Glycosaminoglycans	95-113	amyloid P component, serum	Homo sapiens	28-31
9422374-8	1998	It is interesting that both SAP and proteoglycan binding to A beta fibrils can be inhibited by glycosaminoglycans and Congo red.	Glycosaminoglycans	95-113	amyloid beta precursor protein	Homo sapiens	60-66
9443561-4	1998	The GABA transaminase inhibitor gamma-acetylen GABA (GAG) reduced ambulatory activity and rearing as well as the time spent in the novel environment.	Glycosaminoglycans	53-56	4-aminobutyrate aminotransferase	Mus musculus	4-21
10892427-10	1998	The decline in anti-gag antibody reactivity in CSF is an early indicator of disease progression, reflecting a severe course of neurological impairments.	Glycosaminoglycans	20-23	colony stimulating factor 2	Homo sapiens	47-50
9459305-6	1997	However, senescent HFs produced a greater proportion of PGs containing GlcN-GAG chains and increased the sulphation of the remaining PG fraction with GalN-GAG moieties, yielding a major gain of C6-sulphate groups in the galactosamine residues.	Glycosaminoglycans	155-158	galanin and GMAP prepropeptide	Homo sapiens	150-154
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
10649686-1	1998	The effect of N-acetylglucosamine (NAG) on in vitro synthesis of glycosaminoglycans by human peritoneal mesothelial cells and fibroblasts was studied.	Glycosaminoglycans	65-83	NBAS subunit of NRZ tethering complex	Homo sapiens	14-39
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
9463889-3	1998	PDC-109 displays phosphorylcholine- and heparin-binding activities which are thought to account for its sperm surface coating and glycosaminoglycan-induced sperm capacitating activities, respectively.	Glycosaminoglycans	130-147	seminal plasma protein PDC-109	Bos taurus	0-7
9437731-1	1998	Recently we have shown an evidence that a peptide, corresponding to residues Gln1892 to Gly1910, from the C-terminal heparin-binding domain of fibronectin promotes adhesion of phorbol-12-myristate 13-acetate (PMA)-treated U937 cells and binds to both integrin alpha 4 beta 1 and glycosaminoglycans on U937 cells surface.	Glycosaminoglycans	279-297	fibronectin 1	Homo sapiens	143-154
16793681-5	1998	The formation of complexes between PF4 and heparin or other glycosaminoglycans, leading in some circumstances to the generation of antigenic structures reactive with HIT antibodies, is analysed.	Glycosaminoglycans	60-78	platelet factor 4	Homo sapiens	35-38
9515777-7	1998	Interaction of AT III with heparin-like glycosaminoglycans (GAGs) on the endothelial cell surface appears to be important for this effect.	Glycosaminoglycans	40-58	serpin family C member 1	Homo sapiens	15-21
9407097-5	1997	Here, we have used the above parameters to study the interactions between tau protein and a number of naturally occurring and synthetic glycosaminoglycans.	Glycosaminoglycans	136-154	microtubule associated protein tau	Homo sapiens	74-77
9407097-9	1997	These in vitro interactions between tau protein and sulfated glycosaminoglycans reproduced the known characteristics of paired helical filament-tau from Alzheimer"s disease brain.	Glycosaminoglycans	61-79	microtubule associated protein tau	Homo sapiens	36-39
9407097-9	1997	These in vitro interactions between tau protein and sulfated glycosaminoglycans reproduced the known characteristics of paired helical filament-tau from Alzheimer"s disease brain.	Glycosaminoglycans	61-79	microtubule associated protein tau	Homo sapiens	120-147
9395530-0	1997	Variant exons v6 and v7 together expand the repertoire of glycosaminoglycans bound by CD44.	Glycosaminoglycans	58-76	CD44 molecule (Indian blood group)	Homo sapiens	86-90
9395530-5	1997	Binding to this extended repertoire of glycosaminoglycans by CD44 depends on the inclusion of peptide sequences encoded by the alternatively spliced exons v6 and v7, and occurs both when the CD44 is solubilized from the plasma membrane and when it is expressed on intact cells.	Glycosaminoglycans	39-57	CD44 molecule (Indian blood group)	Homo sapiens	61-65
9388214-7	1997	Interestingly enough, Vpr was found to interact with Gag, NCp15, and NCp7 but not with mature p6 in vitro.	Glycosaminoglycans	53-56	Vpr	Human immunodeficiency virus 1	22-25
9395530-5	1997	Binding to this extended repertoire of glycosaminoglycans by CD44 depends on the inclusion of peptide sequences encoded by the alternatively spliced exons v6 and v7, and occurs both when the CD44 is solubilized from the plasma membrane and when it is expressed on intact cells.	Glycosaminoglycans	39-57	CD44 molecule (Indian blood group)	Homo sapiens	191-195
9395530-6	1997	A single point mutation in the most N-terminal hyaluronate binding motif of CD44 ablates both hyaluronate and chondroitin sulfate binding, suggesting that glycosaminoglycans are bound through a common motif, and that only one of the hyaluronate binding motifs is responsible for the majority of glycosaminoglycan binding by CD44 on the cell surface.	Glycosaminoglycans	155-173	CD44 molecule (Indian blood group)	Homo sapiens	76-80
9395530-6	1997	A single point mutation in the most N-terminal hyaluronate binding motif of CD44 ablates both hyaluronate and chondroitin sulfate binding, suggesting that glycosaminoglycans are bound through a common motif, and that only one of the hyaluronate binding motifs is responsible for the majority of glycosaminoglycan binding by CD44 on the cell surface.	Glycosaminoglycans	155-172	CD44 molecule (Indian blood group)	Homo sapiens	76-80
9390173-2	1997	This study describes the dependence of salt concentration on the binding properties of lysozyme isoforms of different cationic charges, isolated from bovine cartilage, to the two major and structurally similar glycosaminoglycans of cartilage, i.e., chondroitin sulfate and hyaluronan.	Glycosaminoglycans	210-228	lysozyme C, tracheal isozyme	Bos taurus	87-95
9419979-7	1997	A missense mutation (GAG to AAG) at codon 705 of hPMS2 gene was detected in one allele of this patient, which was inherited from his mother without tumors.	Glycosaminoglycans	21-24	PMS1 homolog 2, mismatch repair system component	Homo sapiens	49-54
9461347-1	1997	The influence of ionic strength and composition on the binding and inhibition of human leukocyte elastase by glycosaminoglycans with variable degree and position of sulfation was investigated.	Glycosaminoglycans	109-127	elastase, neutrophil expressed	Homo sapiens	87-105
9511993-5	1997	The major ligand for CD44 is the extracellular matrix glycosaminoglycan, hyaluronic acid (HA).	Glycosaminoglycans	54-71	CD44 molecule (Indian blood group)	Homo sapiens	21-25
9581563-6	1997	Biglycan and decorin were immunoisolated from the second Sepharose CL-4B peak, and had average glycosaminoglycan hydrodynamic sizes of approx.	Glycosaminoglycans	95-112	biglycan	Mus musculus	0-8
9581563-10	1997	The biglycan glycosaminoglycan chains were found to contain a similar ratio of 4-sulphate/6-sulphate, but with approx.	Glycosaminoglycans	13-30	biglycan	Mus musculus	4-12
9348216-8	1997	IGFBP-2 bound in vitro to the glycosaminoglycans chondroitin-4 and -6-sulfate, keratan sulfate, and heparin.	Glycosaminoglycans	30-48	insulin-like growth factor binding protein 2	Rattus norvegicus	0-7
9425437-1	1997	Hurler syndrome (mucopolysaccharidosis IH or MPS IH) is a congenital mucopolysaccharide storage disorder resulting from a genetic deficiency of alpha-L-iduronidase (IDUA), which is required for lysosomal degradation of glycosaminoglycans heparan sulfate and dermatan sulfate.	Glycosaminoglycans	219-237	alpha-L-iduronidase	Homo sapiens	144-163
9425437-1	1997	Hurler syndrome (mucopolysaccharidosis IH or MPS IH) is a congenital mucopolysaccharide storage disorder resulting from a genetic deficiency of alpha-L-iduronidase (IDUA), which is required for lysosomal degradation of glycosaminoglycans heparan sulfate and dermatan sulfate.	Glycosaminoglycans	219-237	alpha-L-iduronidase	Homo sapiens	165-169
9417813-10	1997	The interaction between IL-2 and heparin-like glycosaminoglycans is likely to be an important mechanism for retaining IL-2 close to its sites of secretion, thus giving rise to localized concentration gradients in the tissues.	Glycosaminoglycans	46-64	interleukin 2	Homo sapiens	118-122
9371595-6	1997	The Pr55Gag-Vif interaction is detected (i) in the glutathione S-transferase system, with in vitro-translated proteins demonstrating a critical role of the NC p7 domain of the Gag precursor; (ii) with proteins expressed in infected cells; and (iii) by coimmunoprecipitation experiments.	Glycosaminoglycans	8-11	Vif	Human immunodeficiency virus 1	12-15
9354625-9	1997	The endothelial cell binding sites for IL-8, RANTES, and MCP-1 were deduced to be glycosaminoglycans since competition assays showed the biphasic curves and micromolar IC50 values seen in studies with immobilized heparin, and mRNA for known chemokine receptors was not detected.	Glycosaminoglycans	82-100	C-X-C motif chemokine ligand 8	Homo sapiens	39-43
9354625-9	1997	The endothelial cell binding sites for IL-8, RANTES, and MCP-1 were deduced to be glycosaminoglycans since competition assays showed the biphasic curves and micromolar IC50 values seen in studies with immobilized heparin, and mRNA for known chemokine receptors was not detected.	Glycosaminoglycans	82-100	C-C motif chemokine ligand 5	Homo sapiens	45-51
9354625-9	1997	The endothelial cell binding sites for IL-8, RANTES, and MCP-1 were deduced to be glycosaminoglycans since competition assays showed the biphasic curves and micromolar IC50 values seen in studies with immobilized heparin, and mRNA for known chemokine receptors was not detected.	Glycosaminoglycans	82-100	C-C motif chemokine ligand 2	Homo sapiens	57-62
9354625-12	1997	Removal of glycosaminoglycans from CHO cells expressing chemokine receptors CXCR1, CCR1, or CCR2 resulted in 40-70% decreases in the binding of RANTES, MCP-1, IL-8, and MIP-1alpha.	Glycosaminoglycans	11-29	C-C chemokine receptor type 2	Cricetulus griseus	92-96
9354625-12	1997	Removal of glycosaminoglycans from CHO cells expressing chemokine receptors CXCR1, CCR1, or CCR2 resulted in 40-70% decreases in the binding of RANTES, MCP-1, IL-8, and MIP-1alpha.	Glycosaminoglycans	11-29	C-C motif chemokine ligand 5	Homo sapiens	144-150
9354625-12	1997	Removal of glycosaminoglycans from CHO cells expressing chemokine receptors CXCR1, CCR1, or CCR2 resulted in 40-70% decreases in the binding of RANTES, MCP-1, IL-8, and MIP-1alpha.	Glycosaminoglycans	11-29	C-C motif chemokine ligand 2	Homo sapiens	152-157
9354625-12	1997	Removal of glycosaminoglycans from CHO cells expressing chemokine receptors CXCR1, CCR1, or CCR2 resulted in 40-70% decreases in the binding of RANTES, MCP-1, IL-8, and MIP-1alpha.	Glycosaminoglycans	11-29	C-X-C motif chemokine ligand 8	Homo sapiens	159-163
9386279-2	1997	We postulate that the deposition of glycosaminoglycans in the meninges may impair CSF flow and explain the development of arachnoid cysts also noted in patients with other forms of mucopolysaccharidoses.	Glycosaminoglycans	36-54	colony stimulating factor 2	Homo sapiens	82-85
9397239-2	1997	Measurements were performed both ex vivo and in vivo to validate the in vivo measurements and to estimate the relative contribution of intrinsic and extrinsic influences to ANG II-stimulated GAG synthesis in sodium-fed rats.	Glycosaminoglycans	191-194	angiotensinogen	Rattus norvegicus	173-179
9397239-9	1997	The synergistic effect of ANG II treatment and high sodium diet on GAG synthesis appears to be, in part, arterial pressure independent and vascular tissue specific.	Glycosaminoglycans	67-70	angiotensinogen	Rattus norvegicus	26-32
9334256-1	1997	Serglycin is a family of small proteoglycans with Ser-Gly dipeptide repeats and is modified with various types of glycosaminoglycan side chains.	Glycosaminoglycans	114-131	serglycin	Homo sapiens	0-9
9536291-8	1997	p55, but not p75 TNF-R, expression on chondrocytes was closely related to the susceptibility of explants from the same site to TNF alpha-induced GAG loss.	Glycosaminoglycans	145-148	TNF receptor superfamily member 1A	Homo sapiens	0-3
9536291-8	1997	p55, but not p75 TNF-R, expression on chondrocytes was closely related to the susceptibility of explants from the same site to TNF alpha-induced GAG loss.	Glycosaminoglycans	145-148	tumor necrosis factor	Homo sapiens	127-136
9334256-5	1997	Glycosaminoglycans on these serglycins, which are essential for CD44 binding, are composed of chondroitin 4-sulfate or a mixture of chondroitin 4-sulfate and chondroitin 6-sulfate, but no heparin or heparan sulfate side chain was detected.	Glycosaminoglycans	0-18	CD44 molecule (Indian blood group)	Homo sapiens	64-68
9343372-8	1997	Heparan sulfate affinity chromatography and isothermal titration calorimetry, used to measure binding thermodynamics, demonstrated that a synthetic peptide analogous to the GAG binding site in FGF-1 bound tightly to heparan sulfate.	Glycosaminoglycans	173-176	fibroblast growth factor 1	Homo sapiens	193-198
9378276-8	1997	These data suggest that GAG synthesis in the rainbow trout cartilage is controlled by multiple interactions among stimulative hormones, such as T3 and IGF-I, and inhibitory hormones, such as cortisol.	Glycosaminoglycans	24-27	insulin-like growth factor I	Oncorhynchus mykiss	151-156
9343372-10	1997	A cyclic peptide, expected to be topologically most similar to the triangular GAG binding site in FGF-1, bound with the highest affinity to heparan sulfate.	Glycosaminoglycans	78-81	fibroblast growth factor 1	Homo sapiens	98-103
9343372-11	1997	These data suggest the triangular topology of the GAG binding site in FGF is critical for its interaction with heparan sulfate.	Glycosaminoglycans	50-53	fibroblast growth factor 1	Homo sapiens	70-73
9359432-10	1997	In addition, when the sulphation of glycosaminoglycans (GAGs) is prevented by growing the HepG2 cells in the presence of 30 mM sodium chlorate, TFPI binding is unaffected, whereas the binding of bovine lipoprotein lipase, a protein known to associate with cell-surface GAGs, falls to 50% of control levels.	Glycosaminoglycans	36-54	tissue factor pathway inhibitor	Homo sapiens	144-148
9364929-0	1997	Feline mucopolysaccharidosis type VI: correction of glycosaminoglycan storage in myoblasts by retrovirus-mediated transfer of the feline N-acetylgalactosamine 4-sulfatase gene.	Glycosaminoglycans	52-69	arylsulfatase B	Homo sapiens	137-170
9328841-8	1997	These peptides contained glycosaminoglycan-dependent and -independent binding sites because [125I]DCN binding to VDAVRTEKGFLLLASLRQMKKTRGT and KKTRGTLLALERKDHS was partially reduced upon removal of the glycosaminoglycan chain (65% and 46% inhibition, respectively).	Glycosaminoglycans	25-42	decorin	Homo sapiens	98-101
9349476-4	1997	The gag gene contains conserved splice acceptor and donor sites suggesting that, like human foamy virus, FeFV expresses its pol gene using a spliced mRNA.	Glycosaminoglycans	4-7	hypothetical protein	Feline foamy virus	124-127
9261401-2	1997	While Gag-Gag protein interactions which affect HIV assembly occur in the capsid (CA) domain of Pr55Gag, the nucleocapsid (NC) domain, which functions in viral RNA encapsidation, also appears to participate in virus assembly.	Glycosaminoglycans	6-9	Pr55(Gag)	Human immunodeficiency virus 1	96-103
9350282-9	1997	The glycosaminoglycans heparan sulfate and heparin, which bind SAP, reduced SAPs binding to the virus.	Glycosaminoglycans	4-22	amyloid P component, serum	Homo sapiens	63-66
21528246-3	1997	A point mutation was found in the exon D hormone-binding domain of AR leading to substitution of glutamine (GAG) for wild-type arginine (CGG) at codon 629 in 1 (3.4%) hormone-independent stage D2 patient.	Glycosaminoglycans	108-111	androgen receptor	Homo sapiens	67-69
9261419-2	1997	The requirement for CyP A maps to sequences in the capsid (CA) domain of the structural precursor, Gag.	Glycosaminoglycans	99-102	peptidylprolyl isomerase A	Homo sapiens	20-25
9261401-2	1997	While Gag-Gag protein interactions which affect HIV assembly occur in the capsid (CA) domain of Pr55Gag, the nucleocapsid (NC) domain, which functions in viral RNA encapsidation, also appears to participate in virus assembly.	Glycosaminoglycans	10-13	Pr55(Gag)	Human immunodeficiency virus 1	96-103
9258403-8	1997	On the other hand IL-2 stimulated both glycosaminoglycan (GAG) and prostacyclin syntheses and enhanced the stimulation of both GAG and prostacyclin syntheses induced by AII.	Glycosaminoglycans	39-56	interleukin 2	Homo sapiens	18-22
9387191-9	1997	These results suggest that the collagen-binding activity of vitronectin may play an important role in the progression of liver disease and/or fibrosis through its activation with some glycosaminoglycans.	Glycosaminoglycans	184-202	vitronectin	Homo sapiens	60-71
9264555-3	1997	Treatment with IL-1beta or RA each resulted in &gt;90% GAG loss after 8 days in culture.	Glycosaminoglycans	55-58	interleukin 1 beta	Homo sapiens	15-23
9264555-4	1997	Addition of TIMP or L-758,354 to the culture media inhibited IL-1beta-induced loss of tissue GAG by 40 and 65%, respectively, and inhibited RA-induced GAG loss by 35 and 65%, respectively.	Glycosaminoglycans	93-96	TIMP metallopeptidase inhibitor 1	Homo sapiens	12-16
9264555-4	1997	Addition of TIMP or L-758,354 to the culture media inhibited IL-1beta-induced loss of tissue GAG by 40 and 65%, respectively, and inhibited RA-induced GAG loss by 35 and 65%, respectively.	Glycosaminoglycans	93-96	interleukin 1 beta	Homo sapiens	61-69
9264555-4	1997	Addition of TIMP or L-758,354 to the culture media inhibited IL-1beta-induced loss of tissue GAG by 40 and 65%, respectively, and inhibited RA-induced GAG loss by 35 and 65%, respectively.	Glycosaminoglycans	151-154	TIMP metallopeptidase inhibitor 1	Homo sapiens	12-16
9252349-6	1997	In addition, an auxiliary binding site located COOH-terminal to this fibronectin type III repeat interacted with the glycosaminoglycan component of decorin.	Glycosaminoglycans	117-134	fibronectin 1	Homo sapiens	69-80
9300051-6	1997	Together with the fact that no significant sequence homology exists between p40 and the gag and gag-like proteins, it is likely that the p40 RNP-complex is structurally different from the typical virus and virus-like particles.	Glycosaminoglycans	96-99	interleukin 9	Homo sapiens	137-140
9300051-6	1997	Together with the fact that no significant sequence homology exists between p40 and the gag and gag-like proteins, it is likely that the p40 RNP-complex is structurally different from the typical virus and virus-like particles.	Glycosaminoglycans	96-99	RNA binding region (RNP1, RRM) containing 3	Homo sapiens	141-144
9258403-8	1997	On the other hand IL-2 stimulated both glycosaminoglycan (GAG) and prostacyclin syntheses and enhanced the stimulation of both GAG and prostacyclin syntheses induced by AII.	Glycosaminoglycans	127-130	interleukin 2	Homo sapiens	18-22
9258403-8	1997	On the other hand IL-2 stimulated both glycosaminoglycan (GAG) and prostacyclin syntheses and enhanced the stimulation of both GAG and prostacyclin syntheses induced by AII.	Glycosaminoglycans	127-130	angiotensinogen	Homo sapiens	169-172
9305797-8	1997	The glycosaminoglycan chains on both decorin and biglycan were identified as dermatan sulphate by their susceptibility to chondroitinase-B.	Glycosaminoglycans	4-21	decorin	Bos taurus	37-44
9305797-8	1997	The glycosaminoglycan chains on both decorin and biglycan were identified as dermatan sulphate by their susceptibility to chondroitinase-B.	Glycosaminoglycans	4-21	biglycan	Bos taurus	49-57
9300048-1	1997	We have sequenced the p17 coding regions of the gag gene from 211 patients infected either through injecting drug use (IDU) or by sexual intercourse between men from six cities in Scotland, N. England, N. Ireland, and the Republic of Ireland.	Glycosaminoglycans	48-51	family with sequence similarity 72 member B	Homo sapiens	22-25
9257861-6	1997	First, we assessed the effect of GAG on the second-order rate constant of the inactivation of C1s by C1 inhibitor.	Glycosaminoglycans	33-36	complement C1s	Homo sapiens	94-97
9257861-8	1997	Second, all tested GAG were found to reduce deposition of C4 and C3 on immobilized aggregated human IgG (AHG) and to reduce fluid phase formation of C4b/c and C3b/c in recalcified plasma upon incubation with AHG.	Glycosaminoglycans	19-22	complement C4B (Chido blood group)	Homo sapiens	149-152
9257861-8	1997	Second, all tested GAG were found to reduce deposition of C4 and C3 on immobilized aggregated human IgG (AHG) and to reduce fluid phase formation of C4b/c and C3b/c in recalcified plasma upon incubation with AHG.	Glycosaminoglycans	19-22	complement C3	Homo sapiens	159-162
9258403-8	1997	On the other hand IL-2 stimulated both glycosaminoglycan (GAG) and prostacyclin syntheses and enhanced the stimulation of both GAG and prostacyclin syntheses induced by AII.	Glycosaminoglycans	58-61	interleukin 2	Homo sapiens	18-22
9288934-0	1997	All-transglycolytic synthesis and characterization of sialyl(alpha2-3)galactosyl(beta1-4)xylosyl-p-nitrophenyl(beta1-), an oligosaccharide derivative related to glycosaminoglycan biosynthesis.	Glycosaminoglycans	161-178	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	81-88
9270876-1	1997	Thrombospondin 1 (TSP1), a high molecular weight glycoprotein of the extracellular matrix, interacts with glycosaminoglycan at the cell surface of porcine endothelial cells (Schon et al., Eur.J.	Glycosaminoglycans	106-123	thrombospondin 1	Homo sapiens	0-16
9270876-1	1997	Thrombospondin 1 (TSP1), a high molecular weight glycoprotein of the extracellular matrix, interacts with glycosaminoglycan at the cell surface of porcine endothelial cells (Schon et al., Eur.J.	Glycosaminoglycans	106-123	thrombospondin 1	Homo sapiens	18-22
9270876-14	1997	Purified perlecan bound to TSP1 in a dose-dependent manner and the binding was mediated by its glycosaminoglycan side chains.	Glycosaminoglycans	95-112	thrombospondin 1	Homo sapiens	27-31
9283829-4	1997	The abundance of mRNAs for P0 protein and myelin basic protein of regenerating nerves was also affected by treatment with glycosaminoglycans.	Glycosaminoglycans	122-140	myelin basic protein	Rattus norvegicus	42-62
9288934-0	1997	All-transglycolytic synthesis and characterization of sialyl(alpha2-3)galactosyl(beta1-4)xylosyl-p-nitrophenyl(beta1-), an oligosaccharide derivative related to glycosaminoglycan biosynthesis.	Glycosaminoglycans	161-178	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	81-86
9288934-2	1997	Among these oligosaccharide derivatives, we synthesized the trisaccharide derivative NeuAc(alpha2-3)Gal(beta1-4)Xyl-Np(beta1- as a potential inhibitor of human skin fibroblast glycosaminoglycan biosynthesis.	Glycosaminoglycans	176-193	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	104-111
9288934-2	1997	Among these oligosaccharide derivatives, we synthesized the trisaccharide derivative NeuAc(alpha2-3)Gal(beta1-4)Xyl-Np(beta1- as a potential inhibitor of human skin fibroblast glycosaminoglycan biosynthesis.	Glycosaminoglycans	176-193	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	104-109
9338017-2	1997	Interestingly, Vpu was also shown to enhance the release of capsids produced by gag gene contructs of other retroviruses that lack a Vpu-like activity.	Glycosaminoglycans	80-83	Vpu	Human immunodeficiency virus 1	15-18
9298694-5	1997	CD44 is subject to a wide array of post-translational carbohydrate modifications, including N-linked, O-linked and glycosaminoglycan side chain additions.	Glycosaminoglycans	115-132	CD44 molecule (Indian blood group)	Homo sapiens	0-4
9298694-7	1997	Some glycosaminoglycan modifications also affect ligand binding specificity, allowing CD44 to interact with proteins of the extracellular matrix, such as fibronectin and collagen, and to sequester heparin binding growth factors.	Glycosaminoglycans	5-22	CD44 molecule (Indian blood group)	Homo sapiens	86-90
9298699-5	1997	The major ligand for CD44 is the extracellular matrix glycosaminoglycan, hyaluronic acid (HA).	Glycosaminoglycans	54-71	CD44 molecule (Indian blood group)	Homo sapiens	21-25
9268591-6	1997	Relative proportions of glycosaminoglycans, the natural substrates of beta-glucuronidase and arylsulfatase B, in the retinal pigment epithelium altered with the age of the donors.	Glycosaminoglycans	24-42	glucuronidase beta	Homo sapiens	70-88
9268591-6	1997	Relative proportions of glycosaminoglycans, the natural substrates of beta-glucuronidase and arylsulfatase B, in the retinal pigment epithelium altered with the age of the donors.	Glycosaminoglycans	24-42	arylsulfatase B	Homo sapiens	93-108
9258342-3	1997	The activity, towards bFGF, of heparan sulfate proteoglycans present within the vascular system is likely related to the chemical characteristics of the glycosaminoglycan as well as the structure and pericellular location of the intact proteoglycans.	Glycosaminoglycans	153-170	fibroblast growth factor 2	Homo sapiens	22-26
9217004-3	1997	UDP-glucose dehydrogenase is required for the biosynthesis of UDP-glucuronate, which in turn is utilized in the biosynthesis of glycosaminoglycans.	Glycosaminoglycans	128-146	sugarless	Drosophila melanogaster	0-25
9201990-6	1997	Removal of cell surface GAG chains by treatment of cells with heparinase or heparitinase but not chondroitinase markedly reduced fXa-stimulated 125I-TFPI uptake and degradation.	Glycosaminoglycans	24-27	tissue factor pathway inhibitor	Bos taurus	149-153
9201990-7	1997	Inhibition of GAG sulfation by growth of cells in chlorate-containing medium similarly decreased fXa-stimulated 125I-TFPI degradation.	Glycosaminoglycans	14-17	tissue factor pathway inhibitor	Bos taurus	117-121
9240182-1	1997	OBJECTIVE: To clarify the role of glycosaminoglycans (GAGs) in crystal-surface binding substances (CSBS) on the growth of calcium oxalate crystals in urine.	Glycosaminoglycans	34-52	filamin A	Homo sapiens	99-103
9240182-7	1997	CONCLUSION: Both heparan sulphate and dermatan sulphate may inhibit calcium oxalate crystallization, the former being the predominant GAG in CSBS.	Glycosaminoglycans	134-137	filamin A	Homo sapiens	141-145
9188605-1	1997	The neuroinvasiveness of a chimeric murine retrovirus, CasFrKP (KP), is dependent on the expression of glycosylated Gag (gp85gag).	Glycosaminoglycans	116-119	melanoma antigen	Mus musculus	121-128
9202067-2	1997	Ectopic expression of decorin proteoglycan or protein core as a mutated form lacking any glycosaminoglycan side chains induced growth suppression in neoplastic cells of various histogenetic origins, including tumor cells derived from gastrointestinal, genital, skeletal, cutaneous, or bone marrow tissues.	Glycosaminoglycans	89-106	decorin	Homo sapiens	22-29
9483172-2	1997	In in vitro studies, the prolongation of thrombin clotting time (TCT) by these glycosaminoglycans was completely neutralized by PS, whereas activated partial thromboplastin time (APTT) was relatively resistant to neutralization.	Glycosaminoglycans	79-97	coagulation factor II	Rattus norvegicus	41-49
9276666-3	1997	The deduced primary structure of mouse ryudocan, including the three glycosaminoglycan attachment sites in the extracellular domain as well as the transmembrane and cytoplasmic regions, is highly similar to those of the rat, human, and chicken proteins.	Glycosaminoglycans	69-86	syndecan 4	Mus musculus	39-47
9237673-2	1997	We have examined the glycosaminoglycan specificity of the Link module from the arthritis-associated protein, human TSG-6, by microtitre plate-based assays employing biotinylated-hyaluronan or mono-biotinylated Link module.	Glycosaminoglycans	21-38	TNF alpha induced protein 6	Homo sapiens	115-120
9267850-1	1997	Mucopolysaccharidosis type VII (MPS VII) is caused by a deficiency in the lysosomal enzyme beta-glucuronidase resulting in the accumulation of undegraded glycosaminoglycans in many tissues.	Glycosaminoglycans	154-172	glucuronidase, beta	Mus musculus	91-109
9217327-4	1997	Excess soluble glycosaminoglycans inhibited the binding of tenascin-C to purified fibronectin in ELISA, and completely blocked incorporation into matrix fibrils.	Glycosaminoglycans	15-33	tenascin	Cricetulus griseus	59-69
9199199-0	1997	Glycosaminoglycans can influence fibroblast growth factor-2 mitogenicity without significant growth factor binding.	Glycosaminoglycans	0-18	fibroblast growth factor 2	Homo sapiens	33-59
9185153-11	1997	In the present study the effects of hTGF-beta on the stimulation of DNA and sulfated GAG synthesis and ALP activity were studied.	Glycosaminoglycans	85-88	transforming growth factor beta 1	Homo sapiens	36-45
9169007-1	1997	Two major glycoforms of recombinant antithrombin which differ 10-fold in their affinity for the effector glycosaminoglycan, heparin, were previously shown to be expressed in BHK or CHO mammalian cell lines (I. Bjork, et al., 1992, Biochem.	Glycosaminoglycans	105-122	serpin family C member 1	Homo sapiens	36-48
9184660-12	1997	Thus, morphological and biochemical features in these mice are consistent with those of mucopolysaccharidosis and demonstrate an essential role of beta-hexosaminidase in the degradation of glycosaminoglycans.	Glycosaminoglycans	189-207	O-GlcNAcase	Mus musculus	147-166
9151840-3	1997	We described here the possibility that down-regulation results from the presence of inhibitory elements within the gag-env region of the provirus in fresh peripheral blood mononuclear cells from carriers.	Glycosaminoglycans	115-118	endogenous retrovirus group W member 1, envelope	Homo sapiens	119-122
9160685-8	1997	Finally, we have demonstrated by RT-PCR, flow cytometry, and Western blotting that cultured RS cells, of B and undetermined phenotype, express syndecan-1 mRNA and produce a form of syndecan-1, recognized by the B-B4 MoAb, which is predominantly associated with glycosaminoglycans and is present at the cell surface.	Glycosaminoglycans	261-279	syndecan 1	Homo sapiens	181-191
9215063-13	1997	CONCLUSION: An increase of beta glucuronidase activity might have caused extensive fragmentation of GAG with resultant accumulation in the blood and lens and excretion in urine.	Glycosaminoglycans	100-103	glucuronidase beta	Homo sapiens	27-45
9140562-3	1997	PROCEDURE: Triamcinolone acetonide and IGF-1 effects were evaluated by assessing: matrix responses by sulfated glycosaminoglycan (GAG) assay and [35S]sulfated GAG synthesis; collagen content by hydroxyproline assay; and mitogenic response by [3H]thymidine incorporation into DNA and fluorometric assay of total DNA concentration.	Glycosaminoglycans	111-128	insulin like growth factor 1	Equus caballus	39-44
9140562-3	1997	PROCEDURE: Triamcinolone acetonide and IGF-1 effects were evaluated by assessing: matrix responses by sulfated glycosaminoglycan (GAG) assay and [35S]sulfated GAG synthesis; collagen content by hydroxyproline assay; and mitogenic response by [3H]thymidine incorporation into DNA and fluorometric assay of total DNA concentration.	Glycosaminoglycans	130-133	insulin like growth factor 1	Equus caballus	39-44
9140562-3	1997	PROCEDURE: Triamcinolone acetonide and IGF-1 effects were evaluated by assessing: matrix responses by sulfated glycosaminoglycan (GAG) assay and [35S]sulfated GAG synthesis; collagen content by hydroxyproline assay; and mitogenic response by [3H]thymidine incorporation into DNA and fluorometric assay of total DNA concentration.	Glycosaminoglycans	159-162	insulin like growth factor 1	Equus caballus	39-44
9175930-6	1997	RESULTS: Increased SF 3-B-3 concentrations and 3-B-3/GAG ratio were found in OA, compared with RA or normal knees, with higher 3-B-3 and 3-B-3/GAG in LJOA and NGOA than in CPA.	Glycosaminoglycans	143-146	splicing factor 3b subunit 3	Homo sapiens	19-27
9165101-1	1997	Serum amyloid P component (SAP), a member of the pentraxin family of proteins, binds calcium-dependently to several ligands including glycosaminoglycans (GAG"s).	Glycosaminoglycans	134-152	amyloid P component, serum	Homo sapiens	0-25
9165101-1	1997	Serum amyloid P component (SAP), a member of the pentraxin family of proteins, binds calcium-dependently to several ligands including glycosaminoglycans (GAG"s).	Glycosaminoglycans	134-152	amyloid P component, serum	Homo sapiens	27-30
9165101-2	1997	We have investigated the influence of pH on the Ca2(+)-dependent binding of SAP to solid phase GAG"s and amyloid fibril proteins (AA and beta2M) by ELISA.	Glycosaminoglycans	95-98	amyloid P component, serum	Homo sapiens	76-79
9169588-4	1997	Finally, lipid and glycosaminoglycan modification of tau structure affords yet more complexity for regulation and aggregation.	Glycosaminoglycans	19-36	microtubule associated protein tau	Homo sapiens	53-56
9111037-13	1997	The Tat binding activity of the glycosaminoglycans tested correlates with their capacity to affect the transactivating activity of extracellular Tat, indicating the possibility to design specific heparin/HS-like structures with Tat-antagonist activity.	Glycosaminoglycans	32-50	tyrosine aminotransferase	Homo sapiens	4-7
9111037-13	1997	The Tat binding activity of the glycosaminoglycans tested correlates with their capacity to affect the transactivating activity of extracellular Tat, indicating the possibility to design specific heparin/HS-like structures with Tat-antagonist activity.	Glycosaminoglycans	32-50	tyrosine aminotransferase	Homo sapiens	145-148
9111037-13	1997	The Tat binding activity of the glycosaminoglycans tested correlates with their capacity to affect the transactivating activity of extracellular Tat, indicating the possibility to design specific heparin/HS-like structures with Tat-antagonist activity.	Glycosaminoglycans	32-50	tyrosine aminotransferase	Homo sapiens	145-148
9099729-4	1997	Consistent with previous models of glycosaminoglycan attachment, roughly 50% of the recombinant NG2 fragments containing the central domain have chondroitin sulfate chains attached to the protein core.	Glycosaminoglycans	35-52	chondroitin sulfate proteoglycan 4	Homo sapiens	96-99
9083065-4	1997	Cleavage at the aggrecanase site was observed only at MMP-8 concentrations resulting in complete release of glycosaminoglycan from the cartilage, suggesting that preferential cleavage occurs at a different site.	Glycosaminoglycans	108-125	matrix metallopeptidase 8	Homo sapiens	54-59
9227267-7	1997	The heparin-binding characteristics of HGF would result in increased binding to glycosaminoglycans and other heparin-like matrix components and, therefore, increased growth factor availability to the cognate recptor.	Glycosaminoglycans	80-98	hepatocyte growth factor	Homo sapiens	39-42
9124611-4	1997	The diminished activity of oxidized SLPI could be almost completely restored when an iduronate-containing glycosaminoglycan, such as heparin, heparan sulfate, or dermatan sulfate, was added to the reaction medium.	Glycosaminoglycans	106-123	secretory leukocyte peptidase inhibitor	Homo sapiens	36-40
9148753-1	1997	Decorin (DCN) is a ubiquitous proteoglycan comprised of a core protein attached to a single dermatan/chondroitin sulphate glycosaminoglycan chain.	Glycosaminoglycans	122-139	decorin	Homo sapiens	0-7
9148753-1	1997	Decorin (DCN) is a ubiquitous proteoglycan comprised of a core protein attached to a single dermatan/chondroitin sulphate glycosaminoglycan chain.	Glycosaminoglycans	122-139	decorin	Homo sapiens	9-12
9097952-4	1997	Homozygous Idua -/- mice have no detectable alpha-L-iduronidase enzyme activity and show increased urinary glycosaminoglycan levels.	Glycosaminoglycans	107-124	iduronidase, alpha-L	Mus musculus	11-15
9209286-3	1997	We have recently reported that the reverse transcription of HIV-1 RNA is markedly enhanced by the association of the gag encoded nucleocapsid p15 protein and cellular topoisomerase 1.	Glycosaminoglycans	117-120	Vpr	Human immunodeficiency virus 1	142-145
9209315-3	1997	We have recently reported that the reverse transcription of HIV-1 RNA is markedly enhanced by the association of the gag encoded nucleocapsid p15 protein and cellular topoisomerase I.	Glycosaminoglycans	117-120	Vpr	Human immunodeficiency virus 1	142-145
9209375-4	1997	In viral forms of abl, gag sequences are fused to Abl portions resulting in a deletion of N-terminal sequences.	Glycosaminoglycans	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
9133733-3	1997	The total amount of Gag in whole-cell lysates of scs1/lcb2 mutant cells is greater than in wild-type lysates indicating that the enrichment of the protein in the microsomal fraction of scs1/lcb2 mutant cells may result from increased copy number of the L-A dsRNA virus.	Glycosaminoglycans	20-23	serine palmitoyltransferase long chain base subunit 2	Homo sapiens	54-58
9123868-3	1997	SI overlaps the primer-binding site; and SII contains the palindromic sequence, UCCCUAGGGA, the disruption of which impairs dimer formation; and SIII extends into the gag gene.	Glycosaminoglycans	167-170	elongin B	Homo sapiens	145-149
9124611-6	1997	Kinetic analysis revealed that glycosaminoglycans greatly accelerated the association of oxidized SLPI and HLE, whereas iduronate-containing glycosaminoglycans also stabilized the enzyme-inhibitor complex formed.	Glycosaminoglycans	31-49	secretory leukocyte peptidase inhibitor	Homo sapiens	98-102
9124611-7	1997	Based on these findings, we suggest that oxidized SLPI is a functionally active form of the inhibitor but that expression of its elastase inhibitory activity is regulated by sulfated uronate-containing glycosaminoglycans.	Glycosaminoglycans	202-220	secretory leukocyte peptidase inhibitor	Homo sapiens	50-54
9071714-2	1997	The presence of the glycosaminoglycan side chains of heparan sulfate proteoglycan, an important constituent of the glomerular basement membrane, is decreased in diabetic nephropathy proportionally to the degree of proteinuria.	Glycosaminoglycans	20-37	CD44 molecule (Indian blood group)	Homo sapiens	53-81
9067536-2	1997	In this study the mechanism by which the glycosaminoglycan (GAG) heparin antagonizes the activation of a model endothelium by IFN-gamma was investigated.	Glycosaminoglycans	41-58	interferon gamma	Homo sapiens	126-135
9067536-4	1997	Treatment of the cells with chlorate, a metabolic inhibitor of GAG sulphation, was found to reduce both the subsequent binding of IFN-gamma and its ability to induce expression of class II MHC antigens.	Glycosaminoglycans	63-66	interferon gamma	Homo sapiens	130-139
9067536-7	1997	These results appear to demonstrate that IFN-gamma is sequestered at the surface of endothelial cells by electrostatic interaction between specific basic amino acid residues and sulphated domains on HS, the most abundant endothelial GAG.	Glycosaminoglycans	233-236	interferon gamma	Homo sapiens	41-50
9057648-8	1997	c-Fos protein was shown essential for an optimal transactivation of the HIV-1 long terminal repeat (LTR) by Tat: incubation of Jurkat cells with antisense, but not sense, c-fos oligonucleotides significantly reduced either the Tat-enhanced expression of an LTR-CAT reporter construct or the levels of gag p24 in the culture supernatants of Jurkat cells and PBMC acutely infected with HIV-1.	Glycosaminoglycans	301-304	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5
9057648-8	1997	c-Fos protein was shown essential for an optimal transactivation of the HIV-1 long terminal repeat (LTR) by Tat: incubation of Jurkat cells with antisense, but not sense, c-fos oligonucleotides significantly reduced either the Tat-enhanced expression of an LTR-CAT reporter construct or the levels of gag p24 in the culture supernatants of Jurkat cells and PBMC acutely infected with HIV-1.	Glycosaminoglycans	301-304	Tat	Human immunodeficiency virus 1	108-111
9057648-8	1997	c-Fos protein was shown essential for an optimal transactivation of the HIV-1 long terminal repeat (LTR) by Tat: incubation of Jurkat cells with antisense, but not sense, c-fos oligonucleotides significantly reduced either the Tat-enhanced expression of an LTR-CAT reporter construct or the levels of gag p24 in the culture supernatants of Jurkat cells and PBMC acutely infected with HIV-1.	Glycosaminoglycans	301-304	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	171-176
9032471-12	1997	These data indicate that the sequence VDAVRTEKGFLLLASLRQMKKTRGTLLALERKDHS (residues 60-94) constitutes a GAG-dependent cell adhesive site in the N-terminus of TSP-1.	Glycosaminoglycans	105-108	thrombospondin-1	Cricetulus griseus	159-164
9065996-2	1997	This increase in TFPI activity could be the result of increased thrombin formation and/or altered binding of TFPI to glycosaminoglycans.	Glycosaminoglycans	117-135	tissue factor pathway inhibitor	Homo sapiens	17-21
9065996-2	1997	This increase in TFPI activity could be the result of increased thrombin formation and/or altered binding of TFPI to glycosaminoglycans.	Glycosaminoglycans	117-135	tissue factor pathway inhibitor	Homo sapiens	109-113
9065996-11	1997	It is hypothesized that vascular damage, leading to alterations in glycosaminoglycans, is in part responsible for the changes in TFPI activity, F1 + 2 levels and ETP.	Glycosaminoglycans	67-85	tissue factor pathway inhibitor	Homo sapiens	129-133
9065996-11	1997	It is hypothesized that vascular damage, leading to alterations in glycosaminoglycans, is in part responsible for the changes in TFPI activity, F1 + 2 levels and ETP.	Glycosaminoglycans	67-85	coagulation factor XII	Homo sapiens	144-150
9057969-2	1997	The molecular mass of the glycosaminoglycan chain from pronase digestion of HSPG was estimated to be 30-100 kDa.	Glycosaminoglycans	26-43	syndecan 2	Homo sapiens	76-80
8999938-7	1997	The expression levels of gag correlate with the absence of binding of PABP1 to the INS-1 RNA in cellular extracts.	Glycosaminoglycans	25-28	poly(A) binding protein cytoplasmic 1	Homo sapiens	70-75
8995662-10	1997	The affinity and specificity of gB2 binding to glycosaminoglycans demonstrated in these studies support its role in the initial binding of HSV-2 to cells bearing heparan sulfate or dermatan sulfate glycosaminoglycans.	Glycosaminoglycans	47-65	gamma-aminobutyric acid type B receptor subunit 2	Homo sapiens	32-35
9068944-4	1997	Distribution of glycosaminoglycans (GAGs), the natural substrates of GUSB, in the RPE and fibroblast cell layer and media was examined by cellulose acetate electrophoresis following 72 h of metabolic labeling with Na2(35)SO4.	Glycosaminoglycans	16-34	glucuronidase, beta	Rattus norvegicus	69-73
9068944-4	1997	Distribution of glycosaminoglycans (GAGs), the natural substrates of GUSB, in the RPE and fibroblast cell layer and media was examined by cellulose acetate electrophoresis following 72 h of metabolic labeling with Na2(35)SO4.	Glycosaminoglycans	36-40	glucuronidase, beta	Rattus norvegicus	69-73
9068944-10	1997	Supplementation of the cultured cells with selected GAGs moderately increased the GUSB activity.	Glycosaminoglycans	52-56	glucuronidase, beta	Rattus norvegicus	82-86
9013976-6	1997	Binding of C1q to CSPG was competitively inhibited by free glycosaminoglycans (GAG) in the order dextran sulfate &gt; heparin &gt; heparan sulfate &gt; chondroitin-6-sulfate (CS-C) &gt; dermatan sulfate (CS-B) &gt; chondroitin-4-sulfate (CS-A).	Glycosaminoglycans	59-77	complement C1q A chain	Homo sapiens	11-14
9013976-6	1997	Binding of C1q to CSPG was competitively inhibited by free glycosaminoglycans (GAG) in the order dextran sulfate &gt; heparin &gt; heparan sulfate &gt; chondroitin-6-sulfate (CS-C) &gt; dermatan sulfate (CS-B) &gt; chondroitin-4-sulfate (CS-A).	Glycosaminoglycans	59-77	chorionic somatomammotropin hormone 2	Homo sapiens	204-208
9013976-6	1997	Binding of C1q to CSPG was competitively inhibited by free glycosaminoglycans (GAG) in the order dextran sulfate &gt; heparin &gt; heparan sulfate &gt; chondroitin-6-sulfate (CS-C) &gt; dermatan sulfate (CS-B) &gt; chondroitin-4-sulfate (CS-A).	Glycosaminoglycans	79-82	complement C1q A chain	Homo sapiens	11-14
9013976-6	1997	Binding of C1q to CSPG was competitively inhibited by free glycosaminoglycans (GAG) in the order dextran sulfate &gt; heparin &gt; heparan sulfate &gt; chondroitin-6-sulfate (CS-C) &gt; dermatan sulfate (CS-B) &gt; chondroitin-4-sulfate (CS-A).	Glycosaminoglycans	79-82	chorionic somatomammotropin hormone 2	Homo sapiens	204-208
8995691-2	1997	In the cytoplasm or the nucleus of infected cells as well as in free virus particles, two Gag precursor polypeptides were identified at approximately 72 and 68 kDa, p72 giving rise to p68 by a maturation process.	Glycosaminoglycans	90-93	DEAD-box helicase 17	Homo sapiens	165-168
8995691-2	1997	In the cytoplasm or the nucleus of infected cells as well as in free virus particles, two Gag precursor polypeptides were identified at approximately 72 and 68 kDa, p72 giving rise to p68 by a maturation process.	Glycosaminoglycans	90-93	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	184-187
8999938-7	1997	The expression levels of gag correlate with the absence of binding of PABP1 to the INS-1 RNA in cellular extracts.	Glycosaminoglycans	25-28	forkhead box M1	Homo sapiens	83-88
8999938-8	1997	These results suggest a role for PABP1 in the inhibition of gag expression mediated through INS-1.	Glycosaminoglycans	60-63	poly(A) binding protein cytoplasmic 1	Homo sapiens	33-38
8999938-8	1997	These results suggest a role for PABP1 in the inhibition of gag expression mediated through INS-1.	Glycosaminoglycans	60-63	forkhead box M1	Homo sapiens	92-97
9007059-9	1997	The gag gene of both the maternal and the child"s virus population represented an A/C recombinant sequence (Ap17/Cp24).	Glycosaminoglycans	4-7	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	113-117
9512891-2	1997	The effects of interleukin-1 alpha (IL-1 alpha) on GAG metabolism in normal and otosclerotic human bone cells as well as its capacity to modulate IL-1 alpha, IL-1 beta and IL-6 secretion in both populations was analyzed.	Glycosaminoglycans	51-54	interleukin 1 alpha	Homo sapiens	36-46
9330666-0	1997	Inhibitory effect of pentoxifylline on HLA-DR expression and glycosaminoglycan synthesis of retrobulbar fibroblasts induced by interferon gamma.	Glycosaminoglycans	61-78	interferon gamma	Homo sapiens	127-143
9330666-13	1997	Both spontaneous and IFN-gamma-induced GAG synthesis of REF was inhibited by Ptx (100, 500 and 1000 mg/l, respectively).	Glycosaminoglycans	39-42	interferon gamma	Homo sapiens	21-30
9512891-8	1997	As the activity of neither enzyme was modified by treatment with IL-1 alpha, the cytokine seems to exert its influences on GAG synthesis rather than on the degradation process.	Glycosaminoglycans	123-126	interleukin 1 alpha	Homo sapiens	65-75
9338582-2	1997	Among seven unrelated Northern European kindreds with clinical TPI deficiency studied, a single missense mutation at codon 104 (GAG;Glu--&gt;GAC;Asp) predominated, accounting for 11/14 (79%) mutant alleles.	Glycosaminoglycans	128-131	triosephosphate isomerase 1	Homo sapiens	63-66
8996834-3	1997	Omission of the latter exons in L-APP and L-APLP2 isoforms, respectively, generates a functional recognition sequence for xylosyltransferase-mediated addition of glycosaminoglycans and proteoglycan formation.	Glycosaminoglycans	162-180	amyloid beta precursor like protein 2	Rattus norvegicus	44-49
9595258-5	1997	Recombinant virus constructs having the mutated gag region of tdPH2010 produced a p19 with the same electrophoretic mobility as the p19 of tdPH2010.	Glycosaminoglycans	48-51	interleukin 23 subunit alpha	Homo sapiens	82-85
9469634-4	1997	AT III promotes the endothelial release of prostacyclin by interacting with cell surface glycosaminoglycans in vivo.	Glycosaminoglycans	89-107	serpin family C member 1	Rattus norvegicus	0-6
9061044-1	1997	To investigate the intracellular regulation of glycosaminoglycan (GAG) production induced by basic fibroblast growth factor (bFGF), bovine aortic endothelial cells were cultured with recombinant human bFGF in the presence of [3H]glucosamine or [35S]sulfate.	Glycosaminoglycans	47-64	fibroblast growth factor 2	Bos taurus	93-123
9061044-1	1997	To investigate the intracellular regulation of glycosaminoglycan (GAG) production induced by basic fibroblast growth factor (bFGF), bovine aortic endothelial cells were cultured with recombinant human bFGF in the presence of [3H]glucosamine or [35S]sulfate.	Glycosaminoglycans	47-64	fibroblast growth factor 2	Bos taurus	125-129
9061044-1	1997	To investigate the intracellular regulation of glycosaminoglycan (GAG) production induced by basic fibroblast growth factor (bFGF), bovine aortic endothelial cells were cultured with recombinant human bFGF in the presence of [3H]glucosamine or [35S]sulfate.	Glycosaminoglycans	66-69	fibroblast growth factor 2	Bos taurus	93-123
9061044-1	1997	To investigate the intracellular regulation of glycosaminoglycan (GAG) production induced by basic fibroblast growth factor (bFGF), bovine aortic endothelial cells were cultured with recombinant human bFGF in the presence of [3H]glucosamine or [35S]sulfate.	Glycosaminoglycans	66-69	fibroblast growth factor 2	Bos taurus	125-129
9061044-6	1997	The present data suggested that bFGF may increase the number of GAG chains as a result of enhanced protein synthesis including xylosyl transferase through the lipoxygenase pathway of arachidonic acid metabolism in vascular endothelial cell layer.	Glycosaminoglycans	64-67	fibroblast growth factor 2	Homo sapiens	32-36
9492183-6	1997	rBVs containing gag and p26 genes were found to express high quality and large quantities of Gag and p26 antigens, respectively.	Glycosaminoglycans	16-19	transmembrane p24 trafficking protein 3	Homo sapiens	101-104
9492183-6	1997	rBVs containing gag and p26 genes were found to express high quality and large quantities of Gag and p26 antigens, respectively.	Glycosaminoglycans	93-96	transmembrane p24 trafficking protein 3	Homo sapiens	24-27
21590010-5	1997	Biological roles of S100B in chondroid cells may involve Ca2+-signaling in precalcified tissue, cytoskeletal protein organization and matrix formation since glycosaminoglycan synthesis is mediated by calcium ions.	Glycosaminoglycans	157-174	S100 calcium binding protein B	Homo sapiens	20-25
9337530-3	1997	TFPI is synthesized by vascular endothelial cells and part of it is associated with glycosaminoglycans of these cells.	Glycosaminoglycans	84-102	tissue factor pathway inhibitor	Homo sapiens	0-4
8974075-2	1996	The incorporation of the label into total glycosaminoglycan (GAG) was significantly higher in cells maintained on Co IV compared to those maintained on Fn or Ln.	Glycosaminoglycans	61-64	fibronectin 1	Rattus norvegicus	152-154
8939995-2	1996	In mammals, decorin carries one chondroitin/dermatan sulfate chain as a distinction from its homologue, biglycan, which contains two glycosaminoglycan chains.	Glycosaminoglycans	133-150	decorin	Gallus gallus	12-19
8997260-0	1996	Response of airway smooth muscle cells to TGF-beta 1: effects on growth and synthesis of glycosaminoglycans.	Glycosaminoglycans	89-107	transforming growth factor beta 1	Bos taurus	42-52
8997260-11	1996	TGF-beta 1 also promoted secretion of glycosaminoglycans into culture medium by BASMC with a preferential increase in hyaluronan secretion (4.5-fold) after 24 h. Latent TGF-beta (0.89 +/- 0.06 ng/ml) was also detected in conditioned medium from cultured BASMC, and TGF-beta 1 expression was demonstrated with RNA extracts from BASMC.	Glycosaminoglycans	38-56	transforming growth factor beta 1	Bos taurus	0-10
8997260-11	1996	TGF-beta 1 also promoted secretion of glycosaminoglycans into culture medium by BASMC with a preferential increase in hyaluronan secretion (4.5-fold) after 24 h. Latent TGF-beta (0.89 +/- 0.06 ng/ml) was also detected in conditioned medium from cultured BASMC, and TGF-beta 1 expression was demonstrated with RNA extracts from BASMC.	Glycosaminoglycans	38-56	transforming growth factor beta 1	Bos taurus	0-8
9000088-3	1996	Although both Tera 1 and PA-1 cells express Gag, demethylation upon treatment with 5-azacytidine (5-AZC) or exposure to the chromatin-modifying agent n-butyrate resulted in an increase in Gag protein levels only in Tera 1 cells.	Glycosaminoglycans	44-47	PAXIP1 associated glutamate rich protein 1	Homo sapiens	14-29
9000088-3	1996	Although both Tera 1 and PA-1 cells express Gag, demethylation upon treatment with 5-azacytidine (5-AZC) or exposure to the chromatin-modifying agent n-butyrate resulted in an increase in Gag protein levels only in Tera 1 cells.	Glycosaminoglycans	188-191	PAXIP1 associated glutamate rich protein 1	Homo sapiens	14-29
8970945-6	1996	Importantly, parallel analyses of total lysates of the producer cells revealed that the cell-associated expression levels of Vif are close to those of the Gag proteins.	Glycosaminoglycans	155-158	Vif	Human immunodeficiency virus 1	125-128
9020901-3	1996	TGF-beta 1 increased the release of sulfated proteoglycans into the medium, including the cell-specific melanoma proteoglycan, mel-PG, and induced changes in disaccharide composition and sulfation of the glycosaminoglycan chains.	Glycosaminoglycans	204-221	transforming growth factor beta 1	Homo sapiens	0-10
8970376-3	1996	The results showed that glycosaminoglycan deposition in the lesions of ARDS, BOOP, and IPF corresponded to the deposition of versican.	Glycosaminoglycans	24-41	versican	Homo sapiens	125-133
8939995-2	1996	In mammals, decorin carries one chondroitin/dermatan sulfate chain as a distinction from its homologue, biglycan, which contains two glycosaminoglycan chains.	Glycosaminoglycans	133-150	biglycan	Homo sapiens	104-112
9117350-2	1996	The carboxy-terminal end of vitronectin has a consensus sequence for glycosaminoglycan-binding.	Glycosaminoglycans	69-86	vitronectin	Homo sapiens	28-39
8948051-2	1996	It has been suggested that the highly positively charged carboxy terminal end of heparin releasable TFPI is bound to negatively charged binding molecule(s), presumably glycosaminoglycans (GAGs), on the luminal surface of endothelial cells.	Glycosaminoglycans	168-186	tissue factor pathway inhibitor	Rattus norvegicus	100-104
9049708-5	1996	In the implants treated with AII (2 micrograms) no further increase in angiogenesis was observed, whereas a marked effect was shown in wet weight (326 +/- 15 vs. 424 +/- 27 mg), total protein (18 +/- 1 vs. 25 +/- 1 micrograms/ww) and GAG (98 +/- 10 vs. 160 +/- 13 ng/ww).	Glycosaminoglycans	234-237	arginase type II	Mus musculus	29-32
8895319-4	1996	We have previously shown that IGFBP-5 associates with glycosaminoglycans and binds to proteoglycans that are contained in ECM and basement membranes.	Glycosaminoglycans	54-72	insulin like growth factor binding protein 5	Homo sapiens	30-37
8895319-13	1996	In summary, IGFBP-2 binding to glycosaminoglycans is dependent upon binding of IGF-I and IGF-II to IGFBP-2.	Glycosaminoglycans	31-49	insulin like growth factor binding protein 2	Homo sapiens	12-19
8895319-13	1996	In summary, IGFBP-2 binding to glycosaminoglycans is dependent upon binding of IGF-I and IGF-II to IGFBP-2.	Glycosaminoglycans	31-49	insulin like growth factor 1	Homo sapiens	79-84
8895319-13	1996	In summary, IGFBP-2 binding to glycosaminoglycans is dependent upon binding of IGF-I and IGF-II to IGFBP-2.	Glycosaminoglycans	31-49	insulin like growth factor 2	Homo sapiens	89-95
8808643-1	1996	Heparin and heparan sulfate are related glycosaminoglycans which demonstrate high-affinity interactions with a number of proteins, including antithrombin III.	Glycosaminoglycans	40-58	serine (or cysteine) peptidase inhibitor, clade C (antithrombin), member 1	Mus musculus	141-157
8951806-6	1996	Numerous studies indicate that in the case of thinning of the anionic glycosaminoglycan film on the endothelial surface, the lipoprotein-lipase and antithrombin III activity induced by heparin is reduced, as result of which hyperlipoproteinaemia and increased tendency to thrombosis can only by compensated for to an inadequate extent.	Glycosaminoglycans	70-87	lipoprotein lipase	Homo sapiens	125-143
8951806-6	1996	Numerous studies indicate that in the case of thinning of the anionic glycosaminoglycan film on the endothelial surface, the lipoprotein-lipase and antithrombin III activity induced by heparin is reduced, as result of which hyperlipoproteinaemia and increased tendency to thrombosis can only by compensated for to an inadequate extent.	Glycosaminoglycans	70-87	serpin family C member 1	Homo sapiens	148-164
8849730-0	1996	Assembly of microtubule-associated protein tau into Alzheimer-like filaments induced by sulphated glycosaminoglycans.	Glycosaminoglycans	98-116	microtubule associated protein tau	Homo sapiens	12-46
8849730-5	1996	Here we show that non-phosphorylated recombinant tau isoforms with three microtubule-binding repeats form paired helical-like filaments under physiological conditions in vitro, when incubated with sulphated glycosaminoglycans such as heparin or heparan sulphate.	Glycosaminoglycans	207-225	microtubule associated protein tau	Homo sapiens	49-52
