ライフサイエンスコーパス: OST

1 OST and drug use during HCV therapy did not impact treat

2 OST isoforms with different catalytic subunits (STT3A ve

3 OST was associated with a 45% increase in odds of viral

4 OST was associated with a 69% increase in recruitment on

5 OST, coupled with the eOST software, can be used to sequ

6 2-OST-deficient embryos have reduced GAG chain sulfation a

7 whereas only one histidine (His168) of CS 2-OST is likely to be critical.

8 Embryos in which maternally encoded 2-OST is knocked down have normal activation of several zy

9 This unique feature of HS 2-OST catalytic residues directed us to characterize the D

10 esion and altered cell cycle regulation in 2-OST-deficient embryos are associated with decreased beta

11 , which can be rescued by re-expression of 2-OST protein.

12 Here, we report that 2-O-sulfotransferase (2-OST) is an essential component of canonical Wnt signalin

13 Together, these results indicate that 2-OST functions within the Wnt pathway, downstream of Wnt

14 -syringes distributed per PWID per year; <20 OST recipients per PWID per year).

15 ed via NSP per PWID annually, and 16 (10-24) OST recipients per 100 PWID.

16 3-OST is present in multiple isoforms, and the polysacchar

17 3-OST isoform 1 (3-OST-1) is the key enzyme for the biosyn

18 3-OST-1 binds with micomolar affinity to HS (K(D) = 2.79 m

19 3-OST-1 was treated with acetic anhydride in either the pr

20 3-OST-1-transduced cells gained the ability to bind to ant

21 3-OST-5 functions in the fibroblast growth factor pathway

22 ate D-glucosaminyl 3-O-sulfotransferase-1 (3-OST-1) (EC 2.8.2.23).

23 on between 3-O-sulfotransferase isoform 1 (3-OST-1) and HS have been examined using surface plasmon r

24 paran sulfate (HS) 3-O-sulfotransferase 1 (3-OST-1) gene into Chinese hamster ovary (CHO) cells.

25 by heparan sulfate 3-O-sulfotransferase-1 (3-OST-1) is a key modification step during the biosynthesi

26 3-OST isoform 1 (3-OST-1) is the key enzyme for the biosynthesis of anticoa

27 oding glucosaminyl 3-O-sulfotransferase-1 (3-OST-1) was introduced into wild-type Chinese hamster ova

28 me heparan sulfate 3-O-sulfotransferase-1 (3-OST-1).

29 of the role of ZF 3-OST isoforms (3-OST-1, 3-OST-5, 3-OST-6, and 3-OST-7) in HSV-1 entry.

30 1 homologous genes, designated as 3-OST-2, 3-OST-3A, and 3-OST-3B as described in the accompanying pa

31 406-, and 390-amino acid enzymes 3-OST-2, 3-OST-3A, and 3-OST-3B, respectively.

32 -generating enzyme 3-O sulfotransferase 3 (3-OST-3) but not nectin-1 or nectin-2.

33 First, 3-O-sulfotransferase-3 (3-OST-3) expression in HIS cells promoted HCMV internaliza

34 f human HS 3-O-sulfotransferase isoform 3 (3-OST-3), a key sulfotransferase that transfers a sulfuryl

35 ucosaminyl-3-O-sulfotransferase isoform 3 (3-OST-3), and it provides binding sites for viral glycopro

36 le of ZF 3-OST isoforms (3-OST-1, 3-OST-5, 3-OST-6, and 3-OST-7) in HSV-1 entry.

37 ypes suggesting that HS(act) or additional 3-OST-1-derived structures may serve alternate biologic ro

38 rain predominant expression of 3-OST-4 and 3-OST-2 transcripts, respectively; whereas, 3-OST-3A and 3

39 e heparan sulfates modified by 3-OST-2 and 3-OST-3A, isoforms of 3-OST-1, do not have anticoagulant a

40 enes, designated as 3-OST-2, 3-OST-3A, and 3-OST-3B as described in the accompanying paper.

