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1 Xanthomonas oryzae pv. oryzae, is a tyrosine sulfotransferase.
2 mmobilized HS chain using D-glucosaminyl 3-O-sulfotransferase.
3 racterize the Drosophila heparan sulfate 2-O-sulfotransferase.
4 similarity to vertebrate heparan sulfate 2-O-sulfotransferase.
5 imerase, heparan 6O-sulfotransferase, and 2O-sulfotransferase.
6 otic metabolism using dehydroepiandrosterone sulfotransferase.
7 hat the purified protein functions as an LPS sulfotransferase.
8 e oxidase, catechol O-methyltransferase, and sulfotransferase.
9 rate selection by SULT2A1 and possibly other sulfotransferases.
10 se/N-sulfotransferases and heparan sulfate O-sulfotransferases.
11 s encoding specific glycosyltransferases and sulfotransferases.
12 g heparan sulfate N-sulfotransferase and 6-O-sulfotransferases.
13 the least sequence conservation between TEG sulfotransferases.
14 ferases, heparan sulfate C(5)-epimerase, and sulfotransferases.
15 its homology to vertebrate glycosaminoglycan sulfotransferases.
16 producing the obligatory cosubstrate for all sulfotransferases.
17 in heparan sulfate generated by specific 3-O-sulfotransferases.
18 neral mechanism of action of heparan sulfate sulfotransferases.
19 in heparan sulfate generated by specific 3-O-sulfotransferases.
21 ied with 4-linked sulfate by either GalNAc-4-sulfotransferase 1 (GalNAc-4-ST1) (CHST8) or GalNAc-4-ST
22 ce deficient in both N-acetylglucosamine-6-O-sulfotransferase 1 (GlcNAc6ST-1) and GlcNAc6ST-2 and fou
25 (HS) modifying enzyme GlcNAc N-deacetylase/N-sulfotransferase 1 (Ndst1) exhibit severe developmental
26 the biosynthetic gene GlcNAc N-deacetylase/N-sulfotransferase 1 (Ndst1) in hepatocytes using the Cre-
27 we generated mice lacking Golgi-associated N-sulfotransferase 1 (Ndst1) that catalyzes sulfation of H
32 fation of glucosamine by heparan sulfate 3-O-sulfotransferase-1 (3-OST-1) is a key modification step
34 Mice deficient in N-acetylglucosamine-6-O-sulfotransferase-1 (GlcNAc6ST-1) failed to synthesize su
35 ransferase (Hs2st(f/f)) and glucosaminyl 6-O-sulfotransferase-1 (Hs6st1(f/f)) and the bacterial Cre r
36 ivation of the gene encoding N-deacetylase/N-sulfotransferase-1 (Ndst1), a key enzyme involved in the
37 mpted targeting of lymphatic N-deacetylase/N-sulfotransferase-1 (Ndst1), a major sulfate-modifying he
38 hat the sulfation activity of tyrosylprotein sulfotransferase-1 (TPST-1) is required for Xenopus dors
39 d at position 21 by expressed tyrosylprotein sulfotransferase-1 and unmodified peptide are both disor
41 Mammary tumor cells lacking N-deacetylase/N-sulfotransferase-1 exhibited reduced toxoplasma infectiv
42 lfation of HS resulting from elevated HS 6-O-sulfotransferase-1 expression in IPF HLF accounted, in p
43 enzyme N-acetyl glucosamine N-deacetylase-N-sulfotransferase-1 in endothelial cells and leukocytes,
44 heparan sulfate initiated by N-deacetylase/N-sulfotransferase-1, but 2-O sulfation and 6-O sulfation
45 d invasion were unchanged in N-deacetylase/N-sulfotransferase-1-inactivated cells as well, but replic
46 subjected to enzymatic modifications by 3-O-sulfotransferases-1 (3-OST1) to provide 3-O-sulfated der
47 re, we identified and validated carbohydrate sulfotransferase 10 (CHST10) as a novel RARgamma target
48 allele and the carbohydrate (chondroitin 4) sulfotransferase 11 (CHST11) locus at 12q23, with a reci
49 s to serve as substrates for human cytosolic sulfotransferase 1A1 (hSULT1A1) was assessed by OH-PCB-d
50 DP-glucuronosyltransferase (UGT), and phenol sulfotransferase 1A1 (SULT1A1) were measured in brain of
53 show that heparan sulfate D-glucosaminyl 3-O-sulfotransferase 2 (HS3ST-2) is a marker for specific su
54 d HS 6-O-sulfotransferase 1 (HS6ST-1) or 6-O-sulfotransferase 2 (HS6ST-2) expression in endothelial c
