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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 e oxidase, catechol O-methyltransferase, and sulfotransferase.
7 rate selection by SULT2A1 and possibly other sulfotransferases.
8 se/N-sulfotransferases and heparan sulfate O-sulfotransferases.
9 s encoding specific glycosyltransferases and sulfotransferases.
10 g heparan sulfate N-sulfotransferase and 6-O-sulfotransferases.
11 the least sequence conservation between TEG sulfotransferases.
12 ferases, heparan sulfate C(5)-epimerase, and sulfotransferases.
13 its homology to vertebrate glycosaminoglycan sulfotransferases.
14 producing the obligatory cosubstrate for all sulfotransferases.
15 brid N-glycans that especially interact with sulfotransferases.
17 ied with 4-linked sulfate by either GalNAc-4-sulfotransferase 1 (GalNAc-4-ST1) (CHST8) or GalNAc-4-ST
18 ce deficient in both N-acetylglucosamine-6-O-sulfotransferase 1 (GlcNAc6ST-1) and GlcNAc6ST-2 and fou
22 (HS) modifying enzyme GlcNAc N-deacetylase/N-sulfotransferase 1 (Ndst1) exhibit severe developmental
23 the biosynthetic gene GlcNAc N-deacetylase/N-sulfotransferase 1 (Ndst1) in hepatocytes using the Cre-
24 ulfate biosynthetic gene N-deacetylase and N-sulfotransferase 1 (Ndst1) in murine hepatocytes (Ndst1
25 we generated mice lacking Golgi-associated N-sulfotransferase 1 (Ndst1) that catalyzes sulfation of H
29 and decreased or absent heparan sulfate 2-O-sulfotransferase 1 in two of three fibroblast cell lines
30 y in planta co-expression of tyrosyl protein sulfotransferase 1, we installed O-sulfated tyrosine in
32 the two CS synthetic enzymes chondroitin 4-O-sulfotransferase-1 (C4ST-1/CHST11) and chondroitin 6-O-s
33 ferase-1 (C4ST-1/CHST11) and chondroitin 6-O-sulfotransferase-1 (C6ST-1/CHST3) suppressed cell viabil
35 Mice deficient in N-acetylglucosamine-6-O-sulfotransferase-1 (GlcNAc6ST-1) failed to synthesize su
36 ransferase (Hs2st(f/f)) and glucosaminyl 6-O-sulfotransferase-1 (Hs6st1(f/f)) and the bacterial Cre r
37 ivation of the gene encoding N-deacetylase/N-sulfotransferase-1 (Ndst1), a key enzyme involved in the
38 mpted targeting of lymphatic N-deacetylase/N-sulfotransferase-1 (Ndst1), a major sulfate-modifying he
39 hat the sulfation activity of tyrosylprotein sulfotransferase-1 (TPST-1) is required for Xenopus dors
40 d at position 21 by expressed tyrosylprotein sulfotransferase-1 and unmodified peptide are both disor
42 Mammary tumor cells lacking N-deacetylase/N-sulfotransferase-1 exhibited reduced toxoplasma infectiv
43 lfation of HS resulting from elevated HS 6-O-sulfotransferase-1 expression in IPF HLF accounted, in p
44 enzyme N-acetyl glucosamine N-deacetylase-N-sulfotransferase-1 in endothelial cells and leukocytes,
46 -4-sulfotransferase-1, but not of dermatan-4-sulfotransferase-1, accelerates regeneration of zebrafis
47 heparan sulfate initiated by N-deacetylase/N-sulfotransferase-1, but 2-O sulfation and 6-O sulfation
49 d invasion were unchanged in N-deacetylase/N-sulfotransferase-1-inactivated cells as well, but replic
50 n, we studied the effect of chondroitin 4- O-sulfotransferase-1/carbohydrate sulfotransferase-11 (C4S
51 ferase-11 (C4ST-1/Chst-11) and dermatan 4- O-sulfotransferase-1/Chst-14 (D4ST-1/Chst-14) down-regulat
52 subjected to enzymatic modifications by 3-O-sulfotransferases-1 (3-OST1) to provide 3-O-sulfated der
53 re, we identified and validated carbohydrate sulfotransferase 10 (CHST10) as a novel RARgamma target
54 allele and the carbohydrate (chondroitin 4) sulfotransferase 11 (CHST11) locus at 12q23, with a reci
55 droitin 4- O-sulfotransferase-1/carbohydrate sulfotransferase-11 (C4ST-1/Chst-11) and dermatan 4- O-s
56 s to serve as substrates for human cytosolic sulfotransferase 1A1 (hSULT1A1) was assessed by OH-PCB-d
57 DP-glucuronosyltransferase (UGT), and phenol sulfotransferase 1A1 (SULT1A1) were measured in brain of
59 m-specific inhibitors of the human cytosolic sulfotransferase 1A3 (SULT1A3)-the isoform responsible f
62 pha) phosphorylation plays a pivotal role in sulfotransferase 1E1 gene regulation within mouse liver.
