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3'-phosphoadenylyl sulfate + chondroitin sulfate
?
-
chondroitin sulfate exhibits similar high affinity binding to 3-OST-3A compared to heparan sulfate
-
-
?
3'-phosphoadenylyl sulfate + chondroitin sulfate A
adenosine 3',5'-diphosphate + ?
-
isoform 3A, low activity
-
?
3'-phosphoadenylyl sulfate + GlcA-beta-(1->4)-GlcNS6S-beta-(1->4)-IdoA-beta-(1->4)-GlcNS6S-alpha-(CH2)5NH2
adenosine 3',5'-bisphosphate + GlcA-beta-(1->4)-GlcNS3S6S-beta-(1->4)-IdoA-beta-(1->4)-GlcNS6S-alpha-(CH2)5NH2
-
-
-
-
?
3'-phosphoadenylyl sulfate + GlcA-beta-(1->4)-GlcNS6S-beta-(1->4)-IdoA-beta-(1->4)-GlcNS6S-beta-(1->4)-GlcA-beta-(1->4)-GlcNS6S-alpha-(CH2)5NH2
adenosine 3',5'-bisphosphate + GlcA-beta-(1->4)-GlcNS3S6S-beta-(1->4)-IdoA-beta-(1->4)-GlcNS3S6S-beta-(1->4)-GlcA-beta-(1->4)-GlcNS6S-alpha-(CH2)5NH2
-
-
-
-
?
3'-phosphoadenylyl sulfate + heparin
?
-
heparin exhibits similar high affinity binding to 3-OST-3A compared to heparan sulfate
-
-
?
3'-phosphoadenylyl sulfate + IdoA-beta-(1->4)-GlcNS6S-beta-(1->4)-IdoA-beta-(1->4)-GlcNS6S-alpha-(CH2)5NH2
adenosine 3',5'-bisphosphate + IdoA-beta-(1->4)-GlcNS3S6S-beta-(1->4)-IdoA-beta-(1->4)-GlcNS6S-alpha-(CH2)5NH2
-
-
-
-
?
3'-phosphoadenylyl sulfate + keratan sulfate
adenosine 3',5'-diphosphate + ?
-
isoform 3A, low activity
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
heparan sulfate + 3'-phosphoadenylyl sulfate
3-O-sulfated heparan sulfate + adenosine 3',5'-bisphosphate
-
i.e. PAPS
-
-
?
heparin 3-hydroxy octasaccharide + 3'-phosphoadenylyl sulfate
3-O-sulfated heparin octasaccharide + adenosine 3',5'-bisphosphate
additional information
?
-
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
3-OST-3 forms IdoUA2S-AnMan3S and IdoUA2S-AnMan3S6S disaccharides-containing products, product analysis, overview
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
3-O-sulfation of GlcNH2-containing heparan sulfate by 3-OST-3 provides binding sites for glycoprotein gD of Herpes simplex virus type I and is involved in involved in cyclosporine B, CyPB, binding and viral infection, analysis of heparin sulfate structures involve, overview
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
3-OST-3 is involved in 3-OST-2-mediated HSV-1 entry into cells by catalyzing the preceeding step of 3-O-sulfated heparin sulfate modification of receptors
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
modification of the heparan sulfate of glycoprotein D gD receptors required for entry of Herpes simplex virus simplex 1, 3-OST-3 and the herpesvirus entry mediator are involved, but not nectin-1 or nectin-2, in primary croneal fibroblasts, a natural target cell type, while HeLa cells use nectin-1 as the entry receptor, overview, 3-OS HS is required for HSV-1 glycoprotein-induced cell-to-cell fusion of cultured corneal fibroblasts
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
C5 epimerization of some GlcUA into L-iduronic acid, IdoUA, 2-O-sulfation of IdoUA, and 6-O-sulfation of GlcN units
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
3-OST-3A generates a unique heparan sulfate sequence that is predicted to specifically bind envelope glycoprotein D of Herpes Simplex virus type 1, but not antithrombin III
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
isoform 3A modifies two novel tetrasaccharides of 3-O-sulfated heparan sulfate: deltaUA2S-GlcNS-IdoUA2S-S-GlcNH23S and deltaUA2S-GlcNS-IdoUA2S-3S-GlcNH23S6S
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
3-O-sulfonation of heparan sulfate by isoenzyme 3A and 3B generates binding sites for the HSV-1 glycoprotein gD and initiation of virus entry
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
isoforms 3A and 3B, isoform 3A transfers the sulfate group to IdoA2S-GlcNS, 3-O-sulfonation of glucosamine depends on the saccharide structure around the modified glucosamine residue
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
3-O-sulfonation of heparan sulfate by isoenzyme 3A and 3B generates binding sites for the HSV-1 glycoprotein gD and initiation of virus entry
-
?
