ライフサイエンスコーパス: sulfatase

1 ylsulfatase B (ARSB; N-acetylgalactosamine-4-sulfatase).

2 he steroid hormone-modulating enzyme steroid sulfatase.

3 e, consistent with inhibition of iduronate 2-sulfatase.

4 sulfate and heparin can inhibit iduronate 2-sulfatase.

5 ed de-sulfation, owing to the induction of a sulfatase.

6 ive form and identify it as a specific HSGAG sulfatase.

7 c cysteinyl or seryl residue on the relevant sulfatase.

8 structure-function investigation of the 2-O-sulfatase.

9 g activities of QSulf1, a novel cell surface sulfatase.

10 ase, aryl sulfatase, and galactose-6-sulfate sulfatase.

11 unction, beta-glucocerebrosidase and steroid sulfatase.

12 and one homologous to N-acetylglucosamine-6-sulfatase.

13 one sulfate to estrone by the enzyme estrone sulfatase.

14 ross-feeding mediated by Bacteroides-encoded sulfatases.

15 smaller than those generated by S-O cleaving sulfatases.

16 ytic metalloenzymes such as phosphatases and sulfatases.

17 ted to heparan-specific N-acetyl glucosamine sulfatases.

18 sidue that is also conserved in carbohydrate sulfatases.

19 and remyelination by blocking OPC-expressed sulfatases.

20 ranch that contains all known AP superfamily sulfatases.

21 the polysaccharide utilisation loci encoded sulfatases.

22 emical characterization of four GAG-specific sulfatases.

23 ncy, as shown before for all other lysosomal sulfatases.

24 based on genetically conserved mycobacterial sulfatases.

25 on of the catalytic formylglycine residue in sulfatases.

26 es have proposed a tumor suppressor role for sulfatase 1 (SULF1) in hepatocellular carcinoma (HCC); h

27 Here, we establish that the secreted Sulfatase 1 (Sulf1) is a major component of the mechanis

28 wn that the heparin-degrading endosulfatase, sulfatase 1 (SULF1), functions as a liver tumor suppress

29 as AKT Serine/Threonine Kinase 3 (AKT3) and Sulfatase 1 (SULF1).

30 The recently identified human sulfatase 1 enzyme (SULF1) desulfates cell surface hepar

31 atent TGF-beta-binding protein 2) and Sulf1 (sulfatase 1), which are translationally regulated by EPR

32 Here, we define a new role for SULFATASE 2 (SULF2) in regulating tissue regeneration an

33 network-based transcriptomics, we identified sulfatase 2 (Sulf2) mRNA in activated human primary OPCs

34 Sulfatase 2 (SULF2), an enzyme with 6-O-desulfatase acti

35 ), pleckstrin domain-containing A3 (PHLDA3), sulfatase 2 (SULF2), B cell translocation gene 2 (BTG2),

36 ssor, but the role of the related sulfatase, sulfatase 2 (SULF2), in liver carcinogenesis remains to

37 aining beta-glucuronidase (100 U mL(-1)) and sulfatase (2.5 U mL(-1)) for 5 min (37 degrees C; pH 6)

38 lls) are 5, (IC50(aromatase) = 0.82 nM; IC50(sulfatase) = 39 nM), and 14, (IC50(aromatase) = 0.77 nM;

39 M), and 14, (IC50(aromatase) = 0.77 nM; IC50(sulfatase) = 590 nM).

40 orted specificities for the F. heparinum 2-O-sulfatase, 6-O-sulfatase, and unsaturated glucuronyl hyd

41 tations in the IDS gene encoding iduronate-2-sulfatase, a crucial enzyme in the lysosomal degradation

42 a catalytic formylglycine residue of steroid sulfatases, a residue that is also conserved in carbohyd

43 We developed a sulfatase-activated probe, 7-hydroxy-9H-(1,3-dichloro-9,

44 The machinery responsible for sulfatase activation is poorly understood in prokaryotes

45 ctive site to catalyze oxidase chemistry for sulfatase activation.