8892934-8	1996	These results show that the transforming potential of the axl gene can be activated by truncation of the extracellular domain of the receptor and fusion of the remaining sequence to the gag gene.	Glycosaminoglycans	186-189	AXL receptor tyrosine kinase	Mus musculus	58-61
8892955-9	1996	We conclude that recombination in the gag gene is highly frequent among the major env subtypes and that selection of recombinants is apparently based on particularly beneficial combinations of gag and env gene products.	Glycosaminoglycans	38-41	endogenous retrovirus group K member 20	Homo sapiens	82-85
8896570-7	1996	This result demonstrates that glycosaminoglycans are crucial substrates for beta-hexosaminidase and that their lack of storage in Tay-Sachs and Sandhoff diseases is due to functional redundancy in the beta-hexosaminidase enzyme system.	Glycosaminoglycans	30-48	O-GlcNAcase	Mus musculus	76-95
8896570-7	1996	This result demonstrates that glycosaminoglycans are crucial substrates for beta-hexosaminidase and that their lack of storage in Tay-Sachs and Sandhoff diseases is due to functional redundancy in the beta-hexosaminidase enzyme system.	Glycosaminoglycans	30-48	O-GlcNAcase	Mus musculus	201-220
8824283-3	1996	Human nonpancreatic secretory phospholipase A2 has three regions that may associate with sulfated glycosaminoglycans.	Glycosaminoglycans	98-116	phospholipase A2 group IB	Homo sapiens	30-46
8824283-5	1996	Here we report that human nonpancreatic phospholipase A2 isolated from a transfected cell line binds to glycosaminoglycans secreted by cultured human arterial smooth muscle cells.	Glycosaminoglycans	104-122	phospholipase A2 group IB	Homo sapiens	40-56
8824283-6	1996	A gel mobility shift assay showed that the affinity of phospholipase A2 for glycosaminoglycans from a heparan sulfate/chondroitin sulfate proteoglycan was higher than for chondroitin sulfate glycosaminoglycans from a larger versican-like proteoglycan.	Glycosaminoglycans	76-94	phospholipase A2 group IB	Homo sapiens	55-71
8824283-8	1996	All glycosaminoglycans tested, at concentrations up to 100 microM, increased the activity of phospholipase A2 toward phosphatidylcholine liposomes.	Glycosaminoglycans	4-22	phospholipase A2 group IB	Homo sapiens	93-109
8824283-11	1996	The results indicate that human nonpancreatic secretory phospholipase A2 interacts with proteoglycans via their glycosaminoglycan moiety and that the enzyme activity may be modulated by the association of the enzyme and its substrate to the sulfated polysaccharides.	Glycosaminoglycans	112-129	phospholipase A2 group IB	Homo sapiens	56-72
8831519-1	1996	PURPOSE: Lysozyme destroys the mucopolysaccharide chains of the cell wall of gram-negative bacteria.	Glycosaminoglycans	31-49	lysozyme	Homo sapiens	9-17
9007566-2	1996	On scanning electron microscopy, a corrosion cast of alveolar capillaries in lungs treated with beta APN appeared abnormal in configuration; transmission electron microscopy showed extensive morphological changes in interstitial cells and ECMs, including collagen, elastin, and presumably glycosaminoglycans and, in binding water (GBW).	Glycosaminoglycans	289-307	alanyl aminopeptidase, membrane	Rattus norvegicus	101-104
8892224-5	1996	The core protein of decorin, but not the glycosaminoglycan moiety, was sufficient to induce collagenase expression on both substrates; however, the glycosaminoglycan moiety of decorin as well as the core were required for cell rounding observed in cells adhering to the 120-kDa domain of fibronectin.	Glycosaminoglycans	148-165	decorin	Oryctolagus cuniculus	20-27
9122888-6	1996	In addition, when TGF-beta 2 was exogenously added to limb bud cell culture medium, the synthesis of glycosaminoglycan (GAGs) was reduced even without Am-80 treatment.	Glycosaminoglycans	101-118	transforming growth factor, beta 2	Rattus norvegicus	18-28
8810912-9	1996	These results revealed that the wild-type WT1 binds with slightly higher affinity to sequences with GAG in the finger 2 subsite than sequences with the EGR-1 consensus GCG finger 2 subsite.	Glycosaminoglycans	100-103	WT1 transcription factor	Homo sapiens	42-45
8836130-3	1996	IFN gamma (250 i.u./ml) induced an increase in incorporation of D-[1-3H]glucosamine into glycosaminoglycans, either secreted into the culture medium or associated with the cell layer.	Glycosaminoglycans	89-107	interferon gamma	Homo sapiens	0-9
8879521-0	1996	New preparation and microstructure of the EndoPatch elastin-collagen containing glycosaminoglycans.	Glycosaminoglycans	80-98	elastin	Homo sapiens	52-59
8809074-8	1996	The inhibition of APMA-induced GAG loss by 4 microM TIMP was accompanied by maintenance of streaming potential, electrokinetic coupling coefficient, dynamic stiffness, and equilibrium modulus.	Glycosaminoglycans	31-34	TIMP metallopeptidase inhibitor 1	Homo sapiens	52-56
8806771-6	1996	Characterization of mel-PG purified from the medium from control and TGF-beta 1-treated cells showed that the factor increased slightly the GAG chain length in SK-mel-1.36-1-5 but not in SK-mel-3.44 cells, without modifying the degree of sulfation.	Glycosaminoglycans	140-143	transforming growth factor beta 1	Homo sapiens	69-79
9067256-7	1996	Glycosaminoglycans such as chondroitin sulfate, dermatan sulfate and a chondroitin polysulfate, interacted with myeloblastin as non-essential activators in the presence of peptide substrates (activation up to a 6.7-fold factor) and as partial inhibitors (about 50% inhibition at saturation) in the presence of elastin.	Glycosaminoglycans	0-18	proteinase 3	Homo sapiens	112-124
9067256-7	1996	Glycosaminoglycans such as chondroitin sulfate, dermatan sulfate and a chondroitin polysulfate, interacted with myeloblastin as non-essential activators in the presence of peptide substrates (activation up to a 6.7-fold factor) and as partial inhibitors (about 50% inhibition at saturation) in the presence of elastin.	Glycosaminoglycans	0-18	elastin	Homo sapiens	310-317
9067256-8	1996	This property distinguishes myeloblastin from leukocyte elastase, which is always inhibited by glycosaminoglycans, independently of the substrate.	Glycosaminoglycans	95-113	proteinase 3	Homo sapiens	28-40
9067256-8	1996	This property distinguishes myeloblastin from leukocyte elastase, which is always inhibited by glycosaminoglycans, independently of the substrate.	Glycosaminoglycans	95-113	elastase, neutrophil expressed	Homo sapiens	46-64
8880573-4	1996	The mutation within the FGFR3 transcript was determined by direct sequencing as a specific gcg to gag transversion, resulting in an amino acid substitution ala391glu within the transmembrane region.	Glycosaminoglycans	98-101	fibroblast growth factor receptor 3	Homo sapiens	24-29
8880573-4	1996	The mutation within the FGFR3 transcript was determined by direct sequencing as a specific gcg to gag transversion, resulting in an amino acid substitution ala391glu within the transmembrane region.	Glycosaminoglycans	98-101	glucagon	Homo sapiens	91-94
8892224-5	1996	The core protein of decorin, but not the glycosaminoglycan moiety, was sufficient to induce collagenase expression on both substrates; however, the glycosaminoglycan moiety of decorin as well as the core were required for cell rounding observed in cells adhering to the 120-kDa domain of fibronectin.	Glycosaminoglycans	148-165	decorin	Oryctolagus cuniculus	176-183
8673542-9	1996	Interestingly, there was a paradoxic increase in HIV p24 gag production at low levels of inhibitor; this effect may have been the result of encapsidation of RRE-containing HIV-based retroviral vectors.	Glycosaminoglycans	57-60	transmembrane p24 trafficking protein 2	Homo sapiens	53-56
8752279-7	1996	We have now cloned Fv1: the gene appears to be derived from the gag region of an endogenous retrovirus unrelated to murine leukaemia virus, implying that the Fv1 protein and its target may share functional similarities despite the absence of nucleotide-sequence homology.	Glycosaminoglycans	64-67	Friend virus susceptibility 1	Mus musculus	19-22
8761448-1	1996	Lipoprotein lipase (LPL) has been proposed to play a role in the uptake of chylomicron remnants by hepatocytes by mediating the binding of these lipoproteins to cell-surface glycosaminoglycans and to the low-density-lipoprotein receptor-related protein (LRP).	Glycosaminoglycans	174-192	lipoprotein lipase	Mus musculus	0-18
8702651-7	1996	Glycoforms of biglycan were separated by imidazole gradient elution, under non-denaturing conditions, and comprised: a large proteoglycan form substituted with two chondroitin sulfate chains of molecular mass approximately 34 kDa (HT-1080 cells) or approximately 40 kDa (UMR106 cells); a small proteoglycan form substituted with two chondroitin sulfate chains with a median molecular mass approximately 28 kDa; and a core protein form secreted devoid of glycosaminoglycan chains.	Glycosaminoglycans	454-471	biglycan	Homo sapiens	14-22
8774180-10	1996	Total contents and extractability for GAG were inversely correlated in both controls and joints injected with IL-1 alpha.	Glycosaminoglycans	38-41	interleukin-1 alpha	Oryctolagus cuniculus	110-120
8676442-2	1996	Disruption of cyclophilin A incorporation, either by gag mutations or by cyclosporine A, inhibits virion infectivity, indicating that cyclophilin A plays an essential role in the HIV-1 life cycle.	Glycosaminoglycans	53-56	peptidylprolyl isomerase A	Pan troglodytes	14-27
8693000-9	1996	The results show that alternative splicing of agrin regulates its binding to heparin and suggest that agrin"s interaction with alpha-dystroglycan may be modulated by cell surface glycosaminoglycans in an isoform-dependent manner.	Glycosaminoglycans	179-197	agrin	Homo sapiens	46-51
8693000-9	1996	The results show that alternative splicing of agrin regulates its binding to heparin and suggest that agrin"s interaction with alpha-dystroglycan may be modulated by cell surface glycosaminoglycans in an isoform-dependent manner.	Glycosaminoglycans	179-197	agrin	Homo sapiens	102-107
8755662-2	1996	Mucopolysacchariodosis type VI (MPS VI) is the lysosomal storage disorder caused by the deficient activity of arylsulfatase B (ASB; N-acetylgalactosamine 4-sulfatase) and the subsequent accumulation of the glycosaminoglycan (GAG), dermatan sulfate.	Glycosaminoglycans	206-223	arylsulfatase B	Homo sapiens	110-125
8755662-2	1996	Mucopolysacchariodosis type VI (MPS VI) is the lysosomal storage disorder caused by the deficient activity of arylsulfatase B (ASB; N-acetylgalactosamine 4-sulfatase) and the subsequent accumulation of the glycosaminoglycan (GAG), dermatan sulfate.	Glycosaminoglycans	206-223	arylsulfatase B	Homo sapiens	127-130
8755662-2	1996	Mucopolysacchariodosis type VI (MPS VI) is the lysosomal storage disorder caused by the deficient activity of arylsulfatase B (ASB; N-acetylgalactosamine 4-sulfatase) and the subsequent accumulation of the glycosaminoglycan (GAG), dermatan sulfate.	Glycosaminoglycans	206-223	arylsulfatase B	Homo sapiens	132-165
8755662-2	1996	Mucopolysacchariodosis type VI (MPS VI) is the lysosomal storage disorder caused by the deficient activity of arylsulfatase B (ASB; N-acetylgalactosamine 4-sulfatase) and the subsequent accumulation of the glycosaminoglycan (GAG), dermatan sulfate.	Glycosaminoglycans	225-228	arylsulfatase B	Homo sapiens	110-125
8755662-2	1996	Mucopolysacchariodosis type VI (MPS VI) is the lysosomal storage disorder caused by the deficient activity of arylsulfatase B (ASB; N-acetylgalactosamine 4-sulfatase) and the subsequent accumulation of the glycosaminoglycan (GAG), dermatan sulfate.	Glycosaminoglycans	225-228	arylsulfatase B	Homo sapiens	127-130
8755662-2	1996	Mucopolysacchariodosis type VI (MPS VI) is the lysosomal storage disorder caused by the deficient activity of arylsulfatase B (ASB; N-acetylgalactosamine 4-sulfatase) and the subsequent accumulation of the glycosaminoglycan (GAG), dermatan sulfate.	Glycosaminoglycans	225-228	arylsulfatase B	Homo sapiens	132-165
8829116-3	1996	Metabolic-labeling studies revealed that AngII induced a decrease of HSPG synthesis with decreases in N-sulfation of the glycosaminoglycan side chains.	Glycosaminoglycans	121-138	angiotensinogen	Homo sapiens	41-46
8837392-7	1996	In contrast, sequences of the gag p17 gene and the regulatory genes nef and vif were homogeneous and revealed a very high homology, suggesting that the child had been infected by the mother.	Glycosaminoglycans	30-33	family with sequence similarity 72 member B	Homo sapiens	34-37
8674415-5	1996	This effect was abolished by treatment with the glycosaminoglycan-degrading enzymes heparinase and heparitinase suggesting the specific involvement of heparan sulfate proteoglycan (HSPG) in AR-mediated cell proliferation.	Glycosaminoglycans	48-65	syndecan 2	Mus musculus	151-179
8661411-3	1996	When cells expressing Env proteins in the absence of Gag were examined by immunoelectron microscopy, clusters of Env protein and membrane vesicles containing Env proteins were observed at cell surfaces.	Glycosaminoglycans	53-56	endogenous retrovirus group K member 20	Homo sapiens	22-25
8662979-10	1996	Analysis of a form of syndecan-1 that lacked glycosaminoglycan acceptor sites revealed that covalently attached glycosaminoglycans were not required for cell surface expression, microfilament association, or detergent insolubility.	Glycosaminoglycans	112-130	syndecan 1	Homo sapiens	22-32
8663298-8	1996	Examination of several well characterized glycosaminoglycans to inhibit the binding of heparin to both heparin-binding IGFBP-3 peptides revealed that the most potent inhibitors were heparin, heparan sulfate, and dermatan sulfate; chondroitin sulfate A and hyaluronic acid were intermediate in their inhibitory activities; and chondroitin sulfate C caused no inhibition.	Glycosaminoglycans	42-60	insulin like growth factor binding protein 3	Homo sapiens	119-126
8674529-2	1996	Considering 3H incorporation, we found that IFNgamma increased the production of glycosaminoglycan synthesis, including hyaluronic acid, heparan and chondroitin/dermatan sulfate.	Glycosaminoglycans	81-98	interferon gamma	Homo sapiens	44-52
8725286-5	1996	Inhibition of sulfation of cell surface glycosaminoglycans by treatment with sodium chlorate significantly reduced both the formation of the fibronectin matrix and cell proliferation in response to FGF-2, suggesting an involvement of the low-affinity sulfated glycosaminoglycan FGF receptor system.	Glycosaminoglycans	40-58	fibronectin 1	Gallus gallus	141-152
8725286-5	1996	Inhibition of sulfation of cell surface glycosaminoglycans by treatment with sodium chlorate significantly reduced both the formation of the fibronectin matrix and cell proliferation in response to FGF-2, suggesting an involvement of the low-affinity sulfated glycosaminoglycan FGF receptor system.	Glycosaminoglycans	40-58	fibroblast growth factor 2	Gallus gallus	198-203
8674415-5	1996	This effect was abolished by treatment with the glycosaminoglycan-degrading enzymes heparinase and heparitinase suggesting the specific involvement of heparan sulfate proteoglycan (HSPG) in AR-mediated cell proliferation.	Glycosaminoglycans	48-65	syndecan 2	Mus musculus	181-185
8674415-5	1996	This effect was abolished by treatment with the glycosaminoglycan-degrading enzymes heparinase and heparitinase suggesting the specific involvement of heparan sulfate proteoglycan (HSPG) in AR-mediated cell proliferation.	Glycosaminoglycans	48-65	amphiregulin	Mus musculus	190-192
8648695-2	1996	The 11.2-kb provirus displays a complex expression pattern capable of encoding accessory proteins and is unique in the predicted location of the env initiation codon and signal peptide upstream of gag and the common splice donor site.	Glycosaminoglycans	197-200	endogenous retrovirus group K member 20	Homo sapiens	145-148
8844456-2	1996	A possibility of the pathogenesis of pretibial myxedema is that T cells, reacting with thyrotropin (TSH) receptor, will be targeting to the pretibial fibroblasts where, in the presence of antigen (TSH receptor), they will secrete various cytokines and stimulate fibroblasts to secrete glycosaminoglycans.	Glycosaminoglycans	285-303	thyroid stimulating hormone receptor	Homo sapiens	64-113
8844456-2	1996	A possibility of the pathogenesis of pretibial myxedema is that T cells, reacting with thyrotropin (TSH) receptor, will be targeting to the pretibial fibroblasts where, in the presence of antigen (TSH receptor), they will secrete various cytokines and stimulate fibroblasts to secrete glycosaminoglycans.	Glycosaminoglycans	285-303	thyroid stimulating hormone receptor	Homo sapiens	197-209
8690451-4	1996	In contrast to previous studies, HRG binding was largely inhibited by 50 micrograms/ml heparin, both in the absence and in the presence of zinc, suggesting that HRG interacts primarily through glycosaminoglycans on the T-cell surface.	Glycosaminoglycans	193-211	histidine rich glycoprotein	Homo sapiens	33-36
8690451-4	1996	In contrast to previous studies, HRG binding was largely inhibited by 50 micrograms/ml heparin, both in the absence and in the presence of zinc, suggesting that HRG interacts primarily through glycosaminoglycans on the T-cell surface.	Glycosaminoglycans	193-211	histidine rich glycoprotein	Homo sapiens	161-164
8731217-7	1996	Adding fibroblast growth factor and insulin tripled the rate of cell turnover and doubled the glycosaminoglycan content of seeded implants, but had no effect on their material properties.	Glycosaminoglycans	94-111	insulin	Homo sapiens	36-43
8892045-1	1996	The Accell gene delivery system (gene gun) was used to deliver gold particles coated with HIV-1LAI and SIVmac239 expression constructs into the epidermis of rhesus macaques, resulting in the elicitation of env- and gag-specific humoral responses.	Glycosaminoglycans	215-218	endogenous retrovirus group V member 2 Env polyprotein	Macaca mulatta	206-209
8648699-1	1996	The major 5" splice site of equine infectious anemia virus (EIAV) conforms to the consensus 5" splice site in eight consecutive positions and is located immediately upstream of the gag AUG. Our results show that the presence of this 5" splice site on the EIAV gag mRNA decreases Gag production 30- to 60-fold.	Glycosaminoglycans	181-184	gag protein	Equine infectious anemia virus	279-282
8648699-1	1996	The major 5" splice site of equine infectious anemia virus (EIAV) conforms to the consensus 5" splice site in eight consecutive positions and is located immediately upstream of the gag AUG. Our results show that the presence of this 5" splice site on the EIAV gag mRNA decreases Gag production 30- to 60-fold.	Glycosaminoglycans	260-263	gag protein	Equine infectious anemia virus	279-282
8659115-1	1996	Vpr is one of the auxiliary proteins of HIV-1 and is selectively incorporated into the virion by a process involving the C-terminal p6 portion of the Gag precursor Pr55.	Glycosaminoglycans	150-153	Vpr	Human immunodeficiency virus 1	0-3
8645178-5	1996	CsCl-density-gradient centrifugation after mild treatment of liposome-intercalated 32P-labelled syndecan-2 with trypsin resulted in clear separation of the radioactivity into a bottom fraction containing all the glycosaminoglycans (accounting for 40% of the total radioactivity) and a top fraction containing liposome-associated peptides (60%).	Glycosaminoglycans	212-230	syndecan 2	Mus musculus	96-106
8662679-4	1996	The rate constants of the inactivation of FXIa by C1 inhibitor and by antithrombin III increased up to 117-fold in the presence of glycosaminoglycans.	Glycosaminoglycans	131-149	serpin family C member 1	Homo sapiens	70-86
8662679-8	1996	Thus, physiological glycosaminoglycans selectively enhance inhibition of FXIa without affecting the activity of FXIIa and kallikrein, suggesting that glycosaminoglycans may modulate the biological effects of contact activation, by inhibiting intrinsic coagulation without affecting the fibrinolytic potential of FXIIa/kallikrein.	Glycosaminoglycans	20-38	kallikrein related peptidase 4	Homo sapiens	318-328
8662679-8	1996	Thus, physiological glycosaminoglycans selectively enhance inhibition of FXIa without affecting the activity of FXIIa and kallikrein, suggesting that glycosaminoglycans may modulate the biological effects of contact activation, by inhibiting intrinsic coagulation without affecting the fibrinolytic potential of FXIIa/kallikrein.	Glycosaminoglycans	150-168	kallikrein related peptidase 4	Homo sapiens	318-328
8791281-0	1996	Exogenous glycosaminoglycans (GAG) differentially modulate GAG synthesis by anchorage-independent cultures of the outer cells from neonatal rat calvaria in the absence and presence of TGF-beta.	Glycosaminoglycans	10-28	transforming growth factor, beta 1	Rattus norvegicus	184-192
8791281-0	1996	Exogenous glycosaminoglycans (GAG) differentially modulate GAG synthesis by anchorage-independent cultures of the outer cells from neonatal rat calvaria in the absence and presence of TGF-beta.	Glycosaminoglycans	30-33	transforming growth factor, beta 1	Rattus norvegicus	184-192
8791281-2	1996	Utilizing the same cell population, we have further examined the possibility that glycosaminoglycans (GAG) known to be synthesized and secreted by bone cells might exert feedback effects on GAG synthesis and/or its stimulation by TGF-beta.	Glycosaminoglycans	82-100	transforming growth factor, beta 1	Rattus norvegicus	230-238
8791281-2	1996	Utilizing the same cell population, we have further examined the possibility that glycosaminoglycans (GAG) known to be synthesized and secreted by bone cells might exert feedback effects on GAG synthesis and/or its stimulation by TGF-beta.	Glycosaminoglycans	102-105	transforming growth factor, beta 1	Rattus norvegicus	230-238
8791281-3	1996	Although addition of TGF-beta alone stimulated net synthesis of HA and CS in both AD and anchorage-independent (AI) cultures, significant alterations of basal and TGF-beta-stimulated GAG synthesis by exogenous GAGs were observed only in AI cultures.	Glycosaminoglycans	183-186	transforming growth factor, beta 1	Rattus norvegicus	163-171
8791281-7	1996	Overall, our results indicate specific effects of individual GAGs on basal and TGF-beta-stimulated GAG synthesis in OCP cultures.	Glycosaminoglycans	61-64	transforming growth factor, beta 1	Rattus norvegicus	79-87
8791281-8	1996	We suggest that some of the GAGs in the OCP microenvironment (which with the exception of HA are covalently linked to protein cores of secreted PGs), acting in concert with TGF-beta, may serve as an amplification system for upregulating GAG synthesis in the rapidly growing neonatal calvarium.	Glycosaminoglycans	28-31	transforming growth factor, beta 1	Rattus norvegicus	173-181
8868518-7	1996	One hundred eighty minutes after initiation of dialysis, by which time all patients were receiving heparin there was a further increase in TFPI (to more than 200% of baseline), due to the presence of the glycosaminoglycan.	Glycosaminoglycans	204-221	tissue factor pathway inhibitor	Homo sapiens	139-143
8697103-0	1996	Electrostatic interactions of the butyrylcholinesterase dimer of mucosal cells of rat intestine with glycosaminoglycans.	Glycosaminoglycans	101-119	butyrylcholinesterase	Rattus norvegicus	34-55
8636243-21	1996	Based on these studies, we propose that the normal agonist activity of NK1 and NK2 in mink lung cells is due to an activating interaction with an endogenous glycosaminoglycan.	Glycosaminoglycans	157-174	hepatocyte growth factor	Mus musculus	71-74
8636243-23	1996	Moreover, a preparation of glycosaminoglycans from the surface of mink lung cells induced dimerization of NK1.	Glycosaminoglycans	27-45	hepatocyte growth factor	Mus musculus	106-109
8636243-24	1996	These data show that the activity of NK1 and NK2 can be modulated by heparin and other related glycosaminoglycans to induce proliferation in cells expressing c-Met.	Glycosaminoglycans	95-113	hepatocyte growth factor	Mus musculus	37-40
8636243-24	1996	These data show that the activity of NK1 and NK2 can be modulated by heparin and other related glycosaminoglycans to induce proliferation in cells expressing c-Met.	Glycosaminoglycans	95-113	met proto-oncogene	Mus musculus	158-163
8633029-1	1996	In the foamy virus (FV) subgroup of retroviruses the pol genes are located in the +1 reading frame relative to the gag genes and possess potential ATG initiation codons in their 5" regions.	Glycosaminoglycans	115-118	endogenous retrovirus group W member 4	Homo sapiens	53-56
8613703-10	1996	Chondroitin sulfate-Sepharose was shown to be equally efficient in retaining PF4 from platelet extracts as serglycin-Sepharose indicating that the glycosaminoglycan chains mediate the binding to PF4 in the intact proteoglycan molecule.	Glycosaminoglycans	147-164	platelet factor 4	Homo sapiens	195-198
8613703-12	1996	Affinity measurements using fluoresceinamine-labeled glycosaminoglycans showed that the affinity of heparin for PF4 is on the order of 30 nM, whereas chondroitin sulfate has an affinity of 260 nM.	Glycosaminoglycans	53-71	platelet factor 4	Homo sapiens	112-115
8642655-2	1996	Ligation of 441 nucleotides (nt) containing a splice acceptor (SA) site to the downstream portion of the remaining gag region restored the level of the unspliced message, simultaneously activating a cryptic splice donor (SD) site in the middle of the p30 coding region (between nt 1596 and 1597).	Glycosaminoglycans	115-118	centromere protein V	Homo sapiens	251-254
8796266-6	1996	PCI also binds to GAGs present on the surface of epithelial kidney cells, and GAGs isolated from these cells have a similar effect on PCI activity as heparin.	Glycosaminoglycans	18-22	serpin family A member 5	Homo sapiens	0-3
8796266-6	1996	PCI also binds to GAGs present on the surface of epithelial kidney cells, and GAGs isolated from these cells have a similar effect on PCI activity as heparin.	Glycosaminoglycans	78-82	serpin family A member 5	Homo sapiens	134-137
8708549-12	1996	The results indicate that T3 as well as IGF-I are important modulators of sulfated glycosaminoglycan synthesis in rainbow trout cartilage.	Glycosaminoglycans	83-100	insulin-like growth factor I	Oncorhynchus mykiss	40-45
9172805-1	1996	The CD44 cell surface molecule has been shown to be the principal cell surface receptor for hyaluronan (or hyaluronic acid), a glycosaminoglycan component of marrow extracellular matrix.	Glycosaminoglycans	127-144	CD44 molecule (Indian blood group)	Homo sapiens	4-8
8621620-9	1996	The influence of glycosaminoglycan substitution on CD44 function was specific to keratan sulfate substitution; treatment to remove chondroitin sulfate, heparan sulfate, or hyaluronate did not affect CD44-mediated cell adhesion to hyaluronate.	Glycosaminoglycans	17-34	CD44 molecule (Indian blood group)	Homo sapiens	51-55
8712524-0	1996	Regulation of glycosaminoglycan metabolism by bone morphogenetic protein-2 in equine cartilage explant cultures.	Glycosaminoglycans	14-31	bone morphogenetic protein 2	Equus caballus	46-74
8712524-1	1996	OBJECTIVE: To investigate whether recombinant human bone morphogenetic protein-2 (rhBMP-2) regulates glycosaminoglycan (GAG) synthesis and release from equine articular cartilage explant cultures.	Glycosaminoglycans	101-118	bone morphogenetic protein 2	Homo sapiens	52-80
8712524-1	1996	OBJECTIVE: To investigate whether recombinant human bone morphogenetic protein-2 (rhBMP-2) regulates glycosaminoglycan (GAG) synthesis and release from equine articular cartilage explant cultures.	Glycosaminoglycans	120-123	bone morphogenetic protein 2	Homo sapiens	52-80
8627263-0	1996	Gag-Gag interactions in the C-terminal domain of human immunodeficiency virus type 1 p24 capsid antigen are essential for Gag particle assembly.	Glycosaminoglycans	0-3	transmembrane p24 trafficking protein 2	Homo sapiens	85-88
8627263-0	1996	Gag-Gag interactions in the C-terminal domain of human immunodeficiency virus type 1 p24 capsid antigen are essential for Gag particle assembly.	Glycosaminoglycans	4-7	transmembrane p24 trafficking protein 2	Homo sapiens	85-88
8627263-0	1996	Gag-Gag interactions in the C-terminal domain of human immunodeficiency virus type 1 p24 capsid antigen are essential for Gag particle assembly.	Glycosaminoglycans	4-7	transmembrane p24 trafficking protein 2	Homo sapiens	85-88
8627263-1	1996	Seven internal deletions within the p24 domain of the human immunodeficiency virus type 1 Gag precursor have been assessed for their effect on Gag particle formation following their expression using recombinant baculoviruses.	Glycosaminoglycans	90-93	transmembrane p24 trafficking protein 2	Homo sapiens	36-39
8627263-1	1996	Seven internal deletions within the p24 domain of the human immunodeficiency virus type 1 Gag precursor have been assessed for their effect on Gag particle formation following their expression using recombinant baculoviruses.	Glycosaminoglycans	143-146	transmembrane p24 trafficking protein 2	Homo sapiens	36-39
8642635-9	1996	Binding of PrV to this HSPG in the VOPBA was also dependent on the presence of heparan sulfate, since reactivity was abolished after suppression of glycosaminoglycan biosynthesis with NaClO3 and after heparinase treatment.	Glycosaminoglycans	148-165	syndecan 2	Homo sapiens	23-27
8754146-1	1996	In chronic hepatitis induced by long-term CCl4 administration to rats, there was largely an increase in the formation of malonic dialdehyde and Schiff bases, an elevation of glycosaminoglycans and hydroxyproline in collagen fractions, and proliferation of hepatic fibrous tissue.	Glycosaminoglycans	174-192	C-C motif chemokine ligand 4	Rattus norvegicus	42-46
8636247-0	1996	Interleukin-1 (IL-1) receptor antagonist and soluble IL-1 receptor inhibit IL-1-induced glycosaminoglycan production in cultured human orbital fibroblasts from patients with Graves" ophthalmopathy.	Glycosaminoglycans	88-105	interleukin 1 alpha	Homo sapiens	0-13
8649794-7	1996	In vivo and in situ phosphorylation, phosphoamino acid analysis, immunoprecipitation, 2-dimensional isoelectric focusing/SDS PAGE and immunoblot analysis showed that one of the prominent substrates is p58(gag), a retroviral Gag-like cytoplasmic STP component implicated in stabilizing microfilament-membrane interactions.	Glycosaminoglycans	205-208	protein disulfide isomerase family A, member 3	Rattus norvegicus	201-204
8649794-7	1996	In vivo and in situ phosphorylation, phosphoamino acid analysis, immunoprecipitation, 2-dimensional isoelectric focusing/SDS PAGE and immunoblot analysis showed that one of the prominent substrates is p58(gag), a retroviral Gag-like cytoplasmic STP component implicated in stabilizing microfilament-membrane interactions.	Glycosaminoglycans	224-227	protein disulfide isomerase family A, member 3	Rattus norvegicus	201-204
8649794-9	1996	These results provide further evidence for the constitutive activation of this aggressive mammary tumor and suggest a rote for phosphorylation of p58(gag) in organization of the STP at the membrane-microfilament interface in these cells.	Glycosaminoglycans	150-153	protein disulfide isomerase family A, member 3	Rattus norvegicus	146-149
8660278-1	1996	The small dermatan sulphate protein decorin interacts via its core protein with fibrillar collagens, and its glycosaminoglycan chains were proposed to be capable of self-association.	Glycosaminoglycans	109-126	decorin	Homo sapiens	36-43
8660278-7	1996	A shift in the elution position of [35S]sulphate-labelled decorin-derived glycosaminoglycans by unlabelled decorin could be observed only when the chains were prepared by trypsin.	Glycosaminoglycans	74-92	decorin	Homo sapiens	58-65
8660278-7	1996	A shift in the elution position of [35S]sulphate-labelled decorin-derived glycosaminoglycans by unlabelled decorin could be observed only when the chains were prepared by trypsin.	Glycosaminoglycans	74-92	decorin	Homo sapiens	107-114
8652906-7	1996	The sulphated glycosaminoglycans which were critical in FGF-2-induced proliferation were strictly HSPG, as an addition of heparin in cell culture medium can restore FGF-2 mitogenic activity.	Glycosaminoglycans	14-32	fibroblast growth factor 2	Homo sapiens	56-61
8652906-7	1996	The sulphated glycosaminoglycans which were critical in FGF-2-induced proliferation were strictly HSPG, as an addition of heparin in cell culture medium can restore FGF-2 mitogenic activity.	Glycosaminoglycans	14-32	syndecan 2	Homo sapiens	98-102
8652906-7	1996	The sulphated glycosaminoglycans which were critical in FGF-2-induced proliferation were strictly HSPG, as an addition of heparin in cell culture medium can restore FGF-2 mitogenic activity.	Glycosaminoglycans	14-32	fibroblast growth factor 2	Homo sapiens	165-170
8617726-6	1996	Consistent with these data, a v-Abl mutant encoding only the Gag and SH2 regions was able to bind Shc in vivo.	Glycosaminoglycans	61-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
8617726-6	1996	Consistent with these data, a v-Abl mutant encoding only the Gag and SH2 regions was able to bind Shc in vivo.	Glycosaminoglycans	61-64	SHC adaptor protein 1	Homo sapiens	98-101
8603018-0	1996	Thrombin-mediated activation of endogenous factor XI in plasma in the presence of physiological glycosaminoglycans occurs only with high concentrations of thrombin.	Glycosaminoglycans	96-114	coagulation factor II, thrombin	Homo sapiens	0-8
8603018-0	1996	Thrombin-mediated activation of endogenous factor XI in plasma in the presence of physiological glycosaminoglycans occurs only with high concentrations of thrombin.	Glycosaminoglycans	96-114	coagulation factor XI	Homo sapiens	43-52
8603018-6	1996	We conclude that endogenous FXI in plasma can be activated by thrombin in the presence of various glycosaminoglycans, including the physiological compounds heparan sulphate and dermatan sulphate, but only at very high concentrations of thrombin, corresponding to 100% prothrombin activation in undiluted plasma.	Glycosaminoglycans	98-116	coagulation factor XI	Homo sapiens	28-31
8603018-6	1996	We conclude that endogenous FXI in plasma can be activated by thrombin in the presence of various glycosaminoglycans, including the physiological compounds heparan sulphate and dermatan sulphate, but only at very high concentrations of thrombin, corresponding to 100% prothrombin activation in undiluted plasma.	Glycosaminoglycans	98-116	coagulation factor II, thrombin	Homo sapiens	62-70
8636247-0	1996	Interleukin-1 (IL-1) receptor antagonist and soluble IL-1 receptor inhibit IL-1-induced glycosaminoglycan production in cultured human orbital fibroblasts from patients with Graves" ophthalmopathy.	Glycosaminoglycans	88-105	interleukin 1 alpha	Homo sapiens	15-19
8636247-0	1996	Interleukin-1 (IL-1) receptor antagonist and soluble IL-1 receptor inhibit IL-1-induced glycosaminoglycan production in cultured human orbital fibroblasts from patients with Graves" ophthalmopathy.	Glycosaminoglycans	88-105	interleukin 1 alpha	Homo sapiens	53-57
8636247-0	1996	Interleukin-1 (IL-1) receptor antagonist and soluble IL-1 receptor inhibit IL-1-induced glycosaminoglycan production in cultured human orbital fibroblasts from patients with Graves" ophthalmopathy.	Glycosaminoglycans	88-105	interleukin 1 alpha	Homo sapiens	53-57
8636247-2	1996	Interleukin-1 (IL-1), produced by macrophages and fibroblasts within the diseased orbit, stimulates GAG synthesis by orbital fibroblasts.	Glycosaminoglycans	100-103	interleukin 1 alpha	Homo sapiens	0-13
8601723-1	1996	Whether the chemokines macrophage inflammatory protein-1 beta (MIP-1 beta) and regulated on activation normal T expressed and secreted (RANTES), which interact specifically with glycosaminoglycans and thus mediate the recruitment, attachment, and migration of leukocytes to vascular endothelia and extracellular matrix, are also involved in interactions between CD4+ murine T lymphocytes and keratinocytes was examined.	Glycosaminoglycans	178-196	chemokine (C-C motif) ligand 4	Mus musculus	23-61
8601723-1	1996	Whether the chemokines macrophage inflammatory protein-1 beta (MIP-1 beta) and regulated on activation normal T expressed and secreted (RANTES), which interact specifically with glycosaminoglycans and thus mediate the recruitment, attachment, and migration of leukocytes to vascular endothelia and extracellular matrix, are also involved in interactions between CD4+ murine T lymphocytes and keratinocytes was examined.	Glycosaminoglycans	178-196	chemokine (C-C motif) ligand 4	Mus musculus	63-73
8601723-1	1996	Whether the chemokines macrophage inflammatory protein-1 beta (MIP-1 beta) and regulated on activation normal T expressed and secreted (RANTES), which interact specifically with glycosaminoglycans and thus mediate the recruitment, attachment, and migration of leukocytes to vascular endothelia and extracellular matrix, are also involved in interactions between CD4+ murine T lymphocytes and keratinocytes was examined.	Glycosaminoglycans	178-196	chemokine (C-C motif) ligand 5	Mus musculus	136-142
8601723-1	1996	Whether the chemokines macrophage inflammatory protein-1 beta (MIP-1 beta) and regulated on activation normal T expressed and secreted (RANTES), which interact specifically with glycosaminoglycans and thus mediate the recruitment, attachment, and migration of leukocytes to vascular endothelia and extracellular matrix, are also involved in interactions between CD4+ murine T lymphocytes and keratinocytes was examined.	Glycosaminoglycans	178-196	CD4 antigen	Mus musculus	362-365
8636247-2	1996	Interleukin-1 (IL-1), produced by macrophages and fibroblasts within the diseased orbit, stimulates GAG synthesis by orbital fibroblasts.	Glycosaminoglycans	100-103	interleukin 1 alpha	Homo sapiens	15-19
8636247-6	1996	The addition of IL-1 alone stimulated GAG synthesis by 73-176% (mean, 104%; P &lt; 0.05).	Glycosaminoglycans	38-41	interleukin 1 alpha	Homo sapiens	16-20
8636247-7	1996	Significant inhibition of IL-1-stimulated GAG synthesis was observed after treatment of normal fibroblasts with IL-1ra at a concentration of 5 ng/mL (12.5-fold molar excess; mean, 33%; P &lt; 0.05); essentially complete inhibition was achieved at 40 ng/mL (100-fold molar excess; mean, 86%; P &lt; 0.05).	Glycosaminoglycans	42-45	interleukin 1 alpha	Homo sapiens	26-30
8636247-7	1996	Significant inhibition of IL-1-stimulated GAG synthesis was observed after treatment of normal fibroblasts with IL-1ra at a concentration of 5 ng/mL (12.5-fold molar excess; mean, 33%; P &lt; 0.05); essentially complete inhibition was achieved at 40 ng/mL (100-fold molar excess; mean, 86%; P &lt; 0.05).	Glycosaminoglycans	42-45	interleukin 1 receptor antagonist	Homo sapiens	112-118
8636247-9	1996	IL-1ra and sIL-1R are potent inhibitors of IL-1-induced GAG production by cultured human orbital fibroblasts.	Glycosaminoglycans	56-59	interleukin 1 receptor antagonist	Homo sapiens	0-6
8636247-9	1996	IL-1ra and sIL-1R are potent inhibitors of IL-1-induced GAG production by cultured human orbital fibroblasts.	Glycosaminoglycans	56-59	interleukin 1 alpha	Homo sapiens	0-4
8567685-4	1996	The inhibitory activity was abolished by treating N-syndecan with heparitinase, but it was retained in N-syndecan-derived free glycosaminoglycan chains, suggesting that N-syndecan heparan sulfate at the cell surface is involved in HB-GAM-induced neurite outgrowth.	Glycosaminoglycans	127-144	syndecan 3	Rattus norvegicus	103-113
8567685-4	1996	The inhibitory activity was abolished by treating N-syndecan with heparitinase, but it was retained in N-syndecan-derived free glycosaminoglycan chains, suggesting that N-syndecan heparan sulfate at the cell surface is involved in HB-GAM-induced neurite outgrowth.	Glycosaminoglycans	127-144	syndecan 3	Rattus norvegicus	103-113
8717410-10	1996	We conclude that the decrease of GAG content in the skin of diabetic rats is a result of three co-existing phenomena: decreased circulating IGF-I level, increased plasma content of LMW-BPs and increased proteolytic activity of the skin.	Glycosaminoglycans	33-36	insulin-like growth factor 1	Rattus norvegicus	140-145
8717410-6	1996	We sought to determine whether the insulin-like growth factor-I (IGF-I) and IGF-binding proteins (IGF-BPs) levels are altered in animals with experimental diabetes and might contribute to the decrease in tissue GAG content.	Glycosaminoglycans	211-214	insulin-like growth factor 1	Rattus norvegicus	35-63
8717410-6	1996	We sought to determine whether the insulin-like growth factor-I (IGF-I) and IGF-binding proteins (IGF-BPs) levels are altered in animals with experimental diabetes and might contribute to the decrease in tissue GAG content.	Glycosaminoglycans	211-214	insulin-like growth factor 1	Rattus norvegicus	65-70
9150880-9	1996	Activated TRAP binds to repeated GAG sequences in the leader segment of the trp operon transcript, disrupting an RNA antiterminator and promoting formation of a terminator.	Glycosaminoglycans	33-36	conjugal transfer protein TraP	Escherichia coli	10-14
8573160-3	1996	To identify the Gag sequences directly involved in Vpr binding, we compared the Vpr binding affinities of the 71 amino acid nucleocapsid protein p7, the C-terminal peptide (35-71) p7C and p6gag by affinity chromatography.	Glycosaminoglycans	16-19	Vpr	Human immunodeficiency virus 1	51-54
8922041-5	1996	This decrease was accompanied by significant depletion of insulin-like growth factor-I (IGF-I), known as a stimulator of GAG biosynthesis, and a distinct decrease in the content of high molecular weight IGF-binding proteins (HMW-BPs) with a simultaneous increase in low molecular weight IGF-binding proteins (LMW-BPs) in the sera of diabetic animals.	Glycosaminoglycans	121-124	insulin-like growth factor 1	Rattus norvegicus	58-86
8922041-5	1996	This decrease was accompanied by significant depletion of insulin-like growth factor-I (IGF-I), known as a stimulator of GAG biosynthesis, and a distinct decrease in the content of high molecular weight IGF-binding proteins (HMW-BPs) with a simultaneous increase in low molecular weight IGF-binding proteins (LMW-BPs) in the sera of diabetic animals.	Glycosaminoglycans	121-124	insulin-like growth factor 1	Rattus norvegicus	88-93
8554071-9	1996	Notably, a new IDUA mutation A300T was also identified in the proband, his sister, and his mother, accounting for reduced IDUA activity in these individuals; the asymptomatic sister, whose cells demonstrated normal glycosaminoglycan metabolism, is thus a compound heterozygote for W402X and the new allele.	Glycosaminoglycans	215-232	alpha-L-iduronidase	Homo sapiens	15-19
9150880-10	1996	Activated TRAP also regulates translation of trpG in the folate operon by binding to repeat GAG sequences surrounding the trpG ribosome binding site.	Glycosaminoglycans	92-95	conjugal transfer protein TraP	Escherichia coli	10-14
8550552-1	1996	The tyrosines in the cytoplasmic domain of an oncogenic human insulin-like growth factor I receptor (gag-IGFR) were systematically mutated to phenylalanines to investigate the role of those tyrosines in the enzymatic and biological function of the gag-IGFR.	Glycosaminoglycans	101-104	insulin like growth factor 1 receptor	Homo sapiens	105-109
8550552-8	1996	The transforming potential of the gag-IGFR correlates well with its ability to phosphorylate overall cellular substrates and to activate phosphatidylinositol 3-kinase via insulin receptor substrate 1.	Glycosaminoglycans	34-37	insulin like growth factor 1 receptor	Homo sapiens	38-42
8550552-8	1996	The transforming potential of the gag-IGFR correlates well with its ability to phosphorylate overall cellular substrates and to activate phosphatidylinositol 3-kinase via insulin receptor substrate 1.	Glycosaminoglycans	34-37	insulin receptor substrate 1	Homo sapiens	171-199
9074719-6	1996	By in vitro and ex vivo experiments in mice, heparin and other glycosaminoglycans were shown to stimulate megakaryocytopoiesis by acting synergistically with thrombopoietin and interleukin 6, and in the other hand by neutralizing inhibitors of megakaryocytopoiesis such as platelet factor 4 and transforming growth factor beta.	Glycosaminoglycans	63-81	thrombopoietin	Mus musculus	158-172
9074719-6	1996	By in vitro and ex vivo experiments in mice, heparin and other glycosaminoglycans were shown to stimulate megakaryocytopoiesis by acting synergistically with thrombopoietin and interleukin 6, and in the other hand by neutralizing inhibitors of megakaryocytopoiesis such as platelet factor 4 and transforming growth factor beta.	Glycosaminoglycans	63-81	interleukin 6	Mus musculus	177-190
9112638-1	1996	Heparin cofactor II (HC II) is a plasma glycoprotein which inhibits thrombin but not factor Xa and which requires heparin or other glycosaminoglycans for its activation.	Glycosaminoglycans	131-149	serpin family D member 1	Homo sapiens	0-19
8832951-4	1996	RESULTS: IL-1 beta failed to stimulate glycosaminoglycan synthesis in REM fibroblasts whereas it stimulated glycosaminoglycan synthesis up to 6-fold in control fibroblasts.	Glycosaminoglycans	108-125	interleukin 1 beta	Homo sapiens	9-18
8664897-1	1996	alpha-L-Iduronidase (IDUA) deficiency (mucopolysaccharidosis type I; MPS-I) is an inborn error of lysosomal degradation of glycosaminoglycans that results in storage of undegraded glycosaminoglycans in lysosomes.	Glycosaminoglycans	123-141	alpha-L-iduronidase	Homo sapiens	0-19
8664897-1	1996	alpha-L-Iduronidase (IDUA) deficiency (mucopolysaccharidosis type I; MPS-I) is an inborn error of lysosomal degradation of glycosaminoglycans that results in storage of undegraded glycosaminoglycans in lysosomes.	Glycosaminoglycans	123-141	alpha-L-iduronidase	Homo sapiens	21-25
9112638-1	1996	Heparin cofactor II (HC II) is a plasma glycoprotein which inhibits thrombin but not factor Xa and which requires heparin or other glycosaminoglycans for its activation.	Glycosaminoglycans	131-149	serpin family D member 1	Homo sapiens	21-26
8807725-4	1996	The generation of thrombin seems to be a pivotal event in thrombogenesis, and inactivation of this enzyme has been attempted for many years with heparin, low-molecular-weight heparin, and other glycosaminoglycans.	Glycosaminoglycans	194-212	coagulation factor II, thrombin	Homo sapiens	18-26
8522611-6	1995	Recombinant agrin is a heparan sulfate proteoglycan (HSPG) of more than 400 kD with glycosaminoglycan side chains attached only to the NH2-terminal half.	Glycosaminoglycans	84-101	agrin	Gallus gallus	12-17
8553538-9	1995	Western blot analysis of extracts prepared from IFN-treated HIV-1-infected cells revealed a decreased accumulation of most HIV-1-specific glycoproteins and proteins with the exception of the pr55 gag precursor.	Glycosaminoglycans	196-199	interferon alpha 1	Homo sapiens	48-51
7499838-10	1995	The glycosaminoglycan chain of the growth factor was not only shown to inhibit CSF-1 activity but also to increase the stability of the core protein when the CSF-1-producing osteosarcoma cells were maintained in a collagen lattice.	Glycosaminoglycans	4-21	colony stimulating factor 1	Homo sapiens	79-84
7499838-10	1995	The glycosaminoglycan chain of the growth factor was not only shown to inhibit CSF-1 activity but also to increase the stability of the core protein when the CSF-1-producing osteosarcoma cells were maintained in a collagen lattice.	Glycosaminoglycans	4-21	colony stimulating factor 1	Homo sapiens	158-163
8543022-2	1995	The pol ORF2 of this mobile genetic element was demonstrated to code for an active Reverse Transcriptase (RT) and the ORF1 is expected to code for the structural Gag proteins of the virus-like particles (VLP).	Glycosaminoglycans	162-165	tarsal-less 2A	Drosophila melanogaster	8-12
8543022-2	1995	The pol ORF2 of this mobile genetic element was demonstrated to code for an active Reverse Transcriptase (RT) and the ORF1 is expected to code for the structural Gag proteins of the virus-like particles (VLP).	Glycosaminoglycans	162-165	uncharacterized protein	Drosophila melanogaster	118-122
7490363-1	1995	BACKGROUND: Sunscreen application to the skin of hairless mice is effective in reversing the histologic changes associated with photoaging (solar elastosis, epidermal thickening, collagen depletion, glycosaminoglycan deposition).	Glycosaminoglycans	199-216	lysine demethylase and nuclear receptor corepressor	Mus musculus	49-57
7503744-2	1995	All glycosaminoglycans and dextran derivatives including dextran T-500 and DEAE dextran examined in this study accelerated the conversion of procathepsin L to processed cathepsin L in vitro with different time courses.	Glycosaminoglycans	4-22	cathepsin L	Homo sapiens	144-155
7494002-3	1995	Heparan sulfate (HS)-conjugated gel also bound HGF, and the binding was competitively inhibited by heparin and bovine liver HS, but not by Engelbreth-Holm-Swarm sarcoma HS, pig aorta HS, or other glycosaminoglycans, suggesting the specific structural domain in HS for the binding of HGF.	Glycosaminoglycans	196-214	hepatocyte growth factor	Bos taurus	47-50
8524879-5	1995	However, a functional Rev/RRE interaction increases the amount of Gag present intracellularly and, more strikingly, results in the release of mature ALV particles into the supernatant.	Glycosaminoglycans	66-69	Rev	Human immunodeficiency virus 1	22-25
8746633-9	1995	In the presence of glycosaminoglycans, the maximal thrombin inhibition rate (k2 x 10(-3) M-1 min-1) for rHCII was 10.4 +/- 2.5 at 100 micrograms/ml heparin and 16.0 +/- 4.3 at 1000 micrograms/ml dermatan sulfate compared to 9.0 +/- 0.7 at 200 micrograms/ml heparin and 18.5 +/- 5.3 at 1000 micrograms/ml dermatan sulfate for pHCII.	Glycosaminoglycans	19-37	serpin family D member 1	Rattus norvegicus	104-109
8746633-9	1995	In the presence of glycosaminoglycans, the maximal thrombin inhibition rate (k2 x 10(-3) M-1 min-1) for rHCII was 10.4 +/- 2.5 at 100 micrograms/ml heparin and 16.0 +/- 4.3 at 1000 micrograms/ml dermatan sulfate compared to 9.0 +/- 0.7 at 200 micrograms/ml heparin and 18.5 +/- 5.3 at 1000 micrograms/ml dermatan sulfate for pHCII.	Glycosaminoglycans	19-37	coagulation factor II, thrombin	Homo sapiens	51-59
8594987-10	1995	Results from this assay are in agreement with previous data from our laboratory and reports from other researchers with respect to the specificity of glycosaminoglycan binding to bFGF and the role of 2,3-O- and 6-O-sulfate groups of heparin.	Glycosaminoglycans	150-167	fibroblast growth factor 2	Homo sapiens	179-183
8746633-9	1995	In the presence of glycosaminoglycans, the maximal thrombin inhibition rate (k2 x 10(-3) M-1 min-1) for rHCII was 10.4 +/- 2.5 at 100 micrograms/ml heparin and 16.0 +/- 4.3 at 1000 micrograms/ml dermatan sulfate compared to 9.0 +/- 0.7 at 200 micrograms/ml heparin and 18.5 +/- 5.3 at 1000 micrograms/ml dermatan sulfate for pHCII.	Glycosaminoglycans	19-37	CD59 molecule (CD59 blood group)	Homo sapiens	93-98
7499327-3	1995	The present study was conducted to determine the mechanism of osteoblast binding of IGFBP-5, beginning with the assumption that cell surface glycosaminoglycans may mediate the binding of this heparin binding protein.	Glycosaminoglycans	141-159	insulin-like growth factor binding protein 5	Mus musculus	84-91
7499327-12	1995	Glycosaminoglycans, however, modulate the binding and internalization of IGFBP-5 in a way that may preferentially favor the intracellular accumulation of the carboxyl-truncated form.	Glycosaminoglycans	0-18	insulin-like growth factor binding protein 5	Mus musculus	73-80
7592967-6	1995	To study the role of these amino acid sequences in controlling heparan sulfate synthesis, we have examined the assembly of glycosaminoglycans on Chinese hamster ovary (CHO) cell syndecan-1.	Glycosaminoglycans	123-141	syndecan-1	Cricetulus griseus	178-188
7492555-8	1995	These intermediate IC50 values indicate that human CEase has two structural regions that contribute to is unique inhibition by this sulfated glycosaminoglycan, and these could regulate cholesterol uptake in humans.	Glycosaminoglycans	141-158	carboxyl ester lipase	Homo sapiens	51-56
7499205-7	1995	These data demonstrate that rhIGFBP-3 inhibits IGFBP-4-degrading proteinase activity and binding of IGFs or glycosaminoglycans to IGFBP-3 may induce conformational changes in the binding protein, causing disinhibition of the proteinase.	Glycosaminoglycans	108-126	insulin like growth factor binding protein 3	Homo sapiens	30-37
7499205-7	1995	These data demonstrate that rhIGFBP-3 inhibits IGFBP-4-degrading proteinase activity and binding of IGFs or glycosaminoglycans to IGFBP-3 may induce conformational changes in the binding protein, causing disinhibition of the proteinase.	Glycosaminoglycans	108-126	endogenous retrovirus group K member 10	Homo sapiens	225-235
8578546-5	1995	Observations suggest that AT III may promote the release of PGl2 from endothelial cells by interacting with heparin-like glycosaminoglycans in vivo, consistent with previous observations in cultured endothelial cells.	Glycosaminoglycans	121-139	serpin family C member 1	Rattus norvegicus	26-32
8593487-1	1995	Our previous study has shown that urinary bikunin has four major isomers, which differ with respect to the sulfation ratio in a glycosaminoglycan chain but which do not exhibit any differences in amino acid composition, N-terminal amino acid sequence, C-terminal amino acid, sialic acid and uronic acid content.	Glycosaminoglycans	128-145	alpha-1-microglobulin/bikunin precursor	Homo sapiens	42-49
8593487-4	1995	We conclude that the charge heterogeneity of urinary bikunin is due to only a difference in the sulfation ratio of a glycosaminoglycan chain.	Glycosaminoglycans	117-134	alpha-1-microglobulin/bikunin precursor	Homo sapiens	53-60
7559619-7	1995	Analysis of the interaction between the enhancer and parts of the CPS promoter revealed that, in addition to the TATA box, the GAG box, a motif similar to the GC box near the TATA motif, is instrumental in conferring the enhancer activity.	Glycosaminoglycans	127-130	carbamoyl-phosphate synthase 1	Rattus norvegicus	66-69
8573207-1	1995	Reactivity of 26 synthetic peptides that comprise 12 to 26 amino acid residues corresponding to segments of the gag p19, env gp46, and pol proteins of human T-lymphotropic virus type I toward 31 positive sera was studied using enzyme-linked immunosorbent assay.	Glycosaminoglycans	112-115	interleukin 23 subunit alpha	Homo sapiens	116-119
7670097-3	1995	We also found that IL-1 or TPA-stimulated IL-11 and GM-CSF expression in PU-34 cells can be abolished by heparin, a class of molecules related to extracellular matrix components, glycosaminoglycans.	Glycosaminoglycans	179-197	interleukin-11	Macaca fascicularis	42-47
7589467-1	1995	Human plasma has been shown to contain a low molecular weight factor that potentiates human IGF-I stimulation of glycosaminoglycan synthesis in chick embryo cartilage.	Glycosaminoglycans	113-130	insulin like growth factor 1	Homo sapiens	92-97
7592623-4	1995	FGF-2-dependent attachment of 32D-flg cells was prevented by inclusion of 10 micrograms/ml heparin in the incubation medium and was diminished when CHO mutants in glycosaminoglycan synthesis or wild-type CHO cells treated with heparinase were used, indicating that the attachment occurred through FGF-2 interactions with heparan sulfates on the CHO cells.	Glycosaminoglycans	163-180	fibroblast growth factor 2	Cricetulus griseus	0-5
7559813-3	1995	One, serglycin, was recognized to have a core protein of 31 kDa, an overall molecular mass of 200-300 kDa, and glycosaminoglycan chains of mean size &lt; 25 kDa.	Glycosaminoglycans	111-128	serglycin	Homo sapiens	5-14
8574292-3	1995	The single major peak of purified GAG on a column of TSK gel DEAE got out of order after treatment with streptococcal hyaluronidase or nitrous acid.	Glycosaminoglycans	34-37	tsukushi, small leucine rich proteoglycan	Mus musculus	53-56
7472397-8	1995	Notably, mRNA encoding chondroitin sulfate glycosaminoglycan (CS GAG)-modified forms of APLP2 are enriched in the olfactory epithelium, relative to alternatively-spliced mRNA, encoding CS GAG-free forms of APLP2.	Glycosaminoglycans	65-68	amyloid beta (A4) precursor-like protein 2	Mus musculus	88-93
7561447-5	1995	Sulfur 35-labeled glycosaminoglycans (35S-GAGs) of HUVECs were decreased 1 hour after the incubation of plasmin with HUVECs, and the thrombomodulin (TM) activity of HUVECs measured by protein C activation capacity was decreased 6 hours after the incubation.	Glycosaminoglycans	18-36	plasminogen	Homo sapiens	104-111
7472397-8	1995	Notably, mRNA encoding chondroitin sulfate glycosaminoglycan (CS GAG)-modified forms of APLP2 are enriched in the olfactory epithelium, relative to alternatively-spliced mRNA, encoding CS GAG-free forms of APLP2.	Glycosaminoglycans	65-68	amyloid beta (A4) precursor-like protein 2	Mus musculus	206-211