heparin 3-hydroxy octasaccharide + 3'-phosphoadenylyl sulfate
3-O-sulfated heparin octasaccharide + adenosine 3',5'-bisphosphate
-
i.e. 3-OH octasaccharide, from partially depolymerized heparin, substrate preparation: upscaling by by coupling 3-OST-3 modification with a PAPS regeneration system, overview. Determination of the site of 3-O-sulfation in the octasaccharide at the G6 residue
i.e. DELTAUA2S-GlcNS6S-IdoUA2S-GlcNS6S-IdoUA2S-GlcNS3S6S-IdoUA2SGlcNS6S, where DELTAUA is 4-deoxy-alpha-L-threo-hex-4-enopyranosyluronic acid, GlcN is D-glucosamine, and IdoUA is L-iduronic acid
-
?
heparin 3-hydroxy octasaccharide + 3'-phosphoadenylyl sulfate
3-O-sulfated heparin octasaccharide + adenosine 3',5'-bisphosphate
-
i.e. 3-OH octasaccharide, from partially depolymerized heparin, substrate preparation: upscaling by by coupling 3-OST-3 modification with a PAPS regeneration system, overview. Determination of the site of 3-O-sulfation in the octasaccharide at the G6 residue
i.e. DELTAUA2S-GlcNS6S-IdoUA2S-GlcNS6S-IdoUA2S-GlcNS3S6S-IdoUA2SGlcNS6S, where DELTAUA is 4-deoxy-alpha-L-threo-hex-4-enopyranosyluronic acid, GlcN is D-glucosamine, and IdoUA is L-iduronic acid
-
?
additional information
?
-
-
heparan sulfate chains contain sulfated domains termed the HS fine structure, which gives HS specific binding affinities for extracellular ligands, heparan sulfate 3-O-sulfotransferases catalyze the transfer of sulfate groups to the 3-O position of glucosamine residues of heparan sulfate, a rare, but essential heparan sulfate chain modification required for HS fine structure
-
-
?
additional information
?
-
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HSV-1 glycoprotein-induced cell-to-cell fusion is inhibited by either prior treatment of cells with heparinases or by heparan sulfate preparations enriched in 3-OS HS, expression of HSV-1 gD in cultured corneal fibroblasts renders resistance to HSV-1 entry, overview
-
-
?
additional information
?
-
-
binding to different glycosaminoglycans, overview
-
-
?
additional information
?
-
-
GlcA-beta-(1->4)-GlcNS6S-beta-(1->4)-GlcA-beta-(1->4)-GlcNS6S-alpha-(CH2)5NH2 and GlcA-beta-(1->4)-GlcNS6S-beta-(1->4)-IdoA2S-beta-(1->4)-GlcNS6S-alpha-(CH2)5NH2 are no substrates for isoform 3-OST-3a
-
-
?
additional information
?
-
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isoform 3-OST3a preferentially sulfates the GlcNS6S residue when an iduronic acid residue is located to its reducing side, while 2-O-sulfation of this iduronic acid inhibits the action of isoform 3-OST3a on the target residue
-
-
?
additional information
?
-
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isoform 3OST-3 prefers to sulfate a GlcNS(+/-)6S with an 2-O-sulfo-L-iduronic acid on the nonreducing end
-
-
?
additional information
?
-
usage of a chemoenzymatic synthetic approach to synthesize six 3-O-sulfated oligosaccharides, including three hexasaccharides and three octasaccharides. The synthesis is achieved by rearranging the enzymatic modification sequence to accommodate the substrate specificity of 3-O-sulfotransferase 3, analysis of the impact of 3-O-sulfation on the conformation of the pyranose ring of 2-O-sulfated iduronic acid using NMR spectroscopy, and on the correlation between ring conformation and anticoagulant activity. An octasaccharide interacts with antithrombin and displays anti factor Xa activity. The two 3-O-sulfotransferase (3-OST) isoforms, 3-OST-1 (EC 2.8.2.23) and 3-OST-3, are employed to install the GlcNS3S6S residue into different saccharide sequences. The 3-OST-1 enzyme introduces a sulfation to form a GlcNS3S6S residue that is linked to a GlcA residue at the nonreducing end, forming the disaccharide unit of -GlcAGlcNS3S6S-, whereas the 3-OST-3 enzyme introduces a sulfation to form a GlcNS3S residue that is linked to an IdoA2S residue at the nonreducing end, forming the disaccharide unit of -IdoA2S-GlcNS3S-. Structural and conformational analysis of oligosaccharides, overview
-
-
-
additional information
?