46 Although some GAG-specific bacterial sulfatase activities have been described in the literatu

47 The spectrum of glycosidase and glycoside sulfatase activities in the synovial fluid from patients

48 addition of camalexin complemented both the sulfatase activity and the loss of plant growth promotio

49 The inhibition of MDA-MB-231 cell estrone sulfatase activity by this compound was found to be irre

50 The loss of sulfatase activity has been linked to severe pathophysio

51 N-alkanoyl tyramines to inhibit: (a) estrone sulfatase activity in intact cultures of human breast ca

52 myocardial infarction and detected increased sulfatase activity in myocardial autopsy samples.

53 or diesters, we have measured a promiscuous sulfatase activity in NPP.

54 We observed that sulfatase activity in soil, which can be used as a measu

55 dent microbiota-specific phenotypes: A lower sulfatase activity in the rhizosphere and a loss of plan

56 tic processing is dispensable for hydrolytic sulfatase activity in vitro.

57 normal barrier homeostasis, neither steroid sulfatase activity nor mRNA levels are upregulated follo

58 t compounds (1 microM) inhibited the estrone sulfatase activity of intact MDA-MB-231 cells; however,

59 an metabolic pathways; understanding of endo sulfatase activity questioning the paradigm of how the '

60 the mutant, a significant amount of residual sulfatase activity suggests the presence of FGE-independ

61 SUMF1 demonstrated that the maximum specific sulfatase activity was already attained at lower SUMF1 e

62 The best non-steroidal inhibitor of steroid sulfatase activity was n-lauroyl tryamine phosphate with

63 Although global sulfatase activity was reduced in the mutant, a signific

64 The poorest non-steroidal based inhibitor of sulfatase activity was tetrahydronaphthyl phosphate with

65 ide association analysis of the variation in sulfatase activity we identified a candidate gene encodi

66 NPP exhibits sulfatase activity with k(cat)/K(M) value of 2 x 10(-5)

67 f the requirements for inhibition of estrone sulfatase activity, a number of novel analogues of estro

68 vious observation that AP has a low level of sulfatase activity, further establishing the functional

69 the ability of a compound to inhibit estrone sulfatase activity.

70 the inhibition of breast cancer cell estrone sulfatase activity.

71 ine for the inhibition of MDA-MB-231 estrone sulfatase activity.

72 thesized and tested as inhibitors of steroid sulfatase activity.

73 mbrane vesicles (OMVs) that harbor bacterial sulfatase activity.

74 els were reduced to 85% (aromatase) and 72% (sulfatase) after 24 h.

75 chemical characterization of these potential sulfatases allowed the identification of GAG-specific su

76 The sulfatase also displays a clear kinetic preference for d

77 double mutation, or by overexpression of 6-O sulfatase, an extracellular enzyme which removes 6-O sul

78 In eukaryotic sulfatases, an active site cysteine residue is oxidized

79 hia coli of the Flavobacterium heparinum 2-O-sulfatase and 6-O-sulfatase enzymes that cleave O-sulfat

80 s of the aromatase inhibitor YM511 inhibited sulfatase and aromatase in JEG-3 cells with respective I

81 of the sulfamate derivatives against steroid sulfatase and carbonic anhydrase II (hCAII) was also obs

82 the aqueous medium were then hydrolyzed with sulfatase and extracted with hexane.

83 GALNS, also known as N-acetylgalactosamine-6-sulfatase and GalN6S; E.C. 3.1.6.4) is deficient in pati

84 racterization of 54 glycoside hydrolases, 11 sulfatases and 1 polysaccharide lyase from A. muciniphil

85 ucoidanases, including glycoside hydrolases, sulfatases and carbohydrate esterases, which are primari

86 ases as well as with activators of anaerobic sulfatases and quinohemoprotein amine dehydrogenases.

87 rylsulfatase B (ASB; N-acetylgalactosamine 4-sulfatase) and the subsequent accumulation of the glycos

88 dherin, cyclooxygenase-2, aromatase, steroid sulfatase), and "proliferation factor" (cytokeratin 5, c

89 eta-glucuronidase, alpha-L-iduronidase, aryl sulfatase, and galactose-6-sulfate sulfatase.