57 hemopoietic PGD(2) synthase, N-deacetylase/N-sulfotransferase-2 (enzyme involved in heparin biosynthe
58 ncreased expression of bile acid-detoxifying sulfotransferase 2A (Sult2a) and selected bile acid tran
59 ), UDP-glucuronosyltransferase 1a1 (Ugt1a1), sulfotransferase 2a1 (Sult2a1), and organic anion-transp
61 le specialized sulfotransferases such as 2-O-sulfotransferase (2OST) that transfers the sulfo group t
63 ) heparan sulfate (HS)-generating enzyme 3-O sulfotransferase 3 (3-OST-3) but not nectin-1 or nectin-
65 pathophysiological significance for the 3-O-sulfotransferase 3-OST3A (HS3ST3A), catalyzing the final
66 d demonstrate the clinical value of the HS-O-sulfotransferase 3-OST3A as a prognostic marker in HER2+
69 mine residues in heparan sulfate (HS) by 3-O-sulfotransferase (3-OST) is a key substitution that is p
71 f the rare 3-O sulfation catalyzed by HS 3-O-sulfotransferase (3-OST2) is predominantly restricted to
73 se genes, heparan sulfate d-glucosaminyl 3-O-sulfotransferase 3A1 and hyaluronan synthase 2, are also
74 tidase 2, heparan sulfate d-glucosaminyl 3-O-sulfotransferase 3A1, and hyaluronan synthase 2) that ha
77 to be the only C. elegans cytosolic alcohol sulfotransferase, a family of enzymes that catalyze a su
78 l of the protease cascade relies on the Pipe sulfotransferase, a fly homolog of vertebrate glycosamin
79 cule 1 (GlyCAM-1), and high endothelial cell sulfotransferase, a PNAd-generating enzyme that is a tar
81 longs to the HNK1 family of Golgi-associated sulfotransferases, a group of glycosaminoglycan-modifyin
82 dues Gln255 and Lys368 are essential for the sulfotransferase activity and lie within hydrogen bondin
83 T carrying mutations of these residues lacks sulfotransferase activity and the ability to bind 3'-pho
84 of bacterially expressed SSU-1 demonstrates sulfotransferase activity and thus confirms the function
85 tations at these residues led to the loss of sulfotransferase activity but maintained the ability to
87 thelium can support the requirement for Pipe sulfotransferase activity in embryonic DV patterning.
89 mechanism through which spatially restricted sulfotransferase activity in the developing egg chamber
91 regulator of HS-sulfation, increasing the N-sulfotransferase activity of HS-modifying N-deacetylase/
93 O-sulfation in a C41C4.1 mutant and in vitro sulfotransferase activity of recombinant C41C4.1 protein
94 indicating the presence of an additional LPS sulfotransferase activity(ies) in S. meliloti that can c
99 sed on their structural homology to estrogen sulfotransferase and HS 3-O-sulfotransferase isoform 3 (
101 oduct of the gene C41C4.1 as a C. elegans CS-sulfotransferase and renamed it chst-1 (CarboHydrate Sul
102 e at LGS1 codes for an enzyme annotated as a sulfotransferase and show that functional loss of this g
103 this scheme the curacin A PKS employs tandem sulfotransferase and TE domains to form a terminal alken
104 ymes comprising the localization domain of a sulfotransferase and the catalytic domain of a glycosylt
105 proportion of 6-O-sulfation suggest that 6-O-sulfotransferase and/or 6-O-sulfatase enzymes may also b
107 ncluding exostosin-2 (Ext2), N-deacetylase/N-sulfotransferases and heparan sulfate O-sulfotransferase
108 we found that the activities of only Gal 3-O-sulfotransferases and not sialyltransferases were advers
112 glycosidases, nucleotide-sugar transporters, sulfotransferases, and glycan-bearing protein/lipid scaf
121 Gal6ST and C6ST-1 to determine whether these sulfotransferases are required for the generation of end
122 identify GlyCAM-1 and high endothelial cell sulfotransferase as new IKKalpha-dependent target genes,
125 we show that Drosophila melanogaster HS 3-O sulfotransferase-b (Hs3st-B), which catalyzes HS 3-O sul
126 nsferase and renamed it chst-1 (CarboHydrate SulfoTransferase) based on loss of CS-4-O-sulfation in a