63 show that heparan sulfate D-glucosaminyl 3-O-sulfotransferase 2 (HS3ST-2) is a marker for specific su
64 d HS 6-O-sulfotransferase 1 (HS6ST-1) or 6-O-sulfotransferase 2 (HS6ST-2) expression in endothelial c
67 hemopoietic PGD(2) synthase, N-deacetylase/N-sulfotransferase-2 (enzyme involved in heparin biosynthe
68 ncreased expression of bile acid-detoxifying sulfotransferase 2A (Sult2a) and selected bile acid tran
69 ), UDP-glucuronosyltransferase 1a1 (Ugt1a1), sulfotransferase 2a1 (Sult2a1), and organic anion-transp
71 le specialized sulfotransferases such as 2-O-sulfotransferase (2OST) that transfers the sulfo group t
73 ) heparan sulfate (HS)-generating enzyme 3-O sulfotransferase 3 (3-OST-3) but not nectin-1 or nectin-
75 pathophysiological significance for the 3-O-sulfotransferase 3-OST3A (HS3ST3A), catalyzing the final
76 d demonstrate the clinical value of the HS-O-sulfotransferase 3-OST3A as a prognostic marker in HER2+
79 mine residues in heparan sulfate (HS) by 3-O-sulfotransferase (3-OST) is a key substitution that is p
82 se genes, heparan sulfate d-glucosaminyl 3-O-sulfotransferase 3A1 and hyaluronan synthase 2, are also
83 tidase 2, heparan sulfate d-glucosaminyl 3-O-sulfotransferase 3A1, and hyaluronan synthase 2) that ha
86 and synaptic activity.SIGNIFICANCE STATEMENT Sulfotransferase 4A1 (SULT4A1) is a brain-specific sulfo
88 erred to as rs752084147, in the Carbohydrate Sulfotransferase 9 (CHST9) gene, was detected in two fam
89 to be the only C. elegans cytosolic alcohol sulfotransferase, a family of enzymes that catalyze a su
90 l of the protease cascade relies on the Pipe sulfotransferase, a fly homolog of vertebrate glycosamin
92 T carrying mutations of these residues lacks sulfotransferase activity and the ability to bind 3'-pho
93 of bacterially expressed SSU-1 demonstrates sulfotransferase activity and thus confirms the function
94 tations at these residues led to the loss of sulfotransferase activity but maintained the ability to
96 thelium can support the requirement for Pipe sulfotransferase activity in embryonic DV patterning.