-
-
usage of a chemoenzymatic synthetic approach to synthesize six 3-O-sulfated oligosaccharides, including three hexasaccharides and three octasaccharides. The synthesis is achieved by rearranging the enzymatic modification sequence to accommodate the substrate specificity of 3-O-sulfotransferase 3, analysis of the impact of 3-O-sulfation on the conformation of the pyranose ring of 2-O-sulfated iduronic acid using NMR spectroscopy, and on the correlation between ring conformation and anticoagulant activity. An octasaccharide interacts with antithrombin and displays anti factor Xa activity. The two 3-O-sulfotransferase (3-OST) isoforms, 3-OST-1 (EC 2.8.2.23) and 3-OST-3, are employed to install the GlcNS3S6S residue into different saccharide sequences. The 3-OST-1 enzyme introduces a sulfation to form a GlcNS3S6S residue that is linked to a GlcA residue at the nonreducing end, forming the disaccharide unit of -GlcAGlcNS3S6S-, whereas the 3-OST-3 enzyme introduces a sulfation to form a GlcNS3S residue that is linked to an IdoA2S residue at the nonreducing end, forming the disaccharide unit of -IdoA2S-GlcNS3S-. Structural and conformational analysis of oligosaccharides, overview
-
-
-
additional information
?
-
-
heparan sulfate is a highly sulfated polysaccharide and is present in large quantities on the cell surface and in the extracellular matrix. Herpes simplex virus type 1 utilizes a specialized cell surface HS, known as 3-O-sulfated HS, as an entry receptor to establish infection. 3-O-sulfated octasaccharide has strong activity in blocking HSV-1 infection, stronger than that of the 3-OH octasaccharide, overview
-
-
?
additional information
?
-
-
heparan sulfate is a highly sulfated polysaccharide and is present in large quantities on the cell surface and in the extracellular matrix. Herpes simplex virus type 1 utilizes a specialized cell surface HS, known as 3-O-sulfated HS, as an entry receptor to establish infection. 3-O-sulfated octasaccharide has strong activity in blocking HSV-1 infection, stronger than that of the 3-OH octasaccharide, overview
-
-
?
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3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
heparan sulfate + 3'-phosphoadenylyl sulfate
3-O-sulfated heparan sulfate + adenosine 3',5'-bisphosphate
-
i.e. PAPS
-
-
?
additional information
?
-
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
3-O-sulfation of GlcNH2-containing heparan sulfate by 3-OST-3 provides binding sites for glycoprotein gD of Herpes simplex virus type I and is involved in involved in cyclosporine B, CyPB, binding and viral infection, analysis of heparin sulfate structures involve, overview
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
3-OST-3 is involved in 3-OST-2-mediated HSV-1 entry into cells by catalyzing the preceeding step of 3-O-sulfated heparin sulfate modification of receptors
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
modification of the heparan sulfate of glycoprotein D gD receptors required for entry of Herpes simplex virus simplex 1, 3-OST-3 and the herpesvirus entry mediator are involved, but not nectin-1 or nectin-2, in primary croneal fibroblasts, a natural target cell type, while HeLa cells use nectin-1 as the entry receptor, overview, 3-OS HS is required for HSV-1 glycoprotein-induced cell-to-cell fusion of cultured corneal fibroblasts
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-bisphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
isoform 3A modifies two novel tetrasaccharides of 3-O-sulfated heparan sulfate: deltaUA2S-GlcNS-IdoUA2S-S-GlcNH23S and deltaUA2S-GlcNS-IdoUA2S-3S-GlcNH23S6S
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
3-O-sulfonation of heparan sulfate by isoenzyme 3A and 3B generates binding sites for the HSV-1 glycoprotein gD and initiation of virus entry
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
isoforms 3A and 3B, isoform 3A transfers the sulfate group to IdoA2S-GlcNS, 3-O-sulfonation of glucosamine depends on the saccharide structure around the modified glucosamine residue
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + [heparan sulfate]-glucosamine
adenosine 3',5'-diphosphate + [heparan sulfate]-glucosamine 3-sulfate
3-O-sulfonation of heparan sulfate by isoenzyme 3A and 3B generates binding sites for the HSV-1 glycoprotein gD and initiation of virus entry
-
?
additional information
?