127 Asp-95 are conserved in heparan sulfate 3-O-sulfotransferases but not in heparan N-deacetylase/N-sul
128 ur data provide evidence that Pipe acts as a sulfotransferase, but argue against the hypothesis that
130 ransferases, glutathione S-transferases, and sulfotransferases can protect cells against the toxic an
132 effects have been measured for the estrogen sulfotransferase-catalyzed sulfuryl (SO3) transfer from
134 reased KSPG core protein genes and galactose sulfotransferase CHST1 expressions 2-fold; and reduced K
136 te with specific functions using immobilized sulfotransferases combined with a 3'-phosphoadenosine 5'
137 glucosamine, whereas chondroitin sulfate 2-O-sulfotransferase (CS-2OST) transfers the sulfo group to
138 evels for Gal3st1 (also known as cerebroside sulfotransferase [CST]), known to play a crucial role in
139 dysmyelinated mutants including the ceramide sulfotransferase deficient (CST-/-) mouse, which are mor
140 ansferase 1A1, 1A3, 1A4, 1A6, hydroxysteroid sulfotransferase enzyme 2A1, multidrug resistance protei
143 e report an essential role for the oestrogen sulfotransferase (EST or SULT1E1), a conjugating enzyme
144 his transfer reaction, catalyzed by estrogen sulfotransferase (EST), is investigated here in detail.
148 ities between members of the human cytosolic sulfotransferase family correlate with small-molecule bi
149 m 1A2 (SULT1A2) is a member of the cytosolic sulfotransferase family of phase II detoxification enzym
151 tly sulfates, which indicated conjugation by sulfotransferases followed by efflux from the enterocyte
152 g modes of TBBPA and 3-OH-BDE-47 to estrogen sulfotransferase for comparison with binding of the endo
153 Using the teicoplanin aglycone and the 3 sulfotransferases found in one of these gene clusters, m
155 d kinetic properties of three cloned Gal:3-O-sulfotransferases (Gal3STs) ST-2, ST-3, and ST-4 along w
156 olgi transmembrane N-acetylgalactosamine-4-O-sulfotransferase (GalNAc4-ST1), which we show by immunof
157 on of Ndst1, the predominant N-deacetylase/N-sulfotransferase gene essential for the formation of mat
158 SULT2B1 gene is unique among steroid/sterol sulfotransferase genes in that it encodes for two isofor
159 ulfation of endothelial glycoproteins by the sulfotransferase GlcNAc6ST-2 is a regulatory modificatio
160 We applied this strategy to the GlcNAc-6-sulfotransferases GlcNAc6ST-1 and GlcNAc6ST-2, which col
161 re, mice lacking two N-acetylglucosamine-6-O-sulfotransferases (GlcNAc6ST-1 and GlcNAc6ST-2) demonstr
163 emicals, including cytochromes P450 (P450s), sulfotransferases, glutathione transferases, and UDP-glu
164 Bs, including OH-PCB3s, as the substrates of sulfotransferases have not been studied in many organism
166 h substrate in the absence of a carbohydrate sulfotransferase; however, they produced extended GlcNAc
168 for cranial axon patterning, whilst the 2-O-sulfotransferase HS2ST (also known as HS2ST1) is importa
169 Mutant mouse embryos lacking the heparan sulfotransferases Hs2st or Hs6st1 have severe CC phenoty
170 e functions of the Drosophila HS 2-O and 6-O sulfotransferase (Hs2st and Hs6st) genes in FGF-mediated
171 vious study using Drosophila HS 2-O- and 6-O-sulfotransferase (Hs2st and Hs6st) mutants showed that l
172 xP-flanked conditional alleles of uronyl 2-O-sulfotransferase (Hs2st(f/f)) and glucosaminyl 6-O-sulfo
174 Inactivation of heparan sulfate uronyl 2-O-sulfotransferase (Hs2st) in neutrophils substantially re
177 HS biosynthetic enzyme, heparan sulfate 2-O sulfotransferase (Hs2st; an enzyme which catalyzes the 2
178 etically ablated heparan sulfate 2-O and 6-O sulfotransferases (Hs2st, Hs6st1, and Hs6st2) in develop
181 dues, which is generated by glucosaminyl-6-O-sulfotransferases (HS6STs) and selectively removed by ce