98 mechanism through which spatially restricted sulfotransferase activity in the developing egg chamber
100 regulator of HS-sulfation, increasing the N-sulfotransferase activity of HS-modifying N-deacetylase/
102 O-sulfation in a C41C4.1 mutant and in vitro sulfotransferase activity of recombinant C41C4.1 protein
106 sed on their structural homology to estrogen sulfotransferase and HS 3-O-sulfotransferase isoform 3 (
107 oduct of the gene C41C4.1 as a C. elegans CS-sulfotransferase and renamed it chst-1 (CarboHydrate Sul
108 e at LGS1 codes for an enzyme annotated as a sulfotransferase and show that functional loss of this g
109 this scheme the curacin A PKS employs tandem sulfotransferase and TE domains to form a terminal alken
110 proportion of 6-O-sulfation suggest that 6-O-sulfotransferase and/or 6-O-sulfatase enzymes may also b
112 ncluding exostosin-2 (Ext2), N-deacetylase/N-sulfotransferases and heparan sulfate O-sulfotransferase
113 we found that the activities of only Gal 3-O-sulfotransferases and not sialyltransferases were advers
115 d with increased expression of HS6ST1, a 6-O-sulfotransferase, and GLCE, an epimerase that promotes 6
118 glycosidases, nucleotide-sugar transporters, sulfotransferases, and glycan-bearing protein/lipid scaf
124 Gal6ST and C6ST-1 to determine whether these sulfotransferases are required for the generation of end
125 identify GlyCAM-1 and high endothelial cell sulfotransferase as new IKKalpha-dependent target genes,
128 we show that Drosophila melanogaster HS 3-O sulfotransferase-b (Hs3st-B), which catalyzes HS 3-O sul
129 nsferase and renamed it chst-1 (CarboHydrate SulfoTransferase) based on loss of CS-4-O-sulfation in a
130 ur data provide evidence that Pipe acts as a sulfotransferase, but argue against the hypothesis that
132 ransferases, glutathione S-transferases, and sulfotransferases can protect cells against the toxic an
133 effects have been measured for the estrogen sulfotransferase-catalyzed sulfuryl (SO3) transfer from
135 reased KSPG core protein genes and galactose sulfotransferase CHST1 expressions 2-fold; and reduced K
137 te with specific functions using immobilized sulfotransferases combined with a 3'-phosphoadenosine 5'
138 glucosamine, whereas chondroitin sulfate 2-O-sulfotransferase (CS-2OST) transfers the sulfo group to
139 evels for Gal3st1 (also known as cerebroside sulfotransferase [CST]), known to play a crucial role in
140 dysmyelinated mutants including the ceramide sulfotransferase deficient (CST-/-) mouse, which are mor
141 ISPR-Cas9 screening and identified PAPST1, a sulfotransferase encoded by SLC35B2, as a host entry fac
142 ansferase 1A1, 1A3, 1A4, 1A6, hydroxysteroid sulfotransferase enzyme 2A1, multidrug resistance protei
145 e report an essential role for the oestrogen sulfotransferase (EST or SULT1E1), a conjugating enzyme
146 his transfer reaction, catalyzed by estrogen sulfotransferase (EST), is investigated here in detail.
151 nding cassette subfamily G member 8 [ABCG8], sulfotransferase family 2A member 1, cytochrome P450 7A1
152 ities between members of the human cytosolic sulfotransferase family correlate with small-molecule bi
154 tly sulfates, which indicated conjugation by sulfotransferases followed by efflux from the enterocyte
155 g modes of TBBPA and 3-OH-BDE-47 to estrogen sulfotransferase for comparison with binding of the endo
156 Using the teicoplanin aglycone and the 3 sulfotransferases found in one of these gene clusters, m
158 d kinetic properties of three cloned Gal:3-O-sulfotransferases (Gal3STs) ST-2, ST-3, and ST-4 along w
159 olgi transmembrane N-acetylgalactosamine-4-O-sulfotransferase (GalNAc4-ST1), which we show by immunof
160 on of Ndst1, the predominant N-deacetylase/N-sulfotransferase gene essential for the formation of mat
161 SULT2B1 gene is unique among steroid/sterol sulfotransferase genes in that it encodes for two isofor
162 re, mice lacking two N-acetylglucosamine-6-O-sulfotransferases (GlcNAc6ST-1 and GlcNAc6ST-2) demonstr
164 emicals, including cytochromes P450 (P450s), sulfotransferases, glutathione transferases, and UDP-glu
165 several galactose-sulfurylases, carbohydrate-sulfotransferases, glycosyltransferases, and one family
166 Bs, including OH-PCB3s, as the substrates of sulfotransferases have not been studied in many organism
168 h substrate in the absence of a carbohydrate sulfotransferase; however, they produced extended GlcNAc
170 for cranial axon patterning, whilst the 2-O-sulfotransferase HS2ST (also known as HS2ST1) is importa
171 Mutant mouse embryos lacking the heparan sulfotransferases Hs2st or Hs6st1 have severe CC phenoty