90 the enzymes alpha-l-iduronidase, iduronate-2-sulfatase, and N-acetylgalactosamine-4-sulfatase that ar

91 The neurobiological role of steroid sulfatase, and therefore its potential role in ADHD and

92 ties for the F. heparinum 2-O-sulfatase, 6-O-sulfatase, and unsaturated glucuronyl hydrolase, we are

93 ontrast, our pruned enzymes were ineffective sulfatases, and this limited promiscuity may have provid

94 d a transient increase in plasma iduronate-2-sulfatase approaching normal levels and one MPS I subjec

95 omeostasis, and that basal levels of steroid sulfatase are sufficient to accommodate acute insults to

96 Here we show that sulfatases are essential to the utilization of distal co

97 ctively, these data reveal that carbohydrate sulfatases are highly selective for the glycan component

98 Type I sulfatases are inactivated by aryl sulfamates in a time-

99 We hypothesized that sulfatases are instrumental for this bacterium, and rela

100 Bacterial carbohydrate sulfatases are key enzymes in gut colonization, and they

101 These endo-O-sulfatases are transported onto the cell surface to libe

102 Arylsulfatase B (N-acetylgalactosamine-4-sulfatase; ARSB) removes 4-sulfate groups from chondroit

103 acterized by loss of function of the steroid sulfatase arylsulfatase C (STS), to develop a model of c

104 e sulfatase enzymes, N-acetylgalactosamine-4-sulfatase (arylsulfatase B (ASB)) and galactose-6-sulfat

105 With the acceptance of steroid sulfatase as a target for hormone-dependent cancer, nove

106 vide a framework that enables the use of 6-O-sulfatase as a tool for HSGAG structure-activity studies

107 modification of expression of the lysosomal sulfatases ASB and GALNS regulates the content of CSs.

108 mucopolysaccharidosis type VI caused by aryl sulfatase B (ASB) deficiency.

109 After prior desulfation by an endo-sulfatase, BcSulf, to produce unsulfated chondroitin fro

110 Further, a specific sulfatase (BF3086) and glycosyl hydrolase (BF3134) were

111 r the posttranslational activation of type I sulfatases by oxidation of an active-site cysteine to C(

112 Common to all proposed mechanisms of sulfatase catalysis is a sulfated FGly intermediate.

113 Sulfatases catalyze the cleavage of a variety of cellula

114 Type I sulfatases catalyze the hydrolysis of sulfate esters thr

115 Following sulfatase-catalyzed hydrolysis of the PCB sulfates extra

116 Steroid sulfatase catalyzes the hydrolysis of 3beta-hydroxystero

117 SUMF1, a crucial enzyme in the activation of sulfatases, causes a severe chondrodysplasia by augmenti

118 rmed a cluster within a coleopteran-specific sulfatase clade distant from the previously identified G

119 cal posttranslational modification of type I sulfatases, converting cysteine within the motif CxPxR t

120 an aromatase homology model and the steroid sulfatase crystal structure are presented.

121 achromatic leukodystrophy (MLD) and multiple sulfatase deficiency (MSD) displayed a clear deficit in

122 astrocytes to neurodegeneration in multiple sulfatase deficiency (MSD), a severe lysosomal storage d

123 n the rare but devastating disorder multiple sulfatase deficiency (MSD).

124 ss of B. theta OMVs to host immune cells was sulfatase dependent.

125 s amino terminus, where the highly conserved sulfatase domain is located.

126 Recently, we cloned a novel sulfatase domain-containing downregulated gene, HSulf-1,

127 everely disrupted by sulfatase; in addition, sulfatase dramatically inhibited chordomesodermal cell e

128 use of beta-glucuronidase (EC 3.2.1.31) and sulfatase (EC 3.1.6.1) digestion and liquid chromatograp

129 ylsulfatase B (ARSB; N-acetylgalactosamine 4-sulfatase), either innate or acquired, helps to explain

130 th STS protein expression as well as steroid sulfatase enzymatic activity in proportion to the number

131 ycosylation has a key role in the control of sulfatase enzymatic function.

132 In addition, the steroid sulfatase enzyme (STS) is putatively linked to fear reac

133 zable with a combined beta-glucuronidase and sulfatase enzyme preparation.