182 n of 6-O-sulfate is catalyzed by a family of sulfotransferases (HS6STs), and genetic manipulation of
183 that the HS C-5 epimerase hse-5, the HS 2-O-sulfotransferase hst-2, or the HS 6-O-sulfotransferase h
185 navigation phenotypes in two heparan sulfate sulfotransferase (Hst) mutant embryos, Hs2st-/- and Hs6s
186 C. elegans but also a mutant lacking two HS sulfotransferases (hst-6 hst-2), as we suspected that th
187 ified by co-expression of the human GalNAc 4-sulfotransferase I, which generates SO4-4GalNAcbeta1-4Gl
188 Here we show that inactivation of uronyl 2-O-sulfotransferase in endothelial cells (Hs2st), an enzyme
189 f Toll depends upon the activity of the Pipe sulfotransferase in the ventral region of the follicular
190 ults establish an essential function for the sulfotransferases in L-selectin ligand synthesis and may
191 Human SULT2A1 is one of two predominant sulfotransferases in liver and catalyzes transfer of the
193 ps on HS, which are controlled by various HS sulfotransferases in the Golgi apparatus as well as extr
194 the downregulated genes were chondroitin-4-O-sulfotransferase involved in the synthesis of chondroiti
195 an-1 and hepatocyte-specific inactivation of sulfotransferases involved in heparan sulfate biosynthes
196 for the study of sialyltransferases and 3-O-sulfotransferases involved in the biosynthesis of O-glyc
198 ting that neither of the known galactose 6-O-sulfotransferases is required for ligand synthesis.
200 and kinetics of the interaction between 3-O-sulfotransferase isoform 1 (3-OST-1) and HS have been ex
201 tudy, we report the crystal structure of 3-O-sulfotransferase isoform 1 at 2.5-A resolution in a bina
204 We report a structural study of human HS 3-O-sulfotransferase isoform 3 (3-OST-3), a key sulfotransfe
205 logy to estrogen sulfotransferase and HS 3-O-sulfotransferase isoform 3 (3-OST3), for which crystal s
208 on of both HS3st1 and NDST2 (N-deacetylase/N-sulfotransferase isoform-2) afforded HS with a very low
209 human SULT1A2 that differs from other known sulfotransferase isoforms was developed and used to scre
211 The same vessels also expressed a GlcNAc-6-O-sulfotransferase known as HEC-GlcNAc6ST, which is known
212 Gal6S, namely keratan sulfate galactose 6-O-sulfotransferase (KSGal6ST) and chondroitin 6-O-sulfotra
214 orphisms in UDP-glucuronosyltransferases and sulfotransferases may contribute to variability in phyto
215 sequence and structural similarities, these sulfotransferases modify distinct side chains on the GPA
221 women, indicating changes in N-deacetylase/N-sulfotransferases (NDSTs), the enzymes involved in the i
223 -47) have been suggested to inhibit estrogen sulfotransferase, potentially affecting estrogen metabol
224 form to high-toxicity forms through expanded sulfotransferases, probably as deterrence against predat
226 ided by plastids to serve as a substrate for sulfotransferase reactions in the cytosol and the Golgi
227 ay, the HS structures in the vicinity of the sulfotransferase recognition site are quickly determined
228 structure, we ablated the gene encoding the sulfotransferase responsible for sulfate addition to Gal
229 ession of an engineered human tyrosylprotein sulfotransferase, resulting in antigen-binding and virus
232 chain termination module containing adjacent sulfotransferase (ST) and thioesterase (TE) catalytic do
233 tructure of the ternary complex of bacterial sulfotransferase StaL with the cofactor product 3'-phosp
237 res provide insights into the ability of the sulfotransferase substrate binding pocket to accommodate
238 S biosynthesis involves multiple specialized sulfotransferases such as 2-O-sulfotransferase (2OST) th
239 nsferases but not in heparan N-deacetylase/N-sulfotransferase, suggesting a role for these residues i