-
-
heparan sulfate chains contain sulfated domains termed the HS fine structure, which gives HS specific binding affinities for extracellular ligands, heparan sulfate 3-O-sulfotransferases catalyze the transfer of sulfate groups to the 3-O position of glucosamine residues of heparan sulfate, a rare, but essential heparan sulfate chain modification required for HS fine structure
-
-
?
additional information
?
-
-
HSV-1 glycoprotein-induced cell-to-cell fusion is inhibited by either prior treatment of cells with heparinases or by heparan sulfate preparations enriched in 3-OS HS, expression of HSV-1 gD in cultured corneal fibroblasts renders resistance to HSV-1 entry, overview
-
-
?
additional information
?
-
-
heparan sulfate is a highly sulfated polysaccharide and is present in large quantities on the cell surface and in the extracellular matrix. Herpes simplex virus type 1 utilizes a specialized cell surface HS, known as 3-O-sulfated HS, as an entry receptor to establish infection. 3-O-sulfated octasaccharide has strong activity in blocking HSV-1 infection, stronger than that of the 3-OH octasaccharide, overview
-
-
?
additional information
?
-
-
heparan sulfate is a highly sulfated polysaccharide and is present in large quantities on the cell surface and in the extracellular matrix. Herpes simplex virus type 1 utilizes a specialized cell surface HS, known as 3-O-sulfated HS, as an entry receptor to establish infection. 3-O-sulfated octasaccharide has strong activity in blocking HSV-1 infection, stronger than that of the 3-OH octasaccharide, overview
-
-
?
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Angioedemas, Hereditary
Novel hereditary angioedema linked with a heparan sulfate 3-O-sulfotransferase 6 gene mutation.
Breast Neoplasms
Silencing HS6ST3 inhibits growth and progression of breast cancer cells through suppressing IGF1R and inducing XAF1.
Breast Neoplasms
The heparan sulfate 3-O-sulfotransferases (HS3ST) 2, 3B and 4 enhance proliferation and survival in breast cancer MDA-MB-231 cells.
Breast Neoplasms
The heparan sulfate sulfotransferase 3-OST3A (HS3ST3A) is a novel tumor regulator and a prognostic marker in breast cancer.
Breast Neoplasms
The Pro-Tumoral Activity of Heparan Sulfate 3-O-Sulfotransferase 3B (HS3ST3B) in Breast Cancer MDA-MB-231 Cells Is Dependent on the Expression of Neuropilin-1.
Carcinogenesis
Silencing HS6ST3 inhibits growth and progression of breast cancer cells through suppressing IGF1R and inducing XAF1.
Carcinoma, Hepatocellular
P120ctn overexpression enhances beta-catenin-E-cadherin binding and down regulates expression of survivin and cyclin D1 in BEL-7404 hepatoma cells.
Carcinoma, Non-Small-Cell Lung
Heparan sulfate D-glucosamine 3-O-sulfotransferase 3B1 is a novel regulator of transforming growth factor-beta-mediated epithelial-to-mesenchymal transition and regulated by miR-218 in nonsmall cell lung cancer.
Chondrosarcoma
Cartilage tumour progression is characterized by an increased expression of heparan sulphate 6O-sulphation-modifying enzymes.
Chondrosarcoma
Epigenetics: methylation-associated repression of heparan sulfate 3-O-sulfotransferase gene expression contributes to the invasive phenotype of H-EMC-SS chondrosarcoma cells.
Colonic Neoplasms
Cyclin-dependent kinase 2/cyclin E complex is involved in p120 catenin (p120ctn)-dependent cell growth control: a new role for p120ctn in cancer.
Colorectal Neoplasms
Aberrant methylation of heparan sulfate glucosamine 3-O-sulfotransferase 2 genes as a biomarker in colorectal cancer.