172 e functions of the Drosophila HS 2-O and 6-O sulfotransferase (Hs2st and Hs6st) genes in FGF-mediated
173 vious study using Drosophila HS 2-O- and 6-O-sulfotransferase (Hs2st and Hs6st) mutants showed that l
174 xP-flanked conditional alleles of uronyl 2-O-sulfotransferase (Hs2st(f/f)) and glucosaminyl 6-O-sulfo
176 Inactivation of heparan sulfate uronyl 2-O-sulfotransferase (Hs2st) in neutrophils substantially re
179 HS biosynthetic enzyme, heparan sulfate 2-O sulfotransferase (Hs2st; an enzyme which catalyzes the 2
180 etically ablated heparan sulfate 2-O and 6-O sulfotransferases (Hs2st, Hs6st1, and Hs6st2) in develop
183 dues, which is generated by glucosaminyl-6-O-sulfotransferases (HS6STs) and selectively removed by ce
184 n of 6-O-sulfate is catalyzed by a family of sulfotransferases (HS6STs), and genetic manipulation of
185 that the HS C-5 epimerase hse-5, the HS 2-O-sulfotransferase hst-2, or the HS 6-O-sulfotransferase h
187 navigation phenotypes in two heparan sulfate sulfotransferase (Hst) mutant embryos, Hs2st-/- and Hs6s
188 C. elegans but also a mutant lacking two HS sulfotransferases (hst-6 hst-2), as we suspected that th
189 ified by co-expression of the human GalNAc 4-sulfotransferase I, which generates SO4-4GalNAcbeta1-4Gl
190 Here we show that inactivation of uronyl 2-O-sulfotransferase in endothelial cells (Hs2st), an enzyme
191 f Toll depends upon the activity of the Pipe sulfotransferase in the ventral region of the follicular
192 ults establish an essential function for the sulfotransferases in L-selectin ligand synthesis and may
193 Human SULT2A1 is one of two predominant sulfotransferases in liver and catalyzes transfer of the
195 ps on HS, which are controlled by various HS sulfotransferases in the Golgi apparatus as well as extr
196 target genes, Chst2, encodes a carbohydrate sulfotransferase integral to glycosaminoglycan sulfation
198 the downregulated genes were chondroitin-4-O-sulfotransferase involved in the synthesis of chondroiti
199 an-1 and hepatocyte-specific inactivation of sulfotransferases involved in heparan sulfate biosynthes
200 for the study of sialyltransferases and 3-O-sulfotransferases involved in the biosynthesis of O-glyc
202 ting that neither of the known galactose 6-O-sulfotransferases is required for ligand synthesis.
203 and kinetics of the interaction between 3-O-sulfotransferase isoform 1 (3-OST-1) and HS have been ex
204 logy to estrogen sulfotransferase and HS 3-O-sulfotransferase isoform 3 (3-OST3), for which crystal s
207 on of both HS3st1 and NDST2 (N-deacetylase/N-sulfotransferase isoform-2) afforded HS with a very low
209 Mice deficient in sulfatide (cerebroside sulfotransferase knock-out, CST (-/-)) or complex gangli
210 The same vessels also expressed a GlcNAc-6-O-sulfotransferase known as HEC-GlcNAc6ST, which is known
211 Gal6S, namely keratan sulfate galactose 6-O-sulfotransferase (KSGal6ST) and chondroitin 6-O-sulfotra
213 orphisms in UDP-glucuronosyltransferases and sulfotransferases may contribute to variability in phyto
214 sequence and structural similarities, these sulfotransferases modify distinct side chains on the GPA
220 women, indicating changes in N-deacetylase/N-sulfotransferases (NDSTs), the enzymes involved in the i
222 -47) have been suggested to inhibit estrogen sulfotransferase, potentially affecting estrogen metabol
223 form to high-toxicity forms through expanded sulfotransferases, probably as deterrence against predat
225 ided by plastids to serve as a substrate for sulfotransferase reactions in the cytosol and the Golgi
226 structure, we ablated the gene encoding the sulfotransferase responsible for sulfate addition to Gal
227 ession of an engineered human tyrosylprotein sulfotransferase, resulting in antigen-binding and virus
228 formation of these compounds, we studied the sulfotransferase (SOT) gene family in P trichocarpa (PtS
230 chain termination module containing adjacent sulfotransferase (ST) and thioesterase (TE) catalytic do
231 tructure of the ternary complex of bacterial sulfotransferase StaL with the cofactor product 3'-phosp
234 res provide insights into the ability of the sulfotransferase substrate binding pocket to accommodate
235 S biosynthesis involves multiple specialized sulfotransferases such as 2-O-sulfotransferase (2OST) th
237 CH), on thyroid hormone deiodinase (DIO) and sulfotransferase (SULT) activity were investigated using
239 d mRNA expression levels of five major human sulfotransferase (SULT) enzymes in 10 matched pericarcin
240 osomal prodrug oxamniquine is activated by a sulfotransferase (SULT) in the parasitic flatworm Schist
241 idine glucuronic acid transferase (UGT), and sulfotransferase (SULT)) in their biotransformation.