241 CH), on thyroid hormone deiodinase (DIO) and sulfotransferase (SULT) activity were investigated using
243 d mRNA expression levels of five major human sulfotransferase (SULT) enzymes in 10 matched pericarcin
244 osomal prodrug oxamniquine is activated by a sulfotransferase (SULT) in the parasitic flatworm Schist
249 hether sulfonation of PAH catechols by human sulfotransferases (SULT) could intercept the catechol in
250 ofactors of N,O-acetyltransferases (NAT) and sulfotransferases (SULT) were added to cytosolic samples
251 In primates but not lower order animals, a sulfotransferase (SULT1A3) is present that can rapidly m
252 uced the expression and activity of estrogen sulfotransferase (SULT1E1 or EST), an enzyme important f
253 n by rifampicin (RIF) represses the estrogen sulfotransferase (SULT1E1) gene in human primary hepatoc
254 elopment of specific substrates for estrogen sulfotransferase (SULT1E1) to produce molecular imaging
255 PXR-mediated gene induction of the phase II sulfotransferase Sult2A1 in the livers of 4-month- and 2
259 allosteric regulation of the human cytosolic sulfotransferase (SULTs) family-13 disease-relevant enzy
265 NSAIDs allosterically inhibit cytosolic sulfotransferases (SULTs) with high specificity and ther
269 viii) Just like LNCaPalpha1,2-FT and Gal-3-O-sulfotransferase T2, the cloned alpha2,3(N)ST which modi
270 gene cluster contains three closely related sulfotransferases (Teg12, -13, and -14) that sulfate tei
272 work demonstrates that SSU-1 is a functional sulfotransferase that likely modifies endocrine signalin
273 -sulfotransferase isoform 3 (3-OST-3), a key sulfotransferase that transfers a sulfuryl group to a sp
274 ynthesis of HS includes numerous specialized sulfotransferases that generate a variety of sulfated sa
275 higher organization level of tyrosylprotein sulfotransferases that may serve for substrate selectivi
276 7 Mb) that contained a pair of overexpressed sulfotransferases that were inversely correlated with ge
277 alized glycosyl transferases, epimerase, and sulfotransferases, this approach should mimic the synthe
278 on by using recombinant human tyrosylprotein sulfotransferases TPST-1 and TPST-2 to modify a peptide
279 lfate (PAPS) synthase-coupled tyrosylprotein sulfotransferase (TPST) catalysis system that involves i
282 mediated by one of two Golgi tyrosylprotein sulfotransferases (TPST-1 and -2) expressed in all mamma
283 modification catalyzed by two tyrosylprotein sulfotransferases (TPST-1 and TPST-2) in the trans-Golgi
284 ion is mediated by two Golgi tyrosyl-protein sulfotransferases (TPST-1 and TPST-2) that are widely ex
285 mediated by one of two Golgi tyrosylprotein sulfotransferases (TPST1 and TPST2) that catalyze the tr
288 urylation is catalyzed by the tyrosylprotein sulfotransferases (TPSTs), and in humans there are two i
289 es mediated by purified human tyrosylprotein sulfotransferases (TPSTs), and unambiguously determined
291 Recent evidence indicates that the same two sulfotransferases underlie the formation of functional P
292 for conditional activation of Golgi-resident sulfotransferases using a chemical inducer of dimerizati
295 1 (DS-epi1), together with the 6-O- and 4-O-sulfotransferases, were highly upregulated in ESCC biops
296 ggested that OH-PCB3s were the substrates of sulfotransferases which catalyzed the formation of PCB3
297 tion of ligand formation depends on the Pipe sulfotransferase, which is expressed in ventral cells of
298 dictated by sulfation patterns controlled by sulfotransferases, which add sulfate groups, and sulfata
299 is directly mediated by cytosolic and Golgi sulfotransferases, which use 3'-phosphoadenosine 5'-phos
300 that clearance of the nucleotide product of sulfotransferases within the Golgi plays an important ro
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