Colorectal Neoplasms
Retraction. Aberrant methylation to heparan sulfate glucosamine 3-O-sulfotransferase 2 genes as a biomarker in colorectal cancer.
Diabetic Retinopathy
Association of HS6ST3 gene polymorphisms with obesity and triglycerides: gene x gender interaction.
Hepatitis B
[Down-regulation of hepatitis B virus replication by heparin sulfate-D-glucosaminyl-3-O-sulfotransferase 3B1].
Herpes Simplex
A role for heparan sulfate 3-O-sulfotransferase isoform 2 in herpes simplex virus type 1 entry and spread.
Herpes Simplex
A synthetic heparan sulfate oligosaccharide library reveals the novel enzymatic action of D-glucosaminyl 3-O-sulfotransferase-3a.
Herpes Simplex
Biophysical investigation of human heparan sulfate D-glucosaminyl 3-O-sulfotransferase-3A: a mutual effect of enzyme oligomerisation and glycosaminoglycan ligand binding.
Herpes Simplex
Heparan sulfate 3-O-sulfotransferase isoform 5 generates both an antithrombin-binding site and an entry receptor for herpes simplex virus, type 1.
Herpes Simplex
Portable sulphotransferase domain determines sequence specificity of heparan sulphate 3-O-sulphotransferases.
Herpes Simplex
Structural analysis of the sulfotransferase (3-o-sulfotransferase isoform 3) involved in the biosynthesis of an entry receptor for herpes simplex virus 1.
Herpes Simplex
The heparin/heparan sulfate sequence that interacts with cyclophilin B contains a 3-O-sulfated N-unsubstituted glucosamine residue.
Herpes Simplex
Zebrafish encoded 3-O-sulfotransferase-2 generated heparan sulfate serves as a receptor during HSV-1 entry and spread.
Herpes Simplex
Zebrafish-Encoded 3-O-Sulfotransferase-3 Isoform Mediates Herpes Simplex Virus Type 1 Entry and Spread.
Infections
Heparin sulphate D-glucosaminyl 3-O-sulfotransferase 3B1 plays a role in HBV replication.
Leukemia, Myeloid, Acute
Heparan sulfate D-glucosaminyl 3-O-sulfotransferase-3B1 (HS3ST3B1) promotes angiogenesis and proliferation by induction of VEGF in acute myeloid leukemia cells.
Lung Neoplasms
Heparan sulfate D-glucosamine 3-O-sulfotransferase 3B1 is a novel regulator of transforming growth factor-beta-mediated epithelial-to-mesenchymal transition and regulated by miR-218 in nonsmall cell lung cancer.
Malaria
Environmental Correlation Analysis for Genes Associated with Protection against Malaria.
Mastocytoma
Biosynthesis of heparin. Availability of glucosaminyl 3-O-sulfation sites.
Neoplasm Metastasis
Changes in heparan sulfate sulfotransferases and cell-surface heparan sulfate during SKM-1 cells granulocytic differentiation and A549 cells epithelial-mesenchymal transition.
Neoplasms
Cyclin-dependent kinase 2/cyclin E complex is involved in p120 catenin (p120ctn)-dependent cell growth control: a new role for p120ctn in cancer.
Neoplasms
Establishment of a human lung cancer cell line with high metastatic potential to multiple organs: gene expression associated with metastatic potential in human lung cancer.
Neoplasms
Heparan sulfate D-glucosamine 3-O-sulfotransferase 3B1 is a novel regulator of transforming growth factor-beta-mediated epithelial-to-mesenchymal transition and regulated by miR-218 in nonsmall cell lung cancer.
Neoplasms
Heparan sulfate D-glucosaminyl 3-O-sulfotransferase-3B1, a novel epithelial-mesenchymal transition inducer in pancreatic cancer.
Neoplasms
Heparan sulfate proteoglycans undergo differential expression alterations in right sided colorectal cancer, depending on their metastatic character.
Neoplasms
P120-catenin isoforms 1A and 3A differently affect invasion and proliferation of lung cancer cells.
Neoplasms
Silencing HS6ST3 inhibits growth and progression of breast cancer cells through suppressing IGF1R and inducing XAF1.
Neoplasms
The Emerging Roles of Heparan Sulfate 3-O-Sulfotransferases in Cancer.
Neoplasms
The heparan sulfate sulfotransferase 3-OST3A (HS3ST3A) is a novel tumor regulator and a prognostic marker in breast cancer.