8576935-5	1995	TGF-beta upregulated the synthesis of all these proteoglycans, coincident with elongation of glycosaminoglycan side chains observed for biglycan and decorin.	Glycosaminoglycans	93-110	transforming growth factor, beta 1	Rattus norvegicus	0-8
8576935-5	1995	TGF-beta upregulated the synthesis of all these proteoglycans, coincident with elongation of glycosaminoglycan side chains observed for biglycan and decorin.	Glycosaminoglycans	93-110	biglycan	Rattus norvegicus	136-144
8866672-7	1995	The plasmalogen-selective phospholipase A2 may be regulated by glycosaminoglycans and sialoglycoconjugates and may be involved in the regulation of K+ channels.	Glycosaminoglycans	63-81	LOC104974671	Bos taurus	26-42
7666514-3	1995	We have shown previously that the Gag precursor is able to "rescue" the Gag-Pol precursor into virus-like particles when the two polyproteins are expressed in the same cell by using separate simian virus 40-based plasmid expression vectors.	Glycosaminoglycans	34-37	Gag-Pol	Human immunodeficiency virus 1	72-79
7666514-5	1995	When we tested the abilities of Gag-Pol precursors to be incorporated into particles of Gag by coexpressing the precursors, we found that mutant Gag-Pol precursors lacking a conserved region in retroviral capsid proteins, the major homology region (MHR), were excluded from wild-type Gag particles.	Glycosaminoglycans	32-35	Gag-Pol	Human immunodeficiency virus 1	145-152
7666514-5	1995	When we tested the abilities of Gag-Pol precursors to be incorporated into particles of Gag by coexpressing the precursors, we found that mutant Gag-Pol precursors lacking a conserved region in retroviral capsid proteins, the major homology region (MHR), were excluded from wild-type Gag particles.	Glycosaminoglycans	88-91	Gag-Pol	Human immunodeficiency virus 1	32-39
7666514-5	1995	When we tested the abilities of Gag-Pol precursors to be incorporated into particles of Gag by coexpressing the precursors, we found that mutant Gag-Pol precursors lacking a conserved region in retroviral capsid proteins, the major homology region (MHR), were excluded from wild-type Gag particles.	Glycosaminoglycans	88-91	Gag-Pol	Human immunodeficiency virus 1	145-152
7666514-7	1995	These results suggest that the MHR is critical for interactions between Gag and Gag-Pol molecules.	Glycosaminoglycans	72-75	Gag-Pol	Human immunodeficiency virus 1	80-87
7666514-10	1995	These results indicate that the requirements for Gag particle formation differ from the ones essential for efficient incorporation of the Gag-Pol precursor into these particles.	Glycosaminoglycans	49-52	Gag-Pol	Human immunodeficiency virus 1	138-145
8574287-3	1995	Sequence analysis of the entire coding region of the androgen receptor gene from this patient revealed a single nucleotide substitution (G-->T) at nucleotide position 2676 in exon E (or 5), resulting in conversion of glutamine codon (GAG) to amber stop codon (TAG) at amino acid position 772 within the hormone-binding domain of the androgen receptor.	Glycosaminoglycans	234-237	androgen receptor	Homo sapiens	53-70
8574287-3	1995	Sequence analysis of the entire coding region of the androgen receptor gene from this patient revealed a single nucleotide substitution (G-->T) at nucleotide position 2676 in exon E (or 5), resulting in conversion of glutamine codon (GAG) to amber stop codon (TAG) at amino acid position 772 within the hormone-binding domain of the androgen receptor.	Glycosaminoglycans	234-237	androgen receptor	Homo sapiens	333-350
8530092-1	1995	Versican is a modular proteoglycan harboring a hyaluronan-binding domain at its amino-terminal end and a selectin-like domain at its carboxyl-terminal end, separated by a large intervening region containing the attachment sites for the glycosaminoglycan side chains.	Glycosaminoglycans	236-253	versican	Mus musculus	0-8
7664829-5	1995	In fibroblast phenotype cells, TGF-beta 2, EGF, and bFGF increase the production of glycosaminoglycans from 1.6- to 2.0-fold, with the exception of HS, which is suppressed by the addition of bFGF.	Glycosaminoglycans	84-102	transforming growth factor beta 2	Homo sapiens	31-41
7664829-5	1995	In fibroblast phenotype cells, TGF-beta 2, EGF, and bFGF increase the production of glycosaminoglycans from 1.6- to 2.0-fold, with the exception of HS, which is suppressed by the addition of bFGF.	Glycosaminoglycans	84-102	fibroblast growth factor 2	Homo sapiens	52-56
7664829-5	1995	In fibroblast phenotype cells, TGF-beta 2, EGF, and bFGF increase the production of glycosaminoglycans from 1.6- to 2.0-fold, with the exception of HS, which is suppressed by the addition of bFGF.	Glycosaminoglycans	84-102	fibroblast growth factor 2	Homo sapiens	191-195
7583924-3	1995	In particular, the role of a reported sequence homology between p24 gag and the SmB/B" autoantigen was investigated.	Glycosaminoglycans	68-71	transmembrane p24 trafficking protein 2	Homo sapiens	64-67
7643379-1	1995	The two zinc fingers of the yeast transcription factor Adr1p recognize the 6 bp sequence TTG GAG site in which the first finger, a His-X3-His finger, recognizes the G-rich triplet (GAG) and the second zinc finger, a His-X4-His finger, recognizes the T-rich sequence (TTG).	Glycosaminoglycans	93-96	DNA-binding transcription factor ADR1	Saccharomyces cerevisiae S288C	55-60
7544247-8	1995	Furthermore, anti-gag CTL frequencies determined by limiting dilution analysis were increased by 2- and 10-fold in two asymptomatic patients following IVS plus IL-7 compared with antigen stimulation alone.	Glycosaminoglycans	18-21	interleukin 7	Homo sapiens	160-164
7543138-10	1995	Also, removal of cell surface glycosaminoglycan chains by culture of cells in p-nitrophenyl beta-D-xylopyranoside or treatment with chondroitinase ABC resulted in conversion of cells with an inactive CD44 receptor to an inducible state.	Glycosaminoglycans	30-47	CD44 antigen	Mus musculus	200-204
7543523-6	1995	Glycosylation analysis of purified 33-kDa proMBP indicated that approximately 5 kDa is likely accounted for by the addition of one glycosaminoglycan group, three O-linked, and one N-linked complex type carbohydrate groups.	Glycosaminoglycans	131-148	proteoglycan 2, pro eosinophil major basic protein	Homo sapiens	42-48
7622456-7	1995	We suggest that CS GAG modification of a subset of APP and APLP2 isoforms represents a means of generating functional diversity for these polypeptides.	Glycosaminoglycans	19-22	amyloid beta precursor like protein 2	Homo sapiens	59-64
7618287-5	1995	In addition, the incorporation of the envelope glycoprotein (Env) into the Gag-made particles was investigated.	Glycosaminoglycans	75-78	endogenous retrovirus group K member 20	Homo sapiens	61-64
7629198-7	1995	Scatchard analysis of fibrillar A beta association with proteoglycans indicates a single affinity interaction, and the binding of both HSPG and CSPG to fibrillar A beta is completely inhibited by free glycosaminoglycan chains.	Glycosaminoglycans	201-218	syndecan 2	Homo sapiens	135-139
7629198-7	1995	Scatchard analysis of fibrillar A beta association with proteoglycans indicates a single affinity interaction, and the binding of both HSPG and CSPG to fibrillar A beta is completely inhibited by free glycosaminoglycan chains.	Glycosaminoglycans	201-218	amyloid beta precursor protein	Homo sapiens	162-168
7648625-1	1995	Chick embryo skin fibroblasts release transforming growth factor beta 1 that is able to modulate glycosaminoglycan synthesis and secretion.	Glycosaminoglycans	97-114	transforming growth factor beta 1	Gallus gallus	38-71
7635945-4	1995	DNA sequence analysis of the mutant apoE gene revealed a single-point mutation that resulted in the substitution of glutamic acid (GAG) for lysine (AAG) at residue 146 in the proposed receptor-binding domain of apoE.	Glycosaminoglycans	131-134	apolipoprotein E	Homo sapiens	36-40
7635945-4	1995	DNA sequence analysis of the mutant apoE gene revealed a single-point mutation that resulted in the substitution of glutamic acid (GAG) for lysine (AAG) at residue 146 in the proposed receptor-binding domain of apoE.	Glycosaminoglycans	131-134	apolipoprotein E	Homo sapiens	211-215
7492076-5	1995	The mechanism of antiviral action of the proteinase inhibitor SDZ PRI 0.53 was demonstrated to be inhibition of gag precursor protein processing.	Glycosaminoglycans	112-115	endogenous retrovirus group K member 24	Homo sapiens	41-51
7619084-4	1995	The putative N-terminal ectodomain contains a possible attachment site for heparan sulphate, identical with the comparable glycosaminoglycan-attachment sequence of rat syndecan 2.	Glycosaminoglycans	123-140	syndecan 2	Rattus norvegicus	168-178
7583924-5	1995	Reactivity to HIV-1 p24 gag was slightly but not significantly more frequent in patients with SLE than in controls (25.5% versus 14.0%; P &gt; 0.1), whereas reactivity to HIV-1 p17 gag was significantly more frequent in the former subjects (23.5% versus 8.0%; P = 0.03).	Glycosaminoglycans	24-27	transmembrane p24 trafficking protein 2	Homo sapiens	20-23
7540614-2	1995	Here we demonstrate that the ability of ARIA to induce phosphorylation of its receptor in muscle is blocked by highly charged glycosaminoglycans.	Glycosaminoglycans	126-144	prion protein	Gallus gallus	40-44
7540614-4	1995	Limited proteolysis of ARIA with subtilisin blocks the glycosaminoglycan interaction by degrading this NH2-terminal portion, but preserves the active, EGF-like domain.	Glycosaminoglycans	55-72	prion protein	Gallus gallus	23-27
7647222-4	1995	Together with other data from literature, it seems likely that TFPI is rather specifically released by acidic glycosaminoglycans.	Glycosaminoglycans	110-128	tissue factor pathway inhibitor	Homo sapiens	63-67
7769715-1	1995	We report single-point mutations that are located in the matrix protein domain of the gag gene of human immunodeficiency virus type 1 and that prevent Gag particle formation.	Glycosaminoglycans	151-154	Pr55(Gag)	Human immunodeficiency virus 1	86-89
7779094-3	1995	These data demonstrate that domain I has functional sites for attachment of glycosaminoglycans and indicate that the glycosaminoglycan chains of native perlecan are grouped at its N-terminal end.	Glycosaminoglycans	76-94	LOW QUALITY PROTEIN: basement membrane-specific heparan sulfate proteoglycan core protein	Cricetulus griseus	152-160
7779094-3	1995	These data demonstrate that domain I has functional sites for attachment of glycosaminoglycans and indicate that the glycosaminoglycan chains of native perlecan are grouped at its N-terminal end.	Glycosaminoglycans	76-93	LOW QUALITY PROTEIN: basement membrane-specific heparan sulfate proteoglycan core protein	Cricetulus griseus	152-160
7779094-4	1995	This, in turn, suggests that the likely function of domain I in perlecan would be to provide for the addition of glycosaminoglycan chains to the core protein.	Glycosaminoglycans	113-130	LOW QUALITY PROTEIN: basement membrane-specific heparan sulfate proteoglycan core protein	Cricetulus griseus	64-72
7562769-5	1995	GAG loss from the cartilage into the SF in response to IL-1 injection, as well as other effects of IL-1 challenge, was blocked in a dose dependent manner by IL-1ra administered either intraarticularly (ED50 = 160 ng) or intravenously (iv) (ED50 = 0.09mg/kg).	Glycosaminoglycans	0-3	interleukin-1 receptor antagonist protein	Oryctolagus cuniculus	157-163
7562769-6	1995	In the antigen induced arthritis model, IL-1ra (20 mg/kg, iv -2h) inhibited GAG release by 40%, whereas in polycation induced arthritis no inhibition was observed even with repeated administration of high doses of inhibitor.	Glycosaminoglycans	76-79	interleukin-1 receptor antagonist protein	Oryctolagus cuniculus	40-46
7786019-1	1995	The intracellular compartmentalization of enzyme activities involved in the elongation and sulfation of glycosaminoglycans on aggrecan, decorin, and fibromodulin was investigated using brefeldin A, a compound with known inhibitory action on normal vesicular transport and secretion of macromolecules.	Glycosaminoglycans	104-122	fibromodulin	Bos taurus	149-161
7663435-1	1995	The iduronate-2-sulfatase (IDS) is a lysosomal enzyme that acts on sulphate groups on C-2 positions of the iduronic acid residues of the mucopolysaccharides heparan sulphate and dermatan sulphate.	Glycosaminoglycans	137-156	iduronate 2-sulfatase	Homo sapiens	4-25
7775120-2	1995	To determine, using antisense technology, whether the c-myc protooncogene is involved in cell proliferation and glycosaminoglycan (GAG) synthesis in cultured orbital fibroblasts (OF).	Glycosaminoglycans	112-129	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	54-59
7538130-5	1995	A major portion of the glycosaminoglycan (GAG) chains released from these HSPGs by alkaline beta-elimination rebinds to L-selectin in the presence of calcium, indicating that these saccharides alone can mediate the high affinity recognition.	Glycosaminoglycans	23-40	selectin L	Homo sapiens	120-130
7759513-5	1995	Alternatively spliced pre-mRNAs encode several APLP2 isoforms; the APLP2-751 isoform is a substrate for modifications by a chondroitin sulfate glycosaminoglycan (CS GAG) chain, whereas the APLP2-763 isoform does not undergo CS GAG modification.	Glycosaminoglycans	165-168	amyloid beta precursor like protein 2	Canis lupus familiaris	67-72
7759513-5	1995	Alternatively spliced pre-mRNAs encode several APLP2 isoforms; the APLP2-751 isoform is a substrate for modifications by a chondroitin sulfate glycosaminoglycan (CS GAG) chain, whereas the APLP2-763 isoform does not undergo CS GAG modification.	Glycosaminoglycans	165-168	amyloid beta precursor like protein 2	Canis lupus familiaris	67-72
7759513-9	1995	Our results are consistent with the view that, in MDCK cells, the CS GAG chain of APLP2 has little influence on intracellular trafficking and that the principal basolateral targeting determinants are likely to reside in the APLP2 core protein.	Glycosaminoglycans	69-72	amyloid beta precursor like protein 2	Canis lupus familiaris	82-87
7769275-6	1995	Supernatants from 2 of 9 lines had high titers of p24 gag antigen, which did not seem to interfere with functional properties.	Glycosaminoglycans	54-57	transmembrane p24 trafficking protein 2	Homo sapiens	50-53
7651750-1	1995	Mucolipidosis 4 (ML4) is an autosomal recessive disorder with both lipid and mucopolysaccharide storage.	Glycosaminoglycans	77-95	mucolipin TRP cation channel 1	Homo sapiens	17-20
7784176-0	1995	A gene-type-specific enhancer regulates the carbamyl phosphate synthetase I promoter by cooperating with the proximal GAG activating element.	Glycosaminoglycans	118-121	carbamoyl-phosphate synthase 1	Rattus norvegicus	44-75
7538130-5	1995	A major portion of the glycosaminoglycan (GAG) chains released from these HSPGs by alkaline beta-elimination rebinds to L-selectin in the presence of calcium, indicating that these saccharides alone can mediate the high affinity recognition.	Glycosaminoglycans	42-45	selectin L	Homo sapiens	120-130
7538130-8	1995	However, nitrous acid deamination at pH 4.0 suggests the presence of some unsubstituted amino groups in these L-selectin-binding GAG chains from endothelial cell HSPGs.	Glycosaminoglycans	129-132	selectin L	Homo sapiens	110-120
7538130-11	1995	In both bovine and human endothelial cells, these novel groups are enriched for in the HS-GAG chains which bind to L-selectin.	Glycosaminoglycans	90-93	selectin L	Homo sapiens	115-125
7538130-15	1995	Regardless, these studies shown that HSPGs from cultured endothelial cells which can bind to L-selectin are enriched with unsubstituted amino groups on their GAG chains.	Glycosaminoglycans	158-161	selectin L	Homo sapiens	93-103
7737970-8	1995	The attachment of a glycosaminoglycan chain close to the A beta sequence of APP may affect the proteolytic processing of APP and production of A beta.	Glycosaminoglycans	20-37	amyloid beta precursor protein	Homo sapiens	57-63
7737970-8	1995	The attachment of a glycosaminoglycan chain close to the A beta sequence of APP may affect the proteolytic processing of APP and production of A beta.	Glycosaminoglycans	20-37	amyloid beta precursor protein	Homo sapiens	143-149
7544799-2	1995	We now show that an antiserum raised against the glycoproteins recognises isoforms of CD44, the most abundant of which could be labelled with [35S]sulphate, indicating the presence of glycosaminoglycan side chains.	Glycosaminoglycans	184-201	CD44 molecule (Indian blood group)	Rattus norvegicus	86-90
8589262-0	1995	Interaction of interleukin 7 (IL-7) with glycosaminoglycans and its biological relevance.	Glycosaminoglycans	41-59	interleukin 7	Mus musculus	15-28
8589262-0	1995	Interaction of interleukin 7 (IL-7) with glycosaminoglycans and its biological relevance.	Glycosaminoglycans	41-59	interleukin 7	Mus musculus	30-34
8589262-1	1995	We have investigated the binding of interleukin 7 (IL-7) to sulfated glycosaminoglycans and evaluated its biological consequences.	Glycosaminoglycans	69-87	interleukin 7	Mus musculus	36-49
8589262-1	1995	We have investigated the binding of interleukin 7 (IL-7) to sulfated glycosaminoglycans and evaluated its biological consequences.	Glycosaminoglycans	69-87	interleukin 7	Mus musculus	51-55
7780006-10	1995	Additionally, glycosaminoglycan binding may regulate IL-4 activity in vivo.	Glycosaminoglycans	14-31	interleukin 4	Homo sapiens	53-57
7706380-4	1995	In this study, synthetic oligopeptides were used to explore the capacity of smooth muscle cell-derived glycosaminoglycans to bind to the critical sequences of PDGF and apo B-100.	Glycosaminoglycans	103-121	apolipoprotein B	Homo sapiens	168-177
7706380-10	1995	Like the PDGF-derived oligopeptide, the apo B-100-derived oligopeptide bound to these glycosaminoglycans.	Glycosaminoglycans	86-104	apolipoprotein B	Homo sapiens	40-49
7706382-9	1995	Our results also suggest that expression of different HB-EGF forms in vivo could result in the production of HB-EGFs with divergent responses to sulfated glycosaminoglycans and proteoglycans.	Glycosaminoglycans	154-172	heparin-binding EGF-like growth factor	Mus musculus	54-60
7643748-0	1995	Regulation by basic fibroblast growth factor of glycosaminoglycan biosynthesis in cultured vascular endothelial cells.	Glycosaminoglycans	48-65	fibroblast growth factor 2	Bos taurus	14-44
7643748-1	1995	The alteration of glycosaminoglycans (GAGs) in cultured bovine aortic endothelial cells after exposure to basic fibroblast growth factor (bFGF) was investigated.	Glycosaminoglycans	18-36	fibroblast growth factor 2	Bos taurus	106-136
7643748-1	1995	The alteration of glycosaminoglycans (GAGs) in cultured bovine aortic endothelial cells after exposure to basic fibroblast growth factor (bFGF) was investigated.	Glycosaminoglycans	18-36	fibroblast growth factor 2	Bos taurus	138-142
7706383-6	1995	Thus, as has been suggested for other heparin-binding growth factors such as basic fibroblast growth factor (bFGF), the interaction of AR with an EGF-binding receptor appears to be facilitated by interaction with cell-associated sulfated glycosaminoglycans or proteoglycans.	Glycosaminoglycans	238-256	amphiregulin	Mus musculus	135-137
7535743-3	1995	ITIH1*1 was characterized by GAG (Glu) at codon 551 and CAG (Gln) at codon 561, ITIH1*2, by GTG (Val) and CGG (Arg), and ITIH1*3, by GAG (Glu) and CGG (Arg).	Glycosaminoglycans	29-32	inter-alpha-trypsin inhibitor heavy chain 1	Homo sapiens	0-5
7535743-3	1995	ITIH1*1 was characterized by GAG (Glu) at codon 551 and CAG (Gln) at codon 561, ITIH1*2, by GTG (Val) and CGG (Arg), and ITIH1*3, by GAG (Glu) and CGG (Arg).	Glycosaminoglycans	133-136	inter-alpha-trypsin inhibitor heavy chain 1	Homo sapiens	0-5
7779914-4	1995	Further, biological activity of the transgenic IL-1ra was demonstrated by its ability to inhibit IL-1-induced prostaglandin E2 (PGE2) synthesis in vitro and IL-1-induced glycosaminoglycan (GAG) degradation in vivo.	Glycosaminoglycans	170-187	interleukin 1 receptor antagonist	Homo sapiens	47-53
7699324-6	1995	During subsequent clinical progression to AIDS, loss of Gag-specific CTLp coincided with precipitating CD4+ counts and severe deterioration of T cell function.	Glycosaminoglycans	56-59	CD4 molecule	Homo sapiens	103-106
7743302-13	1995	The mechanism for this has not been defined but may relate to TNF-induced disruption of sulphated glycosaminoglycans.	Glycosaminoglycans	98-116	tumor necrosis factor	Homo sapiens	62-65
7535771-5	1995	The CD44-binding elements on gp600 or serglycin are glycosaminoglycans consisting of chondroitin 4-sulfate.	Glycosaminoglycans	52-70	CD44 antigen	Mus musculus	4-8
7535771-5	1995	The CD44-binding elements on gp600 or serglycin are glycosaminoglycans consisting of chondroitin 4-sulfate.	Glycosaminoglycans	52-70	serglycin	Mus musculus	29-34
7535771-5	1995	The CD44-binding elements on gp600 or serglycin are glycosaminoglycans consisting of chondroitin 4-sulfate.	Glycosaminoglycans	52-70	carbohydrate sulfotransferase 11	Mus musculus	85-98
7890615-6	1995	Using rotation-mediated aggregation assays, we find that aggregation of syndecan-1-transfected cells is dependent on divalent cations and is inhibited by the following: (i) addition of heparin and heparin-like glycosaminoglycans, (ii) removal of heparan sulfate from the cell surface, or (iii) addition of exogenous purified syndecan-1.	Glycosaminoglycans	210-228	syndecan 1	Homo sapiens	72-82
7779914-4	1995	Further, biological activity of the transgenic IL-1ra was demonstrated by its ability to inhibit IL-1-induced prostaglandin E2 (PGE2) synthesis in vitro and IL-1-induced glycosaminoglycan (GAG) degradation in vivo.	Glycosaminoglycans	189-192	interleukin 1 receptor antagonist	Homo sapiens	47-53
7853521-4	1995	A comparison of the sequences of the V1-V2 and the V3 coding regions of the envelope gene and the p17 region of the gag gene showed that the donor-recipient pairs were tightly clustered in all gene segments, but away from local and published transmission controls.	Glycosaminoglycans	116-119	family with sequence similarity 72 member B	Homo sapiens	98-101
8680403-2	1995	These mutations lead to a deficiency of the glycosidase alpha-L-iduronidase (IDUA), which is required for the degradation of heparan sulphate and dermatan sulphate and thus the storage of these glycosaminoglycans in the lysosome.	Glycosaminoglycans	194-212	alpha-L-iduronidase	Homo sapiens	56-75
7877991-7	1995	Golgi-specific glycosaminoglycan sulfation was strongly inhibited in cells overexpressing either holo-PKC epsilon or its zinc-finger domain, while the secretion of sulfated glycosaminoglycans into the medium was impaired in cells expressing the PKC epsilon zinc-finger domain.	Glycosaminoglycans	173-191	protein kinase C, epsilon	Mus musculus	102-113
7831808-3	1995	Pulse-chase and immune precipitation studies showed that both the viral glycoprotein precursor (gp160) and the gag precursor (p57) were cleaved into gp120 and p27, respectively, and both were released into the culture medium of infected cells, although most of the p27 remained cell associated.	Glycosaminoglycans	111-114	cyclin dependent kinase inhibitor 1C	Homo sapiens	126-129
7831808-3	1995	Pulse-chase and immune precipitation studies showed that both the viral glycoprotein precursor (gp160) and the gag precursor (p57) were cleaved into gp120 and p27, respectively, and both were released into the culture medium of infected cells, although most of the p27 remained cell associated.	Glycosaminoglycans	111-114	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	149-154
7831808-3	1995	Pulse-chase and immune precipitation studies showed that both the viral glycoprotein precursor (gp160) and the gag precursor (p57) were cleaved into gp120 and p27, respectively, and both were released into the culture medium of infected cells, although most of the p27 remained cell associated.	Glycosaminoglycans	111-114	interferon alpha inducible protein 27	Homo sapiens	159-162
7831808-3	1995	Pulse-chase and immune precipitation studies showed that both the viral glycoprotein precursor (gp160) and the gag precursor (p57) were cleaved into gp120 and p27, respectively, and both were released into the culture medium of infected cells, although most of the p27 remained cell associated.	Glycosaminoglycans	111-114	interferon alpha inducible protein 27	Homo sapiens	265-268
7574505-4	1995	There is a glycosylated, tetrameric Cu, ZnSOD in the extracellular space that binds to acidic glycosamino-glycans.	Glycosaminoglycans	94-113	Superoxide dismutase 1	Drosophila melanogaster	40-45
7662318-7	1995	Heparan sulphate proteoglycan purified from alveolar macrophages bound strongly to immobilized rTf, thus raising the possibility that the low-affinity interaction of transferrin with these cells may be mediated, at least in part, by this glycosaminoglycan.	Glycosaminoglycans	238-255	transferrin	Rattus norvegicus	166-177
7736647-10	1995	Glycosaminoglycan concentration was significantly increased in cervices treated by LPS, FMLI as well as IL-8 (p &lt; 0.0001, 0.006 and 0.001 respectively).	Glycosaminoglycans	0-17	interleukin-8	Oryctolagus cuniculus	104-108
7871742-2	1995	It has been shown that Vpr incorporation in the virus particle requires only the core protein Gag.	Glycosaminoglycans	94-97	Vpr	Human immunodeficiency virus 1	23-26
7852334-4	1995	Using dose-response experiments, we showed that antithrombin activity via antithrombin III and heparin cofactor II was increased in parallel with GAG plasma levels compared to control.	Glycosaminoglycans	146-149	heparin cofactor 2	Oryctolagus cuniculus	95-114
7539644-5	1995	As inflammatory chemokines (short-range stimulators of lymphocyte migration which trigger integrin activation) are known to bind to endothelial glycosaminoglycans, we propose that the binding of the lymphocyte membrane L-selectin to endothelial glycosaminoglycans may provide a link between the selectin-mediated and integrin-mediated adhesion systems in leukocyte extravasation cascades.	Glycosaminoglycans	144-162	selectin L	Rattus norvegicus	219-229
7539644-5	1995	As inflammatory chemokines (short-range stimulators of lymphocyte migration which trigger integrin activation) are known to bind to endothelial glycosaminoglycans, we propose that the binding of the lymphocyte membrane L-selectin to endothelial glycosaminoglycans may provide a link between the selectin-mediated and integrin-mediated adhesion systems in leukocyte extravasation cascades.	Glycosaminoglycans	245-263	selectin L	Rattus norvegicus	219-229
7744600-5	1995	The role of membrane-associated heparan sulfate in thrombin conversion to an adhesive protein was demonstrated by using CHO cell mutants defective in various aspects of glycosaminoglycan synthesis.	Glycosaminoglycans	169-186	coagulation factor II	Mus musculus	51-59
8689570-4	1995	Various glycosaminoglycans can be recognized by an overlapping set of proteins that include two of the selectins and CD44.	Glycosaminoglycans	8-26	CD44 molecule (Indian blood group)	Homo sapiens	117-121
7721348-5	1995	Furthermore, IRG1 contains the motif for glycosaminoglycan attachment site, implying that IRG1 may be a proteoglycan.	Glycosaminoglycans	41-58	aconitate decarboxylase 1	Mus musculus	13-17
7721348-5	1995	Furthermore, IRG1 contains the motif for glycosaminoglycan attachment site, implying that IRG1 may be a proteoglycan.	Glycosaminoglycans	41-58	aconitate decarboxylase 1	Mus musculus	90-94
8680403-2	1995	These mutations lead to a deficiency of the glycosidase alpha-L-iduronidase (IDUA), which is required for the degradation of heparan sulphate and dermatan sulphate and thus the storage of these glycosaminoglycans in the lysosome.	Glycosaminoglycans	194-212	alpha-L-iduronidase	Homo sapiens	77-81
7983737-6	1995	In addition, the gag gene of HERV-K10 was expressed in the baculovirus system.	Glycosaminoglycans	17-20	keratin 10	Homo sapiens	34-37
11322326-3	1995	After injection of hCG into PMSG-primed immature mice, cumulus and mural granulosa cells adjacent to the antrum synthesized a large amount of such glycosaminoglycan, while the outermost layers layers of mural granulosa cells did not.	Glycosaminoglycans	147-164	hypertrichosis 2 (generalised, congenital)	Homo sapiens	19-22
7798630-0	1995	Oncostatin M stimulates collagen and glycosaminoglycan production by cultured normal dermal fibroblasts: insensitivity of sclerodermal and keloidal fibroblasts.	Glycosaminoglycans	37-54	oncostatin M	Homo sapiens	0-12
7983737-7	1995	Using this recombinant system to test antisera from patients with different diseases and healthy individuals, we were able to detect antibodies against the N-terminal part of HERV-K10 Gag in 2 to 4% of groups of tumor patients with titers ranging between 1:80 and 1:640, while approximately 0.1 to 0.5% of healthy individuals exhibited antibodies with lower titers.	Glycosaminoglycans	184-187	keratin 10	Homo sapiens	180-183
7806495-3	1994	Thrombin is inhibited by the serpins antithrombin and heparin cofactor II (HCiI) in reactions that are accelerated markedly by specific glycosaminoglycans.	Glycosaminoglycans	136-154	coagulation factor II, thrombin	Homo sapiens	0-8
7528742-5	1994	We discovered an additional exon just proximal to the glycosaminoglycan-binding region that was identical to a recently identified splice variant of versican (Dours-Zimmermann, M.T., and Zimmermann, D.R.	Glycosaminoglycans	54-71	versican	Homo sapiens	149-157
7660142-14	1995	The endogenous release of TFPI may contribute to the antithrombotic actions of heparin and related glycosaminoglycans.	Glycosaminoglycans	99-117	tissue factor pathway inhibitor	Homo sapiens	26-30
7806529-0	1994	A novel glycosaminoglycan attachment domain identified in two alternative splice variants of human versican.	Glycosaminoglycans	8-25	versican	Homo sapiens	99-107
7806495-3	1994	Thrombin is inhibited by the serpins antithrombin and heparin cofactor II (HCiI) in reactions that are accelerated markedly by specific glycosaminoglycans.	Glycosaminoglycans	136-154	serpin family C member 1	Homo sapiens	37-49
7806529-1	1994	We have cloned an alternatively spliced glycosaminoglycan attachment domain (GAG-alpha) of human versican from cDNA libraries derived from U251MG glioma cells.	Glycosaminoglycans	40-57	versican	Homo sapiens	97-105
7806495-3	1994	Thrombin is inhibited by the serpins antithrombin and heparin cofactor II (HCiI) in reactions that are accelerated markedly by specific glycosaminoglycans.	Glycosaminoglycans	136-154	serpin family D member 1	Homo sapiens	54-73
7806529-2	1994	Inserted carboxyl-terminal of the hyaluronan-binding region, this domain adds another 987 amino acids to the original versican (V1) core protein giving rise to the large V0 isoform with 3396 amino acids and 17-23 putative glycosaminoglycan attachment sites.	Glycosaminoglycans	222-239	versican	Homo sapiens	118-126
7806529-8	1994	In brain tissue, we identified a short versican variant (V2) including only the GAG-alpha domain.	Glycosaminoglycans	80-83	versican	Homo sapiens	39-47
7806495-3	1994	Thrombin is inhibited by the serpins antithrombin and heparin cofactor II (HCiI) in reactions that are accelerated markedly by specific glycosaminoglycans.	Glycosaminoglycans	136-154	serpin family D member 1	Homo sapiens	75-79
7806495-5	1994	The present study examines the role of anion-binding exosite II of thrombin in the interaction with glycosaminoglycans and HCII.	Glycosaminoglycans	100-118	coagulation factor II, thrombin	Homo sapiens	67-75
7806495-6	1994	Acceleration of thrombin inhibition by serpins in the presence of glycosaminoglycans is proposed to occur by a template mechanism, in which inhibitor and protease bind simultaneously to the same glycosaminoglycan chain, facilitating their interaction.	Glycosaminoglycans	66-84	coagulation factor II, thrombin	Homo sapiens	16-24
7806495-6	1994	Acceleration of thrombin inhibition by serpins in the presence of glycosaminoglycans is proposed to occur by a template mechanism, in which inhibitor and protease bind simultaneously to the same glycosaminoglycan chain, facilitating their interaction.	Glycosaminoglycans	66-83	coagulation factor II, thrombin	Homo sapiens	16-24
7806495-8	1994	Specific mutations in exosite II (R89E, R245E, K248E, and K252E) disrupted thrombin binding to both dermatan sulfate and heparin, indicating that both glycosaminoglycans bind to a common site in exosite II.	Glycosaminoglycans	151-169	coagulation factor II, thrombin	Homo sapiens	75-83
7710270-3	1994	The mode of action of the 2-aminobenzylstatine PR inhibitors was demonstrated to be inhibition of gag precursor processing.	Glycosaminoglycans	98-101	endogenous retrovirus group K member 25	Homo sapiens	47-49
7528540-14	1994	The inhibition of both enzymes is most likely due to interactions with the glycosaminoglycan moiety of PAPP-A/proMBP.	Glycosaminoglycans	75-92	pappalysin 1	Homo sapiens	103-109
7528540-14	1994	The inhibition of both enzymes is most likely due to interactions with the glycosaminoglycan moiety of PAPP-A/proMBP.	Glycosaminoglycans	75-92	proteoglycan 2, pro eosinophil major basic protein	Homo sapiens	110-116
7804447-8	1994	The capacity to synthesize glycosaminoglycan chain in the presence of an artifical acceptor of chain elongation, beta-D-xylodide, was increased significantly by IL-1 beta but not obviously so by TGF-beta.	Glycosaminoglycans	27-44	interleukin 1 beta	Homo sapiens	161-170
7755506-6	1994	Based on these VLP we developed a novel antigen presentation system, which allows the presentation of selected epitopes derived from HIV reading frames other than gag to the immune system.	Glycosaminoglycans	163-166	VHL like	Homo sapiens	15-18
7527332-13	1994	As glycosaminoglycan side-chains are present in proteoglycans that are present in extracellular matrix and on cell surfaces, these side-chains represent a potential mechanism for regulating IGFBP-5 proteolysis in vivo.	Glycosaminoglycans	3-20	insulin like growth factor binding protein 5	Homo sapiens	190-197
7527332-3	1994	In this study we investigated the effects of glycosaminoglycans on IGFBP-5 degradation in fibroblast-conditioned medium.	Glycosaminoglycans	45-63	insulin like growth factor binding protein 5	Homo sapiens	67-74
7804447-8	1994	The capacity to synthesize glycosaminoglycan chain in the presence of an artifical acceptor of chain elongation, beta-D-xylodide, was increased significantly by IL-1 beta but not obviously so by TGF-beta.	Glycosaminoglycans	27-44	transforming growth factor beta 1	Homo sapiens	195-203
7947925-1	1994	It has been proposed that the function of serum amyloid P component (SAP) may closely relate with its binding to polysaccharides, especially glycosaminoglycans.	Glycosaminoglycans	141-159	amyloid P component, serum	Homo sapiens	42-67
7798617-7	1994	These results suggest that excess TNF-alpha (or other mediator) produced in C3H/HeN skin (but not C3H/HeJ skin) in response to UVB exposure is involved in the mast cell increase and partial inhibition of elastin increase, but that neither these mediators nor mast cell products are important mediators for the chronic UVB-induced increases in neutrophils, glycosaminoglycans, and collagen.	Glycosaminoglycans	356-374	tumor necrosis factor	Mus musculus	34-43
7975251-1	1994	The human immunodeficiency virus type 2 gag precursor protein, pr41, self assembles as virus-like particles (VLP) when the gag gene is expressed in insect cells.	Glycosaminoglycans	40-43	VHL like	Homo sapiens	109-112
7975251-1	1994	The human immunodeficiency virus type 2 gag precursor protein, pr41, self assembles as virus-like particles (VLP) when the gag gene is expressed in insect cells.	Glycosaminoglycans	123-126	VHL like	Homo sapiens	109-112
7947945-7	1994	The ATP-elicited release of glycosaminoglycans was also enhanced by interleukin 1 beta, tumour necrosis factor alpha, and transforming growth factor-beta, although only high concentrations of the latter were effective.	Glycosaminoglycans	28-46	interleukin 1 beta	Homo sapiens	68-116
7865478-1	1994	We performed the quantitative and qualitative analysis on the main disaccharide units of glycosaminoglycans produced by human dermal fibroblasts in the 3-dimensional culture supplemented with L-ascorbic acid 2-phosphate (Asc 2-p) comparing with the monolayer culture system.	Glycosaminoglycans	89-107	pyrin domain containing 1	Homo sapiens	221-226
7947925-1	1994	It has been proposed that the function of serum amyloid P component (SAP) may closely relate with its binding to polysaccharides, especially glycosaminoglycans.	Glycosaminoglycans	141-159	amyloid P component, serum	Homo sapiens	69-72
7531724-7	1994	However, binding of CD44 to glycosaminoglycans such as chondroitin 4-sulfate, chondroitin 6-sulfate, and dermatan sulfate was undetectable, suggesting either that a novel chondroitin-type glycosaminoglycan is recognized by CD44 or that a particular configuration of the glycosaminoglycan is required for recognition by CD44.	Glycosaminoglycans	28-45	CD44 antigen	Mus musculus	20-24
7757423-1	1994	In this paper, we report the synthesis of "non-glycosamino" glycan analogues 5-10 of the antithrombin III binding pentasaccharide 1.	Glycosaminoglycans	47-66	serpin family C member 1	Homo sapiens	89-105
7957665-6	1994	A hypothesis is advanced to suggest that when transferrin is bound to a component of macrophage plasmalemma, thought to be the glycosaminoglycan of heparan sulfate, its conformation may change in such a way that it attracts other proteins.	Glycosaminoglycans	127-144	transferrin	Rattus norvegicus	46-57
7531724-6	1994	The gp600 was readily labeled with radioactive sulfate, and treatment of gp600 with chondroitinase ABC or ACII generated a lower molecular weight species (18-22 kDa), suggesting that gp600 consists of a small core protein with chondroitin sulfate glycosaminoglycan side chains.	Glycosaminoglycans	247-264	serglycin	Mus musculus	73-78
7531724-6	1994	The gp600 was readily labeled with radioactive sulfate, and treatment of gp600 with chondroitinase ABC or ACII generated a lower molecular weight species (18-22 kDa), suggesting that gp600 consists of a small core protein with chondroitin sulfate glycosaminoglycan side chains.	Glycosaminoglycans	247-264	serglycin	Mus musculus	73-78
7531724-7	1994	However, binding of CD44 to glycosaminoglycans such as chondroitin 4-sulfate, chondroitin 6-sulfate, and dermatan sulfate was undetectable, suggesting either that a novel chondroitin-type glycosaminoglycan is recognized by CD44 or that a particular configuration of the glycosaminoglycan is required for recognition by CD44.	Glycosaminoglycans	28-46	CD44 antigen	Mus musculus	20-24
7929188-0	1994	Modulation of glycosaminoglycan addition in naturally expressed and recombinant human thrombomodulin.	Glycosaminoglycans	14-31	thrombomodulin	Homo sapiens	86-100
8091672-0	1994	The protein p30, encoded at the gag-pro junction of mouse mammary tumor virus, is a dUTPase fused with a nucleocapsid protein.	Glycosaminoglycans	32-35	centromere protein V	Homo sapiens	12-15
7899138-11	1994	We synthesized N-oleoyl heparin derivative (3 oleoyl groups/one molecule of heparin); such a lipophilic glycosaminoglycan (LipoGAG), although acting as an elastin protecting agent, possessed lower HNE inhibitory capacity as compared with heparin.	Glycosaminoglycans	104-121	elastin	Homo sapiens	155-162
7899138-11	1994	We synthesized N-oleoyl heparin derivative (3 oleoyl groups/one molecule of heparin); such a lipophilic glycosaminoglycan (LipoGAG), although acting as an elastin protecting agent, possessed lower HNE inhibitory capacity as compared with heparin.	Glycosaminoglycans	104-121	elastase, neutrophil expressed	Homo sapiens	197-200
7818994-3	1994	The total urinary GAG in CNF and other nephrotic patients was comparable to controls with all three methods.	Glycosaminoglycans	18-21	NPHS1 adhesion molecule, nephrin	Homo sapiens	25-28
8091672-0	1994	The protein p30, encoded at the gag-pro junction of mouse mammary tumor virus, is a dUTPase fused with a nucleocapsid protein.	Glycosaminoglycans	32-35	Deoxyuridine triphosphatase	Drosophila melanogaster	84-91
8091672-6	1994	By a 1-base insertion, eliminating the gag stop codon and fusing the gag and pro reading frames, a plasmid, pET-3d-NCDU, directing overexpression of p30, was constructed.	Glycosaminoglycans	39-42	centromere protein V	Homo sapiens	149-152
8091672-6	1994	By a 1-base insertion, eliminating the gag stop codon and fusing the gag and pro reading frames, a plasmid, pET-3d-NCDU, directing overexpression of p30, was constructed.	Glycosaminoglycans	69-72	centromere protein V	Homo sapiens	149-152
8071334-4	1994	We report that in stably transfected Chinese hamster ovary and transiently transfected African green monkey kidney (COS-1) cells, APLP2 is modified by glycosaminoglycan (GAG) addition.	Glycosaminoglycans	151-168	amyloid beta (A4) precursor-like protein 2	Mus musculus	130-135
17147647-10	1994	Transforming growth factor-beta(1) was found to cause a dose-dependent increase in glycosaminoglycan synthesis in hypertrophic scar and normal skin but not in normal scar fibroblasts in cell-mediated glycosaminoglycan synthesis; the reverse was observed in cell-free glycosaminoglycan synthesis, where transforming growth factor-beta(1) increased glycosaminoglycan synthesis in normal scar but not in normal skin or hypertrophic scar.	Glycosaminoglycans	83-100	transforming growth factor beta 1	Homo sapiens	0-34
17147647-10	1994	Transforming growth factor-beta(1) was found to cause a dose-dependent increase in glycosaminoglycan synthesis in hypertrophic scar and normal skin but not in normal scar fibroblasts in cell-mediated glycosaminoglycan synthesis; the reverse was observed in cell-free glycosaminoglycan synthesis, where transforming growth factor-beta(1) increased glycosaminoglycan synthesis in normal scar but not in normal skin or hypertrophic scar.	Glycosaminoglycans	83-100	transforming growth factor beta 1	Homo sapiens	302-336
17147647-10	1994	Transforming growth factor-beta(1) was found to cause a dose-dependent increase in glycosaminoglycan synthesis in hypertrophic scar and normal skin but not in normal scar fibroblasts in cell-mediated glycosaminoglycan synthesis; the reverse was observed in cell-free glycosaminoglycan synthesis, where transforming growth factor-beta(1) increased glycosaminoglycan synthesis in normal scar but not in normal skin or hypertrophic scar.	Glycosaminoglycans	200-217	transforming growth factor beta 1	Homo sapiens	0-34
17147647-10	1994	Transforming growth factor-beta(1) was found to cause a dose-dependent increase in glycosaminoglycan synthesis in hypertrophic scar and normal skin but not in normal scar fibroblasts in cell-mediated glycosaminoglycan synthesis; the reverse was observed in cell-free glycosaminoglycan synthesis, where transforming growth factor-beta(1) increased glycosaminoglycan synthesis in normal scar but not in normal skin or hypertrophic scar.	Glycosaminoglycans	200-217	transforming growth factor beta 1	Homo sapiens	0-34
17147647-10	1994	Transforming growth factor-beta(1) was found to cause a dose-dependent increase in glycosaminoglycan synthesis in hypertrophic scar and normal skin but not in normal scar fibroblasts in cell-mediated glycosaminoglycan synthesis; the reverse was observed in cell-free glycosaminoglycan synthesis, where transforming growth factor-beta(1) increased glycosaminoglycan synthesis in normal scar but not in normal skin or hypertrophic scar.	Glycosaminoglycans	200-217	transforming growth factor beta 1	Homo sapiens	0-34
7522446-1	1994	The binding of the 165 amino-acid form of vascular endothelial growth factor (VEGF165) to the VEGF receptors of vascular endothelial cells was potentiated by heparin and heparan-sulfate, but not by other glycosaminoglycans.	Glycosaminoglycans	204-222	vascular endothelial growth factor A	Homo sapiens	42-76
7522446-1	1994	The binding of the 165 amino-acid form of vascular endothelial growth factor (VEGF165) to the VEGF receptors of vascular endothelial cells was potentiated by heparin and heparan-sulfate, but not by other glycosaminoglycans.	Glycosaminoglycans	204-222	vascular endothelial growth factor A	Homo sapiens	78-82
8071334-5	1994	The sensitivity of GAG-modified APLP2 to digestion with chondroitinase AC indicates that chondroitin sulfate (CS) chains are the preponderant GAG on APLP2.	Glycosaminoglycans	142-145	amyloid beta (A4) precursor-like protein 2	Mus musculus	149-154
8071334-6	1994	CS GAG modification of APLP2 occurs in a region with little homology to APP.	Glycosaminoglycans	3-6	amyloid beta (A4) precursor-like protein 2	Mus musculus	23-28
7945307-1	1994	We examined the effect of suramin, an anticancer agent and a functional analog of naturally occuring glycosaminoglycans, on p34cdc2 kinase.	Glycosaminoglycans	101-119	cyclin dependent kinase 1	Homo sapiens	124-131
7945307-7	1994	Therefore, glycosaminoglycans might be physiological regulators of p34cdc2 kinase in vivo.	Glycosaminoglycans	11-29	cyclin dependent kinase 1	Homo sapiens	67-74
8071334-4	1994	We report that in stably transfected Chinese hamster ovary and transiently transfected African green monkey kidney (COS-1) cells, APLP2 is modified by glycosaminoglycan (GAG) addition.	Glycosaminoglycans	170-173	amyloid beta (A4) precursor-like protein 2	Mus musculus	130-135
8071334-7	1994	Contained within this heterologous region is a predicted CS modification site, ENEGSGMAEQ (APLP2 residues 610-619); APLP2 polypeptides harboring a serine-to-alanine substitution at position 614 fail to undergo CS GAG modification.	Glycosaminoglycans	213-216	amyloid beta (A4) precursor-like protein 2	Mus musculus	116-121
8071334-5	1994	The sensitivity of GAG-modified APLP2 to digestion with chondroitinase AC indicates that chondroitin sulfate (CS) chains are the preponderant GAG on APLP2.	Glycosaminoglycans	19-22	amyloid beta (A4) precursor-like protein 2	Mus musculus	32-37
8071334-5	1994	The sensitivity of GAG-modified APLP2 to digestion with chondroitinase AC indicates that chondroitin sulfate (CS) chains are the preponderant GAG on APLP2.	Glycosaminoglycans	19-22	amyloid beta (A4) precursor-like protein 2	Mus musculus	149-154
8093006-7	1994	Tissue-derived biglycan and decorin were less effective competitors for TGF-beta binding than fibromodulin or the non-glycosylated fusion proteins; removal of the chondroitin/dermatan sulphate chains of decorin and biglycan (fibromodulin is a keratan sulphate proteoglycan) increased the activities of decorin and biglycan, suggesting that the glycosaminoglycan chains may hinder the interaction of the core proteins with TGF-beta.	Glycosaminoglycans	344-361	biglycan	Bos taurus	15-23
7841596-18	1994	Whether AT-III in the presence of glycosaminoglycans on cell surfaces expressing TF can function as an auxiliary second physiological regulator is not known.	Glycosaminoglycans	34-52	serpin family C member 1	Homo sapiens	8-14
7841596-18	1994	Whether AT-III in the presence of glycosaminoglycans on cell surfaces expressing TF can function as an auxiliary second physiological regulator is not known.	Glycosaminoglycans	34-52	coagulation factor III, tissue factor	Homo sapiens	81-83
7848837-1	1994	In the present study, we demonstrate that both interleukin-1 (IL-1) and interleukin-6 (IL-6) induced a significant decrease in glycosaminoglycan (GAG) synthesis and, more strikingly, secretion by 7 and 13 day-old chick embryo skin fibroblasts.	Glycosaminoglycans	127-144	interleukin 6	Gallus gallus	72-85
7956830-14	1994	These data suggest that changes in the cytoplasmic domain of PECAM-1 may affect its function during cardiovascular development, and are consistent with our earlier report that systematic truncation of the cytoplasmic domain of human PECAM-1 resulted in changes in its ligand specificity, divalent cation and glycosaminoglycan dependence, as well as its susceptibility to adhesion blocking monoclonal antibodies.	Glycosaminoglycans	308-325	platelet and endothelial cell adhesion molecule 1	Homo sapiens	61-68
7956830-14	1994	These data suggest that changes in the cytoplasmic domain of PECAM-1 may affect its function during cardiovascular development, and are consistent with our earlier report that systematic truncation of the cytoplasmic domain of human PECAM-1 resulted in changes in its ligand specificity, divalent cation and glycosaminoglycan dependence, as well as its susceptibility to adhesion blocking monoclonal antibodies.	Glycosaminoglycans	308-325	platelet and endothelial cell adhesion molecule 1	Homo sapiens	233-240
7848837-1	1994	In the present study, we demonstrate that both interleukin-1 (IL-1) and interleukin-6 (IL-6) induced a significant decrease in glycosaminoglycan (GAG) synthesis and, more strikingly, secretion by 7 and 13 day-old chick embryo skin fibroblasts.	Glycosaminoglycans	127-144	interleukin 6	Gallus gallus	87-91
7848837-1	1994	In the present study, we demonstrate that both interleukin-1 (IL-1) and interleukin-6 (IL-6) induced a significant decrease in glycosaminoglycan (GAG) synthesis and, more strikingly, secretion by 7 and 13 day-old chick embryo skin fibroblasts.	Glycosaminoglycans	146-149	interleukin 6	Gallus gallus	72-85
7848837-1	1994	In the present study, we demonstrate that both interleukin-1 (IL-1) and interleukin-6 (IL-6) induced a significant decrease in glycosaminoglycan (GAG) synthesis and, more strikingly, secretion by 7 and 13 day-old chick embryo skin fibroblasts.	Glycosaminoglycans	146-149	interleukin 6	Gallus gallus	87-91
8074689-6	1994	Our findings support the hypothesis that HSPGs modulate the binding of bFGF to FGFR through the formation of a ternary complex in which the glycosaminoglycan chains interact with bFGF via 2-O- and N-sulfate groups and with FGFR also via 6-O-sulfate groups.	Glycosaminoglycans	140-157	fibroblast growth factor 2	Mus musculus	71-75
7992258-6	1994	In order to determine if a very low molecular weight glycosaminoglycan can release TFPI in plasma, in the present study, we compared plasma TFPI amidolytic activity after intravenous injection in rabbits of pentasaccharide (PS), a synthetic fragment of very low molecular weight and with a strong and exclusive anti Xa activity, and unfractionated heparin (UFH).	Glycosaminoglycans	53-70	tissue factor pathway inhibitor	Oryctolagus cuniculus	83-87
8065455-3	1994	It orchestrates viral assembly via targeting signals that direct the gag precursor polyprotein, p55, to the host cell membrane and it interacts with the transmembrane protein, gp41, to retain the env-encoded proteins in the virus.	Glycosaminoglycans	69-72	phosphoinositide-3-kinase regulatory subunit 3	Homo sapiens	96-99
8065455-3	1994	It orchestrates viral assembly via targeting signals that direct the gag precursor polyprotein, p55, to the host cell membrane and it interacts with the transmembrane protein, gp41, to retain the env-encoded proteins in the virus.	Glycosaminoglycans	69-72	endogenous retrovirus group W member 1, envelope	Homo sapiens	196-199
8074689-6	1994	Our findings support the hypothesis that HSPGs modulate the binding of bFGF to FGFR through the formation of a ternary complex in which the glycosaminoglycan chains interact with bFGF via 2-O- and N-sulfate groups and with FGFR also via 6-O-sulfate groups.	Glycosaminoglycans	140-157	fibroblast growth factor 2	Mus musculus	179-183
7519608-2	1994	This study was designed to determine the role of glycosaminoglycans in altering the formation of the IGF-I.IGFBP complexes.	Glycosaminoglycans	49-67	insulin like growth factor 1	Homo sapiens	101-106
8070564-6	1994	This value remained constant in swim-up sperm and decreased to (7.7 +/- 0.4) x 10(6)/spermatozoon after incubation for 24 h in capacitation medium at 39 degrees C. These data substantiate the hypothesis that PDC-109 may be one of the seminal plasma components that enhance the fertilizing capacity of bull spermatozoa upon interaction with heparin-like glycosaminoglycans present in the female genital tract.	Glycosaminoglycans	353-371	seminal plasma protein PDC-109	Bos taurus	208-215
8043862-9	1994	The binding of CD45 and Mac-1 to the 3T3 cells was similarly blocked by these GAGs.	Glycosaminoglycans	78-82	protein tyrosine phosphatase, receptor type, C	Mus musculus	15-19
8057359-9	1994	In the presence of rev and a functional RRE, there is an increase in the levels of gag and env mRNA in the cytoplasm and a decrease in levels of tat and rev mRNAs.	Glycosaminoglycans	83-86	Rev	Human immunodeficiency virus 1	19-22
8043862-9	1994	The binding of CD45 and Mac-1 to the 3T3 cells was similarly blocked by these GAGs.	Glycosaminoglycans	78-82	integrin alpha M	Mus musculus	24-29
7995378-9	1994	Elastin was also found associated with glycosaminoglycans in the soluble matrix of the aortic wall.	Glycosaminoglycans	39-57	elastin	Homo sapiens	0-7
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
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
8180167-10	1994	The results suggest that protein C inhibitor may be important in the physiological control of acrosin activity, particularly where the presence of heparin-like glycosaminoglycans would stimulate the acrosin-protein C inhibitor reaction.	Glycosaminoglycans	160-178	serpin family A member 5	Homo sapiens	25-44
7528019-1	1994	Interactions between the IGF-binding proteins (IGFBPs) and glycosaminoglycans (GAGs) such as heparin may be involved in the regulatory control of IGF exerted by the IGFBPs at the level of the extracellular matrix and capillary endothelium, although the precise mechanisms of this remain uncertain.	Glycosaminoglycans	59-77	insulin like growth factor binding protein 1	Homo sapiens	165-171
7528019-2	1994	We have searched primary sequences of human, rat and bovine IGFBPs-1 to -6 for putative GAG-binding consensus sequences (XBBXBX and XBBBXXBX, where B represents any basic amino acid and X is undefined).	Glycosaminoglycans	88-91	insulin like growth factor binding protein 1	Bos taurus	60-74
7528019-3	1994	At least one such sequence was identified in each IGFBP examined except human and rat IGFBP-4 and rat IGFBP-6, with IGFBP-5 containing three GAG-binding consensus sequences.	Glycosaminoglycans	141-144	insulin-like growth factor binding protein 5	Rattus norvegicus	116-123
8078307-12	1994	Multiple TGF-beta 1 injections resulted in an increased GAG content in patellar cartilage.	Glycosaminoglycans	56-59	transforming growth factor, beta 1	Mus musculus	9-19
8035817-7	1994	In addition to the full-length RNA, tom is also transcribed into a spliced subgenomic transcript that encodes a protein resulting from the fusion between the amino-terminal region of the first (gag) and the third ORFs.	Glycosaminoglycans	194-197	Twin of m4	Drosophila melanogaster	36-39
8040268-9	1994	Inhibition of bFGF activity by PF 4 could be overcome by exogenous heparin or chondroitin-4-sulfate, suggesting that inhibition of mitogenesis is caused by binding of PF 4 to cell-surface glycosaminoglycans.	Glycosaminoglycans	188-206	fibroblast growth factor 2	Homo sapiens	14-18
8040268-9	1994	Inhibition of bFGF activity by PF 4 could be overcome by exogenous heparin or chondroitin-4-sulfate, suggesting that inhibition of mitogenesis is caused by binding of PF 4 to cell-surface glycosaminoglycans.	Glycosaminoglycans	188-206	platelet factor 4	Homo sapiens	167-171
8030949-0	1994	Scrapie-associated PrP accumulation and its inhibition: revisiting the amyloid-glycosaminoglycan connection.	Glycosaminoglycans	79-96	prion protein	Homo sapiens	19-22
8030949-6	1994	Since protease-resistant PrP amyloid is known to contain sulfated glycosaminoglycans, as do other naturally derived amyloids, we hypothesize that these sulfated inhibitors competitively block binding between PrP and endogenous glycosaminoglycans that is important for its accumulation in a protease-resistant, potentially amyloidogenic state.	Glycosaminoglycans	66-84	prion protein	Homo sapiens	25-28
8030949-6	1994	Since protease-resistant PrP amyloid is known to contain sulfated glycosaminoglycans, as do other naturally derived amyloids, we hypothesize that these sulfated inhibitors competitively block binding between PrP and endogenous glycosaminoglycans that is important for its accumulation in a protease-resistant, potentially amyloidogenic state.	Glycosaminoglycans	66-84	prion protein	Homo sapiens	208-211
8030949-6	1994	Since protease-resistant PrP amyloid is known to contain sulfated glycosaminoglycans, as do other naturally derived amyloids, we hypothesize that these sulfated inhibitors competitively block binding between PrP and endogenous glycosaminoglycans that is important for its accumulation in a protease-resistant, potentially amyloidogenic state.	Glycosaminoglycans	227-245	prion protein	Homo sapiens	25-28