41 ripts, respectively; whereas, 3-OST-3A and 3-OST-3B isoforms show widespread expression of multiple t

42 -amino acid enzymes 3-OST-2, 3-OST-3A, and 3-OST-3B, respectively.

43 T isoforms (3-OST-1, 3-OST-5, 3-OST-6, and 3-OST-7) in HSV-1 entry.

44 of 3-OST-1 homologous genes, designated as 3-OST-2, 3-OST-3A, and 3-OST-3B as described in the accomp

45 r the first time that (i) 3-O-sulfation by 3-OST-1 can occur independently of the 2-O-sulfation of ur

46 However, the heparan sulfates modified by 3-OST-2 and 3-OST-3A, isoforms of 3-OST-1, do not have ant

47 tuted glucosamine and the 3-O-sulfation by 3-OST-3A may provide a clue to the potential biological fu

48 reened 10 genes (HPP1, RUNX3, RIZ1, CRBP1, 3-OST-2, APC, TIMP3, p16, MGMT, p14) for promoter hypermet

49 ations when interacting with the different 3-OST isoforms.

50 the 367-, 406-, and 390-amino acid enzymes 3-OST-2, 3-OST-3A, and 3-OST-3B, respectively.

51 te recognition and catalytic mechanism for 3-OST-3.

52 1 entry and spread, while the other group (3-OST-1, -5, and -7) lacks these properties.

53 of amino acid residues that participate in 3-OST-1 interaction with HS substrate and its catalytic ac

54 of a conformational change that occurs in 3-OST-1 upon binding to heparan sulfate.

55 hr256, and Trp283 in 3-OST-3 and Arg268 in 3-OST-1, play important roles in substrate binding and spe

56 s, including Lys259, Thr256, and Trp283 in 3-OST-3 and Arg268 in 3-OST-1, play important roles in sub

57 ntricular noncontraction phenotype seen in 3-OST-7 depleted embryos.

58 Strikingly, BMP misregulation seen in 3-OST-7 morphants also occurs in multiple cardiac noncontr

59 In 3-OST-7 morphants, ventricular contraction can be rescued

60 We propose that individual 3-OST isozymes create distinct modified domains or 'glycoc

61 Instead, 3-OST-1-deficient mice exhibited unanticipated phenotypes

62 analysis of the role of ZF 3-OST isoforms (3-OST-1, 3-OST-5, 3-OST-6, and 3-OST-7) in HSV-1 entry.

63 hat a group of 3-OST gene family isoforms (3-OST-2, -3, -4, and -6) with conserved catalytic and subs

64 By contrast, a second 3-OST family member, 3-OST-6, does not regulate cilia length, but regulates cil

65 Normal 3-OST-7 activity prevents the expansion of BMP signaling i

66 Multiple isoforms of 3-OST are differentially expressed in tissues of zebrafish

67 ng modes used by the different isoforms of 3-OST for distinguishing the fine structures of saccharide

68 We found that a group of 3-OST gene family isoforms (3-OST-2, -3, -4, and -6) with

69 Six different isoforms of 3-OST have been identified that exhibit different substrat

70 , (iii) 2-O-sulfation blocks the action of 3-OST-1 at glucosamine residues located to the reducing si

71 Expression of 3-OST-1 confers upon CHO cells the ability to produce anti

72 Hs3st1(-/-) animals were devoid of 3-OST-1 enzyme activity in plasma and tissue extracts.

73 and characterized the full-length cDNAs of 3-OST-1 homologous genes, designated as 3-OST-2, 3-OST-3A,

74 athway in vivo when the limiting nature of 3-OST-1 is removed; (ii) HS chains from the mutant cells s

75 up of lysine residues in the C-terminus of 3-OST-1 that become more solvent accessible when 3-OST-1 b

76 A truncated mutant of 3-OST-1 that lacked this C-terminal region was expressed a

77 sing differential chemical modification of 3-OST-1 to measure the solvent accessibility of the lysine

78 sis, a CHO cell clone with three copies of 3-OST-1 was chemically mutagenized.

79 The intrinsic fluorescence of 3-OST-1 was increased in the presence of HS, suggesting a

80 rystal structure of the ternary complex of 3-OST-1, 3'-phosphoadenosine 5'-phosphate, and a heptasacc

81 ified by 3-OST-2 and 3-OST-3A, isoforms of 3-OST-1, do not have anticoagulant activity, although thes

82 the 3-OST isoforms and in the mechanism of 3-OST-1-catalyzed biosynthesis of anticoagulant HS.

83 UA2S-AnMan3S6S) that are representative of 3-OST-3 activity.

84 We have obtained the crystal structure of 3-OST-3 at 1.95 A in a ternary complex with 3'-phosphoaden

85 ons to previously determined structures of 3-OST-3 reveal unique binding modes used by the different

86 articipate in the substrate recognition of 3-OST-3.

87 e to the potential biological functions of 3-OST-3A-modified heparan sulfate.

88 lusive and brain predominant expression of 3-OST-4 and 3-OST-2 transcripts, respectively; whereas, 3-

89 ontraction can be rescued by expression of 3-OST-7 in endocardium, or by genetic loss of bmp4.

90 Knockdown of 3-OST-7 in zebrafish uncouples cardiac ventricular contrac

91 cular sarcomere organization downstream of 3-OST-7.

92 Treatment with 6-OST-1, -3, and/or 3-OST-1 afforded two remodeled heparins that met USP hepar

93 ate in vitro with [(35)S]PAPs and purified 3-OST-1.

94 ride library that was modified by purified 3-OST-3 enzyme.

95 Together these results reveal 3-OST-7 as a key component of a novel pathway that constra

96 By contrast, a second 3-OST family member, 3-OST-6, does not regulate cilia leng

97 Selected 3-OST-1 mutants have provided valuable information of amin

98 is catalyzed by the 3-O-sulfotransferase (3-OST) enzyme.

99 The 3-O-sulfotransferase (3-OST) family catalyzes rare modifications of glycosaminog

100 aran sulfate (HS) by 3-O-sulfotransferase (3-OST) is a key substitution that is present in HS sequenc

101 Heparan sulfate 3-O-sulfotransferase (3-OST) is an enzyme that transfers a sulfo group to the 3-

102 lfate D-glucosaminyl 3-O-sulfotransferase (3-OST-1) is the key modification in anticoagulant heparan

103 of the heparan sulfate chains showed that 3-OST-1 generates sequences containing GlcUA-GlcN(SO(3))3(

104 Here, we show that two members of the 3-OST family are required in distinct signaling pathways t

105 anding the substrate specificity among the 3-OST isoforms and in the mechanism of 3-OST-1-catalyzed b

106 Our results demonstrate that the 3-OST-1 enzyme produces the majority of tissue HS(act).

107 Thus, two 3-OST family members cell-autonomously control LR patterni

108 Two 3-OST-3A-modified tetrasaccharides were purified from the

109 1 that become more solvent accessible when 3-OST-1 binds to HS.

110 -OST-2 transcripts, respectively; whereas, 3-OST-3A and 3-OST-3B isoforms show widespread expression

111 1 entry can be recapitulated by certain ZF 3-OST enzymes, a significant step toward the establishment

112 a comprehensive analysis of the role of ZF 3-OST isoforms (3-OST-1, 3-OST-5, 3-OST-6, and 3-OST-7) in

113 understanding of the interactions between 3-OSTs and HS.

114 needle-syringes distributed per PWID and >40 OST recipients per 100 PWID).

115 To understand how 6-OST and other proteins regulate HS(act) biosynthesis, a

116 We discovered in this study that (i) 6-OST-1 is a limiting enzyme in the HS(act) biosynthetic p

117 (iii) in contradiction to the literature, 6-OST-1 can add 6-O-sulfate to GlcNAc residues, especially

118 ion of HS chains from the mutant with pure 6-OST-1 and 3'-phosphoadenosine 5'-phosphosulfate increase

119 excellent substrate for demonstrating that 6-OST-1 is the limiting factor for HS(act) generation in v

120 Transfection of this mutant with 6-OST-1 created a CHO cell line that makes HS, 50% of whic

121 Treatment with 6-OST-1, -3, and/or 3-OST-1 afforded two remodeled heparin

122 -opioid substitution therapy [OST], n = 984; OST, n = 51) evaluating the once-daily, pan-genotypic re

123 rior to sampling were less likely to have an OST-positive isolate (odds ratio, 0.20; 95% confidence i

124 ere, we report the first cross-linking of an OST subunit to a nascent chain that is undergoing transl

125 significantly associated with recovery of an OST-positive isolate (odds ratio, 7.36; 95% confidence i

126 te syringe coverage, linkage to HIV care and OST.

127 countries with high coverage of both NSP and OST (>200 needle-syringes distributed per PWID and >40 O

128 on HIV testing were sparser than for NSP and OST, and very few data were available to estimate ART ac

129 The coordinated interplay between PMTs and OST in vivo is further shown by a comprehensive mass spe

130 ents had isolates that were OST-positive and OST-negative, respectively.

131 in EACs, with RUNX3, HPP1, CRBP1, RIZ1, and OST-2 representing novel methylation targets in EAC and/

132 docking of the bacterial LLO to a bacterial OST suggests that such orientations can enhance binding

133 irst X-ray structure of a complete bacterial OST enzyme, Campylobacter lari PglB, was recently determ

134 D. gigas PglB, which was the only bacterial OST to glycosylate the Fc domain of human immunoglobulin

135 Overall, we find that a subset of bacterial OSTs follow their own rules for acceptor-site specificit

136 n in OST medium supplemented with TGF-beta1 (OST+TGF-beta1) or basal (CTL) medium for up to 21 days.

137 A connection between OST dysregulation and immune disorders was demonstrated

138 Both OST (adjusted hazard, 0.34; 95% CI, .23, .49) and HAART

139 Both OST and HAART independently protected against HIV-relate

140 While both OST and HAART are life-saving treatments, joint administ

141 lable so far), at least 70% were verified by OSTs.

142 ted in vivo activity for 16 of the candidate OSTs.

143 ally complement the Saccharomyces cerevisiae OST, making it an ideal experimental system to study the

144 We project the impact of combining OST, HCNSP, and antiviral treatment on HCV prevalence/in

145 nalysis to evaluate the impact of concurrent OST use on ART-related outcomes among HIV-infected PWID.

146 report the function of the highly conserved OST subunit OST3/6.

147 g, whereas higher-order complexes containing OST, TRAP, and TRAM were stabilized following substrate

148 Current OST increased from 12.2% to 27.7% (P < .001), and 48.4%

149 1 parC mutation, and 59 (39.6%) demonstrated OST.

150 ene (STT3A or STT3B), resides in a different OST complex and has distinct donor and acceptor substrat

151 ped the individual regions between different OST proteins and identified region 2 to influence the sp

152 confidence interval [CI], 9.8, 15.0) during OST and 30.0 (27.1, 33.1) during periods out of OST.

153 uencing data, a computer program, electronic OST or eOST, was developed to automatically identify can

154 countries, and for 60 countries to estimate OST coverage.

155 n, 3 vs. 1; P<.001) and more often exhibited OST (51% vs. 15%; P<.001).

156 l was developed to identify risk factors for OST positivity among patients with FQREC colonization.

157 s potential role as a tentacle to search for OST.

158 here was limited evidence from 6 studies for OST decreasing mortality for PWID on ART (HR, 0.91; 95%

159 sn-Bpa-Thr peptides served as substrates for OST and that photoactivation of these probes in the pres

160 Removing one Osteocalcin allele from OST-PTP-deficient mice corrects their metabolic phenotyp

161 In addition, we now have OSTs for approximately 4300 predicted genes for which no

162 If OST and HCNSP coverage were increased to 40% each (no co

163 ms and contribution of single amino acids in OST interaction with its substrates.

164 ine two distinct mechanistic roles of EL5 in OST-catalyzed glycosylation.

165 e calvarial osteoblasts (MOBs) were grown in OST medium for 28 days as a known mineralizing model for

166 PAVICs were grown in OST medium supplemented with TGF-beta1 (OST+TGF-beta1) o

167 lcified' nodules formed from PAVICs grown in OST+TGF-beta1 medium do not mineralize after 21 days in

168 oscopy imaging revealed that PAVICs grown in OST+TGF-beta1 medium produced abundant extracellular mat

169 PAVICs grown in OST+TGF-beta1 produced nodular structures staining posit

170 nd demonstrate a remarkable heterogeneity in OST composition that may reflect a means for controlling

171 e composition and the function of individual OST subunits are still ill defined in plants.

172 velpatasvir for hepatitis C virus infection, OST did not impact completion, adherence, sustained viro

173 Inhibiting OST with aclacinomycin corrects the glycan and immune de

174 Full-length OST-PTP protein expressed in COS cells has a molecular m

175 ther with the previously described mammalian OST subunits (ribophorins I and II, OST48, and DAD1) int

176 All known mammalian OST subunits (STT3-A, ribophorin I, ribophorin II, OST48

177 tify two potential new subunits of mammalian OST and demonstrate a remarkable heterogeneity in OST co

178 he composition and organization of mammalian OST remain unclear.

179 ctrometry, we now demonstrate that mammalian OST can be isolated from solubilized, actively engaged r

180 The mouse OST-PTP (mOST-PTP) gene is a single copy gene encompassi

181 zed the structural organization of the mouse OST-PTP cDNA and gene and determined its chromosomal loc

182 Nine OST subunits have been identified in yeast.

183 ocumenting the impact of OST, compared to no OST, on ART outcomes.

184 Regional and global estimates of NSP, OST, and HIV testing coverage were also calculated.

185 al, and global estimates of coverage of NSP, OST, HIV testing, ART, and condom programmes for PWID.

186 which correlated well with the appearance of OST-PTP protein and its associated tyrosine phosphatase

187 had no substantial impact on the capacity of OST mutants to survive within IE vegetations.

188 PWID was used to project the combinations of OST, HCNSP, and antiviral treatment required to achieve

189 If coverage of OST and HCNSP is 50% at baseline, similar prevalence red

190 dentify the independent and joint effects of OST and HAART on all-cause as well as drug- and HIV-rela

191 termine the independent and joint effects of OST and HAART on mortality, by cause, within a populatio

192 and there were 86 countries with evidence of OST implementation.

193 Expression of OST-PTP mRNA in primary rat calvarial osteoblasts is tem

194 Our aim was to evaluate the impact of OST and drug use during therapy on completion, adherence

195 6 to November 2014 documenting the impact of OST, compared to no OST, on ART outcomes.

196 ion, confirming the functional importance of OST-PTP expression in osteoblast development.

197 and 30.0 (27.1, 33.1) during periods out of OST.

198 The prevalence of OST differed across study years (P = .01).

199 ystem to study the fundamental properties of OST activity.

200 rected against the 5' untranslated region of OST-PTP results in abrogation of differentiation, confir

201 valuable data for a better understanding of OST-catalyzed N-glycosylation.

202 These findings support the use of OST, and its integration with HIV services, to improve t

203 Oligosaccharyltransferase (OST) catalyzes the cotranslational transfer of high-mann

204 Oligosaccharyltransferase (OST) catalyzes the en bloc transfer of dolichylpyrophosp

205 Oligosaccharyltransferase (OST) is an integral membrane protein that catalyzes N-li

206 s catalyzed by an oligosaccharyltransferase (OST) in the lumen of the endoplasmic reticulum (ER).

207 e PAF complex and oligosaccharyltransferase (OST) complex.

208 n is catalyzed by oligosaccharyltransferase (OST).

209 cting with the ER oligosaccharyltransferase (OST) complex and stabilizing its catalytic integrity.

210 complex that has oligosaccharyltransferase (OST) activity.

211 CD2ad and a human oligosaccharyltransferase (OST) subunit.

212 three full-length oligosaccharyltransferase (OST) genes; two of which, TbSTT3A and TbSTT3B, are expre

213 by the multimeric oligosaccharyltransferase (OST) enzyme.

214 the substrates of oligosaccharyltransferase (OST), the enzyme that catalyzes the en bloc transfer of

215 hetero-oligomeric oligosaccharyltransferase (OST).

216 membrane protein oligosaccharyltransferase (OST).

217 The oligosaccharyltransferase (OST) complex is associated with the TC, and performs the

218 reticulum by the oligosaccharyltransferase (OST) complex.

219 th members of the oligosaccharyltransferase (OST) complex.

220 tilization by the oligosaccharyltransferase (OST) from Trypanosoma cruzi, Entamoeba histolytica, Tric

221 al protein of the oligosaccharyltransferase (OST) glycosylation complex.

222 The oligosaccharyltransferase (OST) preferentially utilizes the fully assembled dolicho

223 o isoforms of the oligosaccharyltransferase (OST) that have different catalytic subunits (STT3A or ST

224 on pathway is the oligosaccharyltransferase (OST), PglB, which transfers preassembled glycans to spec

225 ic subunit of the oligosaccharyltransferase (OST).

226 3B isoform of the oligosaccharyltransferase (OST).

227 at the translocon-oligosaccharyltransferase (OST) complex.

228 ogeneity or restricting treatment to PWID on OST.

229 itial cells (PAVICs) cultured in osteogenic (OST) medium supplemented with transforming growth factor

230 nt nascent chain photocross-linking to other OST subunits was detected in these fully assembled trans

231 ice lacking the protein tyrosine phosphatase OST-PTP are hypoglycemic and are protected from obesity

232 teo-testicular protein tyrosine phosphatase (OST-PTP), expressed in osteoblasts and testis, is a rece

233 on the composition and function of the plant OST complex.

234 rucei encodes three paralogue single-protein OSTs called TbSTT3A, TbSTT3B, and TbSTT3C that can funct

235 y of the tripeptide acceptor for the protist OST complex is influenced by the structure of the oligos

236 tase (PTP) superfamily, osteotesticular PTP (OST-PTP) is a receptor protein whose expression is highl

237 Although highly homologous to the rat OST-PTP cDNA, the mouse cDNA possesses a 74 bp insert in

238 R, 2.15; 95% CI, 1.25-3.71), never receiving OST (AOR, 4.40; 95% CI, 2.27-8.54), no recent methamphet

239 g those receiving (n = 70) and not receiving OST (n = 1882), there was no difference in treatment com

240 ence interval, 87%, >99%) in those receiving OST.

241 the ION studies, 4% (n = 70) were receiving OST.

242 require higher treatment rates for the same OST and HCNSP coverage.

243 The roles of specific OST subunits remained enigmatic.

244 The STT3A OST isoform is primarily responsible for cotranslational

245 ously reported structure of a single-subunit OST enzyme, the Campylobacter lari protein PglB, reveale

246 tions by heparan sulfate O-sulfotransferase (OST) families.

247 The oligonucleotide signature tag (OST) mutant with insertional inactivation of the gene (p

248 hen sequenced to generate ORF sequence tags (OSTs) as a way to verify identity and splicing.

249 So far, ORF sequence tags (OSTs) obtained for all individual clones have allowed ex

250 Octamer sequencing technology (OST) is a primer-directed sequencing strategy in which a

251 in the presence of microsomes abolished the OST activity.

252 on of TREX1 by fs mutations dysregulated the OST complex, leading to free glycan release from dolicho

253 ese distinct and complementary roles for the OST isoforms allow sequential scanning of polypeptides f

254 3H]chitobiose as the donor substrate for the OST-catalyzed reaction.

255 dicate that the nascent chain portion of the OST active site is located in STT3.

256 Here we use a GFP-tagged subunit of the OST complex (GFP-Dad1) that rescues the temperature-sens

257 tion channel-associated STT3A isoform of the OST complex before chain termination.

258 lum and interacts with other subunits of the OST complex.

259 ion of the SWP1/ribophorin II subunit of the OST complex.

260 The K(m) of the OST for the acceptor tripeptide was only slightly enhanc

261 nsion of transcription-coupled repair of the OST gene.

262 The STT3A isoform of the OST is primarily responsible for co-translational glycos

263 This suggests that GFP-Dad1 as part of the OST remains associated with inactive TCs.

264 , the steady-state kinetic properties of the OST were reinvestigated using a proteoliposome assay sys

265 N-glycosylation by the STT3A isoform of the OST, which lacks MagT1, allows efficient modification of

266 the biotinylated glycopeptide product of the OST-catalyzed reaction.

267 munoprecipitation as the STT3 subunit of the OST.

268 ce of a competitive peptide substrate of the OST.

269 Our results demonstrate that the OST from diverse organisms utilizes the in vivo oligo sa

270 soform-specific knockdowns, we show that the OST isoforms cooperate and act sequentially to mediate p

271 In contrast to the OST, the ATases only modify correctly folded polypetides

272 of the ATases is to work in concert with the OST and "select" correctly folded from unfolded/misfolde

273 strate the association of Pmt1-Pmt2 with the OST, the trimeric Sec61, and the tetrameric Sec63 comple

274 Interestingly, the OSTs from Campylobacter coli, Campylobacter upsaliensis,

275 ed the peptide acceptor specificities of the OSTs in vivo using a transgenic glycoprotein reporter sy

276 le exchange and opiate substitution therapy (OST) alone.

277 entions such as opiate substitution therapy (OST) and high-coverage needle and syringe programs (HCNS

278 suggested that opioid substitution therapy (OST) could facilitate PWID's engagement with HIV service

279 eople receiving opioid substitution therapy (OST), but treatment uptake remains low.

280 ogrammes (NSP), opioid substitution therapy (OST), HIV counselling and testing, HIV antiretroviral th

281 RAL trials (non-opioid substitution therapy [OST], n = 984; OST, n = 51) evaluating the once-daily, p

282 These OSTs have different peptide acceptor and lipid-linked ol

283 The database contains this OST information along with data pertinent to the cloning

284 t of HCV treatment if only delivered through OST programs.

285 orientations can enhance binding of LLOs to OST.

286 s measured by the organic solvent tolerance (OST) assay.

287 arC mutations and organic solvent tolerance (OST).

288 cribed strand in endogenous and translocated OST genes, which indicates that efficient repair in exon

289 the heteromeric organic solute transporter (OST) OSTalpha-OSTbeta was examined in human and rodent e

290 dies identify an organic solute transporter (OST) that is generated when two novel gene products are

291 was through 5 opioid substitution treatment (OST) clinics, 2 community health centers, and 1 Aborigin

292 g, linkage to opioid substitution treatment (OST) programs and HIV care during 5 rounds of respondent

293 ies indicated opioid substitution treatment (OST) reduces mortality risk and improves the odds of acc

294 tecture and detailed function of trypanosome OSTs.

295 Scaling up OST and HCNSP substantially reduces the treatment rate r

296 y active DHFR gene and the adjacent upstream OST gene, both of which have been translocated to two ch

297 and immunoprecipitates of this protein using OST-PTP-specific antisera show strong tyrosine phosphata

298 nd Stt3p), the composition of the vertebrate OST was less well defined.

299 d 45 (50.6%) patients had isolates that were OST-positive and OST-negative, respectively.

300 acterized proteins were also copurified with OST.

301 Combining antiviral treatment with OST with HCNSP is critical for achieving substantial red

302 Although the yeast OST is an octamer assembled from nonhomologous subunits