Neoplasms
The Heparan Sulfate Sulfotransferases HS2ST1 and HS3ST2 Are Novel Regulators of Breast Cancer Stem-Cell Properties.
Neoplasms
The Pro-Tumoral Activity of Heparan Sulfate 3-O-Sulfotransferase 3B (HS3ST3B) in Breast Cancer MDA-MB-231 Cells Is Dependent on the Expression of Neuropilin-1.
Neurodegenerative Diseases
Genome-wide association study of white matter hyperintensity volume in elderly persons without dementia.
Obesity
Association of HS6ST3 gene polymorphisms with obesity and triglycerides: gene x gender interaction.
Obesity
Genome-wide meta-analysis identifies 11 new loci for anthropometric traits and provides insights into genetic architecture.
Obesity
Identification of a novel 43-bp insertion in the heparan sulfate 6-O-sulfotransferase 3 (HS6ST3) gene and its associations with growth and carcass traits in chickens.
Pancreatic Neoplasms
Heparan sulfate D-glucosaminyl 3-O-sulfotransferase-3B1, a novel epithelial-mesenchymal transition inducer in pancreatic cancer.
Pre-Eclampsia
Placental expression of heparan sulfate 3-O-sulfotransferase-3A1 in normotensive and pre-eclamptic pregnancies.
Stomach Neoplasms
Whole genome and transcriptome sequencing of matched primary and peritoneal metastatic gastric carcinoma.
Virus Diseases
Regulation of CCR5 expression in human placenta: insights from a study of mother-to-child transmission of HIV in Malawi.
Virus Diseases
The heparin/heparan sulfate sequence that interacts with cyclophilin B contains a 3-O-sulfated N-unsubstituted glucosamine residue.
Virus Diseases
Zebrafish-Encoded 3-O-Sulfotransferase-3 Isoform Mediates Herpes Simplex Virus Type 1 Entry and Spread.
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evolution
both isozymes, HS3ST3B and HS3ST2 (EC 2.8.2.29), are differently expressed in monocytes and macrophages depending on the inflammatory environment
evolution
HS3STs represent the largest family of HS-modifying enzymes, and yet the reaction of 3-O-sulfation is the rarest maturation step, when compared to other sulfations. Seven HS3STs have been characterized in human, for which the expression is dependent on cell type and tissue environment
evolution
there are several isoforms in every gene family except that HS2ST gene family has only one isoform
malfunction
-
knocking down enzyme receptor in fibroblasts cells significantly reduces HSV-1 entry and glycoprotein D binding to cells
malfunction
enhanced 3-O-sulfation increases binding to antithrombin, which enhances Factor Xa inhibition, and binding of neuropilin-1
malfunction
expression of the genes encoding HS-modifying enzymes is frequently dysregulated in cancer and other diseases. The enzymes show either anti-oncogenic or tumor-promoting effects. Hypermethylation in proximal regions of the HS3ST3A1 gene in chondrosarcoma. Exposure to a demethylating agent restores its expression, confirming that aberrant methylation has affected its transcription. Re-expression of HS3ST3A reduces the proliferative and migratory properties of chondrosarcoma cells, suggesting that silencing of this enzyme may have contributed to tumor cell growth and invasiveness. The HS3ST3A1 gene is epigenetically repressed in breast cancer cell lines representative of the different molecular subgroups, except in the human epidermal growth factor receptor 2-positive (HER2+) cell lines. Re-expression of the enzyme in luminal A-type MCF-7 and triple negative MDA-MB-231 cell lines reduces cell proliferation in vitro. HS3ST3A is also anti-proliferative in MDA-MB-231 cells. Overexpression of HS3ST3A does not have any effects on the proliferation of MDA-MB-231 cells
malfunction
expression of the genes encoding HS-modifying enzymes is frequently dysregulated in cancer and other diseases. The enzymes show either anti-oncogenic or tumor-promoting effects. Re-expression of HS3ST3B in MDA-MB-231 cells leads to an increase in cell viability and invasion, MDA-MB-231 cells carrying HS3ST3B expression display a significant increase in proliferation and survival. High expression of HS3ST3B in U937 leukemia cells enhances cell proliferation and survival, while its silencing has opposite effects
malfunction