8030949-6	1994	Since protease-resistant PrP amyloid is known to contain sulfated glycosaminoglycans, as do other naturally derived amyloids, we hypothesize that these sulfated inhibitors competitively block binding between PrP and endogenous glycosaminoglycans that is important for its accumulation in a protease-resistant, potentially amyloidogenic state.	Glycosaminoglycans	227-245	prion protein	Homo sapiens	208-211
8182050-8	1994	Heparan sulfate, chondroitin sulfate, and dermatan sulfate, three glycosaminoglycans structurally related to heparin, were &gt; or = 80-fold less effective in binding to RMCP-1 than heparin.	Glycosaminoglycans	66-84	mast cell protease 1-like 1	Rattus norvegicus	170-176
7919526-8	1994	Decorin, biglycan, and fibromodulin are closely related in protein structure but differ in glycosaminoglycan composition and function.	Glycosaminoglycans	91-108	biglycan	Homo sapiens	9-17
7919526-8	1994	Decorin, biglycan, and fibromodulin are closely related in protein structure but differ in glycosaminoglycan composition and function.	Glycosaminoglycans	91-108	fibromodulin	Homo sapiens	23-35
7974391-0	1994	Characterization of the binding between tissue factor pathway inhibitor and glycosaminoglycans.	Glycosaminoglycans	76-94	tissue factor pathway inhibitor	Homo sapiens	40-71
7974391-3	1994	We have developed an assay based on the use of heparin-Sepharose micro columns in order to compare small quantities of heparin fractions as well as different glycosaminoglycans on a weight basis for their TFPI binding.	Glycosaminoglycans	158-176	tissue factor pathway inhibitor	Homo sapiens	205-209
7974391-4	1994	In this assay a glycosaminoglycan in solution compete with heparin-Sepharose for TFPI binding.	Glycosaminoglycans	16-33	tissue factor pathway inhibitor	Homo sapiens	81-85
7974391-10	1994	A number of different glycosaminoglycans were tested and the following order of TFPI affinity was found: heparin &gt;&gt; dermatan sulphate &gt; heparan sulphate &gt; chondroitin sulphate C.	Glycosaminoglycans	22-40	tissue factor pathway inhibitor	Homo sapiens	80-84
8195703-1	1994	Based on the premise that naturally occurring glycosaminoglycans could serve as building blocks for synthesizing nontoxic drugs for suppression of tumor necrosis factor (TNF) production by inflammatory cells, we have chemically modified hyaluronic acid (HA) and tested its effects in blocking TNF-alpha and TNF-beta production in vitro.	Glycosaminoglycans	46-64	tumor necrosis factor	Homo sapiens	147-168
8195703-1	1994	Based on the premise that naturally occurring glycosaminoglycans could serve as building blocks for synthesizing nontoxic drugs for suppression of tumor necrosis factor (TNF) production by inflammatory cells, we have chemically modified hyaluronic acid (HA) and tested its effects in blocking TNF-alpha and TNF-beta production in vitro.	Glycosaminoglycans	46-64	tumor necrosis factor	Homo sapiens	170-173
7850270-2	1994	The PCR/restriction endonuclease digestion (RE) assay and PCR/SSCP analysis of the rhodopsin gene in 13 Japanese families with autosomal dominant retinitis pigmentosa (ad RP) revealed a G-A substitution of the first nucleotide of codon 181, replacing Glu (GAG) with Lys (AAG), in one family.	Glycosaminoglycans	256-259	rhodopsin	Homo sapiens	83-92
7950365-9	1994	Recombinant alpha-L-iduronidase was efficiently endocytosed by Hurler fibroblasts utilizing a mannose 6-phosphate-dependent mechanism (half maximal uptake at 0.7 nM) and was "corrective" for abnormal glycosaminoglycan accumulation (half-maximal correction at 0.7 pM).	Glycosaminoglycans	200-217	alpha-L-iduronidase	Cricetulus griseus	12-31
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
8180167-10	1994	The results suggest that protein C inhibitor may be important in the physiological control of acrosin activity, particularly where the presence of heparin-like glycosaminoglycans would stimulate the acrosin-protein C inhibitor reaction.	Glycosaminoglycans	160-178	acrosin	Homo sapiens	94-101
8180167-10	1994	The results suggest that protein C inhibitor may be important in the physiological control of acrosin activity, particularly where the presence of heparin-like glycosaminoglycans would stimulate the acrosin-protein C inhibitor reaction.	Glycosaminoglycans	160-178	acrosin	Homo sapiens	199-206
8180167-10	1994	The results suggest that protein C inhibitor may be important in the physiological control of acrosin activity, particularly where the presence of heparin-like glycosaminoglycans would stimulate the acrosin-protein C inhibitor reaction.	Glycosaminoglycans	160-178	serpin family A member 5	Homo sapiens	207-226
8192680-2	1994	Hepatic lipase may facilitate uptake of these particles, not only as a lipolytic enzyme, but also as a ligand anchored to extracellular glycosaminoglycans.	Glycosaminoglycans	136-154	lipase C, hepatic type	Rattus norvegicus	0-14
8138579-0	1994	Amphiregulin-dependent proliferation of cultured human keratinocytes: autocrine growth, the effects of exogenous recombinant cytokine, and apparent requirement for heparin-like glycosaminoglycans.	Glycosaminoglycans	177-195	amphiregulin	Homo sapiens	0-12
21244893-3	1994	Both heparin cofactor II and thrombin interact with highly negatively charged glycosaminoglycans like heparin and dermatan sulfate, and they both are leukocyte chemoattractants.	Glycosaminoglycans	78-96	coagulation factor II, thrombin	Homo sapiens	29-37
7520722-3	1994	In contrast, Gag particles were found only in low amounts in the culture medium from Vero cells infected with the same HIV gag-pol vaccinia virus recombinant; the Gag precursor remained associated with the infected Vero cells and was efficiently processed.	Glycosaminoglycans	13-16	gag polyprotein;gag-pol fusion polyprotein	Human immunodeficiency virus 2	123-130
8161203-6	1994	The binding was reversible as these glycosaminoglycans were also effective at displacement of bound [125I]bFGF from rat growth plate ECM.	Glycosaminoglycans	36-54	fibroblast growth factor 2	Rattus norvegicus	106-110
7517179-6	1994	gp600 was readily labeled with radioactive sulfate and treatment of gp600 with chondroitinase ABC or AC II generated a lower molecular weight species (18-22 kDa), suggesting that gp600 consists of a small core protein heavily modified with chondroitin sulfate glycosaminoglycan side chains.	Glycosaminoglycans	260-277	serglycin	Mus musculus	68-73
7517179-6	1994	gp600 was readily labeled with radioactive sulfate and treatment of gp600 with chondroitinase ABC or AC II generated a lower molecular weight species (18-22 kDa), suggesting that gp600 consists of a small core protein heavily modified with chondroitin sulfate glycosaminoglycan side chains.	Glycosaminoglycans	260-277	serglycin	Mus musculus	68-73
7517179-7	1994	However, when binding of CD44 was tested in vitro to chondroitinase-sensitive purified glycosaminoglycans, such as chondroitin-4-sulfate, chondroitin-6-sulfate and dermatan sulfate, no binding was demonstrable, suggesting either that a novel type of chondroitinase-sensitive glycosaminoglycan is recognized by CD44 or that association of the glycosaminoglycan with a core protein is required for recognition by CD44.	Glycosaminoglycans	87-105	CD44 antigen	Mus musculus	25-29
8167338-2	1994	Heparan sulfate (HS) is a physiologic endothelial cell surface modulator of normal anticoagulation, containing a specific oligosaccharide sequence that binds antithrombin III with high affinity and also is present in heparin, a related glycosaminoglycan.	Glycosaminoglycans	236-253	serpin family C member 1	Homo sapiens	158-174
8151769-6	1994	We have identified several regions within the env mRNA that inhibit expression of a gag-env hybrid mRNA.	Glycosaminoglycans	84-87	endogenous retrovirus group W member 1, envelope	Homo sapiens	46-49
8151769-6	1994	We have identified several regions within the env mRNA that inhibit expression of a gag-env hybrid mRNA.	Glycosaminoglycans	84-87	endogenous retrovirus group W member 1, envelope	Homo sapiens	88-91
8163535-12	1994	This glycosaminoglycan distribution was identical on mouse syndecan-1 produced by either mouse epithelial (NMuMG) or hamster mesenchymal (CHO) cells, suggesting that site-specific attachment of glycosaminoglycans is independent of cell type.	Glycosaminoglycans	5-22	syndecan 1	Mus musculus	59-69
8166664-3	1994	The 110 kDa phospholipase A2 was much more active with phosphatidylethanolamine and was not affected by glycosaminoglycans, whereas the 39 kDa phospholipase A2 was much more active with ethanolamine plasmalogen and was markedly inhibited by glycosaminoglycans.	Glycosaminoglycans	241-259	LOC104974671	Bos taurus	12-28
8166664-3	1994	The 110 kDa phospholipase A2 was much more active with phosphatidylethanolamine and was not affected by glycosaminoglycans, whereas the 39 kDa phospholipase A2 was much more active with ethanolamine plasmalogen and was markedly inhibited by glycosaminoglycans.	Glycosaminoglycans	241-259	LOC104974671	Bos taurus	143-159
7517179-7	1994	However, when binding of CD44 was tested in vitro to chondroitinase-sensitive purified glycosaminoglycans, such as chondroitin-4-sulfate, chondroitin-6-sulfate and dermatan sulfate, no binding was demonstrable, suggesting either that a novel type of chondroitinase-sensitive glycosaminoglycan is recognized by CD44 or that association of the glycosaminoglycan with a core protein is required for recognition by CD44.	Glycosaminoglycans	87-104	CD44 antigen	Mus musculus	25-29
7812655-5	1994	These results and additional data confirming PrP binding to heparin suggested a possible role for sulfated glycosaminoglycans in the generation of protease-resistant PrP during scrapie infection.	Glycosaminoglycans	107-125	prion protein	Homo sapiens	45-48
7812655-5	1994	These results and additional data confirming PrP binding to heparin suggested a possible role for sulfated glycosaminoglycans in the generation of protease-resistant PrP during scrapie infection.	Glycosaminoglycans	107-125	prion protein	Homo sapiens	166-169
8138579-11	1994	Autocrine and paracrine signaling by amphiregulin may require cellular heparin-like glycosaminoglycans, presumably as matrix or membrane proteoglycans, whereas soluble glycosaminoglycans inhibit signaling, possibly by competing for cytokine binding.	Glycosaminoglycans	84-102	amphiregulin	Homo sapiens	37-49
8204207-4	1994	The env-gag-induced proliferative responses of lymphocytes from normal subjects were significantly suppressed when cultures contained only higher levels of ETOH (0.2% and 0.3%), whereas ETOH even at a lower level (0.1%) produced significant suppression of the env-gag-induced proliferation of lymphocytes only from AIDS patients.	Glycosaminoglycans	8-11	endogenous retrovirus group K member 20	Homo sapiens	4-7
7512120-1	1994	The murine AIDS (MAIDS) virus has a unique sequence in the gag p12 region, which could be responsible for MAIDS development.	Glycosaminoglycans	59-62	CDK2 (cyclin-dependent kinase 2)-associated protein 1	Mus musculus	63-66
7512120-7	1994	The nucleotide sequence in the gag p12 region of the transcript was closely similar to that of the MAIDS virus, but the amino acid sequence was less similar because of frameshifting, even when translated.	Glycosaminoglycans	31-34	CDK2 (cyclin-dependent kinase 2)-associated protein 1	Mus musculus	35-38
7512120-9	1994	To determine whether the gag p12 region of the transcript contains a functional sequence, a recombinant virus was generated by replacing the gag p12 region of a replication-competent BM5eco virus with that of the endogenous transcript.	Glycosaminoglycans	25-28	CDK2 (cyclin-dependent kinase 2)-associated protein 1	Mus musculus	29-32
7999307-7	1994	The similarity of these compounds to sulfated glycosaminoglycans, which are components of all natural amyloids, has led to the hypothesis that the inhibitors act by competitively blocking an interaction between endogenous glycosaminoglycan(s) and PrP that is critical for amyloidogenic PrP accumulation.	Glycosaminoglycans	46-64	prion protein	Mus musculus	247-250
7999307-7	1994	The similarity of these compounds to sulfated glycosaminoglycans, which are components of all natural amyloids, has led to the hypothesis that the inhibitors act by competitively blocking an interaction between endogenous glycosaminoglycan(s) and PrP that is critical for amyloidogenic PrP accumulation.	Glycosaminoglycans	46-64	prion protein	Mus musculus	286-289
7912945-11	1994	The results showed a point mutation in the PrP gene at codon 200; GAG to AAG (Glu--&gt;Lys).	Glycosaminoglycans	66-69	prion protein	Homo sapiens	43-46
7912945-11	1994	The results showed a point mutation in the PrP gene at codon 200; GAG to AAG (Glu--&gt;Lys).	Glycosaminoglycans	66-69	N-methylpurine DNA glycosylase	Homo sapiens	73-76
7913757-6	1994	These and other observations suggest that an interaction of PrP with endogenous sulphated glycosaminoglycans or proteoglycans is important in protease-resistant PrP accumulation, and raise the possibility that therapies for transmissible spongiform encephalopathies and other amyloidoses could be based on blocking (pre)amyloid-glycosaminoglycan interactions.	Glycosaminoglycans	90-108	prion protein	Homo sapiens	60-63
7913757-6	1994	These and other observations suggest that an interaction of PrP with endogenous sulphated glycosaminoglycans or proteoglycans is important in protease-resistant PrP accumulation, and raise the possibility that therapies for transmissible spongiform encephalopathies and other amyloidoses could be based on blocking (pre)amyloid-glycosaminoglycan interactions.	Glycosaminoglycans	90-107	prion protein	Homo sapiens	60-63
8204207-4	1994	The env-gag-induced proliferative responses of lymphocytes from normal subjects were significantly suppressed when cultures contained only higher levels of ETOH (0.2% and 0.3%), whereas ETOH even at a lower level (0.1%) produced significant suppression of the env-gag-induced proliferation of lymphocytes only from AIDS patients.	Glycosaminoglycans	8-11	endogenous retrovirus group K member 20	Homo sapiens	260-263
8204207-4	1994	The env-gag-induced proliferative responses of lymphocytes from normal subjects were significantly suppressed when cultures contained only higher levels of ETOH (0.2% and 0.3%), whereas ETOH even at a lower level (0.1%) produced significant suppression of the env-gag-induced proliferation of lymphocytes only from AIDS patients.	Glycosaminoglycans	264-267	endogenous retrovirus group K member 20	Homo sapiens	4-7
7511714-8	1994	Quantitative analysis of glycosaminoglycans present in tumor tissues showed that the hyaluronic acid content of the P29 tumor was more than 5 times that in the more highly metastatic tumors.	Glycosaminoglycans	25-43	SYF2 homolog, RNA splicing factor (S. cerevisiae)	Mus musculus	116-119
8120455-6	1994	Productive infection of H9 cells was quantitated on subsequent days by measuring p24 gag antigen levels in supernatants by enzyme-linked immunosorbent assay.	Glycosaminoglycans	85-88	transmembrane p24 trafficking protein 2	Homo sapiens	81-84
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
8107246-7	1994	This response was observed in two animals (one VV-Env and one Gag-Env).	Glycosaminoglycans	62-65	endogenous retrovirus group K member 20	Homo sapiens	66-69
8107246-11	1994	Active infection developed in all controls and two of three VV-Gag-Env-immunized animals.	Glycosaminoglycans	63-66	endogenous retrovirus group K member 20	Homo sapiens	67-70
8139581-2	1994	A mutated Bla gene in which the termination codon had been replaced by GAG, was fused in-phase to the cDNA sequence encoding the hinge region, CH2 and CH3 of the human IgG3 heavy chain.	Glycosaminoglycans	71-74	beta-lactamase	Escherichia coli	10-13
8307950-8	1994	These results, in combination with the ability of heparin and chondroitin sulfate to compete for binding to DNs, demonstrate that these two glycosaminoglycans interact with similar or overlapping sites in FN.	Glycosaminoglycans	140-158	fibronectin 1	Homo sapiens	205-207
7508748-3	1994	PAPP-A contains 82 Cys residues, which are all bridged, 14 putative sites for N-glycosylation, and 7 putative sites for attachment of glycosaminoglycan groups.	Glycosaminoglycans	134-151	pappalysin 1	Homo sapiens	0-6
8106553-0	1994	Betaglycan can act as a dual modulator of TGF-beta access to signaling receptors: mapping of ligand binding and GAG attachment sites.	Glycosaminoglycans	112-115	transforming growth factor beta receptor 3	Homo sapiens	0-10
8159018-5	1994	A negative and significant correlation was observed for codons AAG and GAG.	Glycosaminoglycans	71-74	N-methylpurine DNA glycosylase	Homo sapiens	63-66
8106435-1	1994	The proximal promoter of the rat carbamyl phosphate synthetase I gene contains four cis-acting regulatory regions, designated sites GAG, I, II, and III.	Glycosaminoglycans	132-135	carbamoyl-phosphate synthase 1	Rattus norvegicus	33-64
8106435-8	1994	Our results suggest a model in which the carbamyl phosphate synthetase I promoter is controlled by a single activating element, GAG, and by two repressor elements, sites I and III.	Glycosaminoglycans	128-131	carbamoyl-phosphate synthase 1	Rattus norvegicus	41-72
8076974-8	1994	Addition of glycosaminoglycans such as hyaluronic acid, chondroitin sulphate, and heparin into the medium cause significant increase in the synthesis and secretion of [3H]apoB into the medium indicating a possible secretory control of apoB by local reuptake.	Glycosaminoglycans	12-30	apolipoprotein B	Rattus norvegicus	171-175
8076974-8	1994	Addition of glycosaminoglycans such as hyaluronic acid, chondroitin sulphate, and heparin into the medium cause significant increase in the synthesis and secretion of [3H]apoB into the medium indicating a possible secretory control of apoB by local reuptake.	Glycosaminoglycans	12-30	apolipoprotein B	Rattus norvegicus	235-239
8106553-0	1994	Betaglycan can act as a dual modulator of TGF-beta access to signaling receptors: mapping of ligand binding and GAG attachment sites.	Glycosaminoglycans	112-115	transforming growth factor beta 1	Homo sapiens	42-50
8139146-7	1994	Urinary GAG levels correlated positively with urinary albumin levels (r = 0.251, p &lt; 0.05) and urinary N-acetyl-beta-D-glucosaminidase activities in diabetics (r = 0.491, p &lt; 0.01).	Glycosaminoglycans	8-11	O-GlcNAcase	Homo sapiens	106-137
8276871-5	1994	The ectodomain of chicken syndecan-4 core protein contains three potential sites for glycosaminoglycan attachment, two sites for N-glycosylation, and lacks a dibasic protease cleavage site proximal to the membrane-spanning region found in other syndecan family members.	Glycosaminoglycans	85-102	syndecan 4	Gallus gallus	26-36
8292049-0	1994	Regulation of alternative pathway complement activation by glycosaminoglycans: specificity of the polyanion binding site on factor H.	Glycosaminoglycans	59-77	complement factor H	Homo sapiens	124-132
8292049-3	1994	In this study we have analyzed the ability of different glycosaminoglycans and other negatively charged macromolecules to interact with the factor H polyanion recognition site and to enhance binding of H to the C3b-target complex.	Glycosaminoglycans	56-74	complement factor H	Homo sapiens	140-148
8292049-3	1994	In this study we have analyzed the ability of different glycosaminoglycans and other negatively charged macromolecules to interact with the factor H polyanion recognition site and to enhance binding of H to the C3b-target complex.	Glycosaminoglycans	56-74	endogenous retrovirus group K member 3	Homo sapiens	211-214
8292049-9	1994	The results show that the interaction of the polyanion binding site on factor H with glycosaminoglycans depends upon the number, orientation and polymeric arrangement of sulphate groups and suggest that most, but not all, sulphated glycosaminoglycans participate in the protection of host tissues from complement damage by promoting inactivation of tissue-bound C3b.	Glycosaminoglycans	85-103	complement factor H	Homo sapiens	71-79
8292049-9	1994	The results show that the interaction of the polyanion binding site on factor H with glycosaminoglycans depends upon the number, orientation and polymeric arrangement of sulphate groups and suggest that most, but not all, sulphated glycosaminoglycans participate in the protection of host tissues from complement damage by promoting inactivation of tissue-bound C3b.	Glycosaminoglycans	85-103	endogenous retrovirus group K member 3	Homo sapiens	362-365
8292049-9	1994	The results show that the interaction of the polyanion binding site on factor H with glycosaminoglycans depends upon the number, orientation and polymeric arrangement of sulphate groups and suggest that most, but not all, sulphated glycosaminoglycans participate in the protection of host tissues from complement damage by promoting inactivation of tissue-bound C3b.	Glycosaminoglycans	232-250	complement factor H	Homo sapiens	71-79
8186357-2	1994	In vitro, the inhibition of thrombin by antithrombin is very slow; but greatly enhanced by heparin and related glycosaminoglycans.	Glycosaminoglycans	111-129	coagulation factor II, thrombin	Homo sapiens	28-36
7976168-2	1994	An increased incorporation of 3H-thymidine into DNA and of 35S-SO4 into sulfated glycosaminoglycans was observed in cultures supplemented with 1-10 ng/ml TGF-beta and with 1% fetal calf serum.	Glycosaminoglycans	81-99	transforming growth factor beta 1	Homo sapiens	154-162
8186357-2	1994	In vitro, the inhibition of thrombin by antithrombin is very slow; but greatly enhanced by heparin and related glycosaminoglycans.	Glycosaminoglycans	111-129	serpin family C member 1	Homo sapiens	40-52
8306483-6	1994	gamma-interferon, tumour necrosis factor and interleukin-1 stimulated glycosaminoglycan synthesis; this effect was greater in orbital than in dermal fibroblasts with gamma-interferon and interleukin-1 (P &lt; 0.05).	Glycosaminoglycans	70-87	interleukin 1 alpha	Homo sapiens	45-58
8306483-6	1994	gamma-interferon, tumour necrosis factor and interleukin-1 stimulated glycosaminoglycan synthesis; this effect was greater in orbital than in dermal fibroblasts with gamma-interferon and interleukin-1 (P &lt; 0.05).	Glycosaminoglycans	70-87	interleukin 1 alpha	Homo sapiens	187-200
8282346-8	1994	The rate of synthesis of subtypes of glycosaminoglycans in the aorta was proportionately increased by Ang II.	Glycosaminoglycans	37-55	angiotensinogen	Rattus norvegicus	102-108
8282346-7	1994	By 7 to 10 days of Ang II administration (200 ng.kg-1.min-1), glycosaminoglycan synthesis of aorta returned toward baseline (P &lt; .10, &gt; .05).	Glycosaminoglycans	62-79	angiotensinogen	Rattus norvegicus	19-25
8263327-0	1994	Monoclonal antibodies against the protein core and glycosaminoglycan side chain of glomerular basement membrane heparan sulfate proteoglycan: characterization and immunohistological application in human tissues.	Glycosaminoglycans	51-68	CD44 molecule (Indian blood group)	Homo sapiens	112-140
8270859-5	1994	We show that infection of mitogen-activated peripheral blood mononuclear cells (PBMC) with Nef+ HIV results in enhanced replication as evidenced by earlier gag p24 expression when compared with infections performed with nef mutant viruses.	Glycosaminoglycans	156-159	S100 calcium binding protein B	Homo sapiens	91-94
7837760-1	1994	Mucolipidosis IV (ML IV) (McKusick 252650) is an autosomal recessive metabolic disorder that displays signs of both lipid and mucopolysaccharide (glycosaminoglycan) storage.	Glycosaminoglycans	126-144	mucolipin TRP cation channel 1	Homo sapiens	18-23
7598784-2	1994	Analysis of Ig isotypes demonstrated that while IgM was the most frequent early response to gag (p19, p24) and env (r21e) proteins within the first 3 months following transfusion, IgG and IgA responses could also be detected within this period.	Glycosaminoglycans	92-95	interleukin 23 subunit alpha	Homo sapiens	97-100
7837760-1	1994	Mucolipidosis IV (ML IV) (McKusick 252650) is an autosomal recessive metabolic disorder that displays signs of both lipid and mucopolysaccharide (glycosaminoglycan) storage.	Glycosaminoglycans	146-163	mucolipin TRP cation channel 1	Homo sapiens	18-23
8983064-1	1994	The invasion-suppressor molecule E-cadherin (E-CAD) can be regulated at multiple levels: synthesis, processing and stability of mRNA; synthesis, processing and stability of protein; localization and posttranslational modification of protein; binding to catenins (E-CAD-associated proteins); and size and charge of cell surface glycosaminoglycans.	Glycosaminoglycans	327-345	cadherin 1	Mus musculus	33-43
8983064-1	1994	The invasion-suppressor molecule E-cadherin (E-CAD) can be regulated at multiple levels: synthesis, processing and stability of mRNA; synthesis, processing and stability of protein; localization and posttranslational modification of protein; binding to catenins (E-CAD-associated proteins); and size and charge of cell surface glycosaminoglycans.	Glycosaminoglycans	327-345	cadherin 1	Mus musculus	45-50
8057139-1	1994	The effect of mouse interferon alpha/beta (MuIFN alpha/beta) on the production of glycosaminoglycans (GAGs) by mouse glioma G-26 in vitro was evaluated.	Glycosaminoglycans	82-100	interferon alpha B	Mus musculus	20-41
8061921-3	1994	These latter PGs were identified as biglycan and decorin on the basis of analyses of their core protein native size, and glycosaminoglycan composition.	Glycosaminoglycans	121-138	biglycan	Homo sapiens	36-44
7824964-1	1994	GAGs were purified from urine of dogs after intranasal administration of 40 mg/kg ITF 1300.	Glycosaminoglycans	0-4	trefoil factor 3	Canis lupus familiaris	82-85
7598784-2	1994	Analysis of Ig isotypes demonstrated that while IgM was the most frequent early response to gag (p19, p24) and env (r21e) proteins within the first 3 months following transfusion, IgG and IgA responses could also be detected within this period.	Glycosaminoglycans	92-95	transmembrane p24 trafficking protein 2	Homo sapiens	102-105
8165623-6	1993	In vitro studies in blood and seminal plasma showed that heparin stimulated complexation of uPA and tPA with PCI, suggesting that negatively charged glycosaminoglycans in blood vessels and in the reproductive system may regulate PCI reactions with uPA and tPA.	Glycosaminoglycans	149-167	plasminogen activator, urokinase	Homo sapiens	92-95
8165623-6	1993	In vitro studies in blood and seminal plasma showed that heparin stimulated complexation of uPA and tPA with PCI, suggesting that negatively charged glycosaminoglycans in blood vessels and in the reproductive system may regulate PCI reactions with uPA and tPA.	Glycosaminoglycans	149-167	serpin family A member 5	Homo sapiens	109-112
8165623-6	1993	In vitro studies in blood and seminal plasma showed that heparin stimulated complexation of uPA and tPA with PCI, suggesting that negatively charged glycosaminoglycans in blood vessels and in the reproductive system may regulate PCI reactions with uPA and tPA.	Glycosaminoglycans	149-167	serpin family A member 5	Homo sapiens	229-232
8165623-6	1993	In vitro studies in blood and seminal plasma showed that heparin stimulated complexation of uPA and tPA with PCI, suggesting that negatively charged glycosaminoglycans in blood vessels and in the reproductive system may regulate PCI reactions with uPA and tPA.	Glycosaminoglycans	149-167	plasminogen activator, urokinase	Homo sapiens	248-251
8276257-3	1993	In such cells, the product of the first L1Hs open reading frame (ORF), a protein called p40, is detectable; p40 has no apparent similarity to gag proteins, but contains a leucine zipper region which may be responsible for the occurrence of p40 multimers.	Glycosaminoglycans	142-145	interleukin 9	Homo sapiens	88-91
8276257-3	1993	In such cells, the product of the first L1Hs open reading frame (ORF), a protein called p40, is detectable; p40 has no apparent similarity to gag proteins, but contains a leucine zipper region which may be responsible for the occurrence of p40 multimers.	Glycosaminoglycans	142-145	interleukin 9	Homo sapiens	108-111
8276257-3	1993	In such cells, the product of the first L1Hs open reading frame (ORF), a protein called p40, is detectable; p40 has no apparent similarity to gag proteins, but contains a leucine zipper region which may be responsible for the occurrence of p40 multimers.	Glycosaminoglycans	142-145	interleukin 9	Homo sapiens	108-111
8268214-6	1993	These results indicated that charge isomers of urinary bikunin was attributed to the difference on sulfation ratio in a glycosaminoglycan chain.	Glycosaminoglycans	120-137	alpha-1-microglobulin/bikunin precursor	Homo sapiens	55-62
8277293-1	1993	The p55 gag gene of simian immunodeficiency virus macaque strain (SIVmac) and the core p27 gag component linked to a synthetic AUG codon have been cloned into adenovirus type 5 vectors to generate either viable E3-replacement or defective E1-replacement viruses.	Glycosaminoglycans	8-11	H3 histone pseudogene 44	Homo sapiens	4-7
8935075-2	1993	The cells actively synthesize glycosaminoglycan (GAG), a marker of the differentiated phenotype of chondrocytes and respond well to PTH and glucocorticoids.	Glycosaminoglycans	49-52	parathyroid hormone	Oryctolagus cuniculus	132-135
8245966-6	1993	The ability of both A beta(1-28) and A beta(1-40) to bind glycosaminoglycans is pH-dependent, with increasing interaction as the pH values fall below neutrality and very little binding at pH 8.0.	Glycosaminoglycans	58-76	amyloid beta precursor protein	Homo sapiens	20-26
8245966-6	1993	The ability of both A beta(1-28) and A beta(1-40) to bind glycosaminoglycans is pH-dependent, with increasing interaction as the pH values fall below neutrality and very little binding at pH 8.0.	Glycosaminoglycans	58-76	amyloid beta precursor protein	Homo sapiens	37-43
8245966-8	1993	Analysis of the A beta sequence reveals a consensus heparin-binding domain at residues 12-17, and this motif contains histidines at positions 13 and 14 that may be involved in the interaction with glycosaminoglycans.	Glycosaminoglycans	197-215	amyloid beta precursor protein	Homo sapiens	16-22
8245966-3	1993	Here we have examined the ability of synthetic A beta s to bind to and interact with the glycosaminoglycan moieties of proteoglycans.	Glycosaminoglycans	89-106	amyloid beta precursor protein	Homo sapiens	47-53
7692086-7	1993	We conclude that deletion of the carboxyl region of the Gag-IGFR inactivates, instead of activating as in the case with Gag-IR, its transforming activity and the amino acid sequence 1250 to 1310 is essential for PTK and transforming activities.	Glycosaminoglycans	56-59	insulin like growth factor 1 receptor	Homo sapiens	60-64
8106273-4	1993	Inhibition of GAG synthesis prevented elaboration of cortical thymocyte-associated HS, IL-1, and de novo expression of the TCR, CD4, and CD8.	Glycosaminoglycans	14-17	CD4 antigen	Mus musculus	128-131
8274446-7	1993	At the early phase (18-24 h) of androgen stimulation, however, AIGF is mainly associated with the glycosaminoglycan on the cell surface or extracellular matrix.	Glycosaminoglycans	98-115	fibroblast growth factor 8	Homo sapiens	63-67
7692967-9	1993	These results suggest that antithrombin and H-kininogen may play important roles in the regulation of kallikrein activity in the presence of heparin or heparin-like glycosaminoglycans.	Glycosaminoglycans	165-183	serpin family C member 1	Homo sapiens	27-39
7692967-9	1993	These results suggest that antithrombin and H-kininogen may play important roles in the regulation of kallikrein activity in the presence of heparin or heparin-like glycosaminoglycans.	Glycosaminoglycans	165-183	kallikrein related peptidase 4	Homo sapiens	102-112
7692086-7	1993	We conclude that deletion of the carboxyl region of the Gag-IGFR inactivates, instead of activating as in the case with Gag-IR, its transforming activity and the amino acid sequence 1250 to 1310 is essential for PTK and transforming activities.	Glycosaminoglycans	56-59	insulin receptor	Homo sapiens	124-126
7692086-7	1993	We conclude that deletion of the carboxyl region of the Gag-IGFR inactivates, instead of activating as in the case with Gag-IR, its transforming activity and the amino acid sequence 1250 to 1310 is essential for PTK and transforming activities.	Glycosaminoglycans	56-59	protein tyrosine kinase 2 beta	Homo sapiens	212-215
8216207-6	1993	35%) of the total TM still lacked a glycosaminoglycan moiety.	Glycosaminoglycans	36-53	thrombomodulin	Homo sapiens	18-20
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
8397111-8	1993	We conclude that the kinase is distinct from PKA, and PKC, and suggest that changes in glycosaminoglycan and polyamine concentrations during the cell cycle may modulate FGF-2 phosphorylation in the nucleus, or as it is translocated to the nucleus.	Glycosaminoglycans	87-104	fibroblast growth factor 2	Homo sapiens	169-174
8268848-0	1993	Characterization of tumor necrosis factor alpha-induced alteration of glycosaminoglycans in cultured cells: comparison among vascular smooth-muscle cells, vascular endothelial cells, Chang liver cells and LLC-PK1 cells.	Glycosaminoglycans	70-88	tumor necrosis factor	Homo sapiens	20-47
8137133-6	1993	These and other observations suggest that an interaction of PrP with glycosaminoglycans is critical in protease-resistant PrP accumulation and raises the possibility that therapeutic strategies for TSEs and other amyloidoses could be based on blocking (pre)amyloid-glycosaminoglycan interactions.	Glycosaminoglycans	69-87	prion protein	Homo sapiens	60-63
8137133-6	1993	These and other observations suggest that an interaction of PrP with glycosaminoglycans is critical in protease-resistant PrP accumulation and raises the possibility that therapeutic strategies for TSEs and other amyloidoses could be based on blocking (pre)amyloid-glycosaminoglycan interactions.	Glycosaminoglycans	69-87	prion protein	Homo sapiens	122-125
8137133-6	1993	These and other observations suggest that an interaction of PrP with glycosaminoglycans is critical in protease-resistant PrP accumulation and raises the possibility that therapeutic strategies for TSEs and other amyloidoses could be based on blocking (pre)amyloid-glycosaminoglycan interactions.	Glycosaminoglycans	69-86	prion protein	Homo sapiens	60-63
8268848-1	1993	We investigated the alteration of glycosaminoglycans (GAGs) induced by recombinant human tumor necrosis factor alpha (rhTNF alpha) using confluent cultures of bovine aortic smooth-muscle cells, bovine aortic endothelial cells, Chang liver cells and porcine kidney LLC-PK1 cells.	Glycosaminoglycans	34-52	tumor necrosis factor	Homo sapiens	89-116
8340425-0	1993	Platelet/endothelial cell adhesion molecule-1 (CD31)-mediated cellular aggregation involves cell surface glycosaminoglycans.	Glycosaminoglycans	105-123	platelet/endothelial cell adhesion molecule 1	Mus musculus	0-45
8353136-2	1993	When these cells were treated with human recombinant interleukin 1 alpha (hrIL-1), the biosynthesis and secretion of hyaluronate were predominantly accelerated, but those of sulfated glycosaminoglycans were not modulated.	Glycosaminoglycans	183-201	interleukin 1 alpha	Homo sapiens	53-72
8217342-7	1993	In addition to single nucleotide changes, the gag regions encoding the structural protein, p19, of the HTLV-IIb isolates were also found to have a 66-bp deletion that would be expected to result in a p19 protein having a 22-amino acid deletion in the carboxy-terminus region.	Glycosaminoglycans	46-49	interleukin 23 subunit alpha	Homo sapiens	91-94
8217342-7	1993	In addition to single nucleotide changes, the gag regions encoding the structural protein, p19, of the HTLV-IIb isolates were also found to have a 66-bp deletion that would be expected to result in a p19 protein having a 22-amino acid deletion in the carboxy-terminus region.	Glycosaminoglycans	46-49	interleukin 23 subunit alpha	Homo sapiens	200-203
8244397-1	1993	Deficiency of the lysosomal enzyme iduronate-2-sulfatase (IDS; EC 3.1.6.13) results in the storage of the glycosaminoglycans heparan sulfate and dermatan sulfate, which leads to the lysosomal storage disorder mucopolysaccharidosis type II.	Glycosaminoglycans	106-124	iduronate 2-sulfatase	Homo sapiens	35-56
8244397-1	1993	Deficiency of the lysosomal enzyme iduronate-2-sulfatase (IDS; EC 3.1.6.13) results in the storage of the glycosaminoglycans heparan sulfate and dermatan sulfate, which leads to the lysosomal storage disorder mucopolysaccharidosis type II.	Glycosaminoglycans	106-124	iduronate 2-sulfatase	Homo sapiens	58-61
8356792-3	1993	The internal deletions of the latter encompass most of the gag to env region.	Glycosaminoglycans	59-62	endogenous retrovirus group K member 20	Homo sapiens	66-69
8343190-9	1993	All 10 patients with end-stage kidney disease had marked elevations of plasma CTAP-III levels, which stimulated DNA and GAG synthesis by peritoneal cells in culture.	Glycosaminoglycans	120-123	pro-platelet basic protein	Homo sapiens	78-86
8315575-2	1993	In this study, we analyzed the immune response to two recombinant gag proteins, p24 and p17, in order to evaluate their diagnostic or prognostic significance.	Glycosaminoglycans	66-69	transmembrane p24 trafficking protein 2	Homo sapiens	80-83
8315575-2	1993	In this study, we analyzed the immune response to two recombinant gag proteins, p24 and p17, in order to evaluate their diagnostic or prognostic significance.	Glycosaminoglycans	66-69	family with sequence similarity 72 member B	Homo sapiens	88-91
7982369-3	1993	The high degree of homology (94.7-97.5%) among clones (TM-1 and TM-2 from the mother, and TC-1 and TC-2 from the infant) of gag sequence provided a molecular epidemiological evidence for vertical transmission.	Glycosaminoglycans	124-127	transcobalamin 1	Homo sapiens	90-94
7982369-3	1993	The high degree of homology (94.7-97.5%) among clones (TM-1 and TM-2 from the mother, and TC-1 and TC-2 from the infant) of gag sequence provided a molecular epidemiological evidence for vertical transmission.	Glycosaminoglycans	124-127	transcobalamin 2	Homo sapiens	99-103
8340425-0	1993	Platelet/endothelial cell adhesion molecule-1 (CD31)-mediated cellular aggregation involves cell surface glycosaminoglycans.	Glycosaminoglycans	105-123	platelet/endothelial cell adhesion molecule 1	Mus musculus	47-51
8340425-5	1993	Enzymatic removal of cell surface glycosaminoglycans confirmed a PECAM-1-glycosaminoglycan interaction and suggested that this interaction involved glycosaminoglycans on adjacent cells.	Glycosaminoglycans	34-52	platelet/endothelial cell adhesion molecule 1	Mus musculus	65-72
8340425-5	1993	Enzymatic removal of cell surface glycosaminoglycans confirmed a PECAM-1-glycosaminoglycan interaction and suggested that this interaction involved glycosaminoglycans on adjacent cells.	Glycosaminoglycans	148-166	platelet/endothelial cell adhesion molecule 1	Mus musculus	65-72
8340425-10	1993	These results demonstrate that PECAM-1-mediated aggregation is dependent on the binding of PECAM-1 to specific glycosaminoglycans on adjacent cells via a glycosaminoglycan consensus binding sequence in the second immunoglobulin-like homology domain.	Glycosaminoglycans	111-129	platelet/endothelial cell adhesion molecule 1	Mus musculus	31-38
8340425-10	1993	These results demonstrate that PECAM-1-mediated aggregation is dependent on the binding of PECAM-1 to specific glycosaminoglycans on adjacent cells via a glycosaminoglycan consensus binding sequence in the second immunoglobulin-like homology domain.	Glycosaminoglycans	111-129	platelet/endothelial cell adhesion molecule 1	Mus musculus	91-98
8340425-10	1993	These results demonstrate that PECAM-1-mediated aggregation is dependent on the binding of PECAM-1 to specific glycosaminoglycans on adjacent cells via a glycosaminoglycan consensus binding sequence in the second immunoglobulin-like homology domain.	Glycosaminoglycans	111-128	platelet/endothelial cell adhesion molecule 1	Mus musculus	31-38
8340425-10	1993	These results demonstrate that PECAM-1-mediated aggregation is dependent on the binding of PECAM-1 to specific glycosaminoglycans on adjacent cells via a glycosaminoglycan consensus binding sequence in the second immunoglobulin-like homology domain.	Glycosaminoglycans	111-128	platelet/endothelial cell adhesion molecule 1	Mus musculus	91-98
8325651-1	1993	Iduronate sulfatase (IDS; EC 3.1.6.13) is a lysosomal enzyme that acts on sulfate groups on C-2 positions of iduronic acid residues of the mucopolysaccharides dermatan and heparan sulfate.	Glycosaminoglycans	139-158	iduronate 2-sulfatase	Mus musculus	0-19
8318504-5	1993	Incorporation of [35S]sulfate into biglycan glycosaminoglycan (GAG) was maximal by 12 to 18 hours after either PDGF or TGF-beta 1 addition.	Glycosaminoglycans	44-61	biglycan	Homo sapiens	35-43
8510213-3	1993	In contrast, vectors containing additional gag and env sequences were packaged with high efficiency and transduced into CD4-expressing target cells with titers exceeding 10(4) CFU/ml.	Glycosaminoglycans	43-46	CD4 molecule	Homo sapiens	120-123
8331144-5	1993	The second approach consisted of using heparin, a mucopolysaccharide with a strong affinity towards ATIII, coupled to amine-modified or epoxy-activated membranes by reductive amination, for the purification of rATIII.	Glycosaminoglycans	50-68	serpin family C member 1	Homo sapiens	100-105
8329981-0	1993	Embryonic skin fibroblasts release TGF alpha and TGF beta able to influence synthesis and secretion of GAG.	Glycosaminoglycans	103-106	transforming growth factor alpha	Gallus gallus	35-44
8329981-2	1993	The factors responsible for GAG enhancement are TGF alpha and TGF beta because they are trypsin and dithiothreitol sensitive, stable or enhanced by heat and transient acidification.	Glycosaminoglycans	28-31	transforming growth factor alpha	Gallus gallus	48-57
8329981-3	1993	Moreover, Sephadex G-75 fractions of CM active on GAG synthesis contain, when analysed on SDS-polyacrylamide gel electrophoresis, two bands that comigrate with TGF alpha and TGF beta and induce NRK cells clone 49F to form large colonies of mean size &gt; 8.000 microns 2 in soft agar.	Glycosaminoglycans	50-53	transforming growth factor alpha	Gallus gallus	160-169
8329981-7	1993	The contemporaneous addition of TGF alpha and TGF beta to 7 days-old fibroblasts produces a pattern of GAG response similar to CM.	Glycosaminoglycans	103-106	transforming growth factor alpha	Gallus gallus	32-41
8329981-8	1993	These embryonic fibroblasts may control their own GAG synthesis and secretion through autocrine TGF alpha and beta activity.	Glycosaminoglycans	50-53	transforming growth factor alpha	Gallus gallus	96-105
8318504-5	1993	Incorporation of [35S]sulfate into biglycan glycosaminoglycan (GAG) was maximal by 12 to 18 hours after either PDGF or TGF-beta 1 addition.	Glycosaminoglycans	63-66	biglycan	Homo sapiens	35-43
8318504-5	1993	Incorporation of [35S]sulfate into biglycan glycosaminoglycan (GAG) was maximal by 12 to 18 hours after either PDGF or TGF-beta 1 addition.	Glycosaminoglycans	63-66	transforming growth factor beta 1	Homo sapiens	119-129
8519127-5	1993	Similar results were found when muscle tissue was preincubated with 200 micrograms of osteosarcoma-derived BMP/NCP for four hours followed by an incubation period of 14 days in BMP-free medium: GAG synthesis increased significantly, whereas DNA synthesis did not change.	Glycosaminoglycans	194-197	bone morphogenetic protein 1	Homo sapiens	107-110
7685415-6	1993	When the mutant ORF3 included an additional frameshift mutation which extended the ORF beyond the initiation site for the gag, gag-pol, and env proteins, host cells were initially transformed but died soon thereafter.	Glycosaminoglycans	122-125	ankyrin repeat, SAM and basic leucine zipper domain containing 1	Homo sapiens	16-20
8317997-2	1993	In the young intervertebral disc, glycosaminoglycan-containing (glycanated) forms of both biglycan and decorin represented a greater proportion of the total proteoglycan population present in extracts of annulus fibrosus and cartilage end-plate compared with extracts of nucleus pulposus, in which they were barely detectable.	Glycosaminoglycans	34-51	biglycan	Homo sapiens	90-98
8317997-5	1993	Dermatan sulphate was the predominant glycosaminoglycan present on biglycan and decorin in annulus fibrosus extracts, whereas chondroitin 4-sulphate was present in both small proteoglycans isolated from cartilage end-plate.	Glycosaminoglycans	38-55	biglycan	Homo sapiens	67-75
8497055-4	1993	Paradoxically, substantial sequence variability was found in the normally high conserved gag gene (encoding p17) in most of the preseroconversion samples.	Glycosaminoglycans	89-92	family with sequence similarity 72 member B	Homo sapiens	108-111
8508806-0	1993	Biochemical bases of the interaction of human basic fibroblast growth factor with glycosaminoglycans.	Glycosaminoglycans	82-100	fibroblast growth factor 2	Homo sapiens	46-76
8394161-3	1993	We have shown that SIVmac-infected rhesus monkeys expressing the major histocompatibility complex (MHC) class I molecule Mamu-A*01 develop a SIVmac gag-specific CTL response which recognizes a 9 amino acid fragment of the gag protein in association with Mamu-A*01.	Glycosaminoglycans	148-151	major histocompatibility complex, class I, A	Macaca mulatta	121-127
8394161-3	1993	We have shown that SIVmac-infected rhesus monkeys expressing the major histocompatibility complex (MHC) class I molecule Mamu-A*01 develop a SIVmac gag-specific CTL response which recognizes a 9 amino acid fragment of the gag protein in association with Mamu-A*01.	Glycosaminoglycans	148-151	major histocompatibility complex, class I, A	Macaca mulatta	254-260
8508806-7	1993	The capacity of different GAGs to protect bFGF from proteolytic cleavage decreases in the following order: heparin &gt; heparan sulfate &gt; dermatan sulfate = chondroitin sulfates A and C &gt; hyaluronic acid = K5 polysaccharide, indicating that both the degree of sulfation and the backbone structure of GAG modulate its interaction with bFGF.	Glycosaminoglycans	26-29	fibroblast growth factor 2	Homo sapiens	42-46
8508806-7	1993	The capacity of different GAGs to protect bFGF from proteolytic cleavage decreases in the following order: heparin &gt; heparan sulfate &gt; dermatan sulfate = chondroitin sulfates A and C &gt; hyaluronic acid = K5 polysaccharide, indicating that both the degree of sulfation and the backbone structure of GAG modulate its interaction with bFGF.	Glycosaminoglycans	26-29	fibroblast growth factor 2	Homo sapiens	340-344
8508806-9	1993	Moreover, tryptic digestion studies performed with various heparin molecules and dextran sulfates of different size, ranging from 2.0 kDa to 500 kDa, indicate that the number of bFGF molecules which interact with a single molecule of polysaccharide is related to the molecular mass of the GAG and that six hexose residues are sufficient to protect 1-2 molecules bFGF.	Glycosaminoglycans	289-292	fibroblast growth factor 2	Homo sapiens	178-182
8508806-2	1993	In the present study we have attempted a characterization of the biochemical bases of the interaction of human basic fibroblast growth factor (bFGF) with glycosaminoglycans (GAGs) in solution.	Glycosaminoglycans	154-172	fibroblast growth factor 2	Homo sapiens	111-141
8508806-2	1993	In the present study we have attempted a characterization of the biochemical bases of the interaction of human basic fibroblast growth factor (bFGF) with glycosaminoglycans (GAGs) in solution.	Glycosaminoglycans	154-172	fibroblast growth factor 2	Homo sapiens	143-147
8508806-2	1993	In the present study we have attempted a characterization of the biochemical bases of the interaction of human basic fibroblast growth factor (bFGF) with glycosaminoglycans (GAGs) in solution.	Glycosaminoglycans	174-178	fibroblast growth factor 2	Homo sapiens	111-141
8508806-2	1993	In the present study we have attempted a characterization of the biochemical bases of the interaction of human basic fibroblast growth factor (bFGF) with glycosaminoglycans (GAGs) in solution.	Glycosaminoglycans	174-178	fibroblast growth factor 2	Homo sapiens	143-147
8508806-3	1993	This interaction has been evidenced as the capacity of different GAGs and various sulfated compounds to protect bFGF and different bFGF mutants from tryptic cleavage.	Glycosaminoglycans	65-69	fibroblast growth factor 2	Homo sapiens	112-116
8508806-10	1993	In conclusion, our findings indicate that the capacity of GAGs to protect bFGF from tryptic cleavage depends upon their size, sulfation, distribution of the anionic sites along the chain, and structural requirements of the bFGF molecule.	Glycosaminoglycans	58-62	fibroblast growth factor 2	Homo sapiens	74-78
8508806-3	1993	This interaction has been evidenced as the capacity of different GAGs and various sulfated compounds to protect bFGF and different bFGF mutants from tryptic cleavage.	Glycosaminoglycans	65-69	fibroblast growth factor 2	Homo sapiens	131-135
8508806-10	1993	In conclusion, our findings indicate that the capacity of GAGs to protect bFGF from tryptic cleavage depends upon their size, sulfation, distribution of the anionic sites along the chain, and structural requirements of the bFGF molecule.	Glycosaminoglycans	58-62	fibroblast growth factor 2	Homo sapiens	223-227
8508806-7	1993	The capacity of different GAGs to protect bFGF from proteolytic cleavage decreases in the following order: heparin &gt; heparan sulfate &gt; dermatan sulfate = chondroitin sulfates A and C &gt; hyaluronic acid = K5 polysaccharide, indicating that both the degree of sulfation and the backbone structure of GAG modulate its interaction with bFGF.	Glycosaminoglycans	26-30	fibroblast growth factor 2	Homo sapiens	42-46
8508806-7	1993	The capacity of different GAGs to protect bFGF from proteolytic cleavage decreases in the following order: heparin &gt; heparan sulfate &gt; dermatan sulfate = chondroitin sulfates A and C &gt; hyaluronic acid = K5 polysaccharide, indicating that both the degree of sulfation and the backbone structure of GAG modulate its interaction with bFGF.	Glycosaminoglycans	26-30	fibroblast growth factor 2	Homo sapiens	340-344
8489237-0	1993	Effects of heparin and other glycosaminoglycans on elastin production by cultured neonatal rat lung fibroblasts.	Glycosaminoglycans	29-47	elastin	Rattus norvegicus	51-58
8489237-7	1993	The galactosamine-containing glycosaminoglycans, chondroitin sulfate and dermatan sulfate, differ from heparin in that they increase the quantity of soluble elastin in the culture medium and decrease the deposition of insoluble elastin in the extracellular matrix.	Glycosaminoglycans	29-47	elastin	Rattus norvegicus	157-164
8489237-7	1993	The galactosamine-containing glycosaminoglycans, chondroitin sulfate and dermatan sulfate, differ from heparin in that they increase the quantity of soluble elastin in the culture medium and decrease the deposition of insoluble elastin in the extracellular matrix.	Glycosaminoglycans	29-47	elastin	Rattus norvegicus	228-235
8491733-0	1993	Yeast MAK3 N-acetyltransferase recognizes the N-terminal four amino acids of the major coat protein (gag) of the L-A double-stranded RNA virus.	Glycosaminoglycans	101-104	peptide alpha-N-acetyltransferase MAK3	Saccharomyces cerevisiae S288C	6-10
7687596-8	1993	(3) In enzymatically digested cartilage matrix, staining with soybean agglutinin (SBA) may be due to link protein, but not to chondroitin sulphate, because specific breakdown of the glycosaminoglycan chain is required for binding of SBA.	Glycosaminoglycans	182-199	lectin	Glycine max	82-85
8491733-0	1993	Yeast MAK3 N-acetyltransferase recognizes the N-terminal four amino acids of the major coat protein (gag) of the L-A double-stranded RNA virus.	Glycosaminoglycans	101-104	N-acetyltransferase	Saccharomyces cerevisiae S288C	11-30
8491733-2	1993	We show that the first 4 amino acids of the L-A gag protein sequence, MLRF, are a portable signal for N-terminal acetylation by MAK3.	Glycosaminoglycans	48-51	peptide alpha-N-acetyltransferase MAK3	Saccharomyces cerevisiae S288C	128-132
7903507-6	1993	Neo-resistant clones exhibited an integrated viral DNA, low viral mRNA expression and (as in F12 cells) the presence of uncleaved gp160, no gp41 and a small amount of p55 gag precursor.	Glycosaminoglycans	171-174	H3 histone pseudogene 44	Homo sapiens	167-170
8386280-6	1993	Point mutations in the RSV gag intragenic enhancer region, which blocked binding of C/EBP at two of three adjacent C/EBP sites, also reduced virus production significantly.	Glycosaminoglycans	27-30	CCAAT enhancer binding protein alpha	Homo sapiens	84-89
8386280-6	1993	Point mutations in the RSV gag intragenic enhancer region, which blocked binding of C/EBP at two of three adjacent C/EBP sites, also reduced virus production significantly.	Glycosaminoglycans	27-30	CCAAT enhancer binding protein alpha	Homo sapiens	115-120
8483924-8	1993	By heparin affinity chromatography, gp330 and RAP copurify, indicating that the glycosaminoglycan binding site within RAP is accessible when the subunit is complexed with gp330.	Glycosaminoglycans	80-97	LDL receptor related protein 2	Rattus norvegicus	36-41
8483924-8	1993	By heparin affinity chromatography, gp330 and RAP copurify, indicating that the glycosaminoglycan binding site within RAP is accessible when the subunit is complexed with gp330.	Glycosaminoglycans	80-97	LDL receptor related protein associated protein 1	Rattus norvegicus	46-49
8483924-8	1993	By heparin affinity chromatography, gp330 and RAP copurify, indicating that the glycosaminoglycan binding site within RAP is accessible when the subunit is complexed with gp330.	Glycosaminoglycans	80-97	LDL receptor related protein associated protein 1	Rattus norvegicus	118-121
8483924-8	1993	By heparin affinity chromatography, gp330 and RAP copurify, indicating that the glycosaminoglycan binding site within RAP is accessible when the subunit is complexed with gp330.	Glycosaminoglycans	80-97	LDL receptor related protein 2	Rattus norvegicus	171-176
8454874-12	1993	Low levels of HIV-specific CTL activity, especially against gag, were correlated with lower CD4+ cells numbers, suggesting that the loss of CD8+ T cell cytotoxic activity against HIV that has been reported to occur with advancing HIV disease progression may reflect in part the extent of CD4+ cell immunodeficiency in HIV-infected subjects.	Glycosaminoglycans	60-63	CD4 molecule	Homo sapiens	92-95
8386194-7	1993	A TM polypeptide fragment comprising the extracellular domain that includes its naturally occurring anionic glycosaminoglycan (GAG) moiety (TMD-105) is strongly inhibited by MBP, whereas its counterpart lacking the GAG moiety (TMD-75) is not.	Glycosaminoglycans	108-125	myelin basic protein	Oryctolagus cuniculus	174-177
8386194-7	1993	A TM polypeptide fragment comprising the extracellular domain that includes its naturally occurring anionic glycosaminoglycan (GAG) moiety (TMD-105) is strongly inhibited by MBP, whereas its counterpart lacking the GAG moiety (TMD-75) is not.	Glycosaminoglycans	127-130	myelin basic protein	Oryctolagus cuniculus	174-177
8386194-7	1993	A TM polypeptide fragment comprising the extracellular domain that includes its naturally occurring anionic glycosaminoglycan (GAG) moiety (TMD-105) is strongly inhibited by MBP, whereas its counterpart lacking the GAG moiety (TMD-75) is not.	Glycosaminoglycans	215-218	myelin basic protein	Oryctolagus cuniculus	174-177
8340608-7	1993	Similar effects of TGF alpha and TGF beta 1 have been observed on the glycosaminoglycan-([35S]sulfate incorporation) and proteoglycan level ([3H]leucin incorporation into decorin and biglycan).	Glycosaminoglycans	70-87	transforming growth factor alpha	Rattus norvegicus	19-28
8340608-7	1993	Similar effects of TGF alpha and TGF beta 1 have been observed on the glycosaminoglycan-([35S]sulfate incorporation) and proteoglycan level ([3H]leucin incorporation into decorin and biglycan).	Glycosaminoglycans	70-87	transforming growth factor, beta 1	Rattus norvegicus	33-43
8440685-3	1993	In solution, heparin cofactor II inhibition of thrombin is accelerated by intact biglycan or decorin and by the dermatan sulfate-containing glycosaminoglycan (GAG) chains prepared from the proteoglycans, while core protein from cartilage biglycan had no effect.	Glycosaminoglycans	159-162	biglycan	Homo sapiens	238-246
8479152-4	1993	EXPERIMENTAL DESIGN: The identification and structural analyses of the sulfated glycosaminoglycans were made by electrophoresis and degradation with specific enzymes (chondroitinases AC and ABC), identification/quantitation of their disaccharide products by chromatography (paper and HPLC) and chemical determinations.	Glycosaminoglycans	80-98	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	167-193
8384442-0	1993	Role of the glycosaminoglycan component of thrombomodulin in its acceleration of the inactivation of single-chain urokinase-type plasminogen activator by thrombin.	Glycosaminoglycans	12-29	thrombomodulin	Homo sapiens	43-57
8384442-0	1993	Role of the glycosaminoglycan component of thrombomodulin in its acceleration of the inactivation of single-chain urokinase-type plasminogen activator by thrombin.	Glycosaminoglycans	12-29	coagulation factor II, thrombin	Homo sapiens	154-162
8384442-8	1993	Treatment of high-Mr rec-TM with chondroitinase ABC to digest the glycosaminoglycans decreased the accelerating effect to the level of low-Mr rec-TM.	Glycosaminoglycans	66-84	thrombomodulin	Homo sapiens	25-27
8384442-8	1993	Treatment of high-Mr rec-TM with chondroitinase ABC to digest the glycosaminoglycans decreased the accelerating effect to the level of low-Mr rec-TM.	Glycosaminoglycans	66-84	thrombomodulin	Homo sapiens	146-148
8452875-0	1993	Tumor necrosis factor alpha-induced alteration of glycosaminoglycans in cultured vascular smooth-muscle cells.	Glycosaminoglycans	50-68	tumor necrosis factor	Homo sapiens	0-27
8452875-1	1993	We studied alteration of glycosaminoglycans (GAGs) induced by recombinant human tumor necrosis factor alpha (rhTNF alpha) in vascular smooth-muscle cells from bovine aorta in a culture system.	Glycosaminoglycans	25-43	tumor necrosis factor	Homo sapiens	80-107
8339853-7	1993	This study shows an altered fibrinolytic response to increased thrombin activation in Type 1 diabetic patients and suggests that the administration of the glycosaminoglycan, Sulodexide, may help to reduce this phenomenon.	Glycosaminoglycans	155-172	coagulation factor II, thrombin	Homo sapiens	63-71
8501849-8	1993	Urinary apo H levels correlated positively with urinary levels of glycosaminoglycan (r = 0.382, n = 45, p &lt; 0.01), which was regarded as an indicator of the anion loss from glomerular basement membrane to urine, and with urinary N-acetyl-beta-D-glucosaminidase activities (r = 0.378, n = 37, p &lt; 0.05).	Glycosaminoglycans	66-83	apolipoprotein H	Homo sapiens	8-13
8440685-3	1993	In solution, heparin cofactor II inhibition of thrombin is accelerated by intact biglycan or decorin and by the dermatan sulfate-containing glycosaminoglycan (GAG) chains prepared from the proteoglycans, while core protein from cartilage biglycan had no effect.	Glycosaminoglycans	140-157	coagulation factor II, thrombin	Homo sapiens	47-55
8440685-3	1993	In solution, heparin cofactor II inhibition of thrombin is accelerated by intact biglycan or decorin and by the dermatan sulfate-containing glycosaminoglycan (GAG) chains prepared from the proteoglycans, while core protein from cartilage biglycan had no effect.	Glycosaminoglycans	159-162	coagulation factor II, thrombin	Homo sapiens	47-55
8440685-5	1993	Treatment of skin decorin and GAG chains with chondroitinase ABC totally eliminated the ability of these compounds to accelerate thrombin inhibition by heparin cofactor II suggesting that dermatan sulfate was responsible for this action.	Glycosaminoglycans	30-33	coagulation factor II, thrombin	Homo sapiens	129-137
8429008-1	1993	Heparin cofactor II and antithrombin are plasma serine proteinase inhibitors whose ability to inhibit alpha-thrombin is accelerated by glycosaminoglycans.	Glycosaminoglycans	135-153	serpin family C member 1	Homo sapiens	24-36
8439543-9	1993	The results suggest that, with the proper secondary structure induced by the lipid environment, the segment RLTRKRRGLK of apoB-100 is an important determinant of the association of LDL and VLDL with glycosaminoglycans but that probably other basic segments contribute to this interaction.	Glycosaminoglycans	199-217	apolipoprotein B	Homo sapiens	122-130
8429008-1	1993	Heparin cofactor II and antithrombin are plasma serine proteinase inhibitors whose ability to inhibit alpha-thrombin is accelerated by glycosaminoglycans.	Glycosaminoglycans	135-153	coagulation factor II, thrombin	Homo sapiens	28-36
8429040-3	1993	Thrombin is inhibited by the serpins antithrombin III and heparin cofactor II in a reaction that is dramatically accelerated by glycosaminoglycans.	Glycosaminoglycans	128-146	coagulation factor II, thrombin	Homo sapiens	0-8
8429040-3	1993	Thrombin is inhibited by the serpins antithrombin III and heparin cofactor II in a reaction that is dramatically accelerated by glycosaminoglycans.	Glycosaminoglycans	128-146	serpin family C member 1	Homo sapiens	37-53
8429008-7	1993	We also found that heparin cofactor II formed a SDS-resistant bimolecular complex with Quick II and alpha-thrombin at similar rates and the rate of complex formation was accelerated in the presence of glycosaminoglycans.	Glycosaminoglycans	201-219	coagulation factor II, thrombin	Homo sapiens	106-114
8429040-8	1993	In contrast, the rate constant for inhibition by heparin cofactor II without glycosaminoglycan was 4.3 x 10(4) M-1 min-1 for wild-type thrombin; rates were 10-fold slower for thrombin K52E and 2- to 3-fold slower for thrombins R68E and R70E.	Glycosaminoglycans	77-94	coagulation factor II, thrombin	Homo sapiens	135-143
8429040-10	1993	Compared to wild-type thrombin, the rate of inhibition by HCII with glycosaminoglycan was 5- to 15-fold slower for thrombins K52E and R70E and 50- to over 100-fold slower for thrombin R68E.	Glycosaminoglycans	68-85	coagulation factor II, thrombin	Homo sapiens	22-30
8429040-10	1993	Compared to wild-type thrombin, the rate of inhibition by HCII with glycosaminoglycan was 5- to 15-fold slower for thrombins K52E and R70E and 50- to over 100-fold slower for thrombin R68E.	Glycosaminoglycans	68-85	serpin family D member 1	Homo sapiens	58-62
8429040-10	1993	Compared to wild-type thrombin, the rate of inhibition by HCII with glycosaminoglycan was 5- to 15-fold slower for thrombins K52E and R70E and 50- to over 100-fold slower for thrombin R68E.	Glycosaminoglycans	68-85	coagulation factor II, thrombin	Homo sapiens	115-123
8431448-5	1993	In addition, a qualitative analysis was performed by determining the formation of SDS-stable, equimolar complexes between thrombin and PAI-1 in the presence of various glycosaminoglycans.	Glycosaminoglycans	168-186	coagulation factor II, thrombin	Homo sapiens	122-130
8431448-5	1993	In addition, a qualitative analysis was performed by determining the formation of SDS-stable, equimolar complexes between thrombin and PAI-1 in the presence of various glycosaminoglycans.	Glycosaminoglycans	168-186	serpin family E member 1	Homo sapiens	135-140
8429008-9	1993	The importance of heparin cofactor II as a thrombin regulator will depend upon its ability to interact with glycosaminoglycans and the functional availability of thrombin exosites.	Glycosaminoglycans	108-126	coagulation factor II, thrombin	Homo sapiens	43-51
7679511-4	1993	The two aberrant RNAs result from splicing of gag to either exon 3 or 4 of c-myb, depending on the site of proviral integration.	Glycosaminoglycans	46-49	myeloblastosis oncogene	Mus musculus	75-80
8328911-3	1993	The specific proteolytic activity of the recombinant protease on the gag and pol precursor proteins was used for the generation of processed gag (p 17, p 24, p 16) and pol (RT/RNaseH, IN) proteins.	Glycosaminoglycans	69-72	family with sequence similarity 72 member B	Homo sapiens	146-150
8381453-8	1993	Removal of cell surface-associated GAGs by culturing cells in 4-methylumbelliferyl-beta-D-xyloside ablated the effect of heparin on apoE.	Glycosaminoglycans	35-39	apolipoprotein E	Homo sapiens	132-136
8381453-10	1993	The results provide evidence that a heparin-releasable pool of newly synthesized apoE is associated with cell surface GAGs that resemble heparin and/or heparan sulfate.	Glycosaminoglycans	118-122	apolipoprotein E	Homo sapiens	81-85
8446935-1	1993	The mode of action of glycosaminoglycans (GAGs) towards thrombus formation in a rat arteriovenous shunt was studied by simultaneous examination of thrombus weight, platelet consumption and thrombin generation during 45 min of blood circulation.	Glycosaminoglycans	22-40	coagulation factor II	Rattus norvegicus	189-197
8423178-5	1993	In contrast, IGF-I stimulated a maximum incorporation of 35S-sulfate into glycosaminoglycans that was 2.6 times that in the IGF-I serum-free control cultures, while bFGF had no effect or was mildly inhibitory.	Glycosaminoglycans	74-92	insulin-like growth factor 1	Rattus norvegicus	13-18
7678300-9	1993	Since PrP-res amyloid is known to contain sulfated glycosaminoglycans, we reason that these inhibitors may competitively block an interaction between PrP and endogenous glycosaminoglycans that is essential for its accumulation in a protease-resistant, potentially amyloidogenic state.	Glycosaminoglycans	51-69	prion protein	Homo sapiens	6-9
7678300-9	1993	Since PrP-res amyloid is known to contain sulfated glycosaminoglycans, we reason that these inhibitors may competitively block an interaction between PrP and endogenous glycosaminoglycans that is essential for its accumulation in a protease-resistant, potentially amyloidogenic state.	Glycosaminoglycans	51-69	prion protein	Homo sapiens	150-153
7678300-9	1993	Since PrP-res amyloid is known to contain sulfated glycosaminoglycans, we reason that these inhibitors may competitively block an interaction between PrP and endogenous glycosaminoglycans that is essential for its accumulation in a protease-resistant, potentially amyloidogenic state.	Glycosaminoglycans	169-187	prion protein	Homo sapiens	6-9
7678300-9	1993	Since PrP-res amyloid is known to contain sulfated glycosaminoglycans, we reason that these inhibitors may competitively block an interaction between PrP and endogenous glycosaminoglycans that is essential for its accumulation in a protease-resistant, potentially amyloidogenic state.	Glycosaminoglycans	169-187	prion protein	Homo sapiens	150-153
8273556-6	1993	TGF-beta and IGF-I increased the amount of S-GAG in both the medium and cell surface compartments, but did not protect from IL-1-induced release.	Glycosaminoglycans	45-48	insulin like growth factor 1	Homo sapiens	13-18
8427512-3	1993	The loss of glycosaminoglycan by rat and human femoral head cartilage in response to human recombinant interleukin 1 beta (rhIL-1 beta) was established, and the modulation of this loss by the metalloproteinase inhibitor U27391 was investigated.	Glycosaminoglycans	12-29	interleukin 1 beta	Homo sapiens	103-121
8328911-3	1993	The specific proteolytic activity of the recombinant protease on the gag and pol precursor proteins was used for the generation of processed gag (p 17, p 24, p 16) and pol (RT/RNaseH, IN) proteins.	Glycosaminoglycans	69-72	transmembrane p24 trafficking protein 2	Homo sapiens	152-156
8328911-3	1993	The specific proteolytic activity of the recombinant protease on the gag and pol precursor proteins was used for the generation of processed gag (p 17, p 24, p 16) and pol (RT/RNaseH, IN) proteins.	Glycosaminoglycans	69-72	cyclin dependent kinase inhibitor 2A	Homo sapiens	158-162
8419401-9	1993	This was the case also when 125I-bFGF was internalized in the presence of soluble heparin, suggesting that the complexes bFGF-cell surface glycosaminoglycan and bFGF-soluble heparin are maintained during the internalization of the growth factor.	Glycosaminoglycans	139-156	fibroblast growth factor 2	Bos taurus	33-37
8419401-9	1993	This was the case also when 125I-bFGF was internalized in the presence of soluble heparin, suggesting that the complexes bFGF-cell surface glycosaminoglycan and bFGF-soluble heparin are maintained during the internalization of the growth factor.	Glycosaminoglycans	139-156	fibroblast growth factor 2	Bos taurus	121-125
8419401-9	1993	This was the case also when 125I-bFGF was internalized in the presence of soluble heparin, suggesting that the complexes bFGF-cell surface glycosaminoglycan and bFGF-soluble heparin are maintained during the internalization of the growth factor.	Glycosaminoglycans	139-156	fibroblast growth factor 2	Bos taurus	121-125
8302410-1	1993	The relationship between glycosaminoglycans and beta 2-microglobulin, glycosaminoglycans and N-acetyl-beta-D-glucosaminidase as well as the relationship between the chondroitin sulfate/heparan sulfate ratio and SDS electrophoresis in the urine of subjects from the endemic area of Balkan nephropathy was studied in order to establish a method for early detection of this disease.	Glycosaminoglycans	25-43	beta-2-microglobulin	Homo sapiens	48-68
8233684-6	1993	As changes in mucopolysaccharide metabolism may be associated with an increased risk of developing neoplasms, the possibility of an intracranial tumor should be considered in patients with MPS I/H and high-pressure hydrocephalus.	Glycosaminoglycans	14-32	gremlin 1, DAN family BMP antagonist	Homo sapiens	189-196
8321358-8	1993	The glomerular GAG level in ADR-treated rats was greatly reduced as compared to controls; this decrease was partly eliminated in rats on an LPD.	Glycosaminoglycans	15-18	acyl-CoA synthetase bubblegum family member 1	Rattus norvegicus	140-143
8321358-9	1993	These results suggest that an LPD has a direct effect on cellular GAG production and turnover in ADR-induced glomerulonephritis.	Glycosaminoglycans	66-69	acyl-CoA synthetase bubblegum family member 1	Rattus norvegicus	30-33
8446427-3	1993	A partial inactivity of galactosyltransferase I which catalyzes the second glycosyl transfer reaction in the assembly of glycosaminoglycan chains has been shown to represent the primary defect in one of the patients.	Glycosaminoglycans	121-138	beta-1,4-galactosyltransferase 7	Homo sapiens	24-47
8516624-4	1993	Endotoxin-free recombinant mouse LIF was found to produce a dose-dependent increase in sulphated glycosaminoglycan (S-GAG) release (ED50 = 123 U/ml, approx.	Glycosaminoglycans	97-114	leukemia inhibitory factor	Mus musculus	33-36
8516624-7	1993	When pig cartilage was stimulated with maximum concentrations of LIF and either interleukin 1 alpha (IL-1 alpha), interleukin 1 beta (IL-1 beta) or tumour necrosis factor alpha (TNF alpha), in each case a significantly greater release of S-GAGs was observed than with the respective cytokines alone (P &lt; 0.05).	Glycosaminoglycans	238-244	interleukin 1 alpha	Sus scrofa	80-99
8516624-7	1993	When pig cartilage was stimulated with maximum concentrations of LIF and either interleukin 1 alpha (IL-1 alpha), interleukin 1 beta (IL-1 beta) or tumour necrosis factor alpha (TNF alpha), in each case a significantly greater release of S-GAGs was observed than with the respective cytokines alone (P &lt; 0.05).	Glycosaminoglycans	238-244	interleukin-1 beta	Sus scrofa	114-132
1476308-7	1992	Explants obtained from older horses were significantly (P &lt; 0.05) less responsive to interleukin 1, with respect to synthesis and release of glycosaminoglycan.	Glycosaminoglycans	144-161	interleukin 1 alpha	Homo sapiens	88-101
8333147-5	1993	The authors concluded that the simultaneous presence of glycosaminoglycans as matrix substance with BMP-mediated cellular activity of modified myoepithelial cells in the formation of chondroid structures in pleomorphic adenomas of the salivary glands.	Glycosaminoglycans	56-74	bone morphogenetic protein 1	Homo sapiens	100-103
1460291-2	1992	Previous studies have demonstrated that simian immunodeficiency virus of macaques (SIVmac)-infected rhesus monkeys expressing the MHC class I allele Mamu-A*01 reproducibly develop a gag-specific CTL response limited to a 9-amino acid epitope of the SIVmac gag protein (residues 182-190 within peptide 11C).	Glycosaminoglycans	182-185	major histocompatibility complex, class I, A	Macaca mulatta	149-155
1339244-0	1992	Glycosaminoglycans regulate the enzyme specificity of protein C inhibitor.	Glycosaminoglycans	0-18	serpin family A member 5	Homo sapiens	54-73
1333980-2	1992	It is also seen in cultured aortic (Ao) smooth muscle cells (SMC) following the release of the EBP by glycosaminoglycans rich in N-acetylgalactosamine, such as chondroitin sulfate (CS).	Glycosaminoglycans	102-120	3-beta-hydroxysteroid-Delta(8),Delta(7)-isomerase	Ovis aries	95-98
1457283-13	1992	Interleukin-6 has been shown to stimulate fibroblast synthesis of collagen and glycosaminoglycans.	Glycosaminoglycans	79-97	interleukin 6	Homo sapiens	0-13
1329776-9	1992	High UDPGD activity probably reflects a preferential ability to synthesize glycosaminoglycans, including hyaluronan.	Glycosaminoglycans	75-93	UDP-glucose 6-dehydrogenase	Homo sapiens	5-10
1431141-5	1992	Competition studies using purified preparations of the decorin core protein and the glycosaminoglycan chains showed that only the former inhibited binding of decorin to C1q indicating that the interaction is mediated by the decorin core protein.	Glycosaminoglycans	84-101	decorin	Homo sapiens	158-165
1431141-5	1992	Competition studies using purified preparations of the decorin core protein and the glycosaminoglycan chains showed that only the former inhibited binding of decorin to C1q indicating that the interaction is mediated by the decorin core protein.	Glycosaminoglycans	84-101	complement C1q A chain	Homo sapiens	169-172
1431141-5	1992	Competition studies using purified preparations of the decorin core protein and the glycosaminoglycan chains showed that only the former inhibited binding of decorin to C1q indicating that the interaction is mediated by the decorin core protein.	Glycosaminoglycans	84-101	decorin	Homo sapiens	158-165
1429568-6	1992	Internalization of bFGF in CHO cells not expressing FGF receptors was inhibited by heparin, heparan sulfate, and dermatan sulfate, the same glycosaminoglycans that block binding to cell-surface heparin sulfates.	Glycosaminoglycans	140-158	fibroblast growth factor 2	Bos taurus	19-23
1429568-6	1992	Internalization of bFGF in CHO cells not expressing FGF receptors was inhibited by heparin, heparan sulfate, and dermatan sulfate, the same glycosaminoglycans that block binding to cell-surface heparin sulfates.	Glycosaminoglycans	140-158	fibroblast growth factor 2	Bos taurus	20-23
1425926-0	1992	Selective and differential binding of interleukin (IL)-1 alpha, IL-1 beta, IL-2 and IL-6 to glycosaminoglycans.	Glycosaminoglycans	92-110	interleukin 1 alpha	Mus musculus	38-62
1425926-0	1992	Selective and differential binding of interleukin (IL)-1 alpha, IL-1 beta, IL-2 and IL-6 to glycosaminoglycans.	Glycosaminoglycans	92-110	interleukin 1 beta	Mus musculus	64-73
1425926-0	1992	Selective and differential binding of interleukin (IL)-1 alpha, IL-1 beta, IL-2 and IL-6 to glycosaminoglycans.	Glycosaminoglycans	92-110	interleukin 2	Mus musculus	75-79
1425926-0	1992	Selective and differential binding of interleukin (IL)-1 alpha, IL-1 beta, IL-2 and IL-6 to glycosaminoglycans.	Glycosaminoglycans	92-110	interleukin 6	Mus musculus	84-88
1465181-2	1992	In this study, we used this technique to show that acetylcholinesterase localized in either frozen or fixed neocortical tissue sections is removed after treatment with various glycosaminoglycans, heparinases or proteases.	Glycosaminoglycans	176-194	acetylcholinesterase (Cartwright blood group)	Homo sapiens	51-71
1466841-8	1992	RESULTS: Infected cells revealed the presence of gag p24, pol, and env gp41 and gp120 antigens on HIV-1 virions.	Glycosaminoglycans	49-52	transmembrane p24 trafficking protein 2	Homo sapiens	53-56
1404799-8	1992	Two neuropathologically confirmed cases and five of nine at-risk family members had an identical mutation (GAG to AAG, glutamic acid to lysine) in codon 200 of the amyloid gene (PRNP) on chromosome 20.	Glycosaminoglycans	107-110	prion protein	Homo sapiens	178-182
1385448-0	1992	Endothelial cells interact with the core protein of basement membrane perlecan through beta 1 and beta 3 integrins: an adhesion modulated by glycosaminoglycan.	Glycosaminoglycans	141-158	hemoglobin, beta adult major chain	Mus musculus	87-104
1356443-2	1992	Sequence analysis of the DNA of the proband that was amplified by PCR and subcloned, revealed a single substitution of one lysine (AAG) for one glutamic acid (GAG) at position 146, thereby adding two negatively charged units to apo E3.	Glycosaminoglycans	159-162	N-methylpurine DNA glycosylase	Homo sapiens	131-134
1427856-1	1992	Arylsulfatase B (ARSB) is the lysosomal enzyme that catalyzes the hydrolysis of 4-sulfate groups from N-acetylgalactosamine 4-sulfate moieties on the glycosaminoglycans, dermatan sulfate and chondroitin sulfate A.	Glycosaminoglycans	150-168	arylsulfatase B	Homo sapiens	0-15
1427856-1	1992	Arylsulfatase B (ARSB) is the lysosomal enzyme that catalyzes the hydrolysis of 4-sulfate groups from N-acetylgalactosamine 4-sulfate moieties on the glycosaminoglycans, dermatan sulfate and chondroitin sulfate A.	Glycosaminoglycans	150-168	arylsulfatase B	Homo sapiens	17-21
1519362-4	1992	The long open reading frame in the cloned cDNA starts with six gag-derived codons spliced to the myb-specific sequence.	Glycosaminoglycans	63-66	MYB proto-oncogene, transcription factor	Gallus gallus	97-100
1396956-4	1992	However, the expression of the p24 product of the gag gene was markedly decreased after IFN treatment as demonstrated by radio-immunoprecipitation assay.	Glycosaminoglycans	50-53	transmembrane p24 trafficking protein 2	Homo sapiens	31-34
1396956-4	1992	However, the expression of the p24 product of the gag gene was markedly decreased after IFN treatment as demonstrated by radio-immunoprecipitation assay.	Glycosaminoglycans	50-53	interferon alpha 1	Homo sapiens	88-91
1337758-1	1992	The responsiveness of human dental pulp (HDP) cells to parathyroid hormone (PTH) was investigated by measuring their cyclic AMP (cAMP) content, DNA synthesis, alkaline phosphatase activity, collagen synthesis, and glycosaminoglycan (GAG) synthesis.	Glycosaminoglycans	214-231	parathyroid hormone	Homo sapiens	55-74
1337758-1	1992	The responsiveness of human dental pulp (HDP) cells to parathyroid hormone (PTH) was investigated by measuring their cyclic AMP (cAMP) content, DNA synthesis, alkaline phosphatase activity, collagen synthesis, and glycosaminoglycan (GAG) synthesis.	Glycosaminoglycans	233-236	parathyroid hormone	Homo sapiens	55-74
1527075-1	1992	Connective tissue activating peptide-III (CTAP-III) is a component of platelet alpha-granules which elicits a series of responses in connective tissue cells referred to as activation, including increased glucose consumption and mitogenesis and increased secretion of hyaluronic acid and glycosaminoglycans.	Glycosaminoglycans	287-305	pro-platelet basic protein	Homo sapiens	0-40
1527075-1	1992	Connective tissue activating peptide-III (CTAP-III) is a component of platelet alpha-granules which elicits a series of responses in connective tissue cells referred to as activation, including increased glucose consumption and mitogenesis and increased secretion of hyaluronic acid and glycosaminoglycans.	Glycosaminoglycans	287-305	pro-platelet basic protein	Homo sapiens	42-50
1505778-1	1992	The secretory enzyme extracellular-superoxide dismutase (EC-SOD) has affinity for heparin and some other sulfated glycosaminoglycans and is in vivo bound to heparan sulfate proteoglycan.	Glycosaminoglycans	114-132	superoxide dismutase 3	Homo sapiens	21-55
1525174-1	1992	Interferon-gamma binds to the glycosaminoglycan part of basement membrane proteoglycan.	Glycosaminoglycans	30-47	interferon gamma	Homo sapiens	0-16
1477353-2	1992	It was established that IL1a leads to cartilage degradation as shown by an increase of sulphated glycosaminoglycans (sGAG) in culture medium and their decrease in tissue, inhibition of proteoglycan (PG) synthesis by chondrocytes.	Glycosaminoglycans	97-115	interleukin 1 alpha	Homo sapiens	24-28
1505778-1	1992	The secretory enzyme extracellular-superoxide dismutase (EC-SOD) has affinity for heparin and some other sulfated glycosaminoglycans and is in vivo bound to heparan sulfate proteoglycan.	Glycosaminoglycans	114-132	superoxide dismutase 3	Homo sapiens	57-63
1380097-8	1992	Since the sequential order of the viral proteins in the Gag precursor is p10-pp21-p27-p14 and that in Gag-Pro is p10-pp21-p27-p30-protease, our results demonstrate the radial organization of the polypeptide precursors forming the intracytoplasmic A particles.	Glycosaminoglycans	56-59	S100 calcium binding protein A10	Homo sapiens	73-76
1501276-8	1992	Three of the nucleotide substitutions were in the gag gene, resulting in one coding change in p15 and one in p30.	Glycosaminoglycans	50-53	cyclin dependent kinase inhibitor 2B	Homo sapiens	94-97
1380097-8	1992	Since the sequential order of the viral proteins in the Gag precursor is p10-pp21-p27-p14 and that in Gag-Pro is p10-pp21-p27-p30-protease, our results demonstrate the radial organization of the polypeptide precursors forming the intracytoplasmic A particles.	Glycosaminoglycans	56-59	interferon alpha inducible protein 27	Homo sapiens	82-85
1501276-8	1992	Three of the nucleotide substitutions were in the gag gene, resulting in one coding change in p15 and one in p30.	Glycosaminoglycans	50-53	centromere protein V	Homo sapiens	109-112
1380097-8	1992	Since the sequential order of the viral proteins in the Gag precursor is p10-pp21-p27-p14 and that in Gag-Pro is p10-pp21-p27-p30-protease, our results demonstrate the radial organization of the polypeptide precursors forming the intracytoplasmic A particles.	Glycosaminoglycans	56-59	ribonuclease P/MRP subunit p14	Homo sapiens	86-89
1498333-8	1992	The blocking activity of the eluted MP+ HS-PG bands depended partly on the amount of GAG attached to the protein core and presumably partly on the structure of the core itself.	Glycosaminoglycans	85-88	CD44 molecule (Indian blood group)	Homo sapiens	40-45
1394971-1	1992	We have investigated the ability of glycosaminoglycans from embryonic chick brain (15 days old) to interact with basic fibroblast growth factor (bFGF).	Glycosaminoglycans	36-54	fibroblast growth factor 2	Gallus gallus	113-143
1394971-1	1992	We have investigated the ability of glycosaminoglycans from embryonic chick brain (15 days old) to interact with basic fibroblast growth factor (bFGF).	Glycosaminoglycans	36-54	fibroblast growth factor 2	Gallus gallus	145-149
1504096-7	1992	It is a 90-kDa HSPG with a hydrophobic core protein and glycosaminoglycan chains similar in size to those of HS1.	Glycosaminoglycans	56-73	syndecan 2	Rattus norvegicus	15-19
1497618-2	1992	Comparison of the affinity of bFGF to various glycosaminoglycan-conjugated gels showed a direct and specific binding of bFGF to heparan sulphate.	Glycosaminoglycans	46-63	fibroblast growth factor 2	Mus musculus	120-124
1497624-7	1992	of Ca2+ ions before activation of calpain II, which corresponds to half the sum of anion groups in glycosaminoglycan side chains.	Glycosaminoglycans	99-116	calpain 2	Sus scrofa	34-44
1476701-5	1992	The glycosaminoglycans were released from the proteoglycans by treatment with alkaline borohydride, separated from the oligosaccharides by chromatography on Bio-Gel P-30, and isolated by chromatography on DEAE-Sephacel and Sepharose CL-6B.	Glycosaminoglycans	4-22	centromere protein V	Homo sapiens	165-169
1525210-9	1992	Surprisingly, increasing over-expression of IDUA resulted in reduced phenotypic correction of these cells as assayed by intracellular accumulation of 35S-labeled glycosaminoglycan.	Glycosaminoglycans	162-179	alpha-L-iduronidase	Homo sapiens	44-48
1505961-1	1992	In humans, a deficiency of the lysosomal hydrolase alpha-L-iduronidase (IDUA;EC 3.2.1.76) results in the lysosomal storage of the glycosaminoglycans heparan sulfate and dermatan sulfate, thereby causing the lysosomal storage disorder mucopolysaccharidosis type I.	Glycosaminoglycans	130-148	alpha-L-iduronidase	Homo sapiens	51-70
1505961-1	1992	In humans, a deficiency of the lysosomal hydrolase alpha-L-iduronidase (IDUA;EC 3.2.1.76) results in the lysosomal storage of the glycosaminoglycans heparan sulfate and dermatan sulfate, thereby causing the lysosomal storage disorder mucopolysaccharidosis type I.	Glycosaminoglycans	130-148	alpha-L-iduronidase	Homo sapiens	72-76
1377216-2	1992	In this article we present evidence that SAP is capable of blocking the anticoagulant effects of glycosaminoglycans.	Glycosaminoglycans	97-115	amyloid P component, serum	Homo sapiens	41-44
1433977-5	1992	This type of M-CSF has a molecular weight of greater than 200 kDa and consists of a 43 kDa subunit and a 150-200 kDa subunit, the latter of which contains chondroitin sulfate glycosaminoglycan.	Glycosaminoglycans	175-192	colony stimulating factor 1	Homo sapiens	13-18
1433977-6	1992	This proteoglycan type M-CSF binds to extra-cellular matrix at the part of glycosaminoglycan.	Glycosaminoglycans	75-92	colony stimulating factor 1	Homo sapiens	23-28
1377216-6	1992	We conclude that SAP may account for much of the heparin-neutralizing capacity of plasma under some conditions and that basement-membrane-bound SAP may modulate extravascular coagulation by blocking the anticoagulant effects of basement membrane glycosaminoglycans.	Glycosaminoglycans	246-264	amyloid P component, serum	Homo sapiens	144-147
1376317-6	1992	Binding of Lys-plasminogen and active-site-blocked plasmin was at least 10-fold higher in affinity (KD = 85-100 nM) compared to Glu-plasminogen (KD approximately 1 microM) and could be inhibited by lysine analogs but not by glycosaminoglycans or PAI-1, indicating that heteropolar plasmin(ogen) binding of VN occurs to an adjacent segment upstream to the heparin and PAI-1-binding sites.	Glycosaminoglycans	224-242	plasminogen	Homo sapiens	15-22
1529643-3	1992	The HIV-2BEN gag precursor p55, its mature cleavage products p24 and p17 as well as the pol reverse transcriptase (RT) p66 were detected in VV-infected CV-1 cells.	Glycosaminoglycans	13-16	H3 histone pseudogene 44	Homo sapiens	27-30
1376317-6	1992	Binding of Lys-plasminogen and active-site-blocked plasmin was at least 10-fold higher in affinity (KD = 85-100 nM) compared to Glu-plasminogen (KD approximately 1 microM) and could be inhibited by lysine analogs but not by glycosaminoglycans or PAI-1, indicating that heteropolar plasmin(ogen) binding of VN occurs to an adjacent segment upstream to the heparin and PAI-1-binding sites.	Glycosaminoglycans	224-242	plasminogen	Homo sapiens	51-58
1596698-1	1992	Recombinant interleukin-1 (IL-1) alpha and beta stimulated significant loss of glycosaminoglcan (GAG) content from normal (non-arthritic) articular cartilage explants but only after incubation for 14 days and only in specimens from 8/21 (38%) individuals.	Glycosaminoglycans	97-100	interleukin 1 alpha	Homo sapiens	12-25
1606969-2	1992	The activity was analyzed by autoprocessing of the protease itself or by processing of the gag p53 precursor.	Glycosaminoglycans	91-94	tumor protein p53	Homo sapiens	95-98
1596698-1	1992	Recombinant interleukin-1 (IL-1) alpha and beta stimulated significant loss of glycosaminoglcan (GAG) content from normal (non-arthritic) articular cartilage explants but only after incubation for 14 days and only in specimens from 8/21 (38%) individuals.	Glycosaminoglycans	97-100	interleukin 1 alpha	Homo sapiens	27-38
1596698-3	1992	The reduction in GAG induced by IL-1 was also greater for both OA and RA cartilage than normal cartilage.	Glycosaminoglycans	17-20	interleukin 1 alpha	Homo sapiens	32-36
1381850-3	1992	We analyzed the effect of glycosaminoglycans (GAGs) and GAG-binding proteins on the HCII/thrombin interaction in more detail.	Glycosaminoglycans	26-44	serpin family D member 1	Homo sapiens	84-88
1613437-6	1992	More detailed analysis of extracellular-matrix component synthesis showed that basic FGF, IGF-I and insulin each caused significant increases in the synthesis of collagen and sulphated glycosaminoglycans.	Glycosaminoglycans	185-203	insulin like growth factor 1	Homo sapiens	90-95
1613437-6	1992	More detailed analysis of extracellular-matrix component synthesis showed that basic FGF, IGF-I and insulin each caused significant increases in the synthesis of collagen and sulphated glycosaminoglycans.	Glycosaminoglycans	185-203	insulin	Homo sapiens	100-107
1613437-10	1992	The same concentrations of TGF-beta 1 inhibited the ability of IGF-I or insulin to stimulate total protein or collagen synthesis, but were additive to their stimulatory effects on sulphated glycosaminoglycan synthesis.	Glycosaminoglycans	190-207	transforming growth factor beta 1	Homo sapiens	27-37
1376146-0	1992	Activation of the collagen-binding of endogenous serum vitronectin by heating, urea and glycosaminoglycans.	Glycosaminoglycans	88-106	vitronectin	Homo sapiens	55-66
1511700-10	1992	This study shows that IFN-gamma regulates cell behavior in three-dimensional collagen matrices: (i) it decreases protein and specifically glycosaminoglycan synthesis in scleroderma fibroblasts, (ii) it modulates the interactions between cells and matrix that lead to the retraction of the lattice.	Glycosaminoglycans	138-155	interferon gamma	Homo sapiens	22-31
1582808-5	1992	Of the various compounds examined, only interleukin-1 (IL-1) and transforming growth factor (TGF)-beta significantly stimulated [3H]GAG accumulation in a dose- and time-dependent fashion.	Glycosaminoglycans	132-135	interleukin 1 alpha	Homo sapiens	40-53
1582808-5	1992	Of the various compounds examined, only interleukin-1 (IL-1) and transforming growth factor (TGF)-beta significantly stimulated [3H]GAG accumulation in a dose- and time-dependent fashion.	Glycosaminoglycans	132-135	interleukin 1 alpha	Homo sapiens	55-59
1582808-7	1992	In conclusion, both IL-1 and TGF-beta are potent stimulators of [3H]GAG accumulation by retroocular connective tissue and perimysial fibroblasts, as well as by fibroblasts from the dermal sites studied.	Glycosaminoglycans	68-71	interleukin 1 alpha	Homo sapiens	20-24
1582808-7	1992	In conclusion, both IL-1 and TGF-beta are potent stimulators of [3H]GAG accumulation by retroocular connective tissue and perimysial fibroblasts, as well as by fibroblasts from the dermal sites studied.	Glycosaminoglycans	68-71	transforming growth factor beta 1	Homo sapiens	29-37
1555588-12	1992	By the use of p-nitrophenyl beta-D-xyloside (an initiator of GAG synthesis) it could be demonstrated that chain synthesis was also enhanced in TGF-beta-treated cells (approximately twofold).	Glycosaminoglycans	61-64	transforming growth factor beta 1	Homo sapiens	143-151
1315738-8	1992	The ability of glycosaminoglycans to accelerate proteinase inhibition appeared to depend on the formation of a ternary complex of inhibitor, proteinase, and glycosaminoglycan.	Glycosaminoglycans	15-33	endogenous retrovirus group K member 18	Homo sapiens	48-58
1315738-8	1992	The ability of glycosaminoglycans to accelerate proteinase inhibition appeared to depend on the formation of a ternary complex of inhibitor, proteinase, and glycosaminoglycan.	Glycosaminoglycans	15-33	endogenous retrovirus group K member 18	Homo sapiens	141-151
1550122-1	1992	alpha-L-Iduronidase activity is deficient in mucopolysaccharidosis type I (MPS I; Hurler syndrome, Scheie syndrome) patients and results in the disruption of the sequential degradation of the glycosaminoglycans dermatan sulfate and heparan sulfate.	Glycosaminoglycans	192-210	alpha-L-iduronidase	Homo sapiens	0-19
1555588-14	1992	These novel findings indicate that TGF-beta affects proteoglycan synthesis both quantitatively and qualitatively and that it can also change the copolymeric structure of the GAG by affecting the GAG-synthesizing machinery.	Glycosaminoglycans	174-177	transforming growth factor beta 1	Homo sapiens	35-43
1555588-14	1992	These novel findings indicate that TGF-beta affects proteoglycan synthesis both quantitatively and qualitatively and that it can also change the copolymeric structure of the GAG by affecting the GAG-synthesizing machinery.	Glycosaminoglycans	195-198	transforming growth factor beta 1	Homo sapiens	35-43
1740437-5	1992	The putative ectodomain, which has 85% homology to fibroglycan, contains three possible glycosaminoglycan attachment sites that may be occupied by heparan sulfate chains.	Glycosaminoglycans	88-105	syndecan 2	Rattus norvegicus	51-62
1547784-6	1992	These findings strengthen the possibility that amyloid P protein has a central role in amyloidogenic processes: first in formation of focal concentrations of lysosomal enzymes including proteases that generate fibril-forming peptides from amyloidogenic proteins, and second in formation of multicomponent complexes that include sulphoglycolipids as well as glycosaminoglycans.	Glycosaminoglycans	357-375	OCA2 melanosomal transmembrane protein	Homo sapiens	55-64
1740413-4	1992	Interestingly, in the presence of glycosaminoglycans the maximal inhibition rate constants by HC with heparin and dermatan sulfate, respectively, were as follows: 30.0 x 10(7) and 60.5 x 10(7) for alpha-thrombin, 14.6 x 10(7) and 24.3 x 10(7) for epsilon-thrombin, and 0.017 x 10(7) and 0.034 x 10(7) M-1 min-1 for gamma T-thrombin.	Glycosaminoglycans	34-52	coagulation factor II, thrombin	Homo sapiens	203-211
1740413-4	1992	Interestingly, in the presence of glycosaminoglycans the maximal inhibition rate constants by HC with heparin and dermatan sulfate, respectively, were as follows: 30.0 x 10(7) and 60.5 x 10(7) for alpha-thrombin, 14.6 x 10(7) and 24.3 x 10(7) for epsilon-thrombin, and 0.017 x 10(7) and 0.034 x 10(7) M-1 min-1 for gamma T-thrombin.	Glycosaminoglycans	34-52	coagulation factor II, thrombin	Homo sapiens	255-263
1566349-4	1992	Displacement studies were done with glycosaminoglycans to show that the antithrombin III was bound to its glycosaminoglycan anchor via a heparinlike binding site, and replacement studies showed that antithrombin III could be returned to the same endothelial cells from which it was displaced.	Glycosaminoglycans	36-54	serpin family C member 1	Homo sapiens	72-88
1566349-4	1992	Displacement studies were done with glycosaminoglycans to show that the antithrombin III was bound to its glycosaminoglycan anchor via a heparinlike binding site, and replacement studies showed that antithrombin III could be returned to the same endothelial cells from which it was displaced.	Glycosaminoglycans	36-53	serpin family C member 1	Homo sapiens	72-88
1386167-3	1992	Plasmin at 10 mU/ml (approximately 2.7 micrograms/ml) and above significantly increased the release of [35S]sulfate-labeled GAG (35S-GAG) from the cell layer after a 60 min incubation.	Glycosaminoglycans	124-127	plasminogen	Bos taurus	0-7
1386167-3	1992	Plasmin at 10 mU/ml (approximately 2.7 micrograms/ml) and above significantly increased the release of [35S]sulfate-labeled GAG (35S-GAG) from the cell layer after a 60 min incubation.	Glycosaminoglycans	133-136	plasminogen	Bos taurus	0-7
1386167-4	1992	A time course study showed that plasmin at 10 mU/ml significantly increased the 35S-GAG release after 20 min and longer.	Glycosaminoglycans	84-87	plasminogen	Bos taurus	32-39
1386167-6	1992	A characterization of 35S-GAG revealed that plasmin increased both dermatan sulfate and the other 35S-GAG in the medium.	Glycosaminoglycans	26-29	plasminogen	Bos taurus	44-51
1386167-6	1992	A characterization of 35S-GAG revealed that plasmin increased both dermatan sulfate and the other 35S-GAG in the medium.	Glycosaminoglycans	102-105	plasminogen	Bos taurus	44-51
1740413-4	1992	Interestingly, in the presence of glycosaminoglycans the maximal inhibition rate constants by HC with heparin and dermatan sulfate, respectively, were as follows: 30.0 x 10(7) and 60.5 x 10(7) for alpha-thrombin, 14.6 x 10(7) and 24.3 x 10(7) for epsilon-thrombin, and 0.017 x 10(7) and 0.034 x 10(7) M-1 min-1 for gamma T-thrombin.	Glycosaminoglycans	34-52	CD59 molecule (CD59 blood group)	Homo sapiens	305-310
1740413-4	1992	Interestingly, in the presence of glycosaminoglycans the maximal inhibition rate constants by HC with heparin and dermatan sulfate, respectively, were as follows: 30.0 x 10(7) and 60.5 x 10(7) for alpha-thrombin, 14.6 x 10(7) and 24.3 x 10(7) for epsilon-thrombin, and 0.017 x 10(7) and 0.034 x 10(7) M-1 min-1 for gamma T-thrombin.	Glycosaminoglycans	34-52	coagulation factor II, thrombin	Homo sapiens	255-263
1740413-9	1992	Our results suggest that the beta-loop region of anion-binding exosite-I in alpha-thrombin, which is not present in gamma T-thrombin, is essential for the rapid inhibition reaction by HC in the presence of a glycosaminoglycan.	Glycosaminoglycans	208-225	coagulation factor II, thrombin	Homo sapiens	82-90
1633327-4	1992	The analysis of tetrads showed five conserved signals: TTGT, (T/A)(T/A)ATA, A(C/T)(C/A)A in the tRNA genes of fungi, (A/T)TGA of invertebrates and (A/T)GAG of vertebrates.	Glycosaminoglycans	152-155	T-box transcription factor 1	Homo sapiens	122-125
1733926-8	1992	These results are consistent with intracellular proteolytic cleavage of the 80-kDa chondroitin sulfate containing subunits from the membrane spanning CSF-1 precursor at a point carboxyl-terminal to the single consensus sequence for glycosaminoglycan addition and cleavage of the 50-kDa glycoprotein subunit at a position aminoterminal to this site.	Glycosaminoglycans	232-249	colony stimulating factor 1 (macrophage)	Mus musculus	150-155
1332436-0	1992	Thrombomodulin: an anticoagulant cell surface proteoglycan with physiologically relevant glycosaminoglycan moiety.	Glycosaminoglycans	89-106	thrombomodulin	Homo sapiens	0-14
1364220-4	1992	Sequence analysis of the amplified product revealed a GAG &gt; AAG transversion at codon 26, which resulted in an amino acid substitution of lysine for glutamic acid.	Glycosaminoglycans	54-57	N-methylpurine DNA glycosylase	Homo sapiens	63-66
1736810-2	1992	These sequences were the p18/p24 junction in gag, the active site of HIV protease in pol; a sequence from the first exon of the rev gene and S-oligodeoxycytidylic acid controls.	Glycosaminoglycans	45-48	H3 histone pseudogene 12	Homo sapiens	25-28
1736810-2	1992	These sequences were the p18/p24 junction in gag, the active site of HIV protease in pol; a sequence from the first exon of the rev gene and S-oligodeoxycytidylic acid controls.	Glycosaminoglycans	45-48	transmembrane p24 trafficking protein 2	Homo sapiens	29-32
1736810-2	1992	These sequences were the p18/p24 junction in gag, the active site of HIV protease in pol; a sequence from the first exon of the rev gene and S-oligodeoxycytidylic acid controls.	Glycosaminoglycans	45-48	endogenous retrovirus group W member 4	Homo sapiens	85-88
1736810-2	1992	These sequences were the p18/p24 junction in gag, the active site of HIV protease in pol; a sequence from the first exon of the rev gene and S-oligodeoxycytidylic acid controls.	Glycosaminoglycans	45-48	Rev	Human immunodeficiency virus 1	128-131
1420809-3	1992	We have shown that interleukin-1 and transforming growth factor-beta, cytokines released by the local inflammatory cell infiltrate, are capable of stimulating GAG synthesis by retroocular and pretibial fibroblasts.	Glycosaminoglycans	159-162	interleukin 1 alpha	Homo sapiens	19-68
1307735-5	1992	Basic fibroblast growth factor (basic FGF) and transforming growth factor-beta (TGF beta) directly bind to glycosaminoglycan molecules.	Glycosaminoglycans	107-124	transforming growth factor beta 1	Homo sapiens	47-78
1459472-1	1992	Human platelet-derived transforming growth factor-beta (TGF-beta) stimulated the incorporation of [35S]sulfate into glycosaminoglycans (GAGs) both in the medium and on the cell surface of cultured aortic endothelial cells in a dose- and time-dependent manner.	Glycosaminoglycans	116-134	transforming growth factor beta 1	Homo sapiens	56-64
1459472-2	1992	TGF-beta inhibited the suppression of GAG synthesis by other cytokines.	Glycosaminoglycans	38-41	transforming growth factor beta 1	Homo sapiens	0-8
1459472-5	1992	Thus, TGF-beta affected the endothelial GAG metabolism both quantitatively and qualitatively.	Glycosaminoglycans	40-43	transforming growth factor beta 1	Homo sapiens	6-14
1307735-5	1992	Basic fibroblast growth factor (basic FGF) and transforming growth factor-beta (TGF beta) directly bind to glycosaminoglycan molecules.	Glycosaminoglycans	107-124	transforming growth factor beta 1	Homo sapiens	80-88
1584067-2	1992	We found that a mouse monoclonal antibody to p17, V17 recognizes the mature p17 but not the unprocessed Gag proteins containing the entire p17 moiety.	Glycosaminoglycans	104-107	family with sequence similarity 72 member B	Homo sapiens	45-48
1301196-1	1992	Mucopolysaccharidosis type I (MPS-I) is an autosomal recessive genetic disease caused by a deficiency of the glycosidase alpha-L-iduronidase which is required for the lysosomal degradation of the glycosaminoglycans heparan sulfate and dermatan sulfate.	Glycosaminoglycans	196-214	alpha-L-iduronidase	Homo sapiens	121-140
1513064-4	1992	For identifying the types of glycosaminoglycans, enzyme digestion methods were carried out with streptomyces hyaluronidase, chondroitinase AC, chondroitinase ABC, or sialidase (neuraminidase).	Glycosaminoglycans	29-47	neuraminidase 1	Homo sapiens	177-190
1301941-1	1992	Mucopolysaccharidosis type I (MPS-I) is an autosomal recessive genetic disease caused by a deficiency of the glycosidase alpha-L-iduronidase which is required for the lysosomal degradation of the glycosaminoglycans heparan sulfate and dermatan sulfate.	Glycosaminoglycans	196-214	alpha-L-iduronidase	Homo sapiens	121-140
1730747-0	1992	Trans-repressor activity of nuclear glycosaminoglycans on Fos and Jun/AP-1 oncoprotein-mediated transcription.	Glycosaminoglycans	36-54	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	58-61
1730747-0	1992	Trans-repressor activity of nuclear glycosaminoglycans on Fos and Jun/AP-1 oncoprotein-mediated transcription.	Glycosaminoglycans	36-54	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	70-74
1727880-5	1992	Anti-gag p24 antibody was strongly correlated with antibodies to other env products, specifically gp41 and gp160.	Glycosaminoglycans	5-8	transmembrane p24 trafficking protein 2	Homo sapiens	9-12
1727880-5	1992	Anti-gag p24 antibody was strongly correlated with antibodies to other env products, specifically gp41 and gp160.	Glycosaminoglycans	5-8	endogenous retrovirus group K member 20	Homo sapiens	71-74
1727880-5	1992	Anti-gag p24 antibody was strongly correlated with antibodies to other env products, specifically gp41 and gp160.	Glycosaminoglycans	5-8	glutamyl aminopeptidase	Homo sapiens	107-112
1309253-0	1992	Enhancement of transforming potential of human insulinlike growth factor 1 receptor by N-terminal truncation and fusion to avian sarcoma virus UR2 gag sequence.	Glycosaminoglycans	147-150	insulin like growth factor 1	Homo sapiens	47-74
1309253-8	1992	The cDNA sequence coding for part of the beta subunit of hIGFR, including 36 amino acids of the extracellular domain and the entire transmembrane and cytoplasmic domains, was fused to the 5" portion of the gag gene in the UR2 vector to form an avian retrovirus.	Glycosaminoglycans	206-209	insulin like growth factor 1 receptor	Homo sapiens	57-62
1584067-2	1992	We found that a mouse monoclonal antibody to p17, V17 recognizes the mature p17 but not the unprocessed Gag proteins containing the entire p17 moiety.	Glycosaminoglycans	104-107	immunoglobulin lambda variable 2-23	Homo sapiens	50-53
1687064-0	1991	Differential antibody responsiveness to p19 gag results in serological discrimination between human T lymphotropic virus type I and type II.	Glycosaminoglycans	44-47	interleukin 23 subunit alpha	Homo sapiens	40-43
1508900-3	1992	In this study, we have investigated the in vivo relationship of the localization of TGF-beta 1 to various ECM proteins, including glycosaminoglycans (GAGs), fibronectin, collagens I and III and to the enzyme alkaline phosphatase, at the early and late bell stages of rat molar tooth development.	Glycosaminoglycans	130-148	transforming growth factor, beta 1	Rattus norvegicus	84-94
1744125-3	1991	Purified betaglycan has properties similar to betaglycan affinity-labeled in intact cells: it binds TGF-beta 1 and TGF-beta 2 with KD approximately 0.2 nM, contains heparan sulfate and chondroitin sulfate glycosaminoglycan (GAG) chains and N-linked glycans attached to a 110-kDa core protein, and can spontaneously associate with phosphatidylcholine liposomes.	Glycosaminoglycans	224-227	transforming growth factor beta receptor 3	Rattus norvegicus	9-19
1744125-4	1991	The betaglycan core obtained by enzymatic removal of the GAG chains has high affinity for TGF-beta and associates with artificial liposomes, indicating that the core protein binds TGF-beta and anchors to membranes independently of the GAG chains present on the native protein or of any ancillary protein.	Glycosaminoglycans	57-60	transforming growth factor beta receptor 3	Rattus norvegicus	4-14
1744125-4	1991	The betaglycan core obtained by enzymatic removal of the GAG chains has high affinity for TGF-beta and associates with artificial liposomes, indicating that the core protein binds TGF-beta and anchors to membranes independently of the GAG chains present on the native protein or of any ancillary protein.	Glycosaminoglycans	57-60	transforming growth factor, beta 1	Rattus norvegicus	90-98
1744125-4	1991	The betaglycan core obtained by enzymatic removal of the GAG chains has high affinity for TGF-beta and associates with artificial liposomes, indicating that the core protein binds TGF-beta and anchors to membranes independently of the GAG chains present on the native protein or of any ancillary protein.	Glycosaminoglycans	235-238	transforming growth factor beta receptor 3	Rattus norvegicus	4-14
1668174-0	1991	Regulation of glycosaminoglycan synthesis by parathyroid hormone and prostaglandin E2 in cultured dental pulp cells.	Glycosaminoglycans	14-31	parathyroid hormone	Bos taurus	45-64
1282012-7	1992	In contrast, target cells coated with the peptide gag aa 129-135, corresponding to the p17/p24 cleavage region of the gag precursor, were not killed.	Glycosaminoglycans	50-53	family with sequence similarity 72 member B	Homo sapiens	87-90
1282012-7	1992	In contrast, target cells coated with the peptide gag aa 129-135, corresponding to the p17/p24 cleavage region of the gag precursor, were not killed.	Glycosaminoglycans	50-53	transmembrane p24 trafficking protein 2	Homo sapiens	91-94
1282012-7	1992	In contrast, target cells coated with the peptide gag aa 129-135, corresponding to the p17/p24 cleavage region of the gag precursor, were not killed.	Glycosaminoglycans	118-121	family with sequence similarity 72 member B	Homo sapiens	87-90
1282012-7	1992	In contrast, target cells coated with the peptide gag aa 129-135, corresponding to the p17/p24 cleavage region of the gag precursor, were not killed.	Glycosaminoglycans	118-121	transmembrane p24 trafficking protein 2	Homo sapiens	91-94
1744124-6	1991	It is likely, based on the magnitude of the size difference, that these two forms of PG-I/biglycan differ in the number of glycosaminoglycan chains.	Glycosaminoglycans	123-140	glucose-6-phosphate isomerase	Bos taurus	85-89
1744586-3	1991	Using limiting dilution analysis of this effector cell population we confirm that the majority of activated gag-specific CTL circulating in the PBMC of infected hemophilic patients are directed at p24 determinants and are present at frequencies of 1/36,000 to 1/86,000 lymphocytes.	Glycosaminoglycans	108-111	transmembrane p24 trafficking protein 2	Homo sapiens	197-200
1744586-5	1991	HIV gag-specific CTL precursors are identified at frequencies of 1/1700 to 1/17,000 lymphocytes and are made up of cells with both p17 and p24 specificities.	Glycosaminoglycans	4-7	family with sequence similarity 72 member B	Homo sapiens	131-134
1744586-5	1991	HIV gag-specific CTL precursors are identified at frequencies of 1/1700 to 1/17,000 lymphocytes and are made up of cells with both p17 and p24 specificities.	Glycosaminoglycans	4-7	transmembrane p24 trafficking protein 2	Homo sapiens	139-142
1687064-1	1991	A new algorithm based upon the differential antibody responses to two gag gene products (p19 and p24) of human T lymphotropic virus (HTLV) has been suggested for serologic discrimination of HTLV type I (HTLV-I) and type II (HTLV-II) [Lillihoj et al., 1990].	Glycosaminoglycans	70-73	interleukin 23 subunit alpha	Homo sapiens	89-92
1687064-1	1991	A new algorithm based upon the differential antibody responses to two gag gene products (p19 and p24) of human T lymphotropic virus (HTLV) has been suggested for serologic discrimination of HTLV type I (HTLV-I) and type II (HTLV-II) [Lillihoj et al., 1990].	Glycosaminoglycans	70-73	transmembrane p24 trafficking protein 2	Homo sapiens	97-100
1657406-2	1991	As deduced from its cDNA sequence, the 853 amino acid core protein of betaglycan has an extracellular domain with clustered sites for potential attachment of glycosaminoglycan chains.	Glycosaminoglycans	158-175	transforming growth factor beta receptor 3	Homo sapiens	70-80
1658356-9	1991	This observation, particularly in reference to our earlier finding of extensive mutations in the gag gene, reveals a target area for potentially productive homologous recombination upstream of the functional endogenous env gene.	Glycosaminoglycans	97-100	endogenous retrovirus group K member 20	Homo sapiens	219-222
1658378-4	1991	The gag precursor is now mapped as NH2-MA(p10)-p4-CA(p24)-NC(p12)-COOH.	Glycosaminoglycans	4-7	S100 calcium binding protein A10	Homo sapiens	42-45
1658378-4	1991	The gag precursor is now mapped as NH2-MA(p10)-p4-CA(p24)-NC(p12)-COOH.	Glycosaminoglycans	4-7	transmembrane p24 trafficking protein 2	Homo sapiens	53-56
1658378-4	1991	The gag precursor is now mapped as NH2-MA(p10)-p4-CA(p24)-NC(p12)-COOH.	Glycosaminoglycans	4-7	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	61-64
1946389-1	1991	alpha-L-Iduronidase (IDUA; EC 3.2.1.76) is a lysosomal hydrolase in the metabolic pathway responsible for the degradation of the glycosaminoglycans heparan sulfate and dermatan sulfate.	Glycosaminoglycans	129-147	alpha-L-iduronidase	Homo sapiens	0-19
1959638-4	1991	The purified protease processed the natural substrate gag precursor (p53) to form gag p19 and gag p24.	Glycosaminoglycans	54-57	tumor protein p53	Homo sapiens	69-72
1959638-4	1991	The purified protease processed the natural substrate gag precursor (p53) to form gag p19 and gag p24.	Glycosaminoglycans	54-57	interleukin 23 subunit alpha	Homo sapiens	86-89
1959638-4	1991	The purified protease processed the natural substrate gag precursor (p53) to form gag p19 and gag p24.	Glycosaminoglycans	54-57	transmembrane p24 trafficking protein 2	Homo sapiens	98-101
1959638-4	1991	The purified protease processed the natural substrate gag precursor (p53) to form gag p19 and gag p24.	Glycosaminoglycans	82-85	tumor protein p53	Homo sapiens	69-72
1959638-4	1991	The purified protease processed the natural substrate gag precursor (p53) to form gag p19 and gag p24.	Glycosaminoglycans	82-85	interleukin 23 subunit alpha	Homo sapiens	86-89
1959638-4	1991	The purified protease processed the natural substrate gag precursor (p53) to form gag p19 and gag p24.	Glycosaminoglycans	82-85	tumor protein p53	Homo sapiens	69-72
1959638-4	1991	The purified protease processed the natural substrate gag precursor (p53) to form gag p19 and gag p24.	Glycosaminoglycans	82-85	interleukin 23 subunit alpha	Homo sapiens	86-89
1656066-2	1991	Two regions, a 1,295-nucleotide segment in the gag gene (IR-1) and a 1,932-nucleotide segment of the pol gene (IR-2), each inhibited reporter gene expression 10- to 20-fold.	Glycosaminoglycans	47-50	nischarin	Homo sapiens	57-61
1946389-1	1991	alpha-L-Iduronidase (IDUA; EC 3.2.1.76) is a lysosomal hydrolase in the metabolic pathway responsible for the degradation of the glycosaminoglycans heparan sulfate and dermatan sulfate.	Glycosaminoglycans	129-147	alpha-L-iduronidase	Homo sapiens	21-25
1946389-2	1991	A deficiency of IDUA in humans leads to the accumulation of these glycosaminoglycans and results in the lysosomal storage disorder mucopolysaccharidosis type I.	Glycosaminoglycans	66-84	alpha-L-iduronidase	Homo sapiens	16-20
1939083-0	1991	The N-terminal acidic domain of heparin cofactor II mediates the inhibition of alpha-thrombin in the presence of glycosaminoglycans.	Glycosaminoglycans	113-131	serpin family D member 1	Homo sapiens	32-51
1805447-7	1991	From these results, it was suggested that HCII would be activated by glycosaminoglycans (GAGs) such as dermatan sulfate of the cell layers and could inhibit thrombin-induced PGI2 production.	Glycosaminoglycans	69-87	serine (or cysteine) peptidase inhibitor, clade D, member 1	Mus musculus	42-46
1805447-7	1991	From these results, it was suggested that HCII would be activated by glycosaminoglycans (GAGs) such as dermatan sulfate of the cell layers and could inhibit thrombin-induced PGI2 production.	Glycosaminoglycans	69-87	coagulation factor II	Mus musculus	157-165
1805447-7	1991	From these results, it was suggested that HCII would be activated by glycosaminoglycans (GAGs) such as dermatan sulfate of the cell layers and could inhibit thrombin-induced PGI2 production.	Glycosaminoglycans	89-93	serine (or cysteine) peptidase inhibitor, clade D, member 1	Mus musculus	42-46