246 hether sulfonation of PAH catechols by human sulfotransferases (SULT) could intercept the catechol in
247 ofactors of N,O-acetyltransferases (NAT) and sulfotransferases (SULT) were added to cytosolic samples
248 In primates but not lower order animals, a sulfotransferase (SULT1A3) is present that can rapidly m
249 uced the expression and activity of estrogen sulfotransferase (SULT1E1 or EST), an enzyme important f
250 n by rifampicin (RIF) represses the estrogen sulfotransferase (SULT1E1) gene in human primary hepatoc
252 elopment of specific substrates for estrogen sulfotransferase (SULT1E1) to produce molecular imaging
254 PXR-mediated gene induction of the phase II sulfotransferase Sult2A1 in the livers of 4-month- and 2
257 xcept for genes encoding aromatase (cyp19b), sulfotransferase (sult2st3), and cyp2k22 that were induc
258 allosteric regulation of the human cytosolic sulfotransferase (SULTs) family-13 disease-relevant enzy
264 NSAIDs allosterically inhibit cytosolic sulfotransferases (SULTs) with high specificity and ther
268 viii) Just like LNCaPalpha1,2-FT and Gal-3-O-sulfotransferase T2, the cloned alpha2,3(N)ST which modi
269 gene cluster contains three closely related sulfotransferases (Teg12, -13, and -14) that sulfate tei
271 ulfotransferase 4A1 (SULT4A1) is a cytosolic sulfotransferase that is highly conserved across species
272 work demonstrates that SSU-1 is a functional sulfotransferase that likely modifies endocrine signalin
273 ynthesis of HS includes numerous specialized sulfotransferases that generate a variety of sulfated sa
274 higher organization level of tyrosylprotein sulfotransferases that may serve for substrate selectivi
275 and DS in the Golgi apparatus is mediated by sulfotransferases that modify sugar chains through trans
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
279 on by using recombinant human tyrosylprotein sulfotransferases TPST-1 and TPST-2 to modify a peptide
280 lfate (PAPS) synthase-coupled tyrosylprotein sulfotransferase (TPST) catalysis system that involves i
283 mediated by one of two Golgi tyrosylprotein sulfotransferases (TPST-1 and -2) expressed in all mamma
284 modification catalyzed by two tyrosylprotein sulfotransferases (TPST-1 and TPST-2) in the trans-Golgi
285 ion is mediated by two Golgi tyrosyl-protein sulfotransferases (TPST-1 and TPST-2) that are widely ex
286 mediated by one of two Golgi tyrosylprotein sulfotransferases (TPST1 and TPST2) that catalyze the tr
289 urylation is catalyzed by the tyrosylprotein sulfotransferases (TPSTs), and in humans there are two i
290 es mediated by purified human tyrosylprotein sulfotransferases (TPSTs), and unambiguously determined
292 Recent evidence indicates that the same two sulfotransferases underlie the formation of functional P
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