HS3ST3B1 is significantly upregulated in non-small cell lung cancer cell (NSCLC) tissues compared with matched normal tissues. Its expression is also upregulated in mesenchymal phenotype of NSCLC lines compared with epithelial phenotype. When TGF-beta is applied to induce the epithelial phenotype to mesenchymal phenotype, HS3ST3B1 is upregulated compared with previous epithelial cell lines. When HS3ST3B1 is knocked down by specific small interfering RNA in the mesenchymal phenotype, mesenchymal phenotype is transformed to epithelial phenotype. HS3ST3B1 can be targeted by miR-218 in non-small cell lung cancer cells (NSCLC)
malfunction
in HER2+ patients, high level expression of 3-OST3A in tumors is associated with reduced relapse-free survival
metabolism
heparan sulfate (HS) 3-O-sulfation can be catalysed by seven 3-sulfotransferases (HS3STs) in humans, but nevertheless it is the rarest modification in heparan sulfate (HS). Isozymes HS3ST2 (EC 2.8.2.29) and HS3ST3B exhibit the same activity in vitro. But they are differently expressed in macrophages depending on cell environment, which suggests that they may be involved in distinct cellular processes
metabolism
heparan sulfate (HS) is a type of glycosaminoglycan consisting of variably sulfated glucuronic acid or iduronic acid-Nacetylglucosamine repeating disaccharide units, and it can bind plenty of growth factors such as FGF2 and its receptor FGFR1, thereby regulating cancer cell signaling. Divergent fine structures of HS are generated by sulfation catalyzed by HS Ndeacetylase/N-, 2-O-, 6-O-, 3-O-sulfotransferases (correspondingly abbreviated as NDST, HS2ST, HS6ST, HS3ST), epimerization catalyzed by HS C5-epimerase at the Golgi lumen and further desulfation catalyzed by HS 6-O-endosulfatase at the cell surface. There are several isoforms in every gene family except that HS2ST gene family has only one isoform
metabolism
HS3ST-mediated 3-O-sulfation leads to at least two distinct forms of 3-O-sulfated motifs. HS3ST1 and HS3ST5 participate in the generation of anticoagulant-active HS/heparin sequences for antithrombin-III, while HS3ST2, HS3ST3A, HS3ST3B, HS3ST4, and HS3ST6 are described to provide the HS-binding motifs for the glycoprotein gD of herpes simplex virus-1 (HSV-1). HS3ST regulations in cancer cells, cell proliferation, and tumor progression, overview
metabolism
regulation of HS3ST3B1 by miR-218 in cells
metabolism
the sulfation at the 3-OH position of glucosamine is an important modification in forming structural domains for heparan sulfate to enable its biological functions. Seven 3-O-sulfotransferase isoforms in the human genome are involved in the biosynthesis of 3-O-sulfated heparan sulfate
metabolism
ZNF263, a C2H2 zinc finger protein, is a negative transcriptional regulator of heparin and heparan sulfate biosynthesis, which shows distinctively low expression in mast cells compared with other (non-heparin-producing) immune cells. ZNF263 is a transcriptional repressor, and its inactivation or silencing enhances mRNA expression of HS3ST1 (EC 2.8.2.23) and HS3ST3A1, enzymes involved in the formation of binding sites for antithrombin and neuropilin-1 (NRP1) and glycoprotein D of herpes simplex virus, respectively. Heparan sulfate (HS) biosynthetic genes exhibit the ZNF263 consensus motif
physiological function
-
3-O-sulfotransferase-3 isoform mediates Herpes simplex virus type 1 entry and spread
physiological function
-
CHO-K1 cells expressing 3-OST-3 isoform induce membrane protrusions during herpes simplex virus type-1 entry. Enzyme expression is associated with enhanced filopodia induction
physiological function
-
the enzyme is a epithelial-mesenchymal transition inducer in pancreatic cancer. Overexpression of isoform 3-OST-3B1 upregulates Snail expression and triggers its nuclear translocation. The enzyme promotes in vivo angiogenic response
physiological function
-
the enzyme shows a potent inhibitory effect on hepatitis B virus replication and protein expression
physiological function
-
3-OST3A exerts dual activities acting as tumor-suppressor in MCF-7 and MDA-MB-231 cells, or as an oncogenic factor in SKBR-3 cells
physiological function
-
heparan sulfate proteoglycans modified by zebrafish encoded glucosaminyl 3-O sulfotransferase-3 generate a receptor for herpes simplex virus type-1 entry and spread
physiological function
-
isoform 3-OST-3 mediates herpes simplex virus-1 entry and spread
physiological function