1805447-7	1991	From these results, it was suggested that HCII would be activated by glycosaminoglycans (GAGs) such as dermatan sulfate of the cell layers and could inhibit thrombin-induced PGI2 production.	Glycosaminoglycans	89-93	coagulation factor II	Mus musculus	157-165
1805447-8	1991	HCII may be a modulator of thrombin on the physiological functions of vascular smooth muscle cells, reacting to the cell surface GAGs.	Glycosaminoglycans	129-133	serine (or cysteine) peptidase inhibitor, clade D, member 1	Mus musculus	0-4
1805447-8	1991	HCII may be a modulator of thrombin on the physiological functions of vascular smooth muscle cells, reacting to the cell surface GAGs.	Glycosaminoglycans	129-133	coagulation factor II	Mus musculus	27-35
1939083-0	1991	The N-terminal acidic domain of heparin cofactor II mediates the inhibition of alpha-thrombin in the presence of glycosaminoglycans.	Glycosaminoglycans	113-131	coagulation factor II, thrombin	Homo sapiens	85-93
1939083-11	1991	The stimulatory effect of glycosaminoglycans on native rHCII was decreased by a C-terminal hirudin peptide which binds to anion-binding exosite I of alpha-thrombin.	Glycosaminoglycans	26-44	coagulation factor II, thrombin	Homo sapiens	155-163
1939083-12	1991	Furthermore, the ability of native rHCII to inhibit gamma-thrombin, which lacks the binding site for hirudin, was stimulated weakly by glycosaminoglycans.	Glycosaminoglycans	135-153	coagulation factor II, thrombin	Homo sapiens	58-66
1918055-4	1991	When granulosa cells were treated with glycosaminoglycan-degrading enzymes before or after addition of follistatin to the cultures, heparinase and heparitinase treatments resulted in significant suppression of the binding, whereas treatment with chondroitinase ABC had no effect.	Glycosaminoglycans	39-56	follistatin	Rattus norvegicus	103-114
1833819-1	1991	The v-akt oncogene codes for a 105-kilodalton fusion phosphoprotein containing Gag sequences at its amino terminus.	Glycosaminoglycans	79-82	AKT serine/threonine kinase 1	Homo sapiens	6-9
1928304-6	1991	GMCSF also resulted in marked increases in SIV gag protein in culture supernatants.	Glycosaminoglycans	47-50	colony stimulating factor 2	Homo sapiens	0-5
1936596-12	1991	However, IGF-I decreased the ratio of [35S]sulfate to [3H]glucosamine in proteoglycans and their glycosaminoglycan side chains.	Glycosaminoglycans	97-114	insulin like growth factor 1	Homo sapiens	9-14
1940439-3	1991	We found that rhIL-6 mimicked some of the activities of IL-1 beta, as 24-96-h treatment of confluent fibroblast cultures with rhIL-6 caused concentration (10 to 1000 ng/ml)-dependent increases in the production of collagen and the glycosaminoglycans (GAG), hyaluronic acid and chondroitin-4/6-sulfates, but had little effect on fibronectin or total protein production.	Glycosaminoglycans	231-249	interleukin 1 beta	Homo sapiens	56-65
1724753-9	1991	With the help of enzyme-linked immunosorbent assay (ELISA) and iodinated [125I]HABP, it has been shown that kidney HABP binds specifically to hyaluronic acid (HA) amongst all the glycosaminoglycans (GAGs), however, HABP can interact with other matrix proteins, e.g., laminin, fibronectin, and collagen type IV.	Glycosaminoglycans	179-197	hyaluronan binding protein 2	Rattus norvegicus	115-119
1724753-9	1991	With the help of enzyme-linked immunosorbent assay (ELISA) and iodinated [125I]HABP, it has been shown that kidney HABP binds specifically to hyaluronic acid (HA) amongst all the glycosaminoglycans (GAGs), however, HABP can interact with other matrix proteins, e.g., laminin, fibronectin, and collagen type IV.	Glycosaminoglycans	179-197	hyaluronan binding protein 2	Rattus norvegicus	115-119
1748468-8	1991	It is proposed that this conserved polyanion binding site of CD4 interacts with a sulphated glycosaminoglycan chain which is associated with class II major histocompatibility complex (MHC) molecules containing recently processed antigen.	Glycosaminoglycans	92-109	CD4 molecule	Homo sapiens	61-64
1940305-3	1991	Antibodies against the basement membrane-derived HSPG (either protein core or GAG chains) demonstrated a virtually concurrent deposition of HSPGs and amyloid in specific tissue sites regardless of the organ involved (spleen or liver) or the induction protocol used (amyloid enhancing factor + silver nitrate, or daily azocasein injections).	Glycosaminoglycans	78-81	syndecan 2	Mus musculus	49-53
1940439-3	1991	We found that rhIL-6 mimicked some of the activities of IL-1 beta, as 24-96-h treatment of confluent fibroblast cultures with rhIL-6 caused concentration (10 to 1000 ng/ml)-dependent increases in the production of collagen and the glycosaminoglycans (GAG), hyaluronic acid and chondroitin-4/6-sulfates, but had little effect on fibronectin or total protein production.	Glycosaminoglycans	251-254	interleukin 1 beta	Homo sapiens	56-65
1940305-6	1991	In the liver, heparan sulfate GAGs were also immunolocalized to the lysosomal compartment of hepatocytes and/or Kupffer cells adjacent to sites of amyloid deposition, suggesting that these cells are involved in HSPG production and/or degradation.	Glycosaminoglycans	30-34	syndecan 2	Mus musculus	211-215
1940439-4	1991	Although the effective stimulating concentrations of IL-6 were within the range (approximately 100 ng/ml) we found produced by rhIL-1 beta-treated fibroblast cultures, rhIL-1 beta at 0.2-1.0 ng/ml induced significantly greater amounts of collagen and GAG than the maximum effective concentrations of IL-6.	Glycosaminoglycans	251-254	interleukin 6	Homo sapiens	53-57
1892820-5	1991	Other glycosaminoglycans can bind to and inhibit the activity of B-PLA2 toward organized phospholipids, but none tested is as effective as heparin.	Glycosaminoglycans	6-24	phospholipase A2, major isoenzyme	Sus scrofa	67-71
1784840-3	1991	Arylsulfatase B catalyses the desulfation of glycosaminoglycans in the catabolism of the intimal ground substance.	Glycosaminoglycans	45-63	arylsulfatase B	Homo sapiens	0-15
1943985-1	1991	The lysosomal enzyme beta-glucuronidase is involved in the degradation of glycosaminoglycans to monosaccharides.	Glycosaminoglycans	74-92	glucuronidase beta	Homo sapiens	21-39
1720904-2	1991	These antifibrinolytic activities as well as other functions are mediated by the glycosaminoglycan (GAG) binding domain of VN.	Glycosaminoglycans	81-98	vitronectin	Homo sapiens	123-125
1720904-2	1991	These antifibrinolytic activities as well as other functions are mediated by the glycosaminoglycan (GAG) binding domain of VN.	Glycosaminoglycans	100-103	vitronectin	Homo sapiens	123-125
1720904-3	1991	Since the GAG binding region is rich in arginyl and lysyl residues, it is a potential target for enzymes such as plasmin.	Glycosaminoglycans	10-13	plasminogen	Homo sapiens	113-120
1720904-8	1991	Thus, the plasmin-mediated proteolysis of the GAG binding activity of VN could destroy the antifibrinolytic activity of VN during physiologic conditions and during thrombolytic therapy.	Glycosaminoglycans	46-49	plasminogen	Homo sapiens	10-17
1720904-8	1991	Thus, the plasmin-mediated proteolysis of the GAG binding activity of VN could destroy the antifibrinolytic activity of VN during physiologic conditions and during thrombolytic therapy.	Glycosaminoglycans	46-49	vitronectin	Homo sapiens	70-72
1720904-8	1991	Thus, the plasmin-mediated proteolysis of the GAG binding activity of VN could destroy the antifibrinolytic activity of VN during physiologic conditions and during thrombolytic therapy.	Glycosaminoglycans	46-49	vitronectin	Homo sapiens	120-122
1720904-9	1991	Furthermore, other functions of VN in complement and coagulation systems that are mediated by the GAG binding domain may be destroyed by plasmin proteolysis.	Glycosaminoglycans	98-101	vitronectin	Homo sapiens	32-34
1649749-2	1991	In the present study regulation of expression of PTH receptors of the chondrocytes by various growth and differentiation factors and its relation to the synthesis of glycosaminoglycan (GAG), a differentiated phenotype of chondrocytes, were investigated.	Glycosaminoglycans	166-183	parathyroid hormone	Oryctolagus cuniculus	49-52
1649749-2	1991	In the present study regulation of expression of PTH receptors of the chondrocytes by various growth and differentiation factors and its relation to the synthesis of glycosaminoglycan (GAG), a differentiated phenotype of chondrocytes, were investigated.	Glycosaminoglycans	185-188	parathyroid hormone	Oryctolagus cuniculus	49-52
1649749-5	1991	The decrease in the number of PTH receptors was dose and time dependent and parallel to the decrease in GAG synthesis.	Glycosaminoglycans	104-107	parathyroid hormone	Oryctolagus cuniculus	30-33
1649749-9	1991	Treatment with insulin-like growth factor-I, (Bu)2cAMP, and transforming growth factor-beta resulted in increases in GAG synthesis as well as in the number of PTH receptors without any change in their affinity.	Glycosaminoglycans	117-120	insulin-like growth factor I	Oryctolagus cuniculus	15-43
1715343-8	1991	Thus, the autocrine growth factor possesses a different characteristic from aFGF and bFGF in that its bioactivities are negatively modulated by the glycosaminoglycan.	Glycosaminoglycans	148-165	fibroblast growth factor 1	Homo sapiens	76-80
1715343-8	1991	Thus, the autocrine growth factor possesses a different characteristic from aFGF and bFGF in that its bioactivities are negatively modulated by the glycosaminoglycan.	Glycosaminoglycans	148-165	fibroblast growth factor 2	Homo sapiens	85-89
2072910-5	1991	Protein kinase activity associated with constructed p60gag-cot was detected by immune complex kinase assay with anti-gag antiserum.	Glycosaminoglycans	55-58	mitogen-activated protein kinase kinase kinase 8	Mus musculus	59-62
1780805-3	1991	A radioimmunoassay for recombinant (r.) hirudin was used to study the effect of heparin and other glycosaminoglycans (GAG"s) on interactions between hirudin and thrombin.	Glycosaminoglycans	118-123	coagulation factor II, thrombin	Homo sapiens	161-169
1715604-2	1991	All monoclonal antibodies recognized HIV-1IIIB infected MOLT3 cells by fluorescence and gave positive Western blot signals with viral gag peptides (p55 and/or p24).	Glycosaminoglycans	134-137	H3 histone pseudogene 44	Homo sapiens	148-151
1713175-5	1991	This cleavage is stimulated by glycosaminoglycans, which are known to anchor vitronectin to the extracellular matrix.	Glycosaminoglycans	31-49	vitronectin	Homo sapiens	77-88
1677358-6	1991	In one out of the five subjects with the apoA-IV-1/0 phenotype we identified two point mutations: 1) replacing the positively charged lysine (AAG), amino acid 167, with a negatively charged glutamic acid (GAG), and 2) converting the neutral residue 360, glutamine (CAG), to a positively charged histidine (CAT).	Glycosaminoglycans	205-208	apolipoprotein A4	Homo sapiens	41-48
2065891-3	1991	Fixed nucleic acid substitutions in the gag gene appear to be caused by random fixation of selectively neutral mutants, whereas nonrandom fixation of selectively advantageous mutants, as has been observed for MHC molecules and serine protease inhibitors, appears to be operational for some hypervariable env gene regions.	Glycosaminoglycans	40-43	endogenous retrovirus group K member 20	Homo sapiens	304-307
1715884-10	1991	MAbs which recognize conserved epitopes of gag-encoded lentivirus proteins (CA p27 and MA p17) are valuable tools.	Glycosaminoglycans	43-46	interferon alpha inducible protein 27	Homo sapiens	79-82
1715884-10	1991	MAbs which recognize conserved epitopes of gag-encoded lentivirus proteins (CA p27 and MA p17) are valuable tools.	Glycosaminoglycans	43-46	family with sequence similarity 72 member B	Homo sapiens	90-93
1926061-0	1991	Antithrombin III modulates the effect of thrombin on the metabolism of glycosaminoglycans in cultured endothelial cells.	Glycosaminoglycans	71-89	serpin family C member 1	Bos taurus	0-16
1711081-0	1991	Definition of an epitope and MHC class I molecule recognized by gag-specific cytotoxic T lymphocytes in SIVmac-infected rhesus monkeys.	Glycosaminoglycans	64-67	major histocompatibility complex, class I, B	Homo sapiens	29-49
1926061-0	1991	Antithrombin III modulates the effect of thrombin on the metabolism of glycosaminoglycans in cultured endothelial cells.	Glycosaminoglycans	71-89	coagulation factor II, thrombin	Bos taurus	4-12
1926061-6	1991	Although thrombin stimulated the release of 35S-GAG from the cell layer, AT III completely prevented the stimulatory effect.	Glycosaminoglycans	48-51	coagulation factor II, thrombin	Bos taurus	9-17
1926061-1	1991	We previously reported that a treatment of cultures of endothelial cells from bovine aorta with thrombin resulted in a less accumulation of glycosaminoglycans (GAG) in the cell layer.	Glycosaminoglycans	140-158	coagulation factor II, thrombin	Bos taurus	96-104
1926061-7	1991	In conclusion, it was suggested that AT III may inhibit the thrombin action on GAG metabolism of endothelial cells to prevent thrombosis in vivo.	Glycosaminoglycans	79-82	serpin family C member 1	Bos taurus	37-43
1926061-7	1991	In conclusion, it was suggested that AT III may inhibit the thrombin action on GAG metabolism of endothelial cells to prevent thrombosis in vivo.	Glycosaminoglycans	79-82	coagulation factor II, thrombin	Bos taurus	60-68
1926061-1	1991	We previously reported that a treatment of cultures of endothelial cells from bovine aorta with thrombin resulted in a less accumulation of glycosaminoglycans (GAG) in the cell layer.	Glycosaminoglycans	160-163	coagulation factor II, thrombin	Bos taurus	96-104
1674745-7	1991	A second G to A substitution at amino acid 13 led to the exchange of lysine (AAG) for glutamic acid (GAG), thereby adding 2 positive charge units to the protein and producing the apoE-5 variant.	Glycosaminoglycans	101-104	apolipoprotein E	Homo sapiens	179-183
1926061-2	1991	In the present study, we found that thrombin-induced decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) such as heparan sulfate was prevented by antithrombin III (AT III) but not by heparin cofactor II (HC II).	Glycosaminoglycans	106-109	coagulation factor II, thrombin	Bos taurus	36-44
1926061-2	1991	In the present study, we found that thrombin-induced decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) such as heparan sulfate was prevented by antithrombin III (AT III) but not by heparin cofactor II (HC II).	Glycosaminoglycans	106-109	serpin family C member 1	Bos taurus	161-177
1926061-2	1991	In the present study, we found that thrombin-induced decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) such as heparan sulfate was prevented by antithrombin III (AT III) but not by heparin cofactor II (HC II).	Glycosaminoglycans	106-109	serpin family C member 1	Bos taurus	179-185
1926061-2	1991	In the present study, we found that thrombin-induced decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) such as heparan sulfate was prevented by antithrombin III (AT III) but not by heparin cofactor II (HC II).	Glycosaminoglycans	106-109	serpin family D member 1	Bos taurus	198-217
1926061-2	1991	In the present study, we found that thrombin-induced decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) such as heparan sulfate was prevented by antithrombin III (AT III) but not by heparin cofactor II (HC II).	Glycosaminoglycans	106-109	serpin family D member 1	Bos taurus	219-224
1926061-2	1991	In the present study, we found that thrombin-induced decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) such as heparan sulfate was prevented by antithrombin III (AT III) but not by heparin cofactor II (HC II).	Glycosaminoglycans	115-118	coagulation factor II, thrombin	Bos taurus	36-44
1926061-2	1991	In the present study, we found that thrombin-induced decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) such as heparan sulfate was prevented by antithrombin III (AT III) but not by heparin cofactor II (HC II).	Glycosaminoglycans	115-118	serpin family C member 1	Bos taurus	161-177
1926061-2	1991	In the present study, we found that thrombin-induced decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) such as heparan sulfate was prevented by antithrombin III (AT III) but not by heparin cofactor II (HC II).	Glycosaminoglycans	115-118	serpin family C member 1	Bos taurus	179-185
1926061-2	1991	In the present study, we found that thrombin-induced decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) such as heparan sulfate was prevented by antithrombin III (AT III) but not by heparin cofactor II (HC II).	Glycosaminoglycans	115-118	serpin family D member 1	Bos taurus	198-217
1926061-2	1991	In the present study, we found that thrombin-induced decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) such as heparan sulfate was prevented by antithrombin III (AT III) but not by heparin cofactor II (HC II).	Glycosaminoglycans	115-118	serpin family D member 1	Bos taurus	219-224
1834236-2	1991	Plasmin significantly increased the release of [35S]sulphate-labelled GAG (35S-GAG) from the cell layer, although plasminogen did not show such a stimulatory effect.	Glycosaminoglycans	70-73	plasminogen	Bos taurus	0-7
1834236-2	1991	Plasmin significantly increased the release of [35S]sulphate-labelled GAG (35S-GAG) from the cell layer, although plasminogen did not show such a stimulatory effect.	Glycosaminoglycans	79-82	plasminogen	Bos taurus	0-7
1896966-2	1991	It was revealed that the trichloroacetic acid-insoluble [35S]sulfate-labeled GAG (35S-GAG) was decreased by thrombin.	Glycosaminoglycans	77-80	coagulation factor II, thrombin	Bos taurus	108-116
2047761-6	1991	When macrophages from mice stressed 8 days or HCC mice were stimulated in vitro with phorbol myristate acetate (PMA) and IL-1 or PMA and IL-2, a changed PG/GAG synthesis was observed only in macrophages from the HCC animals.	Glycosaminoglycans	156-159	interleukin 1 complex	Mus musculus	121-125
2047761-6	1991	When macrophages from mice stressed 8 days or HCC mice were stimulated in vitro with phorbol myristate acetate (PMA) and IL-1 or PMA and IL-2, a changed PG/GAG synthesis was observed only in macrophages from the HCC animals.	Glycosaminoglycans	156-159	interleukin 2	Mus musculus	137-141
1896966-0	1991	Effect of thrombin on the production of glycosaminoglycans by cultured endothelial cells.	Glycosaminoglycans	40-58	coagulation factor II, thrombin	Bos taurus	10-18
1896966-1	1991	We investigated the effect of thrombin on the production process of glycosaminoglycans (GAG) in cultured bovine aortic endothelial cells.	Glycosaminoglycans	68-86	coagulation factor II, thrombin	Bos taurus	30-38
1896966-2	1991	It was revealed that the trichloroacetic acid-insoluble [35S]sulfate-labeled GAG (35S-GAG) was decreased by thrombin.	Glycosaminoglycans	86-89	coagulation factor II, thrombin	Bos taurus	108-116
1896966-3	1991	The thrombin-induced decrease in the accumulation of 35S-GAG in the cell layer occurred even in the presence of actinomycin D or cycloheximide.	Glycosaminoglycans	57-60	coagulation factor II, thrombin	Bos taurus	4-12
1896966-4	1991	The incorporation of both [35S]sulfate and [3H]glucosamine into the GAG was decreased by thrombin, while the ratio of 35S to 3H was not changed.	Glycosaminoglycans	68-71	coagulation factor II, thrombin	Bos taurus	89-97
1896966-5	1991	Also, the incorporation of both [3H]glucosamine and [14C]UDP-xylose into the GAG was inhibited by thrombin.	Glycosaminoglycans	77-80	coagulation factor II, thrombin	Bos taurus	98-106
1896966-6	1991	From these results, it was suggested that thrombin decreased GAG in the endothelial cell layer through an suppression of formation of polysaccharide chains rather than that of core protein.	Glycosaminoglycans	61-64	coagulation factor II, thrombin	Bos taurus	42-50
2021626-4	1991	The larger species, which migrates as a diffuse band of molecular mass 250-350 kDa on sodium dodecyl sulfate-polyacrylamide electrophoresis gels, is characteristic of the TGF-beta receptor type III, a proteoglycan containing glycosaminoglycan (GAG) chains of chondroitin and heparan sulfate.	Glycosaminoglycans	225-242	transforming growth factor beta receptor 3	Homo sapiens	171-197
2026622-11	1991	Inhibitors of oligosaccharide processing, however, permitted secretion of GAG-substituted DS-PGII that was fully (three chains) or incompletely (one or two chains) substituted with partially processed Asn-linked carbohydrate chains.	Glycosaminoglycans	74-77	decorin	Homo sapiens	93-97
1850037-10	1991	Deletion of regions in gag, which was previously shown to contain a cis-acting negative regulator of splicing, resulted in a corresponding increase of both spliced viral mRNAs and a decrease in unspliced RNA, suggesting that this element suppressed both env and src splicing.	Glycosaminoglycans	23-26	endogenous retrovirus group K member 20	Homo sapiens	254-257
1850037-10	1991	Deletion of regions in gag, which was previously shown to contain a cis-acting negative regulator of splicing, resulted in a corresponding increase of both spliced viral mRNAs and a decrease in unspliced RNA, suggesting that this element suppressed both env and src splicing.	Glycosaminoglycans	23-26	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	262-265
1902471-1	1991	Heparin cofactor II (HC) is a plasma serine proteinase inhibitor (serpin) that inhibits alpha-thrombin in a reaction that is dramatically enhanced by heparin and other glycosaminoglycans/polyanions.	Glycosaminoglycans	168-186	coagulation factor II, thrombin	Homo sapiens	94-102
1902486-0	1991	Stimulation of glycosaminoglycan accumulation by interferon gamma in cultured human retroocular fibroblasts.	Glycosaminoglycans	15-32	interferon gamma	Homo sapiens	49-65
1902486-2	1991	We treated cultured retroocular and dermal fibroblasts with recombinant interferon gamma (100 U/ml) for 16-24h and measured [3H]GAG accumulation.	Glycosaminoglycans	128-131	interferon gamma	Homo sapiens	72-88
1902486-5	1991	These results suggest that retroocular fibroblasts may be uniquely targeted for one action of interferon gamma which involves the modulation of GAG metabolism.	Glycosaminoglycans	144-147	interferon gamma	Homo sapiens	94-110
1707986-3	1991	Immunoblotting assays with a monoclonal antibody (MAb) specific for p24 showed that all three mutant contained a gag precursor, Pr56gag, with AH2 and CA expressing an extra band of about 160 kDa.	Glycosaminoglycans	113-116	transmembrane p24 trafficking protein 2	Homo sapiens	68-71
2021626-4	1991	The larger species, which migrates as a diffuse band of molecular mass 250-350 kDa on sodium dodecyl sulfate-polyacrylamide electrophoresis gels, is characteristic of the TGF-beta receptor type III, a proteoglycan containing glycosaminoglycan (GAG) chains of chondroitin and heparan sulfate.	Glycosaminoglycans	244-247	transforming growth factor beta receptor 3	Homo sapiens	171-197
2018799-4	1991	In soluble complexes, at low and at physiological ionic strength, arterial CSPG and sulfated GAG modify the kinetics of apoB-100 proteolysis by trypsin.	Glycosaminoglycans	93-96	apolipoprotein B	Homo sapiens	120-128
2018799-6	1991	This is indirect evidence that the presence of CSPG and GAG modified the exposure of polar regions of apoB-100 in LDL.	Glycosaminoglycans	56-59	apolipoprotein B	Homo sapiens	102-110
1910328-10	1991	EGF markedly stimulated murine palatal collagens and GAG synthesis between stages T.20-T.22, but had no effect thereafter.	Glycosaminoglycans	53-56	epidermal growth factor	Mus musculus	0-3
1901881-0	1991	Role of glycosaminoglycans in the regulation of T cell proliferation induced by thymic stroma-derived T cell growth factor.	Glycosaminoglycans	8-26	interleukin 2	Homo sapiens	102-122
1901881-1	1991	The present study investigates the regulatory effects of glycosaminoglycans such as heparin and heparan sulfate on T cell proliferation induced by thymic stromal cell monolayer or its derived T cell growth factor (TCGF).	Glycosaminoglycans	57-75	interleukin 2	Homo sapiens	192-212
1901881-1	1991	The present study investigates the regulatory effects of glycosaminoglycans such as heparin and heparan sulfate on T cell proliferation induced by thymic stromal cell monolayer or its derived T cell growth factor (TCGF).	Glycosaminoglycans	57-75	interleukin 2	Homo sapiens	214-218
2007624-16	1991	(c) The polymorphic forms use CD44 and CD44E core proteins, each containing a unique set of potential attachment sites for O- and N-glycosides and glycosaminoglycans.	Glycosaminoglycans	147-165	CD44 molecule (Indian blood group)	Homo sapiens	30-34
1872461-1	1991	The identification of a specific required carbohydrate structure for the antithrombin III binding site on heparin suggests that there may be specific structures in glycosaminoglycan chains which are necessary for other vascular functions of these carbohydrates.	Glycosaminoglycans	164-181	serpin family C member 1	Homo sapiens	73-89
2000940-0	1991	Platelet-derived growth factor-BB and transforming growth factor beta 1 selectively modulate glycosaminoglycans, collagen, and myofibroblasts in excisional wounds.	Glycosaminoglycans	93-111	LOW QUALITY PROTEIN: transforming growth factor beta-1	Oryctolagus cuniculus	38-71
1900310-7	1991	Furthermore, the carboxy-terminal part of the interferon-gamma molecule contains an amino acid cluster, very closely related to a consensus sequence, present in more than 20 proteins known to bind sulfated glycosaminoglycans such as heparin.	Glycosaminoglycans	206-224	interferon gamma	Homo sapiens	46-62
1847668-1	1991	The role of low affinity, heparin-like binding sites for basic fibroblast growth factor (bFGF) was investigated in CHO cells mutant in their metabolism of glycosaminoglycans.	Glycosaminoglycans	155-173	fibroblast growth factor 2	Mus musculus	57-87
1847668-1	1991	The role of low affinity, heparin-like binding sites for basic fibroblast growth factor (bFGF) was investigated in CHO cells mutant in their metabolism of glycosaminoglycans.	Glycosaminoglycans	155-173	fibroblast growth factor 2	Mus musculus	89-93
1905847-2	1991	Incubation of confluent endothelial cell cultures with thrombin at 1.0 NIH U/ml for 8 h and above caused a significant decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) in the cell layer.	Glycosaminoglycans	172-175	coagulation factor II, thrombin	Bos taurus	55-63
1905847-2	1991	Incubation of confluent endothelial cell cultures with thrombin at 1.0 NIH U/ml for 8 h and above caused a significant decrease in the accumulation of [35S]sulfate-labeled GAG (35S-GAG) in the cell layer.	Glycosaminoglycans	181-184	coagulation factor II, thrombin	Bos taurus	55-63
1905847-4	1991	The percentage of 35S-GAG released into the medium during the last 3 h of 24 h incubation was significantly increased by thrombin.	Glycosaminoglycans	22-25	coagulation factor II, thrombin	Bos taurus	121-129
1905847-5	1991	In thrombin-treated cell layer, both heparan sulfate and the other GAG was significantly decreased at the same degree.	Glycosaminoglycans	67-70	coagulation factor II, thrombin	Bos taurus	3-11
1905847-8	1991	From these results, it was suggested that thrombin decreased 35S-GAG in the endothelial cell layer without a nonspecific damage of the cells through mainly an inhibition of GAG production and additionally a stimulation of GAG release.	Glycosaminoglycans	65-68	coagulation factor II, thrombin	Bos taurus	42-50
1905847-8	1991	From these results, it was suggested that thrombin decreased 35S-GAG in the endothelial cell layer without a nonspecific damage of the cells through mainly an inhibition of GAG production and additionally a stimulation of GAG release.	Glycosaminoglycans	173-176	coagulation factor II, thrombin	Bos taurus	42-50
1905847-8	1991	From these results, it was suggested that thrombin decreased 35S-GAG in the endothelial cell layer without a nonspecific damage of the cells through mainly an inhibition of GAG production and additionally a stimulation of GAG release.	Glycosaminoglycans	173-176	coagulation factor II, thrombin	Bos taurus	42-50
2012254-8	1991	Reactivity to three or more gag-encoded proteins was found in 85% (45/53) of ELISA-positive, Western blot-indeterminate sera, and 30% (16/53) reacted to p19 and an env gene product but lacked reactivity to p24.	Glycosaminoglycans	28-31	interleukin 23 subunit alpha	Homo sapiens	153-156
2012254-8	1991	Reactivity to three or more gag-encoded proteins was found in 85% (45/53) of ELISA-positive, Western blot-indeterminate sera, and 30% (16/53) reacted to p19 and an env gene product but lacked reactivity to p24.	Glycosaminoglycans	28-31	endogenous retrovirus group K member 20	Homo sapiens	164-167
2012254-8	1991	Reactivity to three or more gag-encoded proteins was found in 85% (45/53) of ELISA-positive, Western blot-indeterminate sera, and 30% (16/53) reacted to p19 and an env gene product but lacked reactivity to p24.	Glycosaminoglycans	28-31	transmembrane p24 trafficking protein 2	Homo sapiens	206-209
1685643-3	1991	This mutation at codon 200 changes glutamic acid coded by GAG to lysine coded by AAG.	Glycosaminoglycans	58-61	N-methylpurine DNA glycosylase	Homo sapiens	81-84
2001175-4	1991	Immunoprecipitation followed by SDS-polyacrylamide gel electrophoresis (PAGE) showed that the gag precursor protein in L-2 cell clone (type IV) was not cleaved to mature gag proteins, while the env precursor protein on L-3 cell clone (type III) was not cleaved to mature env protein.	Glycosaminoglycans	94-97	endogenous retrovirus group W member 1, envelope	Homo sapiens	194-197
2001175-4	1991	Immunoprecipitation followed by SDS-polyacrylamide gel electrophoresis (PAGE) showed that the gag precursor protein in L-2 cell clone (type IV) was not cleaved to mature gag proteins, while the env precursor protein on L-3 cell clone (type III) was not cleaved to mature env protein.	Glycosaminoglycans	94-97	endogenous retrovirus group W member 1, envelope	Homo sapiens	271-274
1893064-2	1991	vWF interacts with components of the SE such as collagen and heparin-like glycosaminoglycans as well as with two platelet membrane receptors: glycoprotein (GP) Ib and GPIIb/IIIa.	Glycosaminoglycans	74-92	von Willebrand factor	Homo sapiens	0-3
1675281-4	1991	However, when rat femoral head cartilage samples were incubated with 100 ng mL-1 rHu-IL-1 alpha or IL-1 beta for 5 days there was a significant increase in GAG loss from the cartilage into medium, whilst human synovial fluid significantly decreased the loss of GAG from rat cartilage into medium, compared with controls.	Glycosaminoglycans	156-159	L1 cell adhesion molecule	Mus musculus	76-80
1675281-4	1991	However, when rat femoral head cartilage samples were incubated with 100 ng mL-1 rHu-IL-1 alpha or IL-1 beta for 5 days there was a significant increase in GAG loss from the cartilage into medium, whilst human synovial fluid significantly decreased the loss of GAG from rat cartilage into medium, compared with controls.	Glycosaminoglycans	156-159	interleukin 1 alpha	Homo sapiens	85-95
1675281-4	1991	However, when rat femoral head cartilage samples were incubated with 100 ng mL-1 rHu-IL-1 alpha or IL-1 beta for 5 days there was a significant increase in GAG loss from the cartilage into medium, whilst human synovial fluid significantly decreased the loss of GAG from rat cartilage into medium, compared with controls.	Glycosaminoglycans	156-159	interleukin 1 beta	Rattus norvegicus	99-108
1675281-4	1991	However, when rat femoral head cartilage samples were incubated with 100 ng mL-1 rHu-IL-1 alpha or IL-1 beta for 5 days there was a significant increase in GAG loss from the cartilage into medium, whilst human synovial fluid significantly decreased the loss of GAG from rat cartilage into medium, compared with controls.	Glycosaminoglycans	261-264	L1 cell adhesion molecule	Mus musculus	76-80
1675281-4	1991	However, when rat femoral head cartilage samples were incubated with 100 ng mL-1 rHu-IL-1 alpha or IL-1 beta for 5 days there was a significant increase in GAG loss from the cartilage into medium, whilst human synovial fluid significantly decreased the loss of GAG from rat cartilage into medium, compared with controls.	Glycosaminoglycans	261-264	interleukin 1 alpha	Homo sapiens	85-95
1675281-4	1991	However, when rat femoral head cartilage samples were incubated with 100 ng mL-1 rHu-IL-1 alpha or IL-1 beta for 5 days there was a significant increase in GAG loss from the cartilage into medium, whilst human synovial fluid significantly decreased the loss of GAG from rat cartilage into medium, compared with controls.	Glycosaminoglycans	261-264	interleukin 1 beta	Rattus norvegicus	99-108
1646210-1	1991	Dermatan sulphate (DS) is a glycosaminoglycan which catalyses specifically thrombin inhibition by a plasmatic inhibitor, Heparin cofactor II (HCII).	Glycosaminoglycans	28-45	coagulation factor II, thrombin	Homo sapiens	75-83
1646210-1	1991	Dermatan sulphate (DS) is a glycosaminoglycan which catalyses specifically thrombin inhibition by a plasmatic inhibitor, Heparin cofactor II (HCII).	Glycosaminoglycans	28-45	serpin family D member 1	Homo sapiens	121-140
1646210-1	1991	Dermatan sulphate (DS) is a glycosaminoglycan which catalyses specifically thrombin inhibition by a plasmatic inhibitor, Heparin cofactor II (HCII).	Glycosaminoglycans	28-45	serpin family D member 1	Homo sapiens	142-146
1905847-0	1991	Thrombin decreases glycosaminoglycans content of endothelial cells in culture.	Glycosaminoglycans	19-37	coagulation factor II, thrombin	Bos taurus	0-8
1905847-1	1991	The effect of thrombin on the metabolism of glycosaminoglycans (GAG) in cultured bovine aortic endothelial cells was investigated.	Glycosaminoglycans	44-62	coagulation factor II, thrombin	Bos taurus	14-22
1898736-5	1991	This PGP cross-link may be present in other proteins, but could have been overlooked due to the heterogeneous behavior of proteins containing glycosaminoglycan.	Glycosaminoglycans	142-159	phosphoglycolate phosphatase	Homo sapiens	5-8
1824616-1	1991	Recombinant human interleukin-1 alpha (IL-1 alpha) and recombinant human IL-1 beta stimulate matrix proteoglycan degradation and inhibit glycosaminoglycan synthesis in bovine nasal cartilage explants.	Glycosaminoglycans	137-154	interleukin 1 alpha	Homo sapiens	18-37
1824616-1	1991	Recombinant human interleukin-1 alpha (IL-1 alpha) and recombinant human IL-1 beta stimulate matrix proteoglycan degradation and inhibit glycosaminoglycan synthesis in bovine nasal cartilage explants.	Glycosaminoglycans	137-154	interleukin 1 alpha	Homo sapiens	39-49
1824616-1	1991	Recombinant human interleukin-1 alpha (IL-1 alpha) and recombinant human IL-1 beta stimulate matrix proteoglycan degradation and inhibit glycosaminoglycan synthesis in bovine nasal cartilage explants.	Glycosaminoglycans	137-154	interleukin 1 beta	Homo sapiens	73-82
1910328-12	1991	PDGF had no effect on mouse palatal collagen and GAG synthesis whilst TGF-beta 1 inhibited GAG synthesis at T.21.	Glycosaminoglycans	91-94	transforming growth factor, beta 1	Mus musculus	70-80
1726397-4	1991	After evaluating many different technical protocols and experimental procedures, we have found the syncytium inhibition and syncytial focus assays to be particularly useful and have found p24 gag antigen production to be an excellent objective measure of HIV infection under a variety of conditions.	Glycosaminoglycans	192-195	transmembrane p24 trafficking protein 2	Homo sapiens	188-191
2026461-8	1991	DRB1*04.EC is identical to DRB1*04.CB except at codon 74 where GAG encodes glutamic acid instead of GCG encoding alanine.	Glycosaminoglycans	63-66	major histocompatibility complex, class II, DR beta 1	Homo sapiens	0-4
2026461-8	1991	DRB1*04.EC is identical to DRB1*04.CB except at codon 74 where GAG encodes glutamic acid instead of GCG encoding alanine.	Glycosaminoglycans	63-66	major histocompatibility complex, class II, DR beta 1	Homo sapiens	27-31
2064635-4	1991	The activity of many enzymes concerned with the degradation of GAG (hyaluronidase, beta-glucuronidase and cathepsin-D) showed increase in these tissues.	Glycosaminoglycans	63-66	glucuronidase, beta	Rattus norvegicus	83-101
2064635-4	1991	The activity of many enzymes concerned with the degradation of GAG (hyaluronidase, beta-glucuronidase and cathepsin-D) showed increase in these tissues.	Glycosaminoglycans	63-66	cathepsin D	Rattus norvegicus	106-117
1915760-2	1991	This activation reaches different levels and is expressed both by different cell survival and enhanced synthesis of glycosaminoglycans that remain cell-associated (exp.	Glycosaminoglycans	116-134	muscleblind like splicing regulator 1	Homo sapiens	48-51
1905297-2	1991	Combined exposure of pericardial cells to IGF-I and EGF cooperatively increased hyaluronic acid synthesis and the level of hyaluronic acid synthase activity over that seen with or without IGF-I or EGF alone, but did not significantly stimulate the sulfated glycosaminoglycan synthesis.	Glycosaminoglycans	257-274	insulin-like growth factor I	Oryctolagus cuniculus	42-47
1905297-2	1991	Combined exposure of pericardial cells to IGF-I and EGF cooperatively increased hyaluronic acid synthesis and the level of hyaluronic acid synthase activity over that seen with or without IGF-I or EGF alone, but did not significantly stimulate the sulfated glycosaminoglycan synthesis.	Glycosaminoglycans	257-274	pro-epidermal growth factor	Oryctolagus cuniculus	52-55
1943455-0	1991	Calcitonin gene-related peptide increases the production of glycosaminoglycans but not of collagen type I and III in cultures of rat fat-storing cells.	Glycosaminoglycans	60-78	calcitonin-related polypeptide alpha	Rattus norvegicus	0-31
1943455-1	1991	We investigated whether calcitonin gene-related peptide (CGRP) was able to affect the production of collagen and glycosaminoglycans (GAG) in cultures of rat fat-storing cells (FSC).	Glycosaminoglycans	113-131	calcitonin-related polypeptide alpha	Rattus norvegicus	24-55
1943455-1	1991	We investigated whether calcitonin gene-related peptide (CGRP) was able to affect the production of collagen and glycosaminoglycans (GAG) in cultures of rat fat-storing cells (FSC).	Glycosaminoglycans	113-131	calcitonin-related polypeptide alpha	Rattus norvegicus	57-61
1943455-1	1991	We investigated whether calcitonin gene-related peptide (CGRP) was able to affect the production of collagen and glycosaminoglycans (GAG) in cultures of rat fat-storing cells (FSC).	Glycosaminoglycans	133-136	calcitonin-related polypeptide alpha	Rattus norvegicus	24-55
1943455-1	1991	We investigated whether calcitonin gene-related peptide (CGRP) was able to affect the production of collagen and glycosaminoglycans (GAG) in cultures of rat fat-storing cells (FSC).	Glycosaminoglycans	133-136	calcitonin-related polypeptide alpha	Rattus norvegicus	57-61
1943455-2	1991	Rat CGRP (1 nM-1 microM) induced a dose-dependent increase of total GAG production in FSC cultures with an EC50 of 28 nM.	Glycosaminoglycans	68-71	calcitonin-related polypeptide alpha	Rattus norvegicus	4-8
1897296-1	1991	A monodimensional electrophoretic method for the separation of glycosaminoglycans on Titan III Zip Zone cellulose acetate plate based on their different electrophoretic mobilities in barium acetate and different solubilities in ethanol was applied to the Chemetron electrophoretic equipment.	Glycosaminoglycans	63-81	death associated protein kinase 3	Homo sapiens	95-98
2125503-8	1990	Upon secretion of the granule contents induced by immobilized anti-CD3 antibodies, most granzyme A molecules remained complexed with the chondroitin sulfate A glycosaminoglycans, even if synthesis of intact proteoglycans was inhibited.	Glycosaminoglycans	159-177	granzyme A	Homo sapiens	88-98
2175610-1	1990	Interleukin-1 (IL-1) has been shown to regulate glycosaminoglycan (GAG) synthesis.	Glycosaminoglycans	48-65	interleukin 1 alpha	Homo sapiens	15-19
2266131-7	1990	Second, the acidic dimer is instrumental in glycosaminoglycan-mediated activation of hLS2.	Glycosaminoglycans	44-61	serpin family D member 1	Homo sapiens	85-89
2175610-1	1990	Interleukin-1 (IL-1) has been shown to regulate glycosaminoglycan (GAG) synthesis.	Glycosaminoglycans	48-65	interleukin 1 alpha	Homo sapiens	0-13
2175610-1	1990	Interleukin-1 (IL-1) has been shown to regulate glycosaminoglycan (GAG) synthesis.	Glycosaminoglycans	67-70	interleukin 1 alpha	Homo sapiens	0-13
2175610-1	1990	Interleukin-1 (IL-1) has been shown to regulate glycosaminoglycan (GAG) synthesis.	Glycosaminoglycans	67-70	interleukin 1 alpha	Homo sapiens	15-19
2175610-4	1990	Similarly, the decrease in sulfated GAG synthesis induced by IL-1 was reversed by the addition of the IL-1 inhibitor.	Glycosaminoglycans	36-39	interleukin 1 alpha	Homo sapiens	61-65
2175610-4	1990	Similarly, the decrease in sulfated GAG synthesis induced by IL-1 was reversed by the addition of the IL-1 inhibitor.	Glycosaminoglycans	36-39	interleukin 1 receptor antagonist	Homo sapiens	102-116
2127920-1	1990	Appreciable amounts of glycosaminoglycans have been found by immunocytochemistry within mature elastin fibers of human dermis.	Glycosaminoglycans	23-41	elastin	Homo sapiens	95-102
2269670-5	1990	Studies on the NG2-type VI collagen complex suggest that binding between the two molecules is mediated by protein-protein interactions rather than by ionic interactions involving the glycosaminoglycans.	Glycosaminoglycans	183-201	chondroitin sulfate proteoglycan 4	Rattus norvegicus	15-18
1706698-2	1990	The stimulation of endothelial cell growth by HBGF type one (HBGF-1) in particular requires heparin or a similar glycosaminoglycan.	Glycosaminoglycans	113-130	fibroblast growth factor 1	Homo sapiens	61-67
2220820-1	1990	The lysosomal hydrolase alpha-L-iduronidase (IDUA) is one of the enzymes in the metabolic pathway responsible for the degradation of the glycosaminoglycans heparan sulfate and dermatan sulfate.	Glycosaminoglycans	137-155	alpha-L-iduronidase	Homo sapiens	24-43
2258640-9	1990	This is in accord with in vitro studies showing that, while interferons alpha and beta decrease production of glycosaminoglycans, IFN-gamma increases production of glycosaminoglycans.	Glycosaminoglycans	164-182	interferon gamma	Homo sapiens	130-139
2086599-7	1990	Sera reacting to p19 and p24 (both gag) by WB were confirmed positive by RIPA in 75% of the cases.	Glycosaminoglycans	35-38	transmembrane p24 trafficking protein 2	Homo sapiens	25-28
2086599-8	1990	The majority of the indeterminate WB profiles not confirmed by RIPA presented isolated gag reactivity (p15 or p19 or p24).	Glycosaminoglycans	87-90	cyclin dependent kinase inhibitor 2B	Homo sapiens	103-106
2086599-8	1990	The majority of the indeterminate WB profiles not confirmed by RIPA presented isolated gag reactivity (p15 or p19 or p24).	Glycosaminoglycans	87-90	interleukin 23 subunit alpha	Homo sapiens	110-113
2086599-8	1990	The majority of the indeterminate WB profiles not confirmed by RIPA presented isolated gag reactivity (p15 or p19 or p24).	Glycosaminoglycans	87-90	transmembrane p24 trafficking protein 2	Homo sapiens	117-120
2150741-4	1990	When cells were incubated with Interleukin-1 (IL-1), Etodolac still exerted its inhibiting effect on GAG synthesis.	Glycosaminoglycans	101-104	interleukin 1 alpha	Homo sapiens	31-44
2150741-4	1990	When cells were incubated with Interleukin-1 (IL-1), Etodolac still exerted its inhibiting effect on GAG synthesis.	Glycosaminoglycans	101-104	interleukin 1 alpha	Homo sapiens	46-50
2150741-6	1990	IL-1 alone or in combination with Etodolac decreased the synthesis of GAGs suggesting that pretreatment with Etodolac cannot prevent the action of IL-1.	Glycosaminoglycans	70-74	interleukin 1 alpha	Homo sapiens	0-4
2150741-10	1990	In the same experiment, IL-1 alone caused a slight increase of GAG production that was not abolished by Etodolac treatment.	Glycosaminoglycans	63-66	interleukin 1 alpha	Homo sapiens	24-28
2220820-1	1990	The lysosomal hydrolase alpha-L-iduronidase (IDUA) is one of the enzymes in the metabolic pathway responsible for the degradation of the glycosaminoglycans heparan sulfate and dermatan sulfate.	Glycosaminoglycans	137-155	alpha-L-iduronidase	Homo sapiens	45-49
2220820-2	1990	In humans a deficiency of IDUA leads to the accumulation of glycosaminoglycans, resulting in the lysosomal storage disorder mucopolysaccharidosis type I.	Glycosaminoglycans	60-78	alpha-L-iduronidase	Homo sapiens	26-30
1700901-2	1990	This study investigates the regulation, by salt and glycosaminoglycans, of ternary (alpha-beta-gamma) complex formation, measured by incubating radioiodinated alpha-subunit with a mixture of IGF-I and IGFBP-3 and precipitating bound radioactivity with an anti-IGFBP-3 antiserum.	Glycosaminoglycans	52-70	insulin like growth factor 1	Homo sapiens	191-196
2091326-8	1990	Since most gag+ T-cell lines produced lymphotoxin (LT)/tumor necrosis factor alpha (TNF alpha), it is suggested that those T cells are playing important roles in the pathogenesis of HAM.	Glycosaminoglycans	11-14	tumor necrosis factor	Homo sapiens	55-82
2120082-4	1990	TGF-beta 1 at 15 ng/ml for 72 h increased [35S]sulfate incorporation into media glycosaminoglycans to 190% of control levels but did not affect the [35S]sulfate incorporation into cell-associated glycosaminoglycans.	Glycosaminoglycans	80-98	transforming growth factor beta 1	Homo sapiens	0-10
2120082-8	1990	These data suggest that the ability of TGF-beta 1 to modulate hematopoiesis may be due, in part, to its effects on glycosaminoglycan production.	Glycosaminoglycans	115-132	transforming growth factor beta 1	Homo sapiens	39-49
2213021-0	1990	Changes in glycosaminoglycans during the neuritogenesis in PC12 pheochromocytoma cells induced by nerve growth factor.	Glycosaminoglycans	11-29	nerve growth factor	Rattus norvegicus	98-117
2213021-2	1990	Therefore, we carried out quantitative and qualitative analyses of glycosaminoglycans (GAGs), the polysaccharide moiety of proteoglycans, during neuritogenesis in PC12 cells that is induced by nerve growth factor (NGF).	Glycosaminoglycans	67-85	nerve growth factor	Rattus norvegicus	193-212
2213021-2	1990	Therefore, we carried out quantitative and qualitative analyses of glycosaminoglycans (GAGs), the polysaccharide moiety of proteoglycans, during neuritogenesis in PC12 cells that is induced by nerve growth factor (NGF).	Glycosaminoglycans	67-85	nerve growth factor	Rattus norvegicus	214-217
2219727-6	1990	These results indicate that p41 could represent an alternative gag precursor with N-terminal sequences derived from p24 and C-terminal from p15.	Glycosaminoglycans	63-66	erythrocyte membrane protein band 4.1	Homo sapiens	28-31
2219727-6	1990	These results indicate that p41 could represent an alternative gag precursor with N-terminal sequences derived from p24 and C-terminal from p15.	Glycosaminoglycans	63-66	transmembrane p24 trafficking protein 2	Homo sapiens	116-119
2219727-6	1990	These results indicate that p41 could represent an alternative gag precursor with N-terminal sequences derived from p24 and C-terminal from p15.	Glycosaminoglycans	63-66	cyclin dependent kinase inhibitor 2B	Homo sapiens	140-143
2091326-8	1990	Since most gag+ T-cell lines produced lymphotoxin (LT)/tumor necrosis factor alpha (TNF alpha), it is suggested that those T cells are playing important roles in the pathogenesis of HAM.	Glycosaminoglycans	11-14	tumor necrosis factor	Homo sapiens	84-93
1698781-6	1990	Syndecans are known to change their glycosaminoglycan composition yielding tissue-type specific polymorphic forms of syndecan (Sanderson, R., and Bernfield, M. (1988) Proc.	Glycosaminoglycans	36-53	syndecan 1	Homo sapiens	117-125
1698787-13	1990	These results indicate that the exposure of the glycosaminoglycan-binding domain in VN may allow the concomitant binding of PAI-1 and heparin-like molecules to this region of the VN molecule.	Glycosaminoglycans	48-65	vitronectin	Homo sapiens	84-86
1698787-13	1990	These results indicate that the exposure of the glycosaminoglycan-binding domain in VN may allow the concomitant binding of PAI-1 and heparin-like molecules to this region of the VN molecule.	Glycosaminoglycans	48-65	serpin family E member 1	Homo sapiens	124-129
1698787-13	1990	These results indicate that the exposure of the glycosaminoglycan-binding domain in VN may allow the concomitant binding of PAI-1 and heparin-like molecules to this region of the VN molecule.	Glycosaminoglycans	48-65	vitronectin	Homo sapiens	179-181
2226466-1	1990	There is evidence that by catalyzing thrombin inhibition, several glycosaminoglycans can inhibit the thrombin-mediated amplification reactions of coagulation and thereby delay prothrombin activation.	Glycosaminoglycans	66-84	coagulation factor II, thrombin	Homo sapiens	37-45
2226466-1	1990	There is evidence that by catalyzing thrombin inhibition, several glycosaminoglycans can inhibit the thrombin-mediated amplification reactions of coagulation and thereby delay prothrombin activation.	Glycosaminoglycans	66-84	coagulation factor II, thrombin	Homo sapiens	101-109
2223864-3	1990	Other glycosaminoglycans inhibited PLA2 activity to a significantly lesser extent, with a pattern of inhibition: heparin much greater than chondroitin sulfate (CS)-C greater than CS-A greater than CS-B greater than keratan sulfate.	Glycosaminoglycans	6-24	phospholipase A2 group IB	Homo sapiens	35-39
2123631-2	1990	The plasmid, which contained a mutation in the frameshift region, expressed viral proteinase (PR), a pol gene product, in the gag reading frame, resulting in efficient processing of mature CA and other gag-related products.	Glycosaminoglycans	126-129	endogenous retrovirus group K member 24	Homo sapiens	82-92
2123631-2	1990	The plasmid, which contained a mutation in the frameshift region, expressed viral proteinase (PR), a pol gene product, in the gag reading frame, resulting in efficient processing of mature CA and other gag-related products.	Glycosaminoglycans	126-129	endogenous retrovirus group K member 24	Homo sapiens	94-96
2170425-5	1990	These results suggest that bFGF-heparin and/or heparan sulfate complexes may be more effective than bFGF alone in stimulating cells located away from the bFGF source because the bFGF-glycosaminoglycan complex partitions into the soluble phase rather than binding to insoluble glycosaminoglycans in the extracellular matrix.	Glycosaminoglycans	183-200	fibroblast growth factor 2	Bos taurus	27-31
2128618-2	1990	The induced glycosaminoglycan depletion in the extracellular matrix was monitored by immunohistochemistry employing monoclonal antibodies to chondroitin 4- and chondroitin 6-sulfates.	Glycosaminoglycans	12-29	carbohydrate sulfotransferase 11	Mus musculus	141-154
2170425-5	1990	These results suggest that bFGF-heparin and/or heparan sulfate complexes may be more effective than bFGF alone in stimulating cells located away from the bFGF source because the bFGF-glycosaminoglycan complex partitions into the soluble phase rather than binding to insoluble glycosaminoglycans in the extracellular matrix.	Glycosaminoglycans	276-294	fibroblast growth factor 2	Bos taurus	27-31
2170425-6	1990	Thus, the complex of bFGF and glycosaminoglycan may represent one of the active forms of bFGF in vivo.	Glycosaminoglycans	30-47	fibroblast growth factor 2	Bos taurus	89-93
2175954-6	1990	These results indicate that the mechanism of the induction of PGI2 production by ATIII involves heparin-like glycosaminoglycans on HUVEC and the stimulation of synthesis of a protein related to PGI2 production.	Glycosaminoglycans	109-127	serpin family C member 1	Homo sapiens	81-86
2212861-4	1990	Three isoforms (CTAP-III des 1-13, des 1-14, and des 1-15/NAP-2) stimulate [14C]glycosaminoglycan synthesis; two isoforms also promote [3H]DNA synthesis in human fibroblast cultures.	Glycosaminoglycans	80-97	pro-platelet basic protein	Homo sapiens	16-24
2212861-4	1990	Three isoforms (CTAP-III des 1-13, des 1-14, and des 1-15/NAP-2) stimulate [14C]glycosaminoglycan synthesis; two isoforms also promote [3H]DNA synthesis in human fibroblast cultures.	Glycosaminoglycans	80-97	pro-platelet basic protein	Homo sapiens	58-63
1962899-4	1990	The half-life of anti-Factor Xa-like activity increased after repeated administration, indicating that glycosaminoglycans or other compounds are released by LMW heparin into the bloodstream.	Glycosaminoglycans	103-121	coagulation factor X	Homo sapiens	22-31
2121613-1	1990	Serglycin (SGC) is a Ser-Gly-repeat-containing protein, used as a proteoglycan core protein in the parietal yolk sac and in mast cells, where glycosaminoglycan side chains are attached to the serine residues of the repeat region.	Glycosaminoglycans	142-159	serglycin	Mus musculus	11-14
1973689-8	1990	In the apoA-IV-3 allele we identified a single G to A substitution that converts the glutamic acid (GAG) at position 230 of the mature protein to a lysine (AAG), thus adding 2 positive charge units to the apoA-IV-1 isoprotein (pI 4.97) and forming the more basic apoA-IV-3 isoprotein (pI 5.08).	Glycosaminoglycans	100-103	N-methylpurine DNA glycosylase	Homo sapiens	156-159
2224589-1	1990	Tumor necrosis factor alpha (TNF alpha) decreased the synthesis of glycosaminoglycan (GAG) in rabbit costal chondrocytes in culture, but did not stimulate the release of GAG from cell layers.	Glycosaminoglycans	67-84	tumor necrosis factor	Oryctolagus cuniculus	0-27
2224589-1	1990	Tumor necrosis factor alpha (TNF alpha) decreased the synthesis of glycosaminoglycan (GAG) in rabbit costal chondrocytes in culture, but did not stimulate the release of GAG from cell layers.	Glycosaminoglycans	67-84	tumor necrosis factor	Oryctolagus cuniculus	29-38
2224589-1	1990	Tumor necrosis factor alpha (TNF alpha) decreased the synthesis of glycosaminoglycan (GAG) in rabbit costal chondrocytes in culture, but did not stimulate the release of GAG from cell layers.	Glycosaminoglycans	86-89	tumor necrosis factor	Oryctolagus cuniculus	0-27
2224589-1	1990	Tumor necrosis factor alpha (TNF alpha) decreased the synthesis of glycosaminoglycan (GAG) in rabbit costal chondrocytes in culture, but did not stimulate the release of GAG from cell layers.	Glycosaminoglycans	86-89	tumor necrosis factor	Oryctolagus cuniculus	29-38
2200887-1	1990	To obtain a better understanding of the role of the gag gene-encoded matrix (MA) protein in the assembly and maturation of type D retroviruses, we have made five mutants with specific in-frame deletions within the p10-coding region by the use of oligonucleotide-directed mutagenesis.	Glycosaminoglycans	52-55	S100 calcium binding protein A10	Homo sapiens	214-217
2196384-7	1990	At the Tyr/Pro site in gag, processing was severely inhibited by substitutions within the P4, P2, P1, and P2" positions.	Glycosaminoglycans	23-26	solute carrier family 10 member 4	Homo sapiens	90-108
2226352-0	1990	Effect of transforming growth factor beta on synthesis of glycosaminoglycans by human lung fibroblasts.	Glycosaminoglycans	58-76	transforming growth factor beta 1	Homo sapiens	10-41
1973167-4	1990	Using molecular techniques, two point mutations were detected in the coding sequence of the FX Vorarlberg gene: a G----A at base pair 160 in exon II resulting in a change of Gla14 (GAA) to Lys (AAA); a G----A at base pair 424 in exon V resulting in a change from Glu102 (GAG) to Lys (AAG).	Glycosaminoglycans	271-274	alpha glucosidase	Homo sapiens	181-184
2338171-0	1990	Association between collagen and glycosaminoglycans is altered in dermal extracellular matrix of fetal Steel (Sld/Sld) mice.	Glycosaminoglycans	33-51	mucin 19	Mus musculus	110-113
2115154-1	1990	Scheie syndrome is a rare inborn error of metabolism, a mucopolysaccharidosis in which deficiency of the lysosomal enzyme alpha-L-iduronidase leads to tissue accumulation of mucopolysaccharides.	Glycosaminoglycans	174-193	alpha-L-iduronidase	Homo sapiens	122-141
1966669-0	1990	The effect of heparin and other glycosaminoglycans on levels of tissue plasminogen activator and plasminogen activator inhibitor in cultured human umbilical vein endothelial cells.	Glycosaminoglycans	32-50	chromosome 20 open reading frame 181	Homo sapiens	64-92
2338171-0	1990	Association between collagen and glycosaminoglycans is altered in dermal extracellular matrix of fetal Steel (Sld/Sld) mice.	Glycosaminoglycans	33-51	mucin 19	Mus musculus	114-117
2351697-2	1990	Using small plastic implants to treat regions of developing mammary glands in situ, we now report that TGF-beta 1 growth inhibition is associated with an ectopic accumulation of type I collagen messenger RNA and protein, as well as the glycosaminoglycan, chondroitin sulfate.	Glycosaminoglycans	236-253	transforming growth factor, beta 1	Mus musculus	103-113
2112156-7	1990	Finally the monoclonal antibody 4B4 showed cross-reactivity to Sm and p24 gag.	Glycosaminoglycans	74-77	transmembrane p24 trafficking protein 2	Homo sapiens	70-73
2143723-10	1990	In the rat, KS and the trophoblast GAG are E2-dependent and down-regulated by P. The functional significance of the hormone-induced GAG changes, namely the possible role of the E2-dependent KS in implantation, are discussed.	Glycosaminoglycans	35-38	dihydrolipoamide S-acetyltransferase	Rattus norvegicus	43-45
2164263-6	1990	These findings could be due to the different, additional anti-thrombin activities of these glycosaminoglycans and/or to their different anti-prothrombinase activities.	Glycosaminoglycans	91-109	coagulation factor II, thrombin	Homo sapiens	62-70
1976012-4	1990	On the other hand, interaction of MTSP-1 with sulfated glycosaminoglycans, i.e., heparin and chondroitin sulfate, led to increased enzymatic activity and an altered fine specificity of MTSP-1 for peptide substrates.	Glycosaminoglycans	55-73	suppression of tumorigenicity 14 (colon carcinoma)	Mus musculus	34-40
2161655-1	1990	Thrombomodulin, an endothelial cell-surface anticoagulant, has been postulated to contain a glycosaminoglycan.	Glycosaminoglycans	92-109	thrombomodulin	Homo sapiens	0-14
2161655-4	1990	These results support a role for glycosaminoglycans in thrombomodulin function and suggest that beta-D-xylosides can be used to investigate both the anticoagulant mechanisms and the biosynthesis of cell-surface thrombomodulin.	Glycosaminoglycans	33-51	thrombomodulin	Homo sapiens	55-69
2110415-4	1990	The material reacted with monoclonal antibody 9-A-2 after digestion by chondroitinase AC in one case and ABC in both cases, which is consistent with the identification of the glycosaminoglycans chondroitin 4-sulfate and dermatan sulfate.	Glycosaminoglycans	175-193	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	105-108
1976012-4	1990	On the other hand, interaction of MTSP-1 with sulfated glycosaminoglycans, i.e., heparin and chondroitin sulfate, led to increased enzymatic activity and an altered fine specificity of MTSP-1 for peptide substrates.	Glycosaminoglycans	55-73	suppression of tumorigenicity 14 (colon carcinoma)	Mus musculus	185-191
2209468-1	1990	The possible in vivo role of TGF-beta 1 in regulating various proteins of the extracellular matrix, including fibronectin, collagen I and III, and glycosaminoglycans, was examined by immunohistochemical methods during critical stages of lung morphogenesis in the 11- to 18-day-old mouse embryo.	Glycosaminoglycans	147-165	transforming growth factor, beta 1	Mus musculus	29-39
2112771-1	1990	In order to study the hormonal control mechanisms of cervical maturation, we investigated cyclooxygenase and 5-lipoxygenase inhibitors-induced changes in the distribution of glycosaminoglycans (GAG) in pregnant Wistar rat uterine cervices at term.	Glycosaminoglycans	174-192	arachidonate 5-lipoxygenase	Rattus norvegicus	109-123
2164946-0	1990	Beta-glucuronidase mediated pathway essential for retinal pigment epithelial degradation of glycosaminoglycans.	Glycosaminoglycans	92-110	glucuronidase, beta	Rattus norvegicus	0-18
2317527-17	1990	Thus, the amount and type of fatty acids may be important in regulating LPL activity in vivo by affecting both LPL interaction with glycosaminoglycans and with apo C-II.	Glycosaminoglycans	132-150	lipoprotein lipase	Bos taurus	72-75
2318847-1	1990	We investigated the interaction of the human plasma proteinase inhibitor heparin cofactor II (HC) with human neutrophil elastase and cathepsin G in order to examine 1) proteinase inhibition by HC, 2) inactivation of HC, and 3) the effect of glycosaminoglycans on inhibition and inactivation.	Glycosaminoglycans	241-259	endogenous retrovirus group K member 25	Homo sapiens	52-62
2324102-4	1990	108, 1547-1556), the core protein of human syndecan can be divided into three domains: a matrix-interacting ectodomain containing putative glycosaminoglycan attachment sites, a 25-residue hydrophobic membrane-spanning domain, and a 34-residue cytoplasmic domain.	Glycosaminoglycans	139-156	syndecan 1	Homo sapiens	43-51
2317527-17	1990	Thus, the amount and type of fatty acids may be important in regulating LPL activity in vivo by affecting both LPL interaction with glycosaminoglycans and with apo C-II.	Glycosaminoglycans	132-150	lipoprotein lipase	Bos taurus	111-114
2318889-0	1990	On the activation of human leuserpin-2, a thrombin inhibitor, by glycosaminoglycans.	Glycosaminoglycans	65-83	serpin family D member 1	Homo sapiens	27-38
2350374-3	1990	Anti-TGF-beta-neutralisation was effective against increases in both sulphated and non-sulphated GAG.	Glycosaminoglycans	97-100	transforming growth factor beta 1	Homo sapiens	5-13
2350374-10	1990	These findings indicate that TGF-beta alone can account for the changes in SMC GAG synthesis stimulated by ECCM.	Glycosaminoglycans	79-82	transforming growth factor beta 1	Homo sapiens	29-37
2350374-11	1990	It was also found, however, that heat-treated SMC conditioned medium stimulated SMC GAG synthesis, thus SMC may contribute to the control of their own GAG synthesis through autocrine TGF-beta activity.	Glycosaminoglycans	151-154	transforming growth factor beta 1	Homo sapiens	183-191
2180732-3	1990	Certain Pgp-1-positive T and B cell lines show hyaluronic acid binding that is highly specific and is not competed for by other glycosaminoglycans.	Glycosaminoglycans	128-146	CD44 antigen	Mus musculus	8-13
2318889-0	1990	On the activation of human leuserpin-2, a thrombin inhibitor, by glycosaminoglycans.	Glycosaminoglycans	65-83	coagulation factor II, thrombin	Homo sapiens	42-50
2318889-3	1990	One of these regions, which encompasses a dimeric structure enriched in basic amino acids, is required for both glycosaminoglycan binding and glycosaminoglycan-mediated acceleration of thrombin inhibition.	Glycosaminoglycans	112-129	coagulation factor II, thrombin	Homo sapiens	185-193
2318889-3	1990	One of these regions, which encompasses a dimeric structure enriched in basic amino acids, is required for both glycosaminoglycan binding and glycosaminoglycan-mediated acceleration of thrombin inhibition.	Glycosaminoglycans	142-159	coagulation factor II, thrombin	Homo sapiens	185-193
2156859-7	1990	These results suggest that at least two acidic thrombin binding domains are present in rabbit TM, whereby a dermatan sulfate-like glycosaminoglycan moiety constitutes the secondary binding domain for thrombin, eliciting both the direct as well as the AT III-dependent anticoagulant function of rabbit TM (activities b and c) but not protein C activation (activity a).	Glycosaminoglycans	130-147	prothrombin	Oryctolagus cuniculus	200-208
2318889-4	1990	Deletion of another dimeric region, which spans a sequence with a high negative charge density, resulted in a strong reduction in the glycosaminoglycan-enhanced activity of hLS2.	Glycosaminoglycans	134-151	serpin family D member 1	Homo sapiens	173-177
2318889-6	1990	Based on our observations we propose a model for the activation of hLS2 by glycosaminoglycans.	Glycosaminoglycans	75-93	serpin family D member 1	Homo sapiens	67-71
2318889-7	1990	The key feature of this model is the suggestion that the glycosaminoglycan-enhanced reaction between hLS2 and thrombin is mediated by at least two regions of contact, involving both the reactive center region and the acidic domain of hLS2.	Glycosaminoglycans	57-74	serpin family D member 1	Homo sapiens	101-105
2318889-7	1990	The key feature of this model is the suggestion that the glycosaminoglycan-enhanced reaction between hLS2 and thrombin is mediated by at least two regions of contact, involving both the reactive center region and the acidic domain of hLS2.	Glycosaminoglycans	57-74	coagulation factor II, thrombin	Homo sapiens	110-118
2318889-7	1990	The key feature of this model is the suggestion that the glycosaminoglycan-enhanced reaction between hLS2 and thrombin is mediated by at least two regions of contact, involving both the reactive center region and the acidic domain of hLS2.	Glycosaminoglycans	57-74	serpin family D member 1	Homo sapiens	234-238
2318889-8	1990	Binding of glycosaminoglycans to hLS2 is suggested to result first in the release of the acidic region from intramolecular interactions.	Glycosaminoglycans	11-29	serpin family D member 1	Homo sapiens	33-37
2317208-3	1990	The results provide strong evidence that codon 501 in albumin Kashmir is AAG (lysine) instead of GAG (glutamic acid), thus confirming the protein sequences reported.	Glycosaminoglycans	97-100	albumin	Homo sapiens	54-61
1969657-9	1990	The number and size of its glycosaminoglycan chains vary with changes in cell shape and organization yielding tissue type-specific polymorphic forms of syndecan.	Glycosaminoglycans	27-44	syndecan 1	Homo sapiens	152-160
2107976-0	1990	Cathepsin B secretion by rabbit articular chondrocytes: modulation by cycloheximide and glycosaminoglycans.	Glycosaminoglycans	88-106	cathepsin B	Oryctolagus cuniculus	0-11
2107976-4	1990	Glycosaminoglycans added to the culture medium of modulated chondrocytes partially reduced the rate of secretion of cathepsin B, this effect being dependent on their structure, the degree of sulfation, and concentration.	Glycosaminoglycans	0-18	cathepsin B	Oryctolagus cuniculus	116-127
2107976-6	1990	The switching off of cathepsin B release was apparently best favored by a high concentration of negatively charged sulfate groups attached to a polymeric glycosaminoglycan chain; this simulates the natural environment of the chondrocytes in articular cartilage.	Glycosaminoglycans	154-171	cathepsin B	Oryctolagus cuniculus	21-32
1689304-4	1990	In this paper, we show that the highly sulfated glycosaminoglycans (GAGs), dextran sulfate, pentosan polysulfate, and fucoidan effectively augment [14C]putrescine incorporation into VN and cross-linking of VN into high molecular multimers by guinea pig liver transglutaminase (TG).	Glycosaminoglycans	68-72	protein-glutamine gamma-glutamyltransferase 2	Cavia porcellus	277-279
2111930-5	1990	Double staining revealed the presence of gag-coded HIV1 proteins in the above-mentioned CD34+ progenitor cells, in myelopoiesis cells, megakaryocytes and above all, in CD68+/acid phosphatase+ and alkaline phosphatase+ bone marrow reticular cells.	Glycosaminoglycans	41-44	CD34 molecule	Homo sapiens	88-92
1689304-0	1990	Highly sulfated glycosaminoglycans augment the cross-linking of vitronectin by guinea pig liver transglutaminase.	Glycosaminoglycans	16-34	vitronectin	Cavia porcellus	64-75
2083241-1	1990	The effect of purified human plasma fibronectin on LDL-GAG and LDL-PG complex formation was studied.	Glycosaminoglycans	55-58	fibronectin 1	Homo sapiens	36-47
1689304-0	1990	Highly sulfated glycosaminoglycans augment the cross-linking of vitronectin by guinea pig liver transglutaminase.	Glycosaminoglycans	16-34	protein-glutamine gamma-glutamyltransferase 2	Cavia porcellus	96-112
1689304-4	1990	In this paper, we show that the highly sulfated glycosaminoglycans (GAGs), dextran sulfate, pentosan polysulfate, and fucoidan effectively augment [14C]putrescine incorporation into VN and cross-linking of VN into high molecular multimers by guinea pig liver transglutaminase (TG).	Glycosaminoglycans	48-66	protein-glutamine gamma-glutamyltransferase 2	Cavia porcellus	259-275
1689304-4	1990	In this paper, we show that the highly sulfated glycosaminoglycans (GAGs), dextran sulfate, pentosan polysulfate, and fucoidan effectively augment [14C]putrescine incorporation into VN and cross-linking of VN into high molecular multimers by guinea pig liver transglutaminase (TG).	Glycosaminoglycans	48-66	protein-glutamine gamma-glutamyltransferase 2	Cavia porcellus	277-279
1689304-4	1990	In this paper, we show that the highly sulfated glycosaminoglycans (GAGs), dextran sulfate, pentosan polysulfate, and fucoidan effectively augment [14C]putrescine incorporation into VN and cross-linking of VN into high molecular multimers by guinea pig liver transglutaminase (TG).	Glycosaminoglycans	68-72	protein-glutamine gamma-glutamyltransferase 2	Cavia porcellus	259-275
2083241-2	1990	Fibronectin added to LDL or to GAG or even to preformed LDL-GAG-Ca2+ complexes could inhibit complex formation and dissociated preformed complexes.	Glycosaminoglycans	31-34	fibronectin 1	Homo sapiens	0-11
2083241-2	1990	Fibronectin added to LDL or to GAG or even to preformed LDL-GAG-Ca2+ complexes could inhibit complex formation and dissociated preformed complexes.	Glycosaminoglycans	60-63	fibronectin 1	Homo sapiens	0-11
2083241-5	1990	It appears therefore that the protein and GAG portions of PGs may not interact at the same sites of LDL and competition by fibronectin would be more efficient at the GAG binding site.	Glycosaminoglycans	166-169	fibronectin 1	Homo sapiens	123-134
2105740-5	1990	This method is applied to the structure determination of an 18-residue peptide with an amino acid sequence comprising the first zinc fingerlike domain from the gag protein p55 of HIV.	Glycosaminoglycans	160-163	H3 histone pseudogene 44	Homo sapiens	172-175
2159160-1	1990	It has previously been found that the GABA transaminase inhibitors gamma-acetylen GABA (GAG) and sodium valproate reduced intromission behavior in male rats without affecting mounting behavior.	Glycosaminoglycans	88-91	4-aminobutyrate aminotransferase	Rattus norvegicus	38-55
2288400-5	1990	Furthermore, lysozyme hydrolyzes the mucopolysaccharide of the connective tissue and inhibits the virus-DNA replication.	Glycosaminoglycans	37-55	lysozyme	Homo sapiens	13-21
2167058-6	1990	This expression was not tumorigenic and was characterized by the presence of the p28 gag antigen and the absence of the gp52 env antigen, except, however, in mammary glands of elder mice where traces of gp52 were found.	Glycosaminoglycans	85-88	B cell receptor associated protein 31	Mus musculus	81-84
2403210-12	1990	These results suggest that the mucin secreted by the developed Brunner"s glands of human is neutral mucopolysaccharide in nature.	Glycosaminoglycans	100-118	LOC100508689	Homo sapiens	31-36
2083865-8	1990	The activities of thrombin and other serine proteases are modulated by the serine protease inhibitors (serpins), including antithrombin III and heparin cofactor II which are important in regulating the physiological anticoagulant action of glycosaminoglycans at the endothelium and the pharmacological action of heparin.	Glycosaminoglycans	240-258	coagulation factor II, thrombin	Homo sapiens	18-26
2180392-6	1990	The inhibitors used partially stopped the processing of gag-coded polyprotein Pr78gag into core protein p27 as shown in pulse-chase experiments.	Glycosaminoglycans	56-59	interferon alpha inducible protein 27	Homo sapiens	104-107
2285364-6	1990	This effect may be due to the retention of apo E by changed sulfated glycosaminoglycans of aortic connective tissue.	Glycosaminoglycans	69-87	apolipoprotein E	Homo sapiens	43-48
1696488-4	1990	Biochemical analyses of the connective tissue capsule demonstrated that TGF-beta 1 induced a dose-dependent accumulation of glycosaminoglycans (GAGs).	Glycosaminoglycans	124-142	transforming growth factor beta-1 proprotein	Cavia porcellus	72-82
1696488-5	1990	The GAG/DNA ratio also increased as a function of the rate of TGF-beta 1 released, suggesting that the factor increased production of GAGs per cell.	Glycosaminoglycans	4-7	transforming growth factor beta-1 proprotein	Cavia porcellus	62-72
2083865-8	1990	The activities of thrombin and other serine proteases are modulated by the serine protease inhibitors (serpins), including antithrombin III and heparin cofactor II which are important in regulating the physiological anticoagulant action of glycosaminoglycans at the endothelium and the pharmacological action of heparin.	Glycosaminoglycans	240-258	serpin family C member 1	Homo sapiens	123-139
2117000-5	1990	IL-1 beta and TNF-alpha were found to be more efficient than TGF-beta in stimulating the production of GAG by the synovial cells.	Glycosaminoglycans	103-106	interleukin 1 beta	Homo sapiens	0-9
2126195-10	1990	Further studies showed that the tryptophan residue influenced the association of the gag peptide with HLA B27, because the affinity of the gag peptide for B27 was strongly increased after replacing this residue with a leucine or a tyrosine.	Glycosaminoglycans	85-88	major histocompatibility complex, class I, B	Homo sapiens	102-109
2126195-10	1990	Further studies showed that the tryptophan residue influenced the association of the gag peptide with HLA B27, because the affinity of the gag peptide for B27 was strongly increased after replacing this residue with a leucine or a tyrosine.	Glycosaminoglycans	85-88	melanocortin 2 receptor accessory protein	Homo sapiens	106-109
2126195-10	1990	Further studies showed that the tryptophan residue influenced the association of the gag peptide with HLA B27, because the affinity of the gag peptide for B27 was strongly increased after replacing this residue with a leucine or a tyrosine.	Glycosaminoglycans	139-142	major histocompatibility complex, class I, B	Homo sapiens	102-109
2126195-10	1990	Further studies showed that the tryptophan residue influenced the association of the gag peptide with HLA B27, because the affinity of the gag peptide for B27 was strongly increased after replacing this residue with a leucine or a tyrosine.	Glycosaminoglycans	139-142	melanocortin 2 receptor accessory protein	Homo sapiens	106-109
2384297-4	1990	In other long-term culture experiments, IL-1a was shown to enhance fibroblast-induced GAG loss from cartilage.	Glycosaminoglycans	86-89	interleukin 1 alpha	Homo sapiens	40-45
2117000-5	1990	IL-1 beta and TNF-alpha were found to be more efficient than TGF-beta in stimulating the production of GAG by the synovial cells.	Glycosaminoglycans	103-106	tumor necrosis factor	Homo sapiens	14-23
2117000-5	1990	IL-1 beta and TNF-alpha were found to be more efficient than TGF-beta in stimulating the production of GAG by the synovial cells.	Glycosaminoglycans	103-106	transforming growth factor beta 1	Homo sapiens	61-69
2117000-6	1990	IFN-gamma exerted an antagonistic effect on the TGF-beta-induced stimulation of GAG synthesis.	Glycosaminoglycans	80-83	interferon gamma	Homo sapiens	0-9
2117000-6	1990	IFN-gamma exerted an antagonistic effect on the TGF-beta-induced stimulation of GAG synthesis.	Glycosaminoglycans	80-83	transforming growth factor beta 1	Homo sapiens	48-56
33781915-1	2021	In Hunter syndrome (mucopolysaccharidosis II, MPS-II), systemic accumulation of glycosaminoglycans (GAGs) due to a deficiency of iduronate-2-sulfatase (IDS), caused by mutations in the IDS gene, leads to multiple somatic manifestations and, in patients with the severe (neuronopathic) phenotype, also to central nervous system (CNS) involvement.	Glycosaminoglycans	80-98	iduronate 2-sulfatase	Homo sapiens	129-150
2133279-1	1990	The breakdown of rat articular cartilage has been studied in vivo and in vitro to observe the effect of platelet-activating factor (PAF) and interleukin-1 alpha (IL-1 alpha) on the net loss of glycosaminoglycan (GAG).	Glycosaminoglycans	193-210	PCNA clamp associated factor	Rattus norvegicus	104-130
2133279-1	1990	The breakdown of rat articular cartilage has been studied in vivo and in vitro to observe the effect of platelet-activating factor (PAF) and interleukin-1 alpha (IL-1 alpha) on the net loss of glycosaminoglycan (GAG).	Glycosaminoglycans	193-210	interleukin 1 alpha	Rattus norvegicus	141-160
2133279-1	1990	The breakdown of rat articular cartilage has been studied in vivo and in vitro to observe the effect of platelet-activating factor (PAF) and interleukin-1 alpha (IL-1 alpha) on the net loss of glycosaminoglycan (GAG).	Glycosaminoglycans	193-210	interleukin 1 alpha	Rattus norvegicus	162-172
2133279-1	1990	The breakdown of rat articular cartilage has been studied in vivo and in vitro to observe the effect of platelet-activating factor (PAF) and interleukin-1 alpha (IL-1 alpha) on the net loss of glycosaminoglycan (GAG).	Glycosaminoglycans	212-215	interleukin 1 alpha	Rattus norvegicus	141-160
1967187-4	1990	Characterization of the alpha 1AT Mmineral springs gene demonstrated that it differed from the common normal M1(Ala213) allele by a single-base substitution causing the amino acid substitution Gly-67 (GGG)----Glu-67 (GAG).	Glycosaminoglycans	217-220	serpin family A member 1	Homo sapiens	24-33
2157186-1	1990	A bacterial expression vector containing a segment of the v-abl gene from Abelson murine leukemia virus (A-MuLV) was constructed such that the gag region of v-abl was replaced by a sequence encoding the IgG-binding domain of the S. aureus protein A. pabl HP, a fusion protein encoded by this vector was rapidly purified to near homogeneity by affinity chromatography on IgG-Affigel and Mono Q FPLC.	Glycosaminoglycans	143-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-162
33781915-1	2021	In Hunter syndrome (mucopolysaccharidosis II, MPS-II), systemic accumulation of glycosaminoglycans (GAGs) due to a deficiency of iduronate-2-sulfatase (IDS), caused by mutations in the IDS gene, leads to multiple somatic manifestations and, in patients with the severe (neuronopathic) phenotype, also to central nervous system (CNS) involvement.	Glycosaminoglycans	80-98	iduronate 2-sulfatase	Homo sapiens	152-155
33781915-1	2021	In Hunter syndrome (mucopolysaccharidosis II, MPS-II), systemic accumulation of glycosaminoglycans (GAGs) due to a deficiency of iduronate-2-sulfatase (IDS), caused by mutations in the IDS gene, leads to multiple somatic manifestations and, in patients with the severe (neuronopathic) phenotype, also to central nervous system (CNS) involvement.	Glycosaminoglycans	80-98	iduronate 2-sulfatase	Homo sapiens	185-188
33781915-1	2021	In Hunter syndrome (mucopolysaccharidosis II, MPS-II), systemic accumulation of glycosaminoglycans (GAGs) due to a deficiency of iduronate-2-sulfatase (IDS), caused by mutations in the IDS gene, leads to multiple somatic manifestations and, in patients with the severe (neuronopathic) phenotype, also to central nervous system (CNS) involvement.	Glycosaminoglycans	100-104	iduronate 2-sulfatase	Homo sapiens	129-150
33781915-1	2021	In Hunter syndrome (mucopolysaccharidosis II, MPS-II), systemic accumulation of glycosaminoglycans (GAGs) due to a deficiency of iduronate-2-sulfatase (IDS), caused by mutations in the IDS gene, leads to multiple somatic manifestations and, in patients with the severe (neuronopathic) phenotype, also to central nervous system (CNS) involvement.	Glycosaminoglycans	100-104	iduronate 2-sulfatase	Homo sapiens	152-155
33781915-1	2021	In Hunter syndrome (mucopolysaccharidosis II, MPS-II), systemic accumulation of glycosaminoglycans (GAGs) due to a deficiency of iduronate-2-sulfatase (IDS), caused by mutations in the IDS gene, leads to multiple somatic manifestations and, in patients with the severe (neuronopathic) phenotype, also to central nervous system (CNS) involvement.	Glycosaminoglycans	100-104	iduronate 2-sulfatase	Homo sapiens	185-188
19685389-5	2009	The most frequent form of inherited dystonia, according to current knowledge, is early-onset generalized DYT1 dystonia, caused by a deletion of three basepairs, GAG, in the DYT1 (TOR1A) gene.	Glycosaminoglycans	161-164	torsin family 1 member A	Homo sapiens	105-109
33763452-4	2021	Solution of the crystal structure of a C-terminal segment of Arc revealed a striking similarity to the capsid domain of HIV Gag.	Glycosaminoglycans	124-127	activity regulated cytoskeleton associated protein	Homo sapiens	61-64
18418554-1	2009	MPS VI (mucopolysaccharidosis VI, known as Maroteaux-Lamy syndrome) is a multi-systemic inherited disease, resulting from a deficiency of N-acetylgalactosamine-4-sulfatase, causing accumulation of the glycosaminoglycan (GAG) dermatan sulfate in all tissues.	Glycosaminoglycans	201-218	arylsulfatase B	Homo sapiens	138-171
19685389-5	2009	The most frequent form of inherited dystonia, according to current knowledge, is early-onset generalized DYT1 dystonia, caused by a deletion of three basepairs, GAG, in the DYT1 (TOR1A) gene.	Glycosaminoglycans	161-164	torsin family 1 member A	Homo sapiens	173-177
19685389-5	2009	The most frequent form of inherited dystonia, according to current knowledge, is early-onset generalized DYT1 dystonia, caused by a deletion of three basepairs, GAG, in the DYT1 (TOR1A) gene.	Glycosaminoglycans	161-164	torsin family 1 member A	Homo sapiens	179-184
34626798-4	2022	Inhibitory effects of GLPG1972/S201086 on interleukin-1alpha-stimulated glycosaminoglycan release in mouse femoral head cartilage explants, and on interleukin-1beta-stimulated release of an ADAMTS5-derived aggrecan neoepitope (quantified with ELISA) in human articular cartilage explants were determined.	Glycosaminoglycans	72-89	secreted acidic cysteine rich glycoprotein	Mus musculus	39-41
9493284-5	1997	Two of 10 AIDS patients had demonstrable recognition of Gag p24, one of RT and eight patients had no recognition of any of the proteins.	Glycosaminoglycans	56-59	transmembrane p24 trafficking protein 2	Homo sapiens	60-63
16622001-5	2006	We observed that vaccination was associated with the preservation of Gag-specific central memory CD8(+) T cells that were functionally capable of producing IFN-gamma, and effector memory CD8(+) T cells that were capable of producing granzyme B following viral Ag exposure.	Glycosaminoglycans	69-72	CD8a molecule	Homo sapiens	97-100
8510409-5	1993	While in control cells the cell-associated heparan sulfate accounts for about 30% of the total glycosaminoglycans under the influence of bFGF the HS percentage increases to approximately 60%.	Glycosaminoglycans	95-113	fibroblast growth factor 2	Bos taurus	137-141
1309785-10	1992	We examined transport of glycosaminoglycan chains since previous studies have shown that these chains enter the regulated secretory pathways and are packaged along with the hormone adrenocorticotropin (ACTH).	Glycosaminoglycans	25-42	pro-opiomelanocortin-alpha	Mus musculus	202-206
34626798-4	2022	Inhibitory effects of GLPG1972/S201086 on interleukin-1alpha-stimulated glycosaminoglycan release in mouse femoral head cartilage explants, and on interleukin-1beta-stimulated release of an ADAMTS5-derived aggrecan neoepitope (quantified with ELISA) in human articular cartilage explants were determined.	Glycosaminoglycans	72-89	interleukin 1 alpha	Mus musculus	42-60
34643428-1	2022	HIV-1 virion production is driven by Gag and Gag-Pol (GP) proteins, with Gag forming the bulk of the capsid and driving budding while GP binds Gag to deliver the essential virion enzymes Protease, Reverse Transcriptase, and Integrase.	Glycosaminoglycans	37-40	Gag-Pol	Human immunodeficiency virus 1	134-136
34928574-4	2022	This facilitates the subsequent interaction with the cellular glycosaminoglycans through the S1B domain of the spike protein as it binds to the ACE2 receptor.	Glycosaminoglycans	62-80	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	111-116
34928574-4	2022	This facilitates the subsequent interaction with the cellular glycosaminoglycans through the S1B domain of the spike protein as it binds to the ACE2 receptor.	Glycosaminoglycans	62-80	angiotensin converting enzyme 2	Homo sapiens	144-148
34643428-1	2022	HIV-1 virion production is driven by Gag and Gag-Pol (GP) proteins, with Gag forming the bulk of the capsid and driving budding while GP binds Gag to deliver the essential virion enzymes Protease, Reverse Transcriptase, and Integrase.	Glycosaminoglycans	73-76	Gag-Pol	Human immunodeficiency virus 1	45-52
34643428-1	2022	HIV-1 virion production is driven by Gag and Gag-Pol (GP) proteins, with Gag forming the bulk of the capsid and driving budding while GP binds Gag to deliver the essential virion enzymes Protease, Reverse Transcriptase, and Integrase.	Glycosaminoglycans	143-146	Gag-Pol	Human immunodeficiency virus 1	45-52
34643428-1	2022	HIV-1 virion production is driven by Gag and Gag-Pol (GP) proteins, with Gag forming the bulk of the capsid and driving budding while GP binds Gag to deliver the essential virion enzymes Protease, Reverse Transcriptase, and Integrase.	Glycosaminoglycans	143-146	Gag-Pol	Human immunodeficiency virus 1	134-136
34643428-2	2022	Virion GP levels are traditionally thought to reflect the relative abundances of GP and Gag in cells (~1:20), dictated by the frequency of a -1 programmed ribosomal frameshifting (PRF) event occurring in gag-pol mRNAs.	Glycosaminoglycans	88-91	Gag-Pol	Human immunodeficiency virus 1	7-9
34643428-2	2022	Virion GP levels are traditionally thought to reflect the relative abundances of GP and Gag in cells (~1:20), dictated by the frequency of a -1 programmed ribosomal frameshifting (PRF) event occurring in gag-pol mRNAs.	Glycosaminoglycans	88-91	Gag-Pol	Human immunodeficiency virus 1	204-211
34643428-5	2022	Second, we report that GP is more efficiently incorporated into virions when Gag and GP are synthesized in cis (i.e., from the same gag-pol mRNA) relative to trans, suggesting that Gag/GP translation and assembly are spatially coupled processes.	Glycosaminoglycans	77-80	Gag-Pol	Human immunodeficiency virus 1	23-25
34643428-5	2022	Second, we report that GP is more efficiently incorporated into virions when Gag and GP are synthesized in cis (i.e., from the same gag-pol mRNA) relative to trans, suggesting that Gag/GP translation and assembly are spatially coupled processes.	Glycosaminoglycans	77-80	Gag-Pol	Human immunodeficiency virus 1	132-139
34643428-5	2022	Second, we report that GP is more efficiently incorporated into virions when Gag and GP are synthesized in cis (i.e., from the same gag-pol mRNA) relative to trans, suggesting that Gag/GP translation and assembly are spatially coupled processes.	Glycosaminoglycans	77-80	Gag-Pol	Human immunodeficiency virus 1	185-187
34643428-5	2022	Second, we report that GP is more efficiently incorporated into virions when Gag and GP are synthesized in cis (i.e., from the same gag-pol mRNA) relative to trans, suggesting that Gag/GP translation and assembly are spatially coupled processes.	Glycosaminoglycans	181-184	Gag-Pol	Human immunodeficiency virus 1	23-25
34643428-5	2022	Second, we report that GP is more efficiently incorporated into virions when Gag and GP are synthesized in cis (i.e., from the same gag-pol mRNA) relative to trans, suggesting that Gag/GP translation and assembly are spatially coupled processes.	Glycosaminoglycans	181-184	Gag-Pol	Human immunodeficiency virus 1	85-87
34643428-5	2022	Second, we report that GP is more efficiently incorporated into virions when Gag and GP are synthesized in cis (i.e., from the same gag-pol mRNA) relative to trans, suggesting that Gag/GP translation and assembly are spatially coupled processes.	Glycosaminoglycans	181-184	Gag-Pol	Human immunodeficiency virus 1	132-139
34643428-5	2022	Second, we report that GP is more efficiently incorporated into virions when Gag and GP are synthesized in cis (i.e., from the same gag-pol mRNA) relative to trans, suggesting that Gag/GP translation and assembly are spatially coupled processes.	Glycosaminoglycans	181-184	Gag-Pol	Human immunodeficiency virus 1	185-187
34643428-6	2022	Third, we show that, surprisingly, virions exhibit a strong upper limit to trans-delivered GP incorporation; an adaptation that appears to allow the virus to temper defects to GP/Gag cleavage that may negatively impact reverse transcription.	Glycosaminoglycans	179-182	Gag-Pol	Human immunodeficiency virus 1	91-93
34643428-6	2022	Third, we show that, surprisingly, virions exhibit a strong upper limit to trans-delivered GP incorporation; an adaptation that appears to allow the virus to temper defects to GP/Gag cleavage that may negatively impact reverse transcription.	Glycosaminoglycans	179-182	Gag-Pol	Human immunodeficiency virus 1	176-178
34643428-10	2022	Mechanisms dictating GP incorporation into assembling virions are poorly defined, with GP levels in virions traditionally thought to solely reflect relative levels of Gag and GP expressed in cells; dictated by the frequency of a -1 programmed ribosomal frameshifting (PRF) event that occurs in gag-pol mRNAs.	Glycosaminoglycans	167-170	Gag-Pol	Human immunodeficiency virus 1	21-23
34643428-10	2022	Mechanisms dictating GP incorporation into assembling virions are poorly defined, with GP levels in virions traditionally thought to solely reflect relative levels of Gag and GP expressed in cells; dictated by the frequency of a -1 programmed ribosomal frameshifting (PRF) event that occurs in gag-pol mRNAs.	Glycosaminoglycans	167-170	Gag-Pol	Human immunodeficiency virus 1	87-89
34610468-13	2022	Collectively, the results reveal that binding to glycosaminoglycans initiates VLDL remodeling by circulating LpL, and suggest heparin binding as a marker of VLDL functionality and a readout for treatment of metabolic disorders.	Glycosaminoglycans	49-67	lipoprotein lipase	Homo sapiens	109-112
34857342-4	2022	GAG contents were measured in media of endothelial cells (EA.hy926) subjected to various GAG-degrading enzymes, as well as in murine plasma and urine in apolipoprotein E/low-density lipoprotein receptor-deficient (ApoE/LDLR -/-) mice and age-matched wild-type C57BL/6 mice.	Glycosaminoglycans	0-3	low density lipoprotein receptor	Mus musculus	219-223
34784477-2	2021	We show that this naphthoxyloside serves as a substrate for beta4GalT7 and induces the formation of soluble glycosaminoglycan (GAG) chains with physiologically relevant lengths and sulfation patterns.	Glycosaminoglycans	127-130	beta-1,4-galactosyltransferase 7	Homo sapiens	60-70
34092466-1	2022	BACKGROUND/PURPOSE: A heterozygous three-nucleotide (GAG) in-frame deletion in the TOR1A gene causes the rare disease, dystonia (DYT1), which typically presents as focal limb dystonia during adolescence, then spreads to other limbs.	Glycosaminoglycans	53-56	torsin family 1 member A	Homo sapiens	83-88
34092466-1	2022	BACKGROUND/PURPOSE: A heterozygous three-nucleotide (GAG) in-frame deletion in the TOR1A gene causes the rare disease, dystonia (DYT1), which typically presents as focal limb dystonia during adolescence, then spreads to other limbs.	Glycosaminoglycans	53-56	torsin family 1 member A	Homo sapiens	129-133
34934153-0	2021	Publisher Correction: An ultrasensitive planar array p24 Gag ELISA to detect HIV-1 in diverse biological matrixes.	Glycosaminoglycans	57-60	transmembrane p24 trafficking protein 2	Homo sapiens	53-56
34536062-1	2022	HLA-DPA1*01:86 differs from DPA1*01:03:01:05 by a single nucleotide change in codon 94 (AAG>GAG).	Glycosaminoglycans	92-95	major histocompatibility complex, class II, DP alpha 1	Homo sapiens	0-8
34536062-1	2022	HLA-DPA1*01:86 differs from DPA1*01:03:01:05 by a single nucleotide change in codon 94 (AAG>GAG).	Glycosaminoglycans	92-95	N-methylpurine DNA glycosylase	Homo sapiens	88-91
34930890-3	2021	Here, we uncover that TMEM165 deficiency impairs the synthesis of proteoglycans by producing a blockage in the elongation of chondroitin-and heparan-sulfate glycosaminoglycan chains leading to the synthesis of proteoglycans with shorter glycosaminoglycan chains.	Glycosaminoglycans	237-254	transmembrane protein 165	Homo sapiens	22-29
34930890-8	2021	Collectively, our results indicate that TMEM165 plays an important role in proteoglycan synthesis and underline the critical role of glycosaminoglycan chains structure in the regulation of chondrogenesis.	Glycosaminoglycans	133-150	transmembrane protein 165	Homo sapiens	40-47
34916232-3	2021	Arylsulfatase K (ARSK) is a recently characterised lysosomal hydrolase involved in GAG degradation that removes the 2-O-sulfate group from 2-sulfoglucuronate.	Glycosaminoglycans	83-86	arylsulfatase family member K	Homo sapiens	0-15
34916232-3	2021	Arylsulfatase K (ARSK) is a recently characterised lysosomal hydrolase involved in GAG degradation that removes the 2-O-sulfate group from 2-sulfoglucuronate.	Glycosaminoglycans	83-86	arylsulfatase family member K	Homo sapiens	17-21
34956182-4	2021	Properdin can bind directly to microbial targets via DNA, sulfatides and glycosaminoglycans, apoptotic cells, nanoparticles, and well-known viral virulence factors.	Glycosaminoglycans	73-91	complement factor properdin	Homo sapiens	0-9
34902449-10	2022	The sulfated glycosaminoglycan-mediated polymerization of STING also largely depends on MAMDC2.	Glycosaminoglycans	13-30	stimulator of interferon response cGAMP interactor 1	Mus musculus	58-63
34902449-10	2022	The sulfated glycosaminoglycan-mediated polymerization of STING also largely depends on MAMDC2.	Glycosaminoglycans	13-30	MAM domain containing 2	Mus musculus	88-94
34948256-3	2021	The enzyme deficit causes a pathological accumulation of the undegraded glycosaminoglycans dermatan-sulphate and chondroitin-sulphate, natural substrates of ASB activity.	Glycosaminoglycans	72-90	arylsulfatase B	Homo sapiens	157-160
34670126-1	2021	BACKGROUND: Mucopolysaccharidosis type II (MPS II) or Hunter syndrome is a rare X-linked recessive genetic disease resulting from deficient activity of the iduronate-2-sulfatase(IDS) enzyme and the accumulation of glycosaminoglycans in almost all cells, tissues and organs, which makes viscera function impaired.This study retrospectively analyzed the clinical characteristics, leukocyte IDS activity and mutations in the IDS gene of 30 Chinese children with MPS II.	Glycosaminoglycans	214-232	iduronate 2-sulfatase	Homo sapiens	422-425
34887403-8	2021	Our data suggest a multimodal mechanism, in which HHIP can bind two specific sites on the SHH morphogen, alongside multiple GAG interactions, to inhibit SHH signalling.	Glycosaminoglycans	124-127	sonic hedgehog signaling molecule	Homo sapiens	153-156
34880361-0	2021	An ultrasensitive planar array p24 Gag ELISA to detect HIV-1 in diverse biological matrixes.	Glycosaminoglycans	35-38	transmembrane p24 trafficking protein 2	Homo sapiens	31-34
34917926-6	2021	The activity of the heparan sulfate (HS) specific glucuronidase Heparanase-1 (Hpa-1) is elevated in sepsis, resulting in shedding of heparan sulfate (HS), a main GAG of the eGC.	Glycosaminoglycans	162-165	heparanase	Homo sapiens	64-76
34917926-6	2021	The activity of the heparan sulfate (HS) specific glucuronidase Heparanase-1 (Hpa-1) is elevated in sepsis, resulting in shedding of heparan sulfate (HS), a main GAG of the eGC.	Glycosaminoglycans	162-165	heparanase	Homo sapiens	78-83
34696603-3	2021	The feasibility of CA4+-enhanced microCT to visualize and quantify glycosaminoglycans (GAGs) in these different tissues was tested using safranin-O staining and 1,9-dimethylmethylene blue assay.	Glycosaminoglycans	67-85	carbonic anhydrase 4	Bos taurus	19-22
34696603-7	2021	CONCLUSIONS: CA4+-enhanced microCT enables assessment of 3-dimensiona distribution and GAG content in different types of cartilage and has promise as an ex vivo diagnostic technique to monitor matrix development in different tissues over time as well as tissue-engineered constructs.	Glycosaminoglycans	87-90	carbonic anhydrase 4	Bos taurus	13-16
34887403-3	2021	Here, we report the structure of the HHIP N-terminal domain (HHIP-N) in complex with a glycosaminoglycan (GAG).	Glycosaminoglycans	87-104	hedgehog interacting protein	Homo sapiens	37-41
34887403-3	2021	Here, we report the structure of the HHIP N-terminal domain (HHIP-N) in complex with a glycosaminoglycan (GAG).	Glycosaminoglycans	87-104	hedgehog interacting protein	Homo sapiens	61-65
34887403-3	2021	Here, we report the structure of the HHIP N-terminal domain (HHIP-N) in complex with a glycosaminoglycan (GAG).	Glycosaminoglycans	106-109	hedgehog interacting protein	Homo sapiens	37-41
34887403-3	2021	Here, we report the structure of the HHIP N-terminal domain (HHIP-N) in complex with a glycosaminoglycan (GAG).	Glycosaminoglycans	106-109	hedgehog interacting protein	Homo sapiens	61-65
34887403-4	2021	HHIP-N displays a unique bipartite fold with a GAG-binding domain alongside a Cysteine Rich Domain (CRD).	Glycosaminoglycans	47-50	hedgehog interacting protein	Homo sapiens	0-4
34435740-2	2021	It is caused by variants in ARSB, which encodes the lysosomal arylsulfatase B (ARSB) enzyme, part of the degradation process of glycosaminoglycans in lysosomes.	Glycosaminoglycans	128-146	arylsulfatase B	Homo sapiens	28-32
34435740-2	2021	It is caused by variants in ARSB, which encodes the lysosomal arylsulfatase B (ARSB) enzyme, part of the degradation process of glycosaminoglycans in lysosomes.	Glycosaminoglycans	128-146	arylsulfatase B	Homo sapiens	62-77
34435740-2	2021	It is caused by variants in ARSB, which encodes the lysosomal arylsulfatase B (ARSB) enzyme, part of the degradation process of glycosaminoglycans in lysosomes.	Glycosaminoglycans	128-146	arylsulfatase B	Homo sapiens	79-83
34851004-1	2022	Cytokines such as interleukin-8 activate the immune system during infection and interact with sulfated glycosaminoglycans with specific sulfation patterns.	Glycosaminoglycans	103-121	C-X-C motif chemokine ligand 8	Homo sapiens	18-31
34580994-3	2021	Here, using SNAP-tag fluorescent labelling and both fixed and live cell imaging we show that the ESCRT-II component EAP45 colocalises with the HIV protein Gag at the plasma membrane in a temporal and quantitative manner, similar to that previously shown for ALIX and Gag.	Glycosaminoglycans	155-158	vacuolar protein sorting 36 homolog	Homo sapiens	116-121
34255438-1	2021	HLA-B*52:49N has one nucleotide change from HLA-B*52:01:01:01 where 601G (GAG) is changed to T(TAG).	Glycosaminoglycans	74-77	major histocompatibility complex, class I, B	Homo sapiens	0-5
34255438-1	2021	HLA-B*52:49N has one nucleotide change from HLA-B*52:01:01:01 where 601G (GAG) is changed to T(TAG).	Glycosaminoglycans	74-77	major histocompatibility complex, class I, B	Homo sapiens	44-49
34651666-13	2021	Following FABP4 knockdown, the expression of matrix metalloproteinases (MMP3, MMP9 and MMP13) of IL-1beta-induced ATDC5 cells was reduced, and the expression of GAG was promoted.	Glycosaminoglycans	161-164	fatty acid binding protein 4, adipocyte	Mus musculus	10-15
34651666-13	2021	Following FABP4 knockdown, the expression of matrix metalloproteinases (MMP3, MMP9 and MMP13) of IL-1beta-induced ATDC5 cells was reduced, and the expression of GAG was promoted.	Glycosaminoglycans	161-164	interleukin 1 alpha	Mus musculus	97-105
34830113-2	2021	Dysfunction of IDS triggers the lysosomal accumulation of its substrates, glycosaminoglycans, leading to mental retardation and systemic symptoms including skeletal deformities and valvular heart disease.	Glycosaminoglycans	74-92	iduronate 2-sulfatase	Homo sapiens	15-18
34768285-4	2022	We found that AT competitively inhibits the GAG-dependent HRPII-mediated activation of NF-kappaB and expression of intercellular cell adhesion molecule 1 (ICAM1) in endothelial cells.	Glycosaminoglycans	44-47	nuclear factor kappa B subunit 1	Homo sapiens	87-96
34768285-4	2022	We found that AT competitively inhibits the GAG-dependent HRPII-mediated activation of NF-kappaB and expression of intercellular cell adhesion molecule 1 (ICAM1) in endothelial cells.	Glycosaminoglycans	44-47	intercellular adhesion molecule 1	Homo sapiens	155-160
34686680-6	2021	The SHIV-Ag85B-inoculated macaques showed enhancement of Gag-specific monofunctional and polyfunctional CD8+ T cells in the acute phase of the pathogenic SHIV challenge.	Glycosaminoglycans	57-60	CD8a molecule	Homo sapiens	104-107
34651208-0	2021	Discrimination of sulfated isomers of chondroitin sulfate disaccharides by HILIC-MS. Chondroitin sulfate (CS) glycosaminoglycans are biologically active sulfated polysaccharides that pose an analytical challenge for their structural analysis and functional evaluation.	Glycosaminoglycans	110-128	citrate synthase	Homo sapiens	106-108
34647745-1	2021	Cellular binding and entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are mediated by its spike glycoprotein (S protein), which binds with not only the human angiotensin-converting enzyme 2 (ACE2) receptor but also glycosaminoglycans such as heparin.	Glycosaminoglycans	236-254	angiotensin converting enzyme 2	Homo sapiens	179-210
34647745-1	2021	Cellular binding and entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are mediated by its spike glycoprotein (S protein), which binds with not only the human angiotensin-converting enzyme 2 (ACE2) receptor but also glycosaminoglycans such as heparin.	Glycosaminoglycans	236-254	angiotensin converting enzyme 2	Homo sapiens	212-216
34768882-4	2021	BP-3 used at concentrations of 0.1-100 microM caused a number of unfavorable changes in the level of type I collagen, decorin, sulfated glycosaminoglycans, hyaluronic acid, elastin, and expression or activity of matrix metalloproteinases (MMP-1, MMP-2), elastase and hyaluronidase.	Glycosaminoglycans	136-154	BP3	Homo sapiens	0-4
34712574-2	2021	It is caused by bi-allelic loss-of-function mutations in SGSH encoding sulphamidase, a lysosomal enzyme required for heparan sulphate glycosaminoglycan (HS GAG) degradation, that results in the progressive build-up of HS GAGs in multiple tissues most notably the central nervous system (CNS).	Glycosaminoglycans	156-159	N-sulfoglucosamine sulfohydrolase	Homo sapiens	71-83
34746235-2	2021	Mucopolysaccharidosis type I (MPS I) is an autosomal recessive disease characterized by the deficiency of alpha-L-iduronidase (IDUA), an enzyme involved in glycosaminoglycan degradation.	Glycosaminoglycans	156-173	alpha-L-iduronidase	Homo sapiens	106-125
34746235-2	2021	Mucopolysaccharidosis type I (MPS I) is an autosomal recessive disease characterized by the deficiency of alpha-L-iduronidase (IDUA), an enzyme involved in glycosaminoglycan degradation.	Glycosaminoglycans	156-173	alpha-L-iduronidase	Homo sapiens	127-131
34712574-2	2021	It is caused by bi-allelic loss-of-function mutations in SGSH encoding sulphamidase, a lysosomal enzyme required for heparan sulphate glycosaminoglycan (HS GAG) degradation, that results in the progressive build-up of HS GAGs in multiple tissues most notably the central nervous system (CNS).	Glycosaminoglycans	221-225	N-sulfoglucosamine sulfohydrolase	Homo sapiens	71-83
34721397-7	2021	We found that CD29 could be reliably used as a marker to identify CD4+ CTLs in rhesus macaques since CD29hi CD4+ T cells secrete higher cytotoxic and proinflammatory cytokines following PMA/ionomycin or gag stimulation.	Glycosaminoglycans	203-206	CD4 molecule	Macaca mulatta	66-69
34721397-7	2021	We found that CD29 could be reliably used as a marker to identify CD4+ CTLs in rhesus macaques since CD29hi CD4+ T cells secrete higher cytotoxic and proinflammatory cytokines following PMA/ionomycin or gag stimulation.	Glycosaminoglycans	203-206	CD4 molecule	Macaca mulatta	108-111
34721397-11	2021	Lastly, increased functionality of CD29hi CD4+ T cells as depicted by elevated levels of either IL-21 or granzyme B hi T Bet+ gag specific responses were linked to limiting the size of the replication-competent reservoir during cART treatment.	Glycosaminoglycans	126-129	CD4 molecule	Macaca mulatta	42-45
34721397-11	2021	Lastly, increased functionality of CD29hi CD4+ T cells as depicted by elevated levels of either IL-21 or granzyme B hi T Bet+ gag specific responses were linked to limiting the size of the replication-competent reservoir during cART treatment.	Glycosaminoglycans	126-129	granzyme B	Macaca mulatta	105-115
34622797-1	2021	Mucopolysaccharidosis type II (MPS II) is a lysosomal storage disorder caused by deficiency of the iduronate-2-sulfatase (IDS) enzyme, resulting in cellular accumulation of glycosaminoglycans (GAGs) throughout the body.	Glycosaminoglycans	173-191	iduronate 2-sulfatase	Mus musculus	99-120
34680238-5	2021	Therefore, we aimed to reduce angiogenesis through interference with growth factor-HS binding and downstream signaling using a CXCL9-derived peptide with a high affinity for glycosaminoglycans (GAGs), CXCL9(74-103).	Glycosaminoglycans	174-192	C-X-C motif chemokine ligand 9	Rattus norvegicus	127-132
34680238-5	2021	Therefore, we aimed to reduce angiogenesis through interference with growth factor-HS binding and downstream signaling using a CXCL9-derived peptide with a high affinity for glycosaminoglycans (GAGs), CXCL9(74-103).	Glycosaminoglycans	174-192	C-X-C motif chemokine ligand 9	Rattus norvegicus	201-206
34680238-5	2021	Therefore, we aimed to reduce angiogenesis through interference with growth factor-HS binding and downstream signaling using a CXCL9-derived peptide with a high affinity for glycosaminoglycans (GAGs), CXCL9(74-103).	Glycosaminoglycans	194-198	C-X-C motif chemokine ligand 9	Rattus norvegicus	127-132
34680238-5	2021	Therefore, we aimed to reduce angiogenesis through interference with growth factor-HS binding and downstream signaling using a CXCL9-derived peptide with a high affinity for glycosaminoglycans (GAGs), CXCL9(74-103).	Glycosaminoglycans	194-198	C-X-C motif chemokine ligand 9	Rattus norvegicus	201-206
34624021-6	2021	We found that RNA and RNA-binding protein Gag encoded by the telomeric retrotransposon HeT-A interact with Polo and Cdk1 mitotic kinases, which are conserved regulators of centrosome biogenesis and cell cycle.	Glycosaminoglycans	42-45	polo	Drosophila melanogaster	107-111
34622797-1	2021	Mucopolysaccharidosis type II (MPS II) is a lysosomal storage disorder caused by deficiency of the iduronate-2-sulfatase (IDS) enzyme, resulting in cellular accumulation of glycosaminoglycans (GAGs) throughout the body.	Glycosaminoglycans	173-191	iduronate 2-sulfatase	Mus musculus	122-125
34624021-6	2021	We found that RNA and RNA-binding protein Gag encoded by the telomeric retrotransposon HeT-A interact with Polo and Cdk1 mitotic kinases, which are conserved regulators of centrosome biogenesis and cell cycle.	Glycosaminoglycans	42-45	Cyclin-dependent kinase 1	Drosophila melanogaster	116-120
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
34159694-1	2021	Biallelic mutations in B3GALT6, coding for a galactosyltransferase involved in the synthesis of glycosaminoglycans (GAGs), have been associated with various clinical conditions, causing spondyloepimetaphyseal dysplasia with joint laxity type 1 (SEMDJL1 or SEMDJL Beighton type), Al-Gazali syndrome (ALGAZ), and a severe progeroid form of Ehlers-Danlos syndrome (EDSSPD2).	Glycosaminoglycans	96-114	beta-1,3-galactosyltransferase 6	Homo sapiens	23-30
34369597-0	2021	Clonotypic architecture of a Gag-specific CD8+ T-cell response in chronic human HIV-2 infection.	Glycosaminoglycans	29-32	CD8a molecule	Homo sapiens	42-45
34369597-3	2021	To address this question, we undertook a detailed molecular characterization of the clonotypic architecture of an HLA-B*3501 restricted Gag -specific CD8+ T-cell response in donors chronically infected with HIV-2 using a combination of flow cytometry, tetramer-specific CD8+ TCR clonotyping and in vitro assays.	Glycosaminoglycans	136-139	major histocompatibility complex, class I, B	Homo sapiens	114-119
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
34536661-0	2021	Generation of two induced pluripotent stem cell lines with heterozygous and homozygous GAG deletion in TOR1A gene from a healthy hiPSC line.	Glycosaminoglycans	87-90	torsin family 1 member A	Homo sapiens	103-108
34369597-3	2021	To address this question, we undertook a detailed molecular characterization of the clonotypic architecture of an HLA-B*3501 restricted Gag -specific CD8+ T-cell response in donors chronically infected with HIV-2 using a combination of flow cytometry, tetramer-specific CD8+ TCR clonotyping and in vitro assays.	Glycosaminoglycans	136-139	CD8a molecule	Homo sapiens	150-153
34369597-3	2021	To address this question, we undertook a detailed molecular characterization of the clonotypic architecture of an HLA-B*3501 restricted Gag -specific CD8+ T-cell response in donors chronically infected with HIV-2 using a combination of flow cytometry, tetramer-specific CD8+ TCR clonotyping and in vitro assays.	Glycosaminoglycans	136-139	CD8a molecule	Homo sapiens	270-273
34152080-1	2021	BACKGROUND: Stabilin-2 is an endocytic scavenger receptor that mediates the clearance of glycosaminoglycans, phosphatidylserine-expressing cells, and von Willebrand factor-factor VIII complex.	Glycosaminoglycans	89-107	stabilin 2	Mus musculus	12-22
34536661-1	2021	A typical DYT1 dystonia is caused by a heterozygous GAG deletion (c.907-909) in the TOR1A gene (DeltaE, p.Glu303del) and the pathogenesis is not clear.	Glycosaminoglycans	52-55	torsin family 1 member A	Homo sapiens	10-14
34536661-1	2021	A typical DYT1 dystonia is caused by a heterozygous GAG deletion (c.907-909) in the TOR1A gene (DeltaE, p.Glu303del) and the pathogenesis is not clear.	Glycosaminoglycans	52-55	torsin family 1 member A	Homo sapiens	84-89
34552077-3	2021	To minimize genomic damage, p22/p18 interrupts virus-like particle function by interaction with Gag.	Glycosaminoglycans	96-99	calcineurin like EF-hand protein 1	Homo sapiens	28-31
34696365-6	2021	Regardless of cell polarization, Gag colocalizes with and promotes the virion incorporation of a subset of uropod-directed host transmembrane proteins, including CD162, CD43, and CD44.	Glycosaminoglycans	33-36	selectin P ligand	Homo sapiens	162-167
34696365-6	2021	Regardless of cell polarization, Gag colocalizes with and promotes the virion incorporation of a subset of uropod-directed host transmembrane proteins, including CD162, CD43, and CD44.	Glycosaminoglycans	33-36	sialophorin	Homo sapiens	169-173
34696365-6	2021	Regardless of cell polarization, Gag colocalizes with and promotes the virion incorporation of a subset of uropod-directed host transmembrane proteins, including CD162, CD43, and CD44.	Glycosaminoglycans	33-36	CD44 molecule (Indian blood group)	Homo sapiens	179-183
34552077-3	2021	To minimize genomic damage, p22/p18 interrupts virus-like particle function by interaction with Gag.	Glycosaminoglycans	96-99	H3 histone pseudogene 12	Homo sapiens	32-35
34552077-8	2021	Our data provide insight into Ty1 Gag structure and suggest how p22/p18 might function in restriction through a blocking-of-assembly mechanism.	Glycosaminoglycans	34-37	H3 histone pseudogene 12	Homo sapiens	68-71
34552077-8	2021	Our data provide insight into Ty1 Gag structure and suggest how p22/p18 might function in restriction through a blocking-of-assembly mechanism.	Glycosaminoglycans	34-37	calcineurin like EF-hand protein 1	Homo sapiens	64-67
34375459-0	2021	A glycosaminoglycan microarray identifies the binding of SARS-CoV-2 spike protein to chondroitin sulfate E.	Glycosaminoglycans	2-19	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	68-73
34280415-7	2021	Moreover, sHDL-Gag + polyICLC induced robust Simian immunodeficiency virus Gag-specific, polyfunctional CD8+ T cell responses in rhesus macaques and could further amplify the efficacy of recombinant adenovirus-based vaccine.	Glycosaminoglycans	15-18	CD8a molecule	Homo sapiens	104-107
34503301-8	2021	In summary, oncofetal CS is a prognostic biomarker and an actionable glycosaminoglycan target in NSCLC.	Glycosaminoglycans	69-86	citrate synthase	Homo sapiens	22-24
34512672-11	2021	Reactivity to one of these clusters located in gag p17 was inversely correlated with viral load set point in an independent cohort of non-controllers.	Glycosaminoglycans	47-50	family with sequence similarity 72 member B	Homo sapiens	51-54
34502207-6	2021	In addition reduced proteoglycan synthesis and oversulfation of glycosaminoglycan chains were demonstrated, as already observed in primary chondrocytes from the Cant1 knock-out mouse.	Glycosaminoglycans	64-81	calcium activated nucleotidase 1	Mus musculus	161-166
34077555-2	2021	As a protein with homology to the retroviral Gag protein, a particular characteristic of Arc is its capacity to self-assemble into virus-like capsids that can package mRNAs and transfer those transcripts to other cells.	Glycosaminoglycans	45-48	activity regulated cytoskeleton associated protein	Homo sapiens	89-92
34502113-5	2021	Firstly, we observed that ANG II significantly suppressed cell proliferation and glycosaminoglycan content in rat chondrocytic RCS cells.	Glycosaminoglycans	81-98	angiotensinogen	Rattus norvegicus	26-32
34425806-9	2021	In addition, NE significantly inhibited IL-1beta-induced release of glycosaminoglycan (GAG) from cartilage explant culture.	Glycosaminoglycans	68-85	interleukin 1 alpha	Homo sapiens	40-48
34425806-9	2021	In addition, NE significantly inhibited IL-1beta-induced release of glycosaminoglycan (GAG) from cartilage explant culture.	Glycosaminoglycans	87-90	interleukin 1 alpha	Homo sapiens	40-48
34440831-3	2021	Prominent amongst the latter is the large glycosaminoglycan hyaluronan (HA) that can form a bulky glycocalyx on the surface of certain tissue-migrating leucocytes and whose engagement with its key lymphatic receptor LYVE-1 mediates docking and entry of dendritic cells to afferent lymphatics.	Glycosaminoglycans	42-59	lymphatic vessel endothelial hyaluronan receptor 1	Homo sapiens	216-222
34388026-3	2021	This study investigated whether lentivirus-mediated Gag-CASP8 can effectively deliver activated CASP8 into primary human breast cancer cells overexpressing HER-2 to induce apoptosis and explore the underlying mechanism.	Glycosaminoglycans	52-55	caspase 8	Homo sapiens	56-61
34388026-3	2021	This study investigated whether lentivirus-mediated Gag-CASP8 can effectively deliver activated CASP8 into primary human breast cancer cells overexpressing HER-2 to induce apoptosis and explore the underlying mechanism.	Glycosaminoglycans	52-55	caspase 8	Homo sapiens	96-101
34388026-3	2021	This study investigated whether lentivirus-mediated Gag-CASP8 can effectively deliver activated CASP8 into primary human breast cancer cells overexpressing HER-2 to induce apoptosis and explore the underlying mechanism.	Glycosaminoglycans	52-55	erb-b2 receptor tyrosine kinase 2	Homo sapiens	156-161
34409033-1	2021	Chondroitin sulfate (CS) is the most abundant and widely distributed glycosaminoglycan (GAG) in the human body.	Glycosaminoglycans	69-86	citrate synthase	Homo sapiens	21-23
34388026-4	2021	Materials and Methods: HER-2-overexpressing primary human breast cancer cells were infected with lentivirus-like particles carrying Gag-CASP8.	Glycosaminoglycans	132-135	erb-b2 receptor tyrosine kinase 2	Homo sapiens	23-28
34388026-4	2021	Materials and Methods: HER-2-overexpressing primary human breast cancer cells were infected with lentivirus-like particles carrying Gag-CASP8.	Glycosaminoglycans	132-135	caspase 8	Homo sapiens	136-141
34388026-5	2021	Results: After a 48-h infection of primary human breast cancer cells with HER-2 by lentivirus-mediated Gag-CASP8, significant differences were observed in the survival rate, migration ability, S-phase number of cells, apoptosis rate, and intracellular activated CASP8 and caspase-3 levels in tumor cells compared with those in the control group (p < 0.05).	Glycosaminoglycans	103-106	erb-b2 receptor tyrosine kinase 2	Homo sapiens	74-79
34388026-5	2021	Results: After a 48-h infection of primary human breast cancer cells with HER-2 by lentivirus-mediated Gag-CASP8, significant differences were observed in the survival rate, migration ability, S-phase number of cells, apoptosis rate, and intracellular activated CASP8 and caspase-3 levels in tumor cells compared with those in the control group (p < 0.05).	Glycosaminoglycans	103-106	caspase 8	Homo sapiens	107-112
34388026-5	2021	Results: After a 48-h infection of primary human breast cancer cells with HER-2 by lentivirus-mediated Gag-CASP8, significant differences were observed in the survival rate, migration ability, S-phase number of cells, apoptosis rate, and intracellular activated CASP8 and caspase-3 levels in tumor cells compared with those in the control group (p < 0.05).	Glycosaminoglycans	103-106	caspase 8	Homo sapiens	262-267
34388026-5	2021	Results: After a 48-h infection of primary human breast cancer cells with HER-2 by lentivirus-mediated Gag-CASP8, significant differences were observed in the survival rate, migration ability, S-phase number of cells, apoptosis rate, and intracellular activated CASP8 and caspase-3 levels in tumor cells compared with those in the control group (p < 0.05).	Glycosaminoglycans	103-106	caspase 3	Homo sapiens	272-281
34388026-6	2021	Conclusions: Lentivirus-mediated Gag-CASP8 can deliver activated CASP8 into HER-2-overexpressing primary human breast cancer cells and induce apoptosis by activating caspase-3, a downstream apoptotic executive molecule.	Glycosaminoglycans	33-36	caspase 8	Homo sapiens	37-42
34388026-6	2021	Conclusions: Lentivirus-mediated Gag-CASP8 can deliver activated CASP8 into HER-2-overexpressing primary human breast cancer cells and induce apoptosis by activating caspase-3, a downstream apoptotic executive molecule.	Glycosaminoglycans	33-36	caspase 8	Homo sapiens	65-70
34388026-6	2021	Conclusions: Lentivirus-mediated Gag-CASP8 can deliver activated CASP8 into HER-2-overexpressing primary human breast cancer cells and induce apoptosis by activating caspase-3, a downstream apoptotic executive molecule.	Glycosaminoglycans	33-36	erb-b2 receptor tyrosine kinase 2	Homo sapiens	76-81
34388026-6	2021	Conclusions: Lentivirus-mediated Gag-CASP8 can deliver activated CASP8 into HER-2-overexpressing primary human breast cancer cells and induce apoptosis by activating caspase-3, a downstream apoptotic executive molecule.	Glycosaminoglycans	33-36	caspase 3	Homo sapiens	166-175
34388026-7	2021	By blocking the S-phase to inhibit cell proliferation and migration, lentivirus-mediated Gag-CASP8 provides a reference for tumor gene therapy.	Glycosaminoglycans	89-92	caspase 8	Homo sapiens	93-98
34409033-1	2021	Chondroitin sulfate (CS) is the most abundant and widely distributed glycosaminoglycan (GAG) in the human body.	Glycosaminoglycans	88-91	citrate synthase	Homo sapiens	21-23
34312884-2	2022	Transforming growth factor (TGF)-beta stimulates glycosaminoglycan elongation in vascular smooth muscle cells.	Glycosaminoglycans	49-66	protransforming growth factor alpha	Camelus bactrianus	0-37
34417096-6	2022	Severe levels of opacification and GAG accumulation were detected in the eyes of MPS VI Arsb- mice.	Glycosaminoglycans	35-38	arylsulfatase B	Mus musculus	88-92
34289859-1	2021	BACKGROUND: Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked multisystem disorder characterized by glycosaminoglycan (GAG) accumulation, caused by a deficiency of iduronate-2-sulfatase (I2S).	Glycosaminoglycans	121-138	iduronate 2-sulfatase	Homo sapiens	185-206
34452297-4	2021	Herein, we report that the overexpression of APH-2 not only hampered the release of HIV-1 pNL4.3 from 293T cells in a dose-dependent manner but also affected the cellular gag expression.	Glycosaminoglycans	171-174	zinc finger DHHC-type palmitoyltransferase 16	Homo sapiens	45-50
34452297-8	2021	Overall, these findings indicate that the HTLV-2 APH-2 may affect the HIV-1 replication at multiple levels by (a) inhibiting the Tat-mediated transactivation and (b) hampering the virus release by affecting the cellular gag expression.	Glycosaminoglycans	220-223	zinc finger DHHC-type palmitoyltransferase 16	Homo sapiens	49-54
34289859-1	2021	BACKGROUND: Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked multisystem disorder characterized by glycosaminoglycan (GAG) accumulation, caused by a deficiency of iduronate-2-sulfatase (I2S).	Glycosaminoglycans	121-138	iduronate 2-sulfatase	Homo sapiens	208-211
34289859-1	2021	BACKGROUND: Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked multisystem disorder characterized by glycosaminoglycan (GAG) accumulation, caused by a deficiency of iduronate-2-sulfatase (I2S).	Glycosaminoglycans	140-143	iduronate 2-sulfatase	Homo sapiens	185-206
34289859-1	2021	BACKGROUND: Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked multisystem disorder characterized by glycosaminoglycan (GAG) accumulation, caused by a deficiency of iduronate-2-sulfatase (I2S).	Glycosaminoglycans	140-143	iduronate 2-sulfatase	Homo sapiens	208-211
34280958-3	2021	Based on previous findings regarding the modulation of VEGF activity by glycosaminoglycans (GAG), here we explore the interaction of hyaluronan (HA)-based GAG with PDGF and its receptor PDGFR-beta by applying molecular modeling and dynamics simulations in combination with surface plasmon resonance (SPR).	Glycosaminoglycans	155-158	vascular endothelial growth factor A	Homo sapiens	55-59
34280958-3	2021	Based on previous findings regarding the modulation of VEGF activity by glycosaminoglycans (GAG), here we explore the interaction of hyaluronan (HA)-based GAG with PDGF and its receptor PDGFR-beta by applying molecular modeling and dynamics simulations in combination with surface plasmon resonance (SPR).	Glycosaminoglycans	155-158	platelet derived growth factor receptor alpha	Homo sapiens	186-196
34280958-3	2021	Based on previous findings regarding the modulation of VEGF activity by glycosaminoglycans (GAG), here we explore the interaction of hyaluronan (HA)-based GAG with PDGF and its receptor PDGFR-beta by applying molecular modeling and dynamics simulations in combination with surface plasmon resonance (SPR).	Glycosaminoglycans	72-90	vascular endothelial growth factor A	Homo sapiens	55-59
34280958-3	2021	Based on previous findings regarding the modulation of VEGF activity by glycosaminoglycans (GAG), here we explore the interaction of hyaluronan (HA)-based GAG with PDGF and its receptor PDGFR-beta by applying molecular modeling and dynamics simulations in combination with surface plasmon resonance (SPR).	Glycosaminoglycans	72-90	platelet derived growth factor receptor alpha	Homo sapiens	186-196
34280958-3	2021	Based on previous findings regarding the modulation of VEGF activity by glycosaminoglycans (GAG), here we explore the interaction of hyaluronan (HA)-based GAG with PDGF and its receptor PDGFR-beta by applying molecular modeling and dynamics simulations in combination with surface plasmon resonance (SPR).	Glycosaminoglycans	92-95	vascular endothelial growth factor A	Homo sapiens	55-59
34299163-7	2021	Interestingly, CVLS led to identification of two distinct sites of GAG binding on TGF-beta2.	Glycosaminoglycans	67-70	transforming growth factor beta 2	Homo sapiens	82-91
34280958-3	2021	Based on previous findings regarding the modulation of VEGF activity by glycosaminoglycans (GAG), here we explore the interaction of hyaluronan (HA)-based GAG with PDGF and its receptor PDGFR-beta by applying molecular modeling and dynamics simulations in combination with surface plasmon resonance (SPR).	Glycosaminoglycans	92-95	platelet derived growth factor receptor alpha	Homo sapiens	186-196
34189496-2	2021	The majority of the DYT1 dystonia patients have a trinucleotide GAG deletion in DYT1/TOR1A.	Glycosaminoglycans	64-67	torsin family 1 member A	Homo sapiens	20-24
34903995-10	2021	The glycosaminoglycan (GAG) deposition was higher in TGF-beta3, KGN and ASU groups compared to the control group.	Glycosaminoglycans	4-21	transforming growth factor, beta 3	Rattus norvegicus	53-62
34903995-10	2021	The glycosaminoglycan (GAG) deposition was higher in TGF-beta3, KGN and ASU groups compared to the control group.	Glycosaminoglycans	23-26	transforming growth factor, beta 3	Rattus norvegicus	53-62
34222264-5	2021	Recent reports have demonstrated that chondroitin sulfate and heparan sulfate, both of which are glycosaminoglycans, work as physiological ligands on their shared receptor, protein tyrosine phosphatase sigma (PTPsigma).	Glycosaminoglycans	97-115	protein tyrosine phosphatase receptor type S	Homo sapiens	209-217
34087306-3	2021	Herein, we studied the influence of different glycosaminoglycan (i.e., glycan; GAG) molecules on the conformation of a GDNF-derived peptide (GAG binding motif, sixteen amino acid residues at the N-terminus) using both experimental and theoretical studies.	Glycosaminoglycans	79-82	glial cell derived neurotrophic factor	Homo sapiens	119-123
34087306-3	2021	Herein, we studied the influence of different glycosaminoglycan (i.e., glycan; GAG) molecules on the conformation of a GDNF-derived peptide (GAG binding motif, sixteen amino acid residues at the N-terminus) using both experimental and theoretical studies.	Glycosaminoglycans	141-144	glial cell derived neurotrophic factor	Homo sapiens	119-123
34087306-6	2021	Our results revealed that the sulfated GAG molecules bind strongly with GDNF peptide and induce alpha-helical structure in the peptide to some extent.	Glycosaminoglycans	39-42	glial cell derived neurotrophic factor	Homo sapiens	72-76
34193099-5	2021	Gene panel analysis identified two compound heterozygous variants in the B4GALT7 gene: c.641G > A and c.723 + 4A > G. B4GALT7 encodes for galactosyltransferase I, which is required for the initiation of glycosaminoglycan side chain synthesis of proteoglycans.	Glycosaminoglycans	203-220	beta-1,4-galactosyltransferase 7	Homo sapiens	73-80
34193099-5	2021	Gene panel analysis identified two compound heterozygous variants in the B4GALT7 gene: c.641G > A and c.723 + 4A > G. B4GALT7 encodes for galactosyltransferase I, which is required for the initiation of glycosaminoglycan side chain synthesis of proteoglycans.	Glycosaminoglycans	203-220	beta-1,4-galactosyltransferase 7	Homo sapiens	118-125
34193099-5	2021	Gene panel analysis identified two compound heterozygous variants in the B4GALT7 gene: c.641G > A and c.723 + 4A > G. B4GALT7 encodes for galactosyltransferase I, which is required for the initiation of glycosaminoglycan side chain synthesis of proteoglycans.	Glycosaminoglycans	203-220	beta-1,4-galactosyltransferase 7	Homo sapiens	138-161
34139912-15	2021	CONCLUSION: At the early stage of AAA, the current study indicated the importance of glycosaminoglycan degradation and anaerobic metabolism.	Glycosaminoglycans	85-102	AAA1	Homo sapiens	34-37
34203832-2	2021	A highly conserved Pro-(Thr/Ser)-Ala-Pro (P(T/S)AP) motif in the HIV-1 structural polyprotein, Gag, engages a P(T/S)AP-binding pocket in the Tsg101 N-terminal domain.	Glycosaminoglycans	95-98	tumor susceptibility 101	Homo sapiens	141-147
34189496-2	2021	The majority of the DYT1 dystonia patients have a trinucleotide GAG deletion in DYT1/TOR1A.	Glycosaminoglycans	64-67	torsin family 1 member A	Homo sapiens	80-84
34189496-2	2021	The majority of the DYT1 dystonia patients have a trinucleotide GAG deletion in DYT1/TOR1A.	Glycosaminoglycans	64-67	torsin family 1 member A	Homo sapiens	85-90
34346645-3	2021	TSH-receptor expressing fibroblasts lead to by accumulation of subcutaneous glycosaminoglycans, causing the oedema.	Glycosaminoglycans	76-94	thyroid stimulating hormone receptor	Homo sapiens	0-12
34112803-4	2021	Here, we show that microenvironmental cytokines, particularly CCL2, decorate cancer exosomes via binding to surface glycosaminoglycan side chains of proteoglycans, causing exosome accumulation in specific cell subsets and organs.	Glycosaminoglycans	116-133	C-C motif chemokine ligand 2	Homo sapiens	62-66
35314385-7	2022	Girk3-/- chondrocytes were also more responsive to the kappa opioid receptor (KOR) ligand dynorphin, as evidenced by greater pCREB expression, greater cAMP and GAG production, and upregulation of Col2a1 and Sox9 transcripts.	Glycosaminoglycans	160-163	potassium inwardly-rectifying channel, subfamily J, member 9	Mus musculus	0-5
34067470-2	2021	This study aimed to assess the glycosaminoglycan (GAG) content of IVDs of patients with adolescent idiopathic scoliosis (AIS) and healthy controls using GAG chemical exchange saturation transfer (gagCEST) imaging.	Glycosaminoglycans	31-48	IS1	Homo sapiens	121-124
34067470-2	2021	This study aimed to assess the glycosaminoglycan (GAG) content of IVDs of patients with adolescent idiopathic scoliosis (AIS) and healthy controls using GAG chemical exchange saturation transfer (gagCEST) imaging.	Glycosaminoglycans	50-53	IS1	Homo sapiens	121-124
34067470-2	2021	This study aimed to assess the glycosaminoglycan (GAG) content of IVDs of patients with adolescent idiopathic scoliosis (AIS) and healthy controls using GAG chemical exchange saturation transfer (gagCEST) imaging.	Glycosaminoglycans	153-156	IS1	Homo sapiens	121-124
34195596-11	2021	These findings suggest that versican is cleaved within each GAG-bearing domain during web regression, and affirms that proteolysis in the GAGbeta domain, via generation of versikine, has an essential role in interdigital web regression.	Glycosaminoglycans	60-63	versican	Mus musculus	28-36
34200372-11	2021	The glycosaminoglycans heparan sulphate and dermatan sulphate, but not chondroitin sulphate, also inhibited the binding of spike protein, indicating that it might bind to one or both of these glycosaminoglycans on the surface of target cells.	Glycosaminoglycans	4-22	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	123-128
34200372-11	2021	The glycosaminoglycans heparan sulphate and dermatan sulphate, but not chondroitin sulphate, also inhibited the binding of spike protein, indicating that it might bind to one or both of these glycosaminoglycans on the surface of target cells.	Glycosaminoglycans	192-210	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	123-128
34807422-4	2021	Spondylodysplastic EDS is caused by pathogenic variants in B4GALT7 or B3GALT6, both of which encode key enzymes that initiate glycosaminoglycan synthesis.	Glycosaminoglycans	126-143	beta-1,4-galactosyltransferase 7	Homo sapiens	59-66
34807422-4	2021	Spondylodysplastic EDS is caused by pathogenic variants in B4GALT7 or B3GALT6, both of which encode key enzymes that initiate glycosaminoglycan synthesis.	Glycosaminoglycans	126-143	beta-1,3-galactosyltransferase 6	Homo sapiens	70-77
34248012-6	2021	The phosphorylation levels of PLC, PLA)2), PKC and p38MAPK in rat platelets were also inhibited by GAG and P)2)Y)1) receptor blocker MRS2179 (p<0.05, p<0.01).	Glycosaminoglycans	99-102	protein kinase C, gamma	Rattus norvegicus	43-46
34248012-6	2021	The phosphorylation levels of PLC, PLA)2), PKC and p38MAPK in rat platelets were also inhibited by GAG and P)2)Y)1) receptor blocker MRS2179 (p<0.05, p<0.01).	Glycosaminoglycans	99-102	mitogen activated protein kinase 14	Rattus norvegicus	51-58
35527471-0	2022	Endothelin-1 dependent expression of GAG genes involves NOX and p38 mediated Smad linker region phosphorylation.	Glycosaminoglycans	37-40	endothelin 1	Homo sapiens	0-12
35527471-0	2022	Endothelin-1 dependent expression of GAG genes involves NOX and p38 mediated Smad linker region phosphorylation.	Glycosaminoglycans	37-40	mitogen-activated protein kinase 14	Homo sapiens	64-67
35527471-1	2022	Endothelin-1 (ET-1) is implicated in the development of atherosclerosis and mediates glycosaminoglycan (GAG) chain hyperelongation on proteoglycans.	Glycosaminoglycans	85-102	endothelin 1	Homo sapiens	0-12
35527471-1	2022	Endothelin-1 (ET-1) is implicated in the development of atherosclerosis and mediates glycosaminoglycan (GAG) chain hyperelongation on proteoglycans.	Glycosaminoglycans	85-102	endothelin 1	Homo sapiens	14-18
35527471-1	2022	Endothelin-1 (ET-1) is implicated in the development of atherosclerosis and mediates glycosaminoglycan (GAG) chain hyperelongation on proteoglycans.	Glycosaminoglycans	104-107	endothelin 1	Homo sapiens	0-12
35527471-1	2022	Endothelin-1 (ET-1) is implicated in the development of atherosclerosis and mediates glycosaminoglycan (GAG) chain hyperelongation on proteoglycans.	Glycosaminoglycans	104-107	endothelin 1	Homo sapiens	14-18
35527471-2	2022	Our aim was to identify the ET-1-mediated signalling pathway involving NADPH oxidase (NOX), p38 MAP kinsae and Smad2 linker region phosphorylation (phospho-Smad2L) regulate GAG synthesizing enzymes mRNA expression (C4ST-1 and ChSy1) involved in GAG chains hyperelongation in human vascular smooth muscle cells (VSMCs).	Glycosaminoglycans	173-176	endothelin 1	Homo sapiens	28-32
35527471-2	2022	Our aim was to identify the ET-1-mediated signalling pathway involving NADPH oxidase (NOX), p38 MAP kinsae and Smad2 linker region phosphorylation (phospho-Smad2L) regulate GAG synthesizing enzymes mRNA expression (C4ST-1 and ChSy1) involved in GAG chains hyperelongation in human vascular smooth muscle cells (VSMCs).	Glycosaminoglycans	173-176	SMAD family member 2	Homo sapiens	111-116
35527471-2	2022	Our aim was to identify the ET-1-mediated signalling pathway involving NADPH oxidase (NOX), p38 MAP kinsae and Smad2 linker region phosphorylation (phospho-Smad2L) regulate GAG synthesizing enzymes mRNA expression (C4ST-1 and ChSy1) involved in GAG chains hyperelongation in human vascular smooth muscle cells (VSMCs).	Glycosaminoglycans	173-176	carbohydrate sulfotransferase 11	Homo sapiens	215-221
35527471-2	2022	Our aim was to identify the ET-1-mediated signalling pathway involving NADPH oxidase (NOX), p38 MAP kinsae and Smad2 linker region phosphorylation (phospho-Smad2L) regulate GAG synthesizing enzymes mRNA expression (C4ST-1 and ChSy1) involved in GAG chains hyperelongation in human vascular smooth muscle cells (VSMCs).	Glycosaminoglycans	173-176	chondroitin sulfate synthase 1	Homo sapiens	226-231
35527471-2	2022	Our aim was to identify the ET-1-mediated signalling pathway involving NADPH oxidase (NOX), p38 MAP kinsae and Smad2 linker region phosphorylation (phospho-Smad2L) regulate GAG synthesizing enzymes mRNA expression (C4ST-1 and ChSy1) involved in GAG chains hyperelongation in human vascular smooth muscle cells (VSMCs).	Glycosaminoglycans	245-248	endothelin 1	Homo sapiens	28-32
35527471-2	2022	Our aim was to identify the ET-1-mediated signalling pathway involving NADPH oxidase (NOX), p38 MAP kinsae and Smad2 linker region phosphorylation (phospho-Smad2L) regulate GAG synthesizing enzymes mRNA expression (C4ST-1 and ChSy1) involved in GAG chains hyperelongation in human vascular smooth muscle cells (VSMCs).	Glycosaminoglycans	245-248	SMAD family member 2	Homo sapiens	111-116
35527471-7	2022	The gene expression levels of GAG synthesizing enzymes post-ET-1 treatment were increased compared to untreated controls (P<0.01).	Glycosaminoglycans	30-33	endothelin 1	Homo sapiens	60-64
35527471-9	2022	ET-1-mediated signalling to GAG synthesizing enzymes gene expression occurs via transactivation-dependent pathway involving NOX, p38 MAP kinsae and Smad2 linker region phosphorylation.	Glycosaminoglycans	28-31	endothelin 1	Homo sapiens	0-4
35527471-9	2022	ET-1-mediated signalling to GAG synthesizing enzymes gene expression occurs via transactivation-dependent pathway involving NOX, p38 MAP kinsae and Smad2 linker region phosphorylation.	Glycosaminoglycans	28-31	mitogen-activated protein kinase 14	Homo sapiens	129-132
35527471-9	2022	ET-1-mediated signalling to GAG synthesizing enzymes gene expression occurs via transactivation-dependent pathway involving NOX, p38 MAP kinsae and Smad2 linker region phosphorylation.	Glycosaminoglycans	28-31	SMAD family member 2	Homo sapiens	148-153
35561285-10	2022	IL-1beta challenge had little effect on cell viability, proliferation, or protein synthesis but induced over 40% GAG loss in 10 days and 61% collagen loss in 6 weeks.	Glycosaminoglycans	113-116	interleukin 1 alpha	Bos taurus	0-8
35561285-11	2022	For the overloaded samples, IL-1beta induced greater degrees of degradation, with 68% GAG loss in 10 days and 80% collagen loss in 6 weeks.	Glycosaminoglycans	86-89	interleukin 1 alpha	Bos taurus	28-36
35537249-6	2022	We demonstrated that GPER1 and OXTR aggregates might be formed due to interactions with GAGs rather than arising from changes of levels of these proteins in cells.	Glycosaminoglycans	88-92	G protein-coupled estrogen receptor 1	Homo sapiens	21-26
35334413-0	2022	Pigment epithelium-derived factor engineered to increase glycosaminoglycan affinity while maintaining bioactivity.	Glycosaminoglycans	57-74	serpin family F member 1	Homo sapiens	0-33
35552402-10	2022	Hyperglycemia in RRMECs caused a significant increase in the mRNA levels of the enzymes involved in GAG biosynthesis (including EXTL-1,2,3, EXT-1,2, ChSY-1,3, and HAS-2,3), with these increases potentially being compensatory responses to overall glycocalyx loss.	Glycosaminoglycans	100-103	exostosin-like glycosyltransferase 1	Rattus norvegicus	128-138
35552402-10	2022	Hyperglycemia in RRMECs caused a significant increase in the mRNA levels of the enzymes involved in GAG biosynthesis (including EXTL-1,2,3, EXT-1,2, ChSY-1,3, and HAS-2,3), with these increases potentially being compensatory responses to overall glycocalyx loss.	Glycosaminoglycans	100-103	exostosin glycosyltransferase 1	Rattus norvegicus	140-147
35552402-10	2022	Hyperglycemia in RRMECs caused a significant increase in the mRNA levels of the enzymes involved in GAG biosynthesis (including EXTL-1,2,3, EXT-1,2, ChSY-1,3, and HAS-2,3), with these increases potentially being compensatory responses to overall glycocalyx loss.	Glycosaminoglycans	100-103	chondroitin sulfate synthase 1	Rattus norvegicus	149-155
35552402-10	2022	Hyperglycemia in RRMECs caused a significant increase in the mRNA levels of the enzymes involved in GAG biosynthesis (including EXTL-1,2,3, EXT-1,2, ChSY-1,3, and HAS-2,3), with these increases potentially being compensatory responses to overall glycocalyx loss.	Glycosaminoglycans	100-103	hyaluronan synthase 2	Rattus norvegicus	163-168
35568060-13	2022	CONCLUSIONS: Patients with the neuronopathic form and lack of IDS protein expression were most at risk to develop sustained anti-IDS titers, which inhibited IDS uptake and/or activity in vitro, and the efficacy of ERT in patients by lowering urinary glycosaminoglycan levels.	Glycosaminoglycans	250-267	iduronate 2-sulfatase	Homo sapiens	62-65
35568060-13	2022	CONCLUSIONS: Patients with the neuronopathic form and lack of IDS protein expression were most at risk to develop sustained anti-IDS titers, which inhibited IDS uptake and/or activity in vitro, and the efficacy of ERT in patients by lowering urinary glycosaminoglycan levels.	Glycosaminoglycans	250-267	iduronate 2-sulfatase	Homo sapiens	129-132
35620518-7	2022	On the other hand, ELN shows promising attributes as a biomarker in adolescent and adult Morquio A. Plasma/urine keratan sulfate (KS), and urinary glycosaminoglycan (GAG) levels were significantly higher in Morquio A patients (p < 0.001) which decreased with age of patients.	Glycosaminoglycans	147-164	elastin	Homo sapiens	19-22
35620518-7	2022	On the other hand, ELN shows promising attributes as a biomarker in adolescent and adult Morquio A. Plasma/urine keratan sulfate (KS), and urinary glycosaminoglycan (GAG) levels were significantly higher in Morquio A patients (p < 0.001) which decreased with age of patients.	Glycosaminoglycans	166-169	elastin	Homo sapiens	19-22
35543974-4	2022	Herein, to avoid denaturation of BMP-2 and enhance therapeutic action via localized delivery, a complex coacervate consisting of fucoidan, a marine-derived glycosaminoglycan, and poly-l-lysine (PLL) is fabricated.	Glycosaminoglycans	156-173	bone morphogenetic protein 2	Homo sapiens	33-38
35532170-10	2022	Downregulation of full length FN1 and concomitant increased FN1-208 ratio resulted in decreased sulphated glycosaminoglycan deposition, as well as decreased ACAN and COL2A1 and increased ADAMTS-5, ITGB1, and ITGB5 gene expression levels.	Glycosaminoglycans	106-123	fibronectin 1	Homo sapiens	30-33
35532170-10	2022	Downregulation of full length FN1 and concomitant increased FN1-208 ratio resulted in decreased sulphated glycosaminoglycan deposition, as well as decreased ACAN and COL2A1 and increased ADAMTS-5, ITGB1, and ITGB5 gene expression levels.	Glycosaminoglycans	106-123	fibronectin 1	Homo sapiens	60-63
35537249-6	2022	We demonstrated that GPER1 and OXTR aggregates might be formed due to interactions with GAGs rather than arising from changes of levels of these proteins in cells.	Glycosaminoglycans	88-92	oxytocin receptor	Homo sapiens	31-35
35533513-0	2022	Generation of gene-corrected isogenic control cell lines from a DYT1 dystonia patient iPSC line carrying a heterozygous GAG mutation in TOR1A gene.	Glycosaminoglycans	120-123	torsin family 1 member A	Homo sapiens	136-141
35533513-1	2022	Childhood-onset torsin dystonia (DYT1) is a rare hereditary movement disorder and usually caused by a heterozygous GAG deletion (c.907-909) in the TOR1A gene (DeltaE, p.Glu303del).	Glycosaminoglycans	115-118	torsin family 1 member A	Homo sapiens	33-37
35533513-1	2022	Childhood-onset torsin dystonia (DYT1) is a rare hereditary movement disorder and usually caused by a heterozygous GAG deletion (c.907-909) in the TOR1A gene (DeltaE, p.Glu303del).	Glycosaminoglycans	115-118	torsin family 1 member A	Homo sapiens	147-152
35573229-13	2022	Under induction of TGF-beta3, PBMSCs/DCBM composites expressed glycosaminoglycan (GAG), and the related gene expression also increased.	Glycosaminoglycans	63-80	transforming growth factor beta 3	Homo sapiens	19-28
35416346-5	2022	Unexpectedly, when SIRT1 was activated, while ACAN was enhanced, glycosaminoglycans (GAGs) were reduced, paralleled by down regulation of gene expression for N-acetylgalactosaminyltransferase type 1 (GALNT1) responsible for GAG chain initiation/elongation.	Glycosaminoglycans	224-227	sirtuin 1	Homo sapiens	19-24
35416346-5	2022	Unexpectedly, when SIRT1 was activated, while ACAN was enhanced, glycosaminoglycans (GAGs) were reduced, paralleled by down regulation of gene expression for N-acetylgalactosaminyltransferase type 1 (GALNT1) responsible for GAG chain initiation/elongation.	Glycosaminoglycans	224-227	aggrecan	Homo sapiens	46-50
35416346-7	2022	In conclusion, SIRT1 activation positively impacts on the expression of the main ECM proteins, while altering ECM composition and suppressing GAG content during human cartilage development.	Glycosaminoglycans	142-145	sirtuin 1	Homo sapiens	15-20
35416346-8	2022	These results suggest that SIRT1 activity has a differential effect on GAGs and proteins in developing hESC-chondrocytes and could only be beneficial to cartilage development and matrix protein synthesis if balanced by addition of positive GAG mediators.	Glycosaminoglycans	71-75	sirtuin 1	Homo sapiens	27-32
35093450-11	2022	Furthermore, quercetin could relieve the decrease of cell viability and the increase of apoptosis that induced by IL-1beta, and promote the synthesis of IL-1beta-inhibited mucopolysaccharide in chondrocytes.	Glycosaminoglycans	172-190	interleukin 1 alpha	Rattus norvegicus	153-161
35563245-1	2022	Mucopolysaccharidosis type II (Hunter Syndrome) is a rare, x-linked recessive, progressive, multi-system, lysosomal storage disease caused by the deficiency of iduronate-2-sulfatase (IDS), which leads to the pathological storage of glycosaminoglycans in nearly all cell types, tissues and organs.	Glycosaminoglycans	232-250	iduronate 2-sulfatase	Homo sapiens	160-181
35563245-1	2022	Mucopolysaccharidosis type II (Hunter Syndrome) is a rare, x-linked recessive, progressive, multi-system, lysosomal storage disease caused by the deficiency of iduronate-2-sulfatase (IDS), which leads to the pathological storage of glycosaminoglycans in nearly all cell types, tissues and organs.	Glycosaminoglycans	232-250	iduronate 2-sulfatase	Homo sapiens	183-186
35231604-3	2022	We have recently developed an immunogen (CaV11), tandemly connected overlapping 11-mer peptides spanning the simian immunodeficiency virus (SIV) Gag capsid and Vif proteins, to selectively induce Gag- and Vif-specific CD8+ T cells but not CD4+ T cells.	Glycosaminoglycans	196-199	calcium voltage-gated channel subunit alpha1 S	Homo sapiens	41-46
35231604-3	2022	We have recently developed an immunogen (CaV11), tandemly connected overlapping 11-mer peptides spanning the simian immunodeficiency virus (SIV) Gag capsid and Vif proteins, to selectively induce Gag- and Vif-specific CD8+ T cells but not CD4+ T cells.	Glycosaminoglycans	196-199	vif protein	Simian immunodeficiency virus	160-163
35231604-3	2022	We have recently developed an immunogen (CaV11), tandemly connected overlapping 11-mer peptides spanning the simian immunodeficiency virus (SIV) Gag capsid and Vif proteins, to selectively induce Gag- and Vif-specific CD8+ T cells but not CD4+ T cells.	Glycosaminoglycans	196-199	vif protein	Simian immunodeficiency virus	205-208
35231604-3	2022	We have recently developed an immunogen (CaV11), tandemly connected overlapping 11-mer peptides spanning the simian immunodeficiency virus (SIV) Gag capsid and Vif proteins, to selectively induce Gag- and Vif-specific CD8+ T cells but not CD4+ T cells.	Glycosaminoglycans	196-199	CD8a molecule	Homo sapiens	218-221
35231604-3	2022	We have recently developed an immunogen (CaV11), tandemly connected overlapping 11-mer peptides spanning the simian immunodeficiency virus (SIV) Gag capsid and Vif proteins, to selectively induce Gag- and Vif-specific CD8+ T cells but not CD4+ T cells.	Glycosaminoglycans	196-199	CD4 molecule	Homo sapiens	239-242
35573229-13	2022	Under induction of TGF-beta3, PBMSCs/DCBM composites expressed glycosaminoglycan (GAG), and the related gene expression also increased.	Glycosaminoglycans	82-85	transforming growth factor beta 3	Homo sapiens	19-28
35631323-0	2022	Pleiotrophin Interaction with Synthetic Glycosaminoglycan Mimetics.	Glycosaminoglycans	40-57	pleiotrophin	Homo sapiens	0-12
35548440-1	2022	Glycosaminoglycans (GAGs) pooling has long been considered as one of the histopathological characteristics defining thoracic aortic aneurysm (TAA) together with smooth muscle cells (SMCs) apoptosis and elastin fibers degradation.	Glycosaminoglycans	0-18	elastin	Mus musculus	202-209
35459923-5	2022	DEMs between ADNS-ADF were enriched in the nervous system, glycosaminoglycan biosynthesis-keratan sulfate (KS) and Quorum sensing pathways.	Glycosaminoglycans	59-76	destrin	Mus musculus	18-21
35438526-16	2022	In this study, we report that SGK1 inhibits the replication of prototype foamy virus by affecting the function of the transcription activator, Tas, and reducing the stability of the structural protein, Gag.	Glycosaminoglycans	202-205	serum/glucocorticoid regulated kinase 1	Homo sapiens	30-34
35631323-4	2022	The results agree with the data for larger GAG (glycosaminoglycans) sequences and confirm our hypothesis that a synthetic tetrasaccharide is long enough to fully interact with PTN.	Glycosaminoglycans	43-46	pleiotrophin	Homo sapiens	176-179
35631323-4	2022	The results agree with the data for larger GAG (glycosaminoglycans) sequences and confirm our hypothesis that a synthetic tetrasaccharide is long enough to fully interact with PTN.	Glycosaminoglycans	48-66	pleiotrophin	Homo sapiens	176-179
35440680-2	2022	In addition to protein receptors, the SARS-CoV-2 spike (S) protein also interacts with heparan sulfate, a negatively charged glycosaminoglycan (GAG) attached to certain membrane proteins on the cell surface.	Glycosaminoglycans	125-142	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	49-54
35440680-2	2022	In addition to protein receptors, the SARS-CoV-2 spike (S) protein also interacts with heparan sulfate, a negatively charged glycosaminoglycan (GAG) attached to certain membrane proteins on the cell surface.	Glycosaminoglycans	125-142	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	56-57
35440680-2	2022	In addition to protein receptors, the SARS-CoV-2 spike (S) protein also interacts with heparan sulfate, a negatively charged glycosaminoglycan (GAG) attached to certain membrane proteins on the cell surface.	Glycosaminoglycans	144-147	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	49-54
35440680-2	2022	In addition to protein receptors, the SARS-CoV-2 spike (S) protein also interacts with heparan sulfate, a negatively charged glycosaminoglycan (GAG) attached to certain membrane proteins on the cell surface.	Glycosaminoglycans	144-147	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	56-57
35220018-0	2022	Targeting angiogenic growth factors using therapeutic glycosaminoglycans on doppel-expressing endothelial cells for blocking angiogenic signaling in cancer.	Glycosaminoglycans	54-72	prion like protein doppel	Homo sapiens	76-82
35410161-5	2022	We applied this approach to mouse CTCF ChIP-seq data and identified the known binding preferences of CTCF ZFs 3-11 as well as a putative GAG binding motif for ZF 1.	Glycosaminoglycans	137-140	CCCTC-binding factor	Mus musculus	34-38
35458529-12	2022	The subdomain p18 in gag, the reverse transcriptase/ribonuclease H in pol, and the surface (SU) in the env protein were the most polymorphic in genomic comparisons.	Glycosaminoglycans	21-24	H3 histone pseudogene 12	Homo sapiens	14-17
35220018-5	2022	In this work, we investigated the effect of a GAG-based biomaterial, which binds to the tumor endothelial cells (TEC), on the interaction among vascular endothelial growth factor (VEGF), its receptors-VEGFR2 and HS-and angiogenesis.	Glycosaminoglycans	46-49	vascular endothelial growth factor A	Homo sapiens	144-178
35220018-5	2022	In this work, we investigated the effect of a GAG-based biomaterial, which binds to the tumor endothelial cells (TEC), on the interaction among vascular endothelial growth factor (VEGF), its receptors-VEGFR2 and HS-and angiogenesis.	Glycosaminoglycans	46-49	vascular endothelial growth factor A	Homo sapiens	180-184
35220018-5	2022	In this work, we investigated the effect of a GAG-based biomaterial, which binds to the tumor endothelial cells (TEC), on the interaction among vascular endothelial growth factor (VEGF), its receptors-VEGFR2 and HS-and angiogenesis.	Glycosaminoglycans	46-49	kinase insert domain receptor	Homo sapiens	201-207
35284671-1	2022	Mucopolysaccharidosis type II (MPS II), also known as Hunter syndrome, is a rare X-linked recessive disease caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase (IDS), which activates intracellular accumulation of nonmetabolized glycosaminoglycans such as heparan sulfate and dermatan sulfate.	Glycosaminoglycans	245-263	iduronate 2-sulfatase	Mus musculus	178-181
35051794-8	2022	On all the flat/patterned surfaces modified with GAG-like polymers, the adsorption of human vascular endothelial growth factor (VEGF) and human basic fibroblast growth factor (bFGF) was improved, and the amount of VEGF and bFGF absorbed on patterned surfaces containing sulfonate units decreased with pattern dimensions.	Glycosaminoglycans	49-52	vascular endothelial growth factor A	Homo sapiens	92-126
35051794-8	2022	On all the flat/patterned surfaces modified with GAG-like polymers, the adsorption of human vascular endothelial growth factor (VEGF) and human basic fibroblast growth factor (bFGF) was improved, and the amount of VEGF and bFGF absorbed on patterned surfaces containing sulfonate units decreased with pattern dimensions.	Glycosaminoglycans	49-52	vascular endothelial growth factor A	Homo sapiens	128-132
35051794-8	2022	On all the flat/patterned surfaces modified with GAG-like polymers, the adsorption of human vascular endothelial growth factor (VEGF) and human basic fibroblast growth factor (bFGF) was improved, and the amount of VEGF and bFGF absorbed on patterned surfaces containing sulfonate units decreased with pattern dimensions.	Glycosaminoglycans	49-52	fibroblast growth factor 2	Homo sapiens	144-174
35051794-8	2022	On all the flat/patterned surfaces modified with GAG-like polymers, the adsorption of human vascular endothelial growth factor (VEGF) and human basic fibroblast growth factor (bFGF) was improved, and the amount of VEGF and bFGF absorbed on patterned surfaces containing sulfonate units decreased with pattern dimensions.	Glycosaminoglycans	49-52	fibroblast growth factor 2	Homo sapiens	176-180
35051794-8	2022	On all the flat/patterned surfaces modified with GAG-like polymers, the adsorption of human vascular endothelial growth factor (VEGF) and human basic fibroblast growth factor (bFGF) was improved, and the amount of VEGF and bFGF absorbed on patterned surfaces containing sulfonate units decreased with pattern dimensions.	Glycosaminoglycans	49-52	vascular endothelial growth factor A	Homo sapiens	214-218
35051794-8	2022	On all the flat/patterned surfaces modified with GAG-like polymers, the adsorption of human vascular endothelial growth factor (VEGF) and human basic fibroblast growth factor (bFGF) was improved, and the amount of VEGF and bFGF absorbed on patterned surfaces containing sulfonate units decreased with pattern dimensions.	Glycosaminoglycans	49-52	fibroblast growth factor 2	Homo sapiens	223-227
34982346-0	2022	Endothelin-1 mediated glycosaminoglycan synthesizing gene expression involves NOX-dependent transactivation of the transforming growth factor-beta receptor.	Glycosaminoglycans	22-39	endothelin 1	Homo sapiens	0-12
34982346-1	2022	G protein-coupled receptor (GPCR) agonist endothelin-1 (ET-1) through transactivation of the transforming growth factor (TGF) beta receptor (TGFBR1) stimulates glycosaminoglycan (GAG) elongation on proteoglycans.	Glycosaminoglycans	160-177	endothelin 1	Homo sapiens	42-54
34982346-1	2022	G protein-coupled receptor (GPCR) agonist endothelin-1 (ET-1) through transactivation of the transforming growth factor (TGF) beta receptor (TGFBR1) stimulates glycosaminoglycan (GAG) elongation on proteoglycans.	Glycosaminoglycans	160-177	endothelin 1	Homo sapiens	56-60
34982346-1	2022	G protein-coupled receptor (GPCR) agonist endothelin-1 (ET-1) through transactivation of the transforming growth factor (TGF) beta receptor (TGFBR1) stimulates glycosaminoglycan (GAG) elongation on proteoglycans.	Glycosaminoglycans	160-177	transforming growth factor beta receptor 1	Homo sapiens	141-147
35199120-5	2022	Concurrently, an in vitro model of OA using primary mouse chondrocytes demonstrated that the release of berberine at a concentration as low as 1 mug mL-1 is sufficient to restore the production of sulphated glycosaminoglycans (sGAG) to levels comparable to healthy chondrocytes while avoiding the cytotoxic concentrations (IC50 = 33 mug mL-1) on skin keratinocytes.	Glycosaminoglycans	207-225	L1 cell adhesion molecule	Mus musculus	149-153
35199120-5	2022	Concurrently, an in vitro model of OA using primary mouse chondrocytes demonstrated that the release of berberine at a concentration as low as 1 mug mL-1 is sufficient to restore the production of sulphated glycosaminoglycans (sGAG) to levels comparable to healthy chondrocytes while avoiding the cytotoxic concentrations (IC50 = 33 mug mL-1) on skin keratinocytes.	Glycosaminoglycans	207-225	L1 cell adhesion molecule	Mus musculus	337-341
35392101-6	2022	We previously demonstrated the adaptation of circulating strains of HIV-1 to the HLA-A*02 molecule by identifying mutations under positive selection located in GC9 and SL9 epitopes derived from the Gag protein.	Glycosaminoglycans	198-201	major histocompatibility complex, class I, A	Homo sapiens	81-86
35142364-8	2022	Our results demonstrate a novel function of GPC3-associated heparan sulfate, and provide a framework for the functional dissection of glycosaminoglycans by in vivo biochemical complementation.	Glycosaminoglycans	134-152	glypican 3	Homo sapiens	44-48
35330115-5	2022	The only gag-related gene has been found in the Drosophila genome-Gagr.	Glycosaminoglycans	9-12	Gag-related	Drosophila melanogaster	66-70
34982346-1	2022	G protein-coupled receptor (GPCR) agonist endothelin-1 (ET-1) through transactivation of the transforming growth factor (TGF) beta receptor (TGFBR1) stimulates glycosaminoglycan (GAG) elongation on proteoglycans.	Glycosaminoglycans	179-182	endothelin 1	Homo sapiens	42-54
34982346-1	2022	G protein-coupled receptor (GPCR) agonist endothelin-1 (ET-1) through transactivation of the transforming growth factor (TGF) beta receptor (TGFBR1) stimulates glycosaminoglycan (GAG) elongation on proteoglycans.	Glycosaminoglycans	179-182	endothelin 1	Homo sapiens	56-60
34982346-1	2022	G protein-coupled receptor (GPCR) agonist endothelin-1 (ET-1) through transactivation of the transforming growth factor (TGF) beta receptor (TGFBR1) stimulates glycosaminoglycan (GAG) elongation on proteoglycans.	Glycosaminoglycans	179-182	transforming growth factor beta receptor 1	Homo sapiens	141-147
34982346-5	2022	In this study, we investigated the involvement of NOX in ET-1/ET receptor-mediated transactivation of TGFBR1 to stimulate mRNA expression of GAG chain synthesizing enzymes chondroitin 4-O-sulfotransferase 1 (C4ST-1) and chondroitin sulfate synthase 1 (ChSy-1).	Glycosaminoglycans	141-144	endothelin 1	Homo sapiens	57-61
34982346-5	2022	In this study, we investigated the involvement of NOX in ET-1/ET receptor-mediated transactivation of TGFBR1 to stimulate mRNA expression of GAG chain synthesizing enzymes chondroitin 4-O-sulfotransferase 1 (C4ST-1) and chondroitin sulfate synthase 1 (ChSy-1).	Glycosaminoglycans	141-144	transforming growth factor beta receptor 1	Homo sapiens	102-108
34982346-5	2022	In this study, we investigated the involvement of NOX in ET-1/ET receptor-mediated transactivation of TGFBR1 to stimulate mRNA expression of GAG chain synthesizing enzymes chondroitin 4-O-sulfotransferase 1 (C4ST-1) and chondroitin sulfate synthase 1 (ChSy-1).	Glycosaminoglycans	141-144	carbohydrate sulfotransferase 11	Homo sapiens	172-206
34982346-9	2022	ET-1 mediated mRNA expression of GAG synthesizing enzymes C4ST-1 and ChSy-1 was also blocked by TGBFR1 antagonists, SB431542, broad spectrum ET receptor antagonist bosentan, DPI and ROS scavenger N-acetyl-L-cysteine.	Glycosaminoglycans	33-36	endothelin 1	Homo sapiens	0-4
34982346-9	2022	ET-1 mediated mRNA expression of GAG synthesizing enzymes C4ST-1 and ChSy-1 was also blocked by TGBFR1 antagonists, SB431542, broad spectrum ET receptor antagonist bosentan, DPI and ROS scavenger N-acetyl-L-cysteine.	Glycosaminoglycans	33-36	carbohydrate sulfotransferase 11	Homo sapiens	58-64
34982346-9	2022	ET-1 mediated mRNA expression of GAG synthesizing enzymes C4ST-1 and ChSy-1 was also blocked by TGBFR1 antagonists, SB431542, broad spectrum ET receptor antagonist bosentan, DPI and ROS scavenger N-acetyl-L-cysteine.	Glycosaminoglycans	33-36	chondroitin sulfate synthase 1	Homo sapiens	69-75
34982346-10	2022	This work shows that NOX and ROS play an important role in ET-1 mediated transactivation of the TGFBR1 and downstream gene targets associated with GAG chain elongation.	Glycosaminoglycans	147-150	endothelin 1	Homo sapiens	59-63
34982346-10	2022	This work shows that NOX and ROS play an important role in ET-1 mediated transactivation of the TGFBR1 and downstream gene targets associated with GAG chain elongation.	Glycosaminoglycans	147-150	transforming growth factor beta receptor 1	Homo sapiens	96-102
35346191-12	2022	Pathway enrichment analysis showed that most DEGs were significantly enriched in BMP signal pathway, transmembrane receptor protein serine/threonine kinase signal pathway, extracellular matrix, basement membrane, glycosaminoglycan binding, sulfur compound binding and so on.	Glycosaminoglycans	213-230	delta 4-desaturase, sphingolipid 1	Homo sapiens	45-49
35201897-11	2022	These genetic defects were concentrated in the env region compared to gag and pol, likely a reflection of viral immune escape in env during untreated HIV-1 infection.	Glycosaminoglycans	70-73	endogenous retrovirus group K member 20	Homo sapiens	129-132
35312866-0	2022	GRASP depletion-mediated Golgi fragmentation impairs glycosaminoglycan synthesis, sulfation, and secretion.	Glycosaminoglycans	53-70	trafficking regulator and scaffold protein tamalin	Homo sapiens	0-5
35312866-1	2022	Synthesis of glycosaminoglycans, such as heparan sulfate (HS) and chondroitin sulfate (CS), occurs in the lumen of the Golgi, but the relationship between Golgi structural integrity and glycosaminoglycan synthesis is not clear.	Glycosaminoglycans	13-31	citrate synthase	Homo sapiens	87-89
35312866-1	2022	Synthesis of glycosaminoglycans, such as heparan sulfate (HS) and chondroitin sulfate (CS), occurs in the lumen of the Golgi, but the relationship between Golgi structural integrity and glycosaminoglycan synthesis is not clear.	Glycosaminoglycans	186-203	citrate synthase	Homo sapiens	87-89
35307777-8	2022	Epitope mapping showed that all Nbs recognize the Arc C-terminal region containing the retroviral Gag capsid homology domain, comprised of tandem N- and C-lobes.	Glycosaminoglycans	98-101	nucleolar protein 3	Rattus norvegicus	50-53
35284671-1	2022	Mucopolysaccharidosis type II (MPS II), also known as Hunter syndrome, is a rare X-linked recessive disease caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase (IDS), which activates intracellular accumulation of nonmetabolized glycosaminoglycans such as heparan sulfate and dermatan sulfate.	Glycosaminoglycans	245-263	iduronate 2-sulfatase	Mus musculus	155-176
35205150-6	2022	Moreover, glycosaminoglycan degradation and lysosome-associated functions were involved in the functional mechanisms of S100A7.	Glycosaminoglycans	10-27	S100 calcium binding protein A7	Homo sapiens	120-126
35281253-6	2022	Hydrogen-deuterium exchange mass spectrometry (HDX-MS) was used to study the glycosaminoglycan (GAG)-peptide complex and identified V12HHQKL17 as the binding site of GAG at Abeta.	Glycosaminoglycans	77-94	amyloid beta precursor protein	Homo sapiens	173-178
35281253-6	2022	Hydrogen-deuterium exchange mass spectrometry (HDX-MS) was used to study the glycosaminoglycan (GAG)-peptide complex and identified V12HHQKL17 as the binding site of GAG at Abeta.	Glycosaminoglycans	96-99	amyloid beta precursor protein	Homo sapiens	173-178
35281253-6	2022	Hydrogen-deuterium exchange mass spectrometry (HDX-MS) was used to study the glycosaminoglycan (GAG)-peptide complex and identified V12HHQKL17 as the binding site of GAG at Abeta.	Glycosaminoglycans	166-169	amyloid beta precursor protein	Homo sapiens	173-178
35177103-10	2022	RESULTS: Our findings represented that a combination of the SMMSCs/secretome/PRP had a considerable effect on glycosaminoglycans (GAGs) and collagen II contents, articular cartilage preservation, compared with other groups.	Glycosaminoglycans	110-128	proline rich protein 2-like 1	Rattus norvegicus	77-80
35216110-6	2022	We propose a model whereby progressive accumulation of glycosaminoglycans elicits an innate immune response, initiated by the Toll-like receptor 4 pathway, but also precipitated by secondary storage components.	Glycosaminoglycans	55-73	toll like receptor 4	Homo sapiens	126-146
35082297-1	2022	HIV elite controllers maintain a population of CD4 + T cells endowed with high avidity for Gag antigens and potent effector functions.	Glycosaminoglycans	91-94	CD4 molecule	Homo sapiens	47-50
35215917-5	2022	Nevertheless, in these last decades, progress in novel bioimaging microscopic approaches (as FFS, FRAP, TIRF, and wide-field microscopy) have allowed for the tracking of retroviral Gag and gRNA in living cells, thus providing important insights at high spatial and temporal resolution of the events regulating the late phases of the retroviral life cycle.	Glycosaminoglycans	181-184	mechanistic target of rapamycin kinase	Homo sapiens	98-102
35242620-1	2022	Chondroitin sulfate (CS) is a glycosaminoglycan with a broad range of applications being a popular dietary supplement for osteoarthritis.	Glycosaminoglycans	30-47	citrate synthase	Homo sapiens	21-23
35140938-4	2022	Because of its high density of net positive charges at physiological pH, CXCL9(74-103) competes with full-length chemokines for glycosaminoglycan (GAG) binding.	Glycosaminoglycans	128-145	C-X-C motif chemokine ligand 9	Homo sapiens	73-78
35140938-4	2022	Because of its high density of net positive charges at physiological pH, CXCL9(74-103) competes with full-length chemokines for glycosaminoglycan (GAG) binding.	Glycosaminoglycans	147-150	C-X-C motif chemokine ligand 9	Homo sapiens	73-78
35140938-12	2022	The anti-fibrotic and anti-inflammatory effects of CXCL9(74-103) were mediated by competition with chemokines and growth factors for GAG binding.	Glycosaminoglycans	133-136	C-X-C motif chemokine ligand 9	Homo sapiens	51-56
35082297-3	2022	Ex vivo characterization of single Gag-specific CD4 + T cells reveals an advanced Th1 differentiation pattern in controllers, except for the CCR5 marker, which is downregulated compared to specific cells of treated patients.	Glycosaminoglycans	35-38	CD4 molecule	Homo sapiens	48-51
35082297-3	2022	Ex vivo characterization of single Gag-specific CD4 + T cells reveals an advanced Th1 differentiation pattern in controllers, except for the CCR5 marker, which is downregulated compared to specific cells of treated patients.	Glycosaminoglycans	35-38	C-C motif chemokine receptor 5	Homo sapiens	141-145
35092850-10	2022	The GAG stained area was thickest for age 1 d to 4 weeks in Postn+/+ and for age 2 to 6 weeks in Postn-/-.	Glycosaminoglycans	4-7	periostin, osteoblast specific factor	Mus musculus	60-65
35118118-1	2021	Mucopolysaccharidosis VI (MPS VI) is an autosomal recessive lysosomal storage disease caused by mutations in the arylsulfatase B gene (ARSB) and consequent deficient activity of ARSB, a lysosomal enzyme involved in the glycosaminoglycan (s) (GAGs) metabolism.	Glycosaminoglycans	219-236	arylsulfatase B	Homo sapiens	135-139
35078524-1	2022	BACKGROUND: Mucopolysaccharidosis VI, or Maroteaux-Lamy disease, is an autosomal recessive disease characterized by deficiency of the enzyme arylsulfatase B in the lysosomal catabolism of glycosaminoglycans.	Glycosaminoglycans	188-206	arylsulfatase B	Homo sapiens	141-156
35118118-1	2021	Mucopolysaccharidosis VI (MPS VI) is an autosomal recessive lysosomal storage disease caused by mutations in the arylsulfatase B gene (ARSB) and consequent deficient activity of ARSB, a lysosomal enzyme involved in the glycosaminoglycan (s) (GAGs) metabolism.	Glycosaminoglycans	219-236	arylsulfatase B	Homo sapiens	178-182
35057081-10	2022	In addition, farnesol drastically increased the synthesis of COL II (2.5-fold) and GAG (15-fold) on interleukin-1beta-induced dedifferentiated chondrocytes.	Glycosaminoglycans	83-86	interleukin 1 beta	Homo sapiens	100-117
34842271-4	2022	We found that reduced sulfation of glycosaminoglycans interacts with heterozygosity for the Lp allele of Vangl2 (a core PCP gene), to cause craniorachischisis in cultured mouse embryos, with rescue by exogenous sulphate.	Glycosaminoglycans	35-53	VANGL planar cell polarity 2	Mus musculus	105-111
34999954-5	2022	SLC10A7-CDG patients presented skeletal dysplasia with multiple large joint dislocations, short stature and amelogenesis imperfecta likely mediated by glycosaminoglycan (GAG) defects.	Glycosaminoglycans	151-168	solute carrier family 10 member 7	Homo sapiens	0-7
34999954-5	2022	SLC10A7-CDG patients presented skeletal dysplasia with multiple large joint dislocations, short stature and amelogenesis imperfecta likely mediated by glycosaminoglycan (GAG) defects.	Glycosaminoglycans	170-173	solute carrier family 10 member 7	Homo sapiens	0-7
34999954-6	2022	Although it has been demonstrated that the transporter and substrate specificities of SLC10A7, if any, differ from those of the main members of the protein family, SLC10A7 seems to play a role in Ca2+ regulation and is involved in proper glycosaminoglycan biosynthesis, especially heparan-sulfate, and N-glycosylation.	Glycosaminoglycans	238-255	solute carrier family 10 member 7	Homo sapiens	86-93
34999954-6	2022	Although it has been demonstrated that the transporter and substrate specificities of SLC10A7, if any, differ from those of the main members of the protein family, SLC10A7 seems to play a role in Ca2+ regulation and is involved in proper glycosaminoglycan biosynthesis, especially heparan-sulfate, and N-glycosylation.	Glycosaminoglycans	238-255	solute carrier family 10 member 7	Homo sapiens	164-171
34581306-5	2022	The HIV-specific T-cell responses among PECs were characterized by high-frequency Gag-specific CD4+ T-cell activity, and markedly more polyfunctional Gag-specific CD8+ activity, compared with PNPs and progressors.	Glycosaminoglycans	150-153	CD8a molecule	Homo sapiens	163-166
35141043-5	2022	In the present study, we further improved the technique by transferring the system to the alpharetroviral vector platform (a.Gag.MS2), which significantly increased CRISPR-Cas9 delivery into target cells and allowed efficient targeted knockout of endogenous TP53/Trp53 genes in primary murine fibroblasts as well as primary human fibroblasts, hepatocytes, and cord-blood-derived CD34+ stem and progenitor cells.	Glycosaminoglycans	125-128	CD34 molecule	Homo sapiens	379-383
34626400-1	2022	The ubiquitous extracellular glycosaminoglycan hyaluronan (HA) is a polymer composed of repeated disaccharide units of alternating D-glucuronic acid and D-N-acetylglucosamine residues linked via alternating beta-1,4 and beta-1,3 glycosidic bonds.	Glycosaminoglycans	29-46	immunoglobulin kappa variable 6D-41 (non-functional)	Homo sapiens	207-215
34626400-1	2022	The ubiquitous extracellular glycosaminoglycan hyaluronan (HA) is a polymer composed of repeated disaccharide units of alternating D-glucuronic acid and D-N-acetylglucosamine residues linked via alternating beta-1,4 and beta-1,3 glycosidic bonds.	Glycosaminoglycans	29-46	immunoglobulin kappa variable 2D-18 (pseudogene)	Homo sapiens	220-228
34980815-5	2022	Nonclinical studies showed that pabinafusp alfa was distributed in the brain of hTfR knock-in mice and monkeys after intravenous administration, and dose-dependently decreased heparan sulfate (HS) glycosaminoglycan deposited in major organs including the brain of MPS II mice.	Glycosaminoglycans	197-214	transferrin receptor	Homo sapiens	80-84
35059272-4	2022	Sequencing analysis revealed a heterozygous GAG (glutamic acid)   AAG (lysine) mutation at amino acid position 23 of the alpha2-globin gene.	Glycosaminoglycans	44-47	hemoglobin subunit alpha 2	Homo sapiens	121-134