134 ational evidence that R/PMH is the first non-sulfatase enzyme shown to use a formylglycine as the cat

135 he use of mixtures of beta-glucuronidase and sulfatase enzymes from different sources was investigate

136 suggest that 6-O-sulfotransferase and/or 6-O-sulfatase enzymes may also be implicated.

137 avobacterium heparinum 2-O-sulfatase and 6-O-sulfatase enzymes that cleave O-sulfate groups from spec

138 The sulfatase enzymes, N-acetylgalactosamine-4-sulfatase (ar

139 r activity for lignans, when used with other sulfatase enzymes.

140 ost-translational activation of all B. theta sulfatase enzymes.

141 ities of beta-glucocerebrosidase and steroid sulfatase, enzymes previously linked to barrier maturati

142 Estrone sulfatase (ES; 562 amino acids), one of the key enzymes

143 oliferator-activated receptor-gamma, steroid sulfatase, estrogen sulfonotransferase, and cytochrome P

144 The sulfatase EUD-1 was previously discovered to execute a p

145 ively, these data suggest that WT1-dependent sulfatase expression plays a critical role in maintainin

146 The human sulfatase family has 17 members, 13 of which have been c

147 FGly is the key catalytic residue of the sulfatase family, comprising 17 nonredundant enzymes in

148 equence homology to other members of a large sulfatase family, especially within its amino terminus,

149 dues are conserved to some degree within the sulfatase family.

150 led that mycobacterial strains have distinct sulfatase fingerprints that can be used to judge both th

151 tissue samples with beta-d-glucuronidase and sulfatase, followed by extraction with ethyl acetate and

152 erization of the heparin/heparan sulfate 2-O-sulfatase from Flavobacterium heparinum.

153 A sulfatase from Helix pomatia was purified by affinity ch

154 tensive structure-function analysis of a 6-O-sulfatase from the Gram-negative bacterium Flavobacteriu

155 wise report the molecular cloning of the 2-O-sulfatase from the same bacterium and its recombinant ex

156 , we use structural biology to determine how sulfatases from the human gut microbiota recognize sulfa

157 se caused by N-acetylgalactosamine-6-sulfate sulfatase (GALNS) deficiency.

158 me caused by N-acetylgalactosamine-6-sulfate sulfatase (GALNS) deficiency.

159 tase (arylsulfatase B (ASB)) and galactose-6-sulfatase (GALNS) hydrolyze sulfate groups of CS.

160 eficiency of N-acetylgalactosamine-6-sulfate sulfatase (GALNS), a lysosomal enzyme required for the s

161 eficiency of N-acetylgalactosamine-6-sulfate sulfatase (GALNS), leading to accumulation of keratan su

162 somal enzyme N-acetylgalactosamine-6-sulfate sulfatase (GALNS).

163 The human lysosomal enzyme galactosamine-6-sulfatase (GALNS, also known as N-acetylgalactosamine-6-

164 ica, Europe, and East Asia, whereas Shinella sulfatase gene signatures were first detected in 2020.

165 Bosea/Chelatococcus sulfatase gene signatures were regularly found from 2013

166 Deletions spanning the STS (steroid sulfatase) gene at Xp22.31 are associated with X-linked

167 ed on our previous study, we investigated 10 sulfatase genes induced in the presence of host glycans.

168 Silencing glucosinolate sulfatase genes resulted in the systemic accumulation of

169 methanol/hexane (2 ml/5 ml) and an overnight sulfatase/glucuronidase hydrolysis.

170 converted to its unconjugated counterpart by sulfatase/glucuronidase.

171 whether brief incubation of the plasma with sulfatases/glucuronidases results in complete deconjugat

172 tified 2 autoantigens, N-acetylglucosamine-6-sulfatase (GNS) and filamin A (FLNA), as targets of T an

173 protein extracts revealed that glucosinolate sulfatase (GSS) activity is associated with the gut memb

174 Thus, inhibitors of estrone sulfatase have potential for the treatment of estrogen-d

175 order structures in idursulfase (iduronate-2-sulfatase, I2S) has been accomplished through the use of

176 tide sequence with that of human iduronate 2-sulfatase (IDS) achieved higher transgene expression.