isoform HS3ST3B1 positively contributes to acute myeloid leukemia progression. The enzyme increases vascular endothelial growth factor expression and release by leukemia cells and promotes the activation of the Notch-1-Jagged-1, PI3K-AKT and ERK pathways
physiological function
-
the enzyme is involved in bone marrow mesenchymal stromal cell differentiation
physiological function
the enzyme plays a role in pre-eclampsia-associated placental dysfunction
physiological function
heparan sulfate D-glucosamine 3-O-sulfotransferase 3B1 (HS3ST3B1) participates in the biosynthetic steps of heparan sulfate (HS) and targets vascular endothelial growth factor (VEGF) in acute myeloid leukemia (AML) cells, thus contributing to angiogenesis and proliferation of AML cells. HS3ST3B1 plays a role in angiogenesis and the proliferation of cancer cells. Heparan sulfate D-glucosamine 3-O-sulfotransferase 3B1 is a regulator of transforming growth factor-beta-mediated epithelial-to-mesenchymal transition and regulated by miR-218 in nonsmall cell lung cancer
physiological function
heparan sulfate sulfotransferase 3-OST3A (HS3ST3A) is a tumor regulator and a prognostic marker in breast cancer. Heparan sulfate (HS) proteoglycan chains are key components of the breast tumor microenvironment that critically influence the behavior of cancer cells. It is established that abnormal synthesis and processing of HS play a prominent role in tumorigenesis. HS function is mainly controlled by sulfotransferases, cellular and pathophysiological significance for the 3-O-sulfotransferase 3-OST3A (HS3ST3A), catalyzing the final maturation step of HS, in breast cancer, overview. OST3A exert dual activities acting as tumor-suppressor in lumA-michigan cancer foundation (MCF)-7 and triple negative-MD Anderson (MDA) metastatic breast (MB)-231 cells, or as an oncogenic factor in HER2+-SKBR3 cells. Mechanistically, fluorescence-resonance energy transfer-fluorescence-lifetime imaging microscopy experiments indicate that the effects of 3-OST3A in MCF-7 cells are mediated by altered interactions between HS and fibroblast growth factor-7 (FGF-7). This interplay between HS and FGF-7 modulates downstream ERK, AKT and p38 cascades, suggesting that altering 3-O-sulfation affects FGFR2IIIb-mediated signaling
physiological function
isozyme HS3ST3A may have a restricted substrate specificity, making it incapable of synthesizing 3-O-sulfated heparan sulfate (HS) with a tumor-promoting property in MDA-MB-231 cells
physiological function
isozymes HS3ST2, HS3ST3B, and HS3ST4 may exhibit a broader selectivity. In pancreatic cancer cells, high level expression of HS3ST3B is reported to induce epithelial-mesenchymal transition (EMT) and to enhance cell invasiveness in vitro. HS3ST3B is related to an increase in the production of vascular endothelial growth factor (VEGF) and activation of downstream signalling pathways. The tumor-promoting effects of HS3ST2, HS3ST3B, and HS3ST4 are related to sustained activation of Src, Akt, and NF-kappaB, and upregulation of the anti-apoptotic proteins survivin and XIAP. Importantly, all these signalling molecules have been well described to play a critical role in promoting tumor growth and resistance to apoptosis. The tumor-promoting effect of HS3ST3B in leukemia cells is dependent on an autocrine activation of VEGF-dependent signalling pathways. HS3ST3B is described as a regulator of TGF-beta-mediated EMT in NSCLC cells. The tumor-promoting properties of HS3ST3B can be dependent on the formation of signalling complexes containing Nrp1
additional information
to date, only a few ligands are known to selectively interact with 3-O-sulfated motifs, whereas hundreds of HS-binding proteins have been identified
additional information
to date, only a few ligands are known to selectively interact with 3-O-sulfated motifs, whereas hundreds of HS-binding proteins have been identified
additional information
-
to date, only a few ligands are known to selectively interact with 3-O-sulfated motifs, whereas hundreds of HS-binding proteins have been identified
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Multiple isoforms of heparan sulfate D-glucosaminyl 3-O-sulfotransferase
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Cell
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The heparan sulfate sulfotransferase 3-OST3A (HS3ST3A) is a novel tumor regulator and a prognostic marker in breast cancer
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