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

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

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

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

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

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

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

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

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

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

15 s provided clinical data for a total of 2466 OST patients.

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

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

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

25 3-OST isoform 1 (3-OST-1) is the key enzyme for the biosynthesis of anticoa

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

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

28 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.

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

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

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

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

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

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

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

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

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

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

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

40 1 entry and spread, while the other group (3-OST-1, -5, and -7) lacks these properties.

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

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

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

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

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

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

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

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

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

50 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 1 that become more solvent accessible when 3-OST-1 binds to HS.

90 1 entry can be recapitulated by certain ZF 3-OST enzymes, a significant step toward the establishment

91 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

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

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

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

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

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

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

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

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

100 of OST, HCV testing, and HCV treatment among OST patients are important public health strategies for

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

102 nagement via telemedicine integrated into an OST program is a feasible model with excellent virologic

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

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

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

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

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

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

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

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

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

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

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

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

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

116 A connection between OST dysregulation and immune disorders was demonstrated

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

118 Both OST and HAART independently protected against HIV-relate

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

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

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

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

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

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

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

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

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

128 1 parC mutation, and 59 (39.6%) demonstrated OST.

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

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

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

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

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

134 d to drastically reduce monitoring costs for OST-based sanitation systems.

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

136 uman embryonic kidney 293 knockout lines for OST isoform-specific catalytic and accessory subunits.

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

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

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

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

141 Because host OSTs attach HSV-1 glycans, NGI-1 might have anti-HSV-1 a

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

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

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

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

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

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

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

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

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

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

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

153 Inhibiting OST with aclacinomycin corrects the glycan and immune de

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

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

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

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

158 he composition and organization of mammalian OST remain unclear.

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

160 ults indicate that it is feasible to monitor OSTs with unmaintained sensors and without plant-specifi

161 Nine OST subunits have been identified in yeast.

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

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

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

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

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

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

168 oyment, younger age, and shorter duration of OST and opioid dependence.

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

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

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

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

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

174 6 to November 2014 documenting the impact of OST, compared to no OST, on ART outcomes.

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

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

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

178 ystem to study the fundamental properties of OST activity.

179 Scaling up the provision of OST, HCV testing, and HCV treatment among OST patients a

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

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

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

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

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

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

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

187 e PAF complex and oligosaccharyltransferase (OST) complex.

188 n is catalyzed by oligosaccharyltransferase (OST).

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

190 CD2ad and a human oligosaccharyltransferase (OST) subunit.

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

192 by the multimeric oligosaccharyltransferase (OST) enzyme.

193 cule inhibitor of oligosaccharyltransferase (OST) complexes STT3A-OST and STT3B-OST, which catalyze c

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

195 hetero-oligomeric oligosaccharyltransferase (OST).

196 membrane protein oligosaccharyltransferase (OST).

197 a subunit of the oligosaccharyltransferase (OST) complex and more specifically of the STT3B complex.

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

199 th members of the oligosaccharyltransferase (OST) complex.

200 reticulum by the oligosaccharyltransferase (OST) complex.

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

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

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

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

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

206 3B isoform of the oligosaccharyltransferase (OST).

207 ic subunit of the oligosaccharyltransferase (OST).

208 at the translocon-oligosaccharyltransferase (OST) complex.

209 nce, and discontinuation between patients on OST and controls as well as between PWID and controls.

210 V treatment outcomes in PWID and patients on OST are similar to those in patients without a history o

211 reatment outcomes among PWID and patients on OST in comparison to control cohorts.

212 HCV reinfection rates among patients on OST ranged from 0.0 to 12.5 per 100 person-years.

213 erence abstracts comprising 1702 patients on OST, 538 PWID, and 19 723 patients who served as control

214 Among patients on OST, the pooled SVR was 90% (95% confidence interval [CI

215 and HCV reinfection in PWID and patients on OST.

216 ogeneity or restricting treatment to PWID on OST.

217 hieve robustness when extrapolating from one OST to another in the absence of plant-specific fine-tun

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

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

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

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

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

223 On-site wastewater treatment plants (OSTs) are usually unattended, so failures often remain u

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

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

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

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

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

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

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

231 er 2014 and June 2016 from randomly selected OST facilities in Germany.

232 The roles of specific OST subunits remained enigmatic.

233 The STT3A OST isoform is primarily responsible for cotranslational

234 gosaccharyltransferase (OST) complexes STT3A-OST and STT3B-OST, which catalyze cotranslational and po

235 date 3) and thus solely dependent upon STT3A-OST for N-glycosylation, NGI-1 treatment resulted in HSV

236 C and gD) was primarily dependent upon STT3A-OST, but to a large extent replaceable by STT3B-OST.

237 nsferase (OST) complexes STT3A-OST and STT3B-OST, which catalyze cotranslational and post-translation

238 , but to a large extent replaceable by STT3B-OST.

239 However, with cells lacking STT3B-OST activity (missing the catalytic subunit STT3B or the

240 Knockouts impairing STT3A- or STT3B-OST activity, by themselves, did not appreciably affect

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

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

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

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

245 valence and HCV incidence rates confirm that OST in Germany is an effective setting both for treating

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

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

248 3H]chitobiose as the donor substrate for the OST-catalyzed reaction.

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

250 conserved interface due to occupation of the OST binding site by the Sec63 protein.

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

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

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

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

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

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

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

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

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

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

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

262 munoprecipitation as the STT3 subunit of the OST.

263 ce of a competitive peptide substrate of the OST.

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

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

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

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

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

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

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

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

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

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

274 and patients on opioid substitution therapy (OST) is still low despite treatment guidelines that advo

275 emedicine in an opioid substitution therapy (OST) program.

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

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

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

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

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

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

282 orientations can enhance binding of LLOs to OST.

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

284 arC mutations and organic solvent tolerance (OST).

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

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

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

288 nts receiving opioid substitution treatment (OST) are needed to estimate the current and future burde

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

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

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

292 tecture and detailed function of trypanosome OSTs.

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

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

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

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

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

298 acterized proteins were also copurified with OST.

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

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

301 protein structures indicates that the yeast OST is unable to interact with the yeast heptameric Sec