177 mass spectrometry based assay of iduronate-2-sulfatase (IdS) activity for the neonatal detection of m

178 duronidase (IDUA) deficiency and iduronate-2-sulfatase (IDS) deficiency, respectively.

179 TfR-targeted platforms fused to iduronate 2-sulfatase (IDS), a lysosomal enzyme deficient in mucopol

180 axis as a novel downstream effector for this sulfatase in a liver model of tissue regeneration.

181 d the physiological function of the Shinella sulfatase in acesulfame hydrolysis.

182 Both 5 and 14 inhibit aromatase and sulfatase in PMSG pretreated adult female Wistar rats po

183 Here, we describe a new acesulfame sulfatase in Shinella strains isolated from wastewater t

184 rotein gels, allowing the rapid detection of sulfatases in mycobacterial lysates.

185 ity suggests the presence of FGE-independent sulfatases in this organism.

186 rulation movements are severely disrupted by sulfatase; in addition, sulfatase dramatically inhibited

187 s proposed end-products of sulfamate-induced sulfatase inactivation highlights that an imine N-sulfat

188 with established k(cat) values of bacterial sulfatases indicates that these enzymes produce rate enh

189 the therapeutic potential of dual aromatase-sulfatase inhibition in hormone-dependent breast cancer

190 brain cholinergic function and that steroid sulfatase inhibition may become an important tool for en

191 Importantly, pharmacological sulfatase inhibition using PI-88 accelerated oligodendro

192 s studies have demonstrated that the steroid sulfatase inhibitor (p-O-sulfamoyl)-N-tetradecanoyl tyra

193 Administration of the non-steroidal steroid sulfatase inhibitor (p-O-sulfamoyl)-N-tetradecanoyl tyra

194 t of these animals for 24 h with the steroid sulfatase inhibitor COUMATE at a dose (10 mg/kg, p.o.) s

195 e escape latency suggesting that the steroid sulfatase inhibitor did not alter motivation or locomoti

196 innovative dual-targeting aromatase-steroid sulfatase inhibitors (DASIs) and as multitargeting agent

197 pendent cancer, novel dual aromatase-steroid sulfatase inhibitors (DASIs) containing a sulfamate grou

198 ), two series of single agent dual aromatase-sulfatase inhibitors (DASIs) were generated.

199 n the structural diversity of dual aromatase-sulfatase inhibitors (DASIs), we introduced the steroid

200 tor to give a series of novel dual aromatase-sulfatase inhibitors (DASIs).

201 Steroid sulfatase inhibitors can alter the metabolism of neurost

202 Steroid sulfatase inhibitors can enhance the concentration of th

203 t that the chronic administration of steroid sulfatase inhibitors enhance learning and spatial memory

204 upport the concept that nonsteroidal estrone sulfatase inhibitors may be useful as therapeutic agents

205 suggest that the arylsulfamate based steroid sulfatase inhibitors such as COUMATE interfere with the

206 (1) has been studied as a model for steroid sulfatase inhibitors such as Coumate, 667 Coumate, and E

207 have been developed that are potent estrone sulfatase inhibitors, most notably estrone-3-O-sulfamate

208 N-alkanoyl tyramines as nonsteroidal estrone sulfatase inhibitors.

209 By introducting the steroid sulfatase inhibitory pharmacophore into aromatase inhibi

210 Injection of hydrolytic sulfatase into the blastocoels of gastrula stage embryos

211 LSD caused by a deficiency in sulfamidase, a sulfatase involved in the stepwise degradation of glycos

212 s were similar to those of several lysosomal sulfatases involved in degradation of sulfated glycosami

213 al and biochemical studies indicate that 6-O-sulfatase is a predominantly exolytic enzyme that specif

214 Hydrolysis of estrone 3-sulfate by steroid sulfatase is an important additional source of tumor est

215 ype of anteroposterior reduction elicited by sulfatase is distinctly different from commonly generate

216 This type of sulfatase is the first one to be identified in a bacteri

217 ylglycine in the catalytic site of mammalian sulfatases is deficient in the rare but devastating diso

218 l sequence identity of ARSK with other human sulfatases is low (18-22%).

219 The sulfatase isozyme S gene constitutes a functional and po

220 enzymes beta-glucocerebrosidase and steroid sulfatase, markers of barrier maturation, were reduced i

221 We deleted the anaerobic sulfatase maturating enzyme (anSME) from B. theta, which

222 re we present the structures of an anaerobic sulfatase maturating enzyme (anSME), both with and witho

223 tilosin, pyrroloquinoline quinone, anaerobic sulfatase maturating enzyme, and mycofactocin), all of w

224 ture of a SPASM-containing enzyme, anaerobic sulfatase-maturating enzyme (anSME), revealed unexpected

225 The anaerobic sulfatase-maturating enzyme from Clostridium perfringens

226 produced in CHO cell lines: native GALNS and sulfatase-modifier-factor 1 (SUMF1) modified GALNS.

227 storage disorder caused by mutations in the sulfatase modifying factor 1 (SUMF1) gene.

228 atases that are activated by another enzyme, Sulfatase-Modifying Factor 1 (SUMF1), whose inactivation

229 st & Microbe, Hickey et al. (2015) show that sulfatases of Bacteroides thetaiotaomicron are required

230 Desulfation of mucin by pure sulfatase or the sulfatase-producing commensal Bacteroid

231 on of existing kinetic data reveals that the sulfatase PaAstA catalyzes the hydrolysis of sulfamate e

232 the functional interrelationships among the sulfatases, phosphatases, and phosphodiesterases within

233 We recently reported that sulfatases play a key role in the adaptation of a major

234 At the protein level, the flavobacterial 2-O-sulfatase possesses considerable sequence homology to ot

235 esulfation of mucin by pure sulfatase or the sulfatase-producing commensal Bacteroides thetaiotaomicr

236 marked sequence homology with epitopes from sulfatase proteins of the Prevotella sp. and Parabactero

237 d Sulf-2, which are extracellular neutral-pH sulfatases, provide a novel post-synthetic mechanism for

238 1) of the developmentally regulated putative sulfatases QSulf-1 and RSulfFP1 as well as a cDNA encodi

239 at the levels of r2/3 and r7 expressing the sulfatase QSulf1 in quail, or the orthologue CSulf1 in c

240 pothesized that hSulf1, a recently described sulfatase, regulates growth signaling in HCCs.

241 ent classes of enzymes (amylase, lipase, and sulfatase), relying on two distinct mechanisms for coupl

242 Inhibition of S1P1 tyrosine sulfation or sulfatase removal of S1P1 sulfate in mouse CD4 T cells s

243 Type I sulfatases require an unusual co- or post-translational

244 G (ARSG) is the long-sought glucosamine-3-O-sulfatase required to complete the degradation of hepara

245 Bmx nonreceptor tyrosine kinase and steroid sulfatase, respectively) partially regulate the elevated

246 , betaine aldehyde dehydrogenase and choline sulfatase, respectively, are involved in choline metabol

247 Treatment with sulfatase resulted in recovery of this peak as p-cresol,

248 ble to bind both Hep and HS, and periplasmic sulfatases reveal the major specificity determinants for

249 They further suggest that the amount of sulfatase secreted by mucin-foraging bacteria such as B.

250 s allowed the identification of GAG-specific sulfatases selective for the type of saccharide residue

251 ison of the structure of GALNS to paralogous sulfatases shows a wide variety of active-site geometrie

252 fied bioinformatically through its conserved sulfatase signature sequence directing posttranslational

253 mis and hydrolyzed to cholesterol by steroid sulfatase (SSase) in the SC.

254 Mutations in the gene for steroid sulfatase (SSase), are responsible for recessive x-linke

255 S232-homologous repeats flanking the steroid sulfatase ( STS ) gene results in STS deletion, which is

256 approach for the dual inhibition of steroid sulfatase (STS) and 17beta-hydroxysteroid dehydrogenase

257 lecular candidate for this effect is Steroid sulfatase (Sts) as this is located in the pseudoautosoma

258 X-linked ichthyosis is the result of steroid sulfatase (STS) deficiency.

259 sized and evaluated as inhibitors of estrone sulfatase (STS) in comparison to a lead inhibitor, estro

260 linked STS gene, encoding the enzyme steroid sulfatase (STS) influences risk for ADHD.

261 A is exemplified in the discovery of steroid sulfatase (STS) inhibiting lanostane triterpenes (LTTs)

262 gration was blocked by aromatase and steroid sulfatase (STS) inhibitors confirming intracrine synthes

263 nhibitors (DASIs), we introduced the steroid sulfatase (STS) inhibitory pharmacophore to letrozole.

264 Steroid sulfatase (STS) is a key enzyme involved in the biosynth

265 Steroid sulfatase (STS) is a new target for the endocrine therap

266 diol-3,17-O,O-bis-sulfamates inhibit steroid sulfatase (STS), carbonic anhydrase (CA), and, when subs

267 The steroid sulfatase (STS)-mediated desulfation is a critical metab

268 by dual inhibition of aromatase and steroid sulfatase (STS).

269 tial hormone-dependent cancer target steroid sulfatase (STS).

270 IRI was prevented by pretreatment with aryl sulfatase, suggesting the presence of a critical sulfo e

271 in 2), JAG1 (jagged 1), SULF2 (extracellular sulfatase Sulf-2), and TIGAR (TP53-inducible glycolysis

272 in 2), JAG1 (jagged 1), SULF2 (extracellular sulfatase Sulf-2), and TIGAR (TP53-inducible glycolysis

273 otransferases, which add sulfate groups, and sulfatases (Sulf), which remove 6-O-sulfates.

274 Human endo-O-sulfatases (Sulf-1 and Sulf-2) are extracellular heparan

275 philic domain (HD) of the human cell-surface sulfatase Sulf1 against its physiological glycosaminogly

276 The expression of the extracellular sulfatase SULF2 has been associated with increased hepat

277 We identified the sulfatase SULF2 in an in silico secretome analysis in bo

278 tudy, we demonstrated that the extracellular sulfatase, SULF2, an enzyme that regulates multiple HSPG

279 umor suppressor, but the role of the related sulfatase, sulfatase 2 (SULF2), in liver carcinogenesis

280 The extracellular sulfatases (Sulfs) are an evolutionally conserved family

281 e evolved more sophisticated and diverse GAG sulfatases than anticipated and establishes how B. theta

282 ate-2-sulfatase, and N-acetylgalactosamine-4-sulfatase that are used for newborn screening of mucopol

283 G (ARSG) is a recently identified lysosomal sulfatase that was shown to be responsible for the degra

284 Sulf-1 and Sulf-2 are novel extracellular sulfatases that act on internal glucosamine 6-O-sulfate

285 ry step for their degradation, is exerted by sulfatases that are activated by another enzyme, Sulfata

286 c challenge to the polysaccharide lyases and sulfatases that mediate degradation.

287 e sulfated glycans by deploying carbohydrate sulfatases that remove sulfate esters.

288 Despite the biological importance of sulfatases, the mechanisms underlying their ability to r

289 Sulf1 encodes a sulfatase thought to be involved in wingless (Wg) signal

290 he substrate-product relationship of the 2-O-sulfatase to the Delta4,5-glycuronidase and the analytic

291 rts a specific cysteine in newly synthesized sulfatases to formylglycine (FGly).

292 triction restores hepatic expression of this sulfatase towards normal.

293 Sulfatase-treated urine extracts lost >80% of their acti

294 cted values for controls prepared by spiking sulfatase-treated urine with MHPG sulfate.

295 Although some sulfatases undergo maturation via mechanisms in which ox

296 Sulfatases use a unique formylglycine nucleophile, forme

297 the oxidation of Ser72 on AtsA, its cognate sulfatase, via an oxygen-independent mechanism.

298 n with glucuronidase and mixed glucuronidase/sulfatase were used to validate the accuracy of the quan

299 ed Carbohydrate-Active enzymes (CAZymes) and sulfatases were tested, individually or combined, accord

300 ts glucosylceramide to ceramide, and steroid sulfatase, which desulfates cholesterol sulfate, also in

301 lfamates is ineffective against carbohydrate sulfatases, yet can inhibit human gut microbiota (HGM) s