ライフサイエンスコーパス: sulfatase

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

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

3 c cysteinyl or seryl residue on the relevant sulfatase.

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

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

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

7 unction, beta-glucocerebrosidase and steroid sulfatase.

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

9 one sulfate to estrone by the enzyme estrone sulfatase.

10 he steroid hormone-modulating enzyme steroid sulfatase.

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

12 sulfate and heparin can inhibit iduronate 2-sulfatase.

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

14 ytic metalloenzymes such as phosphatases and sulfatases.

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

16 ranch that contains all known AP superfamily sulfatases.

17 emical characterization of four GAG-specific sulfatases.

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

19 based on genetically conserved mycobacterial sulfatases.

20 on of the catalytic formylglycine residue in sulfatases.

21 ross-feeding mediated by Bacteroides-encoded sulfatases.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 the inhibition of breast cancer cell estrone sulfatase activity.

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

56 thesized and tested as inhibitors of steroid sulfatase activity.

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

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

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

60 The sulfatase also displays a clear kinetic preference for d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 Sulfatases catalyze the cleavage of a variety of cellula

87 Type I sulfatases catalyze the hydrolysis of sulfate esters thr

88 Steroid sulfatase catalyzes the hydrolysis of 3beta-hydroxystero

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 converted to its unconjugated counterpart by sulfatase/glucuronidase.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 Steroid sulfatase inhibitors can alter the metabolism of neurost

157 Steroid sulfatase inhibitors can enhance the concentration of th

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

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

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

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

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

163 N-alkanoyl tyramines as nonsteroidal estrone sulfatase inhibitors.

164 By introducting the steroid sulfatase inhibitory pharmacophore into aromatase inhibi

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

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

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

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

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

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

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

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

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

174 The sulfatase isozyme S gene constitutes a functional and po

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

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

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

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

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

180 The anaerobic sulfatase-maturating enzyme from Clostridium perfringens

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

206 fied bioinformatically through its conserved sulfatase signature sequence directing posttranslational

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

236 triction restores hepatic expression of this sulfatase towards normal.

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

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

239 Although some sulfatases undergo maturation via mechanisms in which ox

240 Sulfatases use a unique formylglycine nucleophile, forme

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

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

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