ライフサイエンスコーパス: PTS

1 PTS developed in 44 (32.6%) of the 135 patients randomiz

2 PTS scores >/=1, as per the Modified Villalta Scale, wer

3 PTS(Ntr) constitutes a switch through which carbon and n

4 PTS(Ntr) is widely conserved in proteobacteria, highligh

5 PTS-mediated regulation of Mga activity appears to be im

6 generated a mutant strain that lacks all 13 PTS transporters, and from this strain, we created a pan

7 Using our 13 PTS transporter mutant, we also provide the first clear

8 Some proteins lacking a PTS are imported by piggy-backing onto PTS-containing pr

9 of therapy were independent predictors of a PTS score >/=2.

10 In addition to the classic PTS system, a PTS-independent secondary system has been described in w

11 o important concerns in PTS drug design: (a) PTS selectivity and (b) stability to amine oxidases.

12 olved in the utilization of three additional PTS sugars: cellobiose, mannitol, and N-acetyl-D-galacto

13 Here we report two additional PTS-based biofilm regulatory pathways that are active in

14 CES do not offer a better protection against PTS than below-knee CES and are less well tolerated.

15 red component, EI, which is required for all PTS transport, and numerous carbohydrate uptake transpor

16 ored by expressing atxA from an alternative, PTS-independent, promoter.

17 Although PTS affects numerous physiological and pathological proc

18 aqueous micelles derived from the amphiphile PTS are described.

19 d) were large for depression (d = 1.16) and PTS (d = 1.19); moderate for impaired function (d = 0.63

20 impairing its functions in cargo binding and PTS protein import in human cells.

21 adapted standard measures of depression and PTS (primary outcomes) and functional impairment, anxiet

22 n this PTS and measured bacterial growth and PTS gene expression in minimal medium supplemented with

23 s describing the dynamics of nucleotides and PTS (Ntr) enzymes.

24 n identifying gait deviations between PT and PTS was similar and better than Novices.

25 PTS supports the hypothesis that the PTS and PTS-dependent substrates have a central role in sensing

26 outs of genes relating to PEP synthetase and PTS components.

27 eloping recurrent venous thromboembolism and PTS.

28 the two-component regulators, CovR, WalR and PTS/HPr regulation of Mga.

29 e insertionally inactivated the 14 annotated PTS EIIC-encoding genes in the GAS MGAS5005 genome and s

30 sertional mutant library of all 14 annotated PTS permease (EIIC) genes in MGAS5005, the annotated bet

31 senger regulatory network with the bacterial PTS (Ntr) system and investigates how bacteria respond t

32 stic simulation model based on the bacterial PTS system that it is not possible to shorten the lag-ph

33 ignaling, such as cross-talk with the carbon PTS system, here we present our first effort to develop

34 ype 1 or 2 (PTS1/2), three proteins carrying PTS-related peptides, and four proteins that lack conven

35 that a previously uncharacterized cellobiose PTS system is involved in central nervous system infecti

36 We found that the cellobiose-PTS system is induced by cellobiose and characterized th

37 e and galactosyl-glycerol via the cellobiose-PTS system together with a bifunctional 6-phospho-beta-g

38 vantage of the promiscuity of the cellobiose-PTS system.

39 Our findings reveal that the V. cholerae PTS is an additional modulator of the ToxT regulon and d

40 In addition to the classic PTS system, a PTS-independent secondary system has been

41 We found the highly conserved PTS ManLMN contributes to growth on glucose and is also

42 The ability to control PTS, so-called conditional protein splicing (CPS), has l

43 we demonstrate that signals from cytoplasmic PTS components are transmitted directly to the sensory c

44 ts with deep venous thrombosis still develop PTS.

45 own primates exhibit more strongly developed PTS cam mechanisms than extant primates.

46 ormation (MuGENT), we systematically dissect PTS transport in V. cholerae.

47 In Vibrio cholerae, there are 13 distinct PTS transporters.

48 t encode for densely O-glycosylated domains (PTS-repeats) with microbe-binding properties.

49 a result of this study, the percentage of E-PTS sequences similar to functionally annotated ones (BL

50 mbers of the trans-polyprenyl transferase (E-PTS) subgroup in the isoprenoid synthase superfamily, wh

51 fined the carbohydrate specificities of each PTS transporter.

52 ultimeric polyamine derivatives as efficient PTS ligands.

53 Here, we further elucidate PTS control of Vibrio cholerae carbohydrate transport an

54 e thus improve the applicability of existing PTS methods and should enable future efforts to engineer

55 drate metabolism in general, and E. faecalis PTS-gluconate in particular, during inflammation may ide

56 unction recessive mutations of USP18 in five PTS patients from two unrelated families.

57 a relative standard uncertainty of 4.2% for PTS- and 2.4% for RM-based spectral correction when meas

58 depression, -0.43 (95% CI: -0.51, -0.35) for PTS, -0.42 (95% CI: -0.58, -0.27) for functional impairm

59 of 76% and 41% for anxiety, 75% and 37% for PTS, 67% and 22% for functional impairment, and 71% and

60 8, 24, and 36 months, they were assessed for PTS manifestations according to the Villalta scale.

61 Therefore, competition for PTS substrates may be a dominant force in the success of

62 Rs are transcriptional regulators, named for PTS Regulatory Domains (PRDs) subject to phosphorylation

63 51 amino acids (CT51), which is required for PTS protein import.

64 Since the fructose PTS has been shown to impact virulence in several strept

65 Therefore, a functional PTS is not required for subcutaneous skin infection in m

66 where on the chromosome to form a functional PTS transporter.

67 Further, PTS increased the expression of Nrf2 downstream target g

68 transport systems for galactose, a galactose-PTS system and an ABC galactose transporter.

69 involvement of PTS permeases and the general PTS proteins enzyme I and HPr was developed that reveals

70 coding the permease dgaABCD (d-glucosaminate PTS permease components EIIA, EIIB, EIIC, and EIID).

71 l findings that loss of LacR altered glucose-PTS activity and expression of the gene for glucokinase.

72 and di-saccharides that involve the glucose-PTS or glucokinase in their catabolism.

73 ssary for growth in other non-beta-glucoside PTS sugars, such as fructose and mannose.

74 es in MGAS5005, the annotated beta-glucoside PTS transporter (bglP) was found to be crucial for GAS g

75 our results indicate that the beta-glucoside PTS transports salicin and its metabolism can differenti

76 In this study, we harness PTS by rendering association of split intein fragments c

77 fur source along with the formation of [hmim]PTS as probed by NMR, ESI-MS, DART-MS, and HPLC studies.

78 However, PTS-mediated phosphorylation inhibited Mga-dependent tra

79 hotransferase systems, one for sugar import (PTS(sugar)) and one for nitrogen regulation (PTS(Ntr)),

80 re-orientation of leucine 410 side chain in PTS might facilitate the creation of a 2-pocket active s

81 hesized to address two important concerns in PTS drug design: (a) PTS selectivity and (b) stability t

82 ls of the injury and its aftermath influence PTS development.

83 vity that make it more robust than any known PTS system.

84 IIBC (EIIBC(Glc)) in defined media that lack PTS substrates.

85 The glucose- and lactose-PTS permeases, EII(Man) and EII(Lac), respectively, were

86 ering event, and DVT resolution predicted LE-PTS in our cohort.

87 We also demonstrated that deletion of Man-PTS system from a sensitive strain made the cells partia

88 stant to mutacin IV, indicating that the Man-PTS system plays a role in mutacin IV recognition.

89 el) components, and certain fructose/mannose-PTS permeases in the transcriptional regulation of the c

90 Many PTS components are repressed at the transcriptional leve

91 , limiting the general applicability of many PTS-based methods.

92 Because V. cholerae possesses many PTS-independent carbohydrate transporters, the PTS is no

93 he proposal that HPr is not optimal for most PTS permeases but instead represents a compromise with s

94 compromise with suboptimal activity for most PTS permeases.

95 CPr14 shows decreased activity with most PTS permeases relative to HPr, but increases activity wi

96 ection in the primate lineage; and (iv) MUC7 PTS-repeats have evolved recurrently and under adaptive

97 ylation of HPr, inhibited growth on multiple PTS sugars.

98 grow on multiple carbon sources (PTS and non-PTS).

99 Daily administration of PTS disturbed Nrf2/Keap1 interaction and reduced complem

100 this model does not consider all aspects of PTS (Ntr) signaling, such as cross-talk with the carbon

101 ardi-Goutieres syndrome, which is a cause of PTS.

102 re, the time and concentration dependence of PTS performed in nucleo enabled us to examine difference

103 ncy represents the first genetic disorder of PTS caused by dysregulation of the response to type I IF

104 ompression therapy are necessary elements of PTS prevention efforts, but are not sufficient to preven

105 y significant difference in the frequency of PTS (P = .04; 62.5%, 40.0%, and 46.3% in Non-LR, LRneona

106 The cumulative incidence of PTS was 14.2% in active ECS versus 12.7% in placebo ECS

107 and that this requirement is independent of PTS regulation of biofilm formation.

108 n these data, a model for the involvement of PTS permeases and the general PTS proteins enzyme I and

109 there was no difference in the occurrence of PTS (Villalta scale >=5 or ulcer: 49% PCDT versus 51% No

110 is, PCDT did not influence the occurrence of PTS or recurrent venous thromboembolism.

111 ith placebo stockings, for the prevention of PTS.

112 th with below-knee CES for the prevention of PTS.

113 At W2, passersby had the highest rate of PTS symptoms (23.2% [95% CI, 21.4%-25.0%]).

114 set of the conditions in which repression of PTS components is observed, we conclude that additional

115 ce was associated with increased severity of PTS (P < 0.001; RR: 1.6, 95% CI: 1.4-2.2).

116 will not only facilitate cellular studies of PTS, but also paves the way for economical production of

117 , V. cholerae Mlc represses transcription of PTS components in both defined medium and LB broth and t

118 ecent progress, our current understanding of PTS is still in its infancy.

119 operon that exhibited the most influence on PTS sugar metabolism, including mannose.

120 t a few EIIs had a very limited influence on PTS sugar metabolism, whereas others were fairly promisc

121 ing a PTS are imported by piggy-backing onto PTS-containing proteins.

122 from the ubiquitination described for other PTS receptors.

123 nding and is thought to regulate the overall PTS.

124 any bacterial genomes also encode a parallel PTS pathway that includes the EI homolog EI(Ntr), the HP

125 t, maladaptive coping strategies, and parent PTS symptoms.

126 ted HPr functions in concert with particular PTS permeases to prioritize carbohydrate utilization by

127 Modified Villalta Scale (MVS; for pediatric PTS) scores >1; there was an interaction between DVT tri

128 te of PEDOT with poly(ethyleneglycol) (PEDOT(PTS):PEG) in the presence of IL mixtures containing trii

129 ared to the theoretical capacitance of PEDOT(PTS), due to the formation of additional double-layer ca

130 PEG film expands up to ~100% while the PEDOT(PTS) film expanded ~50%.

131 In presence of the mixtures, the PEDOT(PTS):PEG film expands up to ~100% while the PEDOT(PTS) f

132 We examined 12 PEP-PTS transporter component mutants by needle inoculation

133 However, the functional roles of PEP-PTS and AC in the infectious cycle of Borrelia have not

134 oenolpyruvate phosphotransferase system (PEP-PTS) and adenylate cyclase (AC) IV (encoded by BB0723 [c

135 oenolpyruvate phosphotransferase system (PEP-PTS) and for their impact on virulence gene expression.

136 nfection in mice, while all other tested PEP-PTS mutants retained infectivity.

137 organisms, the regulatory effects of the PEP-PTS are mediated by adenylate cyclase and cyclic AMP (cA

138 Overall, the PEP-PTS glucose transporter PtsG appears to play important r

139 hological treatment of severe and persistent PTS via trauma-focused cognitive behavioral therapy; evi

140 studies identify risk factors for persistent PTS, including preinjury psychological problems, peritra

141 f the nitrogen-regulated phosphotransferase (PTS(Ntr)) system, as being important for cyclic-di-GMP p

142 ECS did not prevent PTS after a first proximal DVT, hence our findings do no

143 rsus placebo ECS used for 2 years to prevent PTS after a first proximal DVT in centres in Canada and

144 n efforts, but are not sufficient to prevent PTS in many DVT patients.

145 astic compression stockings (ECS) to prevent PTS were small, single-centre studies without placebo co

146 rious Nrf2 activators tested, pterostilbene (PTS) showed effective Nrf2 activation, as seen by lumino

147 Using 2 recognized PTS scales, clinically significant PTS was reported in 2

148 ly leg symptoms and, over 24 months, reduced PTS severity scores, reduced the proportion of patients

149 PCDT led to reduced PTS severity as shown by lower mean Villalta and Venous

150 PTS(sugar)) and one for nitrogen regulation (PTS(Ntr)), that utilize proteins enzyme I(sugar) (EI(sug

151 play a key role in preventing injury-related PTS by providing "trauma-informed" pediatric care (ie, r

152 Secondary prevention of injury-related PTS often involves parents and focuses on promoting adap

153 These are the first reported PTS transporters in the Thermotogales.

154 As in Escherichia coli, the Rlv3841 PTS(Ntr) system also regulates K(+) homeostasis by trans

155 The promoter targeting sequences (PTS) from Abd-B locus overcome the enhancer blocking eff

156 Severe PTS developed in 3 patients in each group.

157 0.65; 95% CI, 0.45-0.94; P=0.021) or severe PTS (Villalta scale >=15 or ulcer: 8.7% versus 15%; risk

158 , and fewer patients with moderate-or-severe PTS (Villalta scale >=10 or ulcer: 18% versus 28%; risk

159 of patients who developed moderate-or-severe PTS, and resulted in greater improvement in venous disea

160 kle, known as the posterior trochlear shelf (PTS), is well-regarded as a derived crown primate trait,

161 by either the peroxisomal targeting signal (PTS) type 1 or PTS2 pathway.

162 racterized as peroxisomal targeting signals (PTS) residing either at the C terminus (PTS1) or close t

163 Two peroxisomal targeting signals (PTS), the C-terminal PTS1 and the N-terminal PTS2, media

164 of two common peroxisomal targeting signals (PTS).

165 ing one of two peroxisome-targeting signals (PTSs) into the organelle.

166 roteins carry peroxisomal targeting signals (PTSs), PTS1 or PTS2, and are imported into the organelle

167 depend on the peroxisomal targeting signals (PTSs), which require the PTS receptor PEX5, whose defici

168 elated thrombosis and clinically significant PTS 2 years later.

169 ecognized PTS scales, clinically significant PTS was reported in 2 children (1 symptomatic, 1 asympto

170 s unable to grow on multiple carbon sources (PTS and non-PTS).

171 Components of the carbohydrate-specific PTS include the general cytoplasmic components enzyme I

172 show that EIIA(Glc) of the glucose-specific PTS system is also required for the normal decay of thes

173 The mannitol-specific PTS catalyze the uptake and phosphorylation of d-mannito

174 ugh a process called protein trans splicing (PTS).

175 The protein trans-splicing (PTS) activity of naturally split inteins has found wides

176 Protein trans-splicing (PTS) by split inteins has found widespread use in chemic

177 ular chromatin using protein trans-splicing (PTS).

178 ugh a process termed protein trans-splicing (PTS).

179 es by evaluating physical transfer standard (PTS)-based and reference material (RM)-based calibration

180 nts develop persistent posttraumatic stress (PTS) symptoms that are linked to poorer physical and fun

181 for depression and/or posttraumatic stress (PTS).

182 with less clinical experience (PT students [PTS] and Novices).

183 dent in strains containing an intact sucrose PTS.

184 A paralog of EIIA of the sugar PTS system known as ptsN has been purported to regulate

185 Protein tyrosine O-sulfation (PTS) plays a crucial role in extracellular biomolecular

186 Protein tyrosine sulfation (PTS) is a widespread posttranslational modification that

187 llar catalysis using the designer surfactant PTS.

188 lue of sPECAM-1 for postthrombotic syndrome (PTS) after acute DVT.

189 LE-DVT) can lead to postthrombotic syndrome (PTS) and other adverse events.

190 DT) did not prevent postthrombotic syndrome (PTS) in patients with acute proximal deep vein thrombosi

191 (UE-DVT) and of UE postthrombotic syndrome (PTS) is still lacking.

192 e prevention of the postthrombotic syndrome (PTS), a substantial number of patients with deep venous

193 plications, such as postthrombotic syndrome (PTS), from asymptomatic CVC-related thrombosis is unknow

194 prevention of the post-thrombotic syndrome (PTS) in patients with deep vein thrombosis (DVT).

195 Post-thrombotic syndrome (PTS) is a common and burdensome complication of deep ven

196 ns and symptoms of post thrombotic syndrome (PTS), and the risk factors were recorded.

197 Pseudo-TORCH syndrome (PTS) is characterized by microcephaly, enlarged ventricl

198 sphate with recombinant patchoulol synthase (PTS) from Pogostemon cablin afforded a 65:35 mixture of

199 using a nitrogen phosphotransferase system (PTS (Ntr)).

200 e-dependent sugar phosphotransferase system (PTS II transport enzyme).

201 nitrogen-related phosphotransferase system (PTS(Ntr)) of Rhizobium leguminosarum bv.

202 cal nitrogen-type phosphotransferase system (PTS(Ntr)).

203 yruvate-dependent phosphotransferase system (PTS) and an unsaturated glucuronyl hydrolase (Ugl) encod

204 bility to use the phosphotransferase system (PTS) as regulatory machinery to control the energy condi

205 vate-carbohydrate phosphotransferase system (PTS) consists of cascading phosphotransferases that coup

206 The phosphotransferase system (PTS) couples the import of carbohydrates with their phos

207 osphoenolpyruvate phosphotransferase system (PTS) enzymes.

208 yruvate-dependent phosphotransferase system (PTS) exhibited Streptolysin S (SLS)-mediated hemolysis d

209 vate carbohydrate phosphotransferase system (PTS) for cellobiose.

210 ated pathway is a phosphotransferase system (PTS) in E. faecalis strain OG1RF that phosphorylates glu

211 ugar-transporting phosphotransferase system (PTS) in many bacteria.

212 nolpyruvate:sugar phosphotransferase system (PTS) in prokaryotes mediates the uptake and phosphorylat

213 osphoenolpyruvate-phosphotransferase system (PTS) is a global regulatory network connecting sugar upt

214 osphoenolpyruvate phosphotransferase system (PTS) is a highly conserved phosphotransfer cascade that

215 osphoenolpyruvate phosphotransferase system (PTS) is a highly conserved phosphotransfer cascade whose

216 The phosphoenol phosphotransferase system (PTS) is a multicomponent signal transduction cascade tha

217 The bacterial phosphotransferase system (PTS) is a signal transduction pathway that couples phosp

218 osphoenolpyruvate phosphotransferase system (PTS) is the primary mechanism by which bacteria transpor

219 ng a carbohydrate phosphotransferase system (PTS) permease (biofilm and endocarditis-associated perme

220 se-specific sugar phosphotransferase system (PTS) permease (EII(Cel)).

221 ed mannose family phosphotransferase system (PTS) permease, and we designate the genes encoding the p

222 e-dependent sugar:phosphotransferase system (PTS) permeases.

223 tains homology to phosphotransferase system (PTS) regulatory domains (PRDs) found in sugar operon reg

224 apparent fructose phosphotransferase system (PTS) sugar transporter.

225 signals, such as phosphotransferase system (PTS) sugars, biotin, and amino acids, especially cystein

226 The phosphotransferase system (PTS), encompassing EI, HPr, and assorted EII proteins, u

227 r permease of the phosphotransferase system (PTS), which are predicted to compose a Bgl-like sensory

228 vate:carbohydrate phosphotransferase system (PTS).

229 osphoenolpyruvate phosphotransferase system (PTS).

230 ncodes a putative phosphotransferase system (PTS).

231 of the bacterial phosphotransferase system (PTS).

232 ate: carbohydrate phosphotransferase system (PTS).

233 yruvate-dependent phosphotransferase system (PTS).

234 of the bacterial phosphoryl transfer system (PTS).

235 hosphoenolpyruvate:sugar transferase system (PTS).

236 The polyamine transport system (PTS) is a therapeutically relevant target, as it can pro

237 AB pathway (sugar-phosphotransferase system [PTS] permease and sucrose-6-PO(4) hydrolase) constitute

238 ruvate-dependent phosphotransferase systems (PTS).

239 large family of phosphotransferase systems (PTSs).

240 is resistant to the stress, indicating that PTS transporters encoded by both SgrS targets are involv

241 The PTS is initiated by the binding of phosphoenolpyruvate (

242 The PTS locus was widespread in isolates from hospital outbr

243 The PTS modulates virulence gene expression by regulating ex

244 e Frontabdominal-8 (Fab-8) insulator and the PTS element.

245 s that bridge these two subcomplexes and the PTS receptor-recycling machinery.

246 Because the PTS plays a role in colonization of environmental surfac

247 there is no principal difference between the PTS-exerted mechanisms controlling the activities of Bgl

248 We found that the delay is caused by the PTS and an insulator, and it is not specific to the enha

249 that Mga was phosphorylated in vitro by the PTS components EI/HPr at conserved PRD histidines.

250 evidence that carbohydrate transport by the PTS is not essential during infection in an infant mouse

251 o different mechanisms for activation by the PTS were proposed.

252 vailability and positively controlled by the PTS.

253 As a cam, the PTS may increase grasping efficiency in dorsiflexed foot

254 mary route of glucose uptake in E. coli, the PTS plays a key role in regulating central carbon metabo

255 opose a novel biomechanical function for the PTS and model the talus as a cam mechanism.

256 veloped that reveals a critical role for the PTS in CcpA-independent catabolite repression and induct

257 We analyze the model and demonstrate how the PTS (Ntr) system influences (p)ppGpp, c-di-GMP, GMP and

258 To identify the PTS components responsible for this phenotype, we insert

259 dependent biofilm regulatory circuits in the PTS supports the hypothesis that the PTS and PTS-depende

260 In the PTS, phosphoryl groups are transferred from phosphoenolp

261 Comparison of the PTS amino acid sequence with those of other sesquiterpen

262 part due to the regulatory activities of the PTS elements and chromatin boundaries.

263 We then define the role of the PTS in V. cholerae colonization of the adult germfree mo

264 highlighting the possible versatility of the PTS to adapt to strain-specific needs.

265 stablish one of the first known roles of the PTS(Ntr) in P. aeruginosa.

266 Mutation of ptsP encoding EI(Ntr) of the PTS(Ntr) system in Rhizobium leguminosarum strain Rlv384

267 PtsN), the putative regulatory module of the PTS(Ntr).

268 l as with other cytoplasmic complexes of the PTS, highlights a unifying mechanism for recognition of

269 A phosphoryl transfer protein of the PTS, NPr, homologous to HPr, functions to regulate nitro

270 that is common to all sugar branches of the PTS.

271 cid similarity to Enzyme IIB proteins of the PTS.

272 ocation into peroxisomes depends only on the PTS receptors and Pex14p and not on intraperoxisomal Pex

273 targeting signals (PTSs), which require the PTS receptor PEX5, whose deficiency causes fatal human p

274 dditionally, malate utilization requires the PTS transporter EI enzyme (PtsI), as a PtsI(-) mutant fa

275 that despite different modes of sensing, the PTS- and receptor-mediated signals have similar regulato

276 in the PTS supports the hypothesis that the PTS and PTS-dependent substrates have a central role in

277 However, we find that the PTS is essential for colonization of the germfree adult

278 r closest relatives, we demonstrate that the PTS is most strongly developed in extant taxa that habit

279 Therefore, we propose that the PTS permease BepA is directly implicated in E. faecium p

280 vironmental changes communicated through the PTS (Ntr) system.

281 n the absence of phosphotransfer through the PTS(Ntr), but only in the presence of enzyme II (PtsN),

282 S-independent carbohydrate transporters, the PTS is not essential for bacterial growth in vitro.

283 approaches that support a model in which the PTS proteins HPr and Enzyme I (EI) are required for tran

284 containing deletions/point mutations in this PTS and measured bacterial growth and PTS gene expressio

285 In this PTS(Ntr), the protein HPr is phosphorylated on histidine

286 ted to encode the enzyme IID subunit of this PTS, significantly impaired the ability of E. faecium to

287 We hypothesize that this PTS permits growth in gluconate, facilitates E. faecalis

288 Thus, PTS-mediated phosphorylation of Mga may allow the bacter

289 ing is essential for efficient chemotaxis to PTS substrates and may be common to most bacteria.

290 Survival analysis showed that the time to PTS score >/=1 significantly differed among group (log-r

291 for five conserved histidine residues in two PTS regulatory domains and an EIIA-like domain also prov

292 rence, characteristics, and predictors of UE-PTS in a cohort of children with objectively confirmed U

293 In conclusion, pediatric UE-PTS frequency and severity depend on UE-DVT pathogenesis

294 Line-related UE-PTS has a more benign course, particularly in neonates.

295 Finally, we used PTS to semisynthesize a native histone modification, H2B

296 P-dependent transport might be regulated via PTS(Ntr) responding to the cellular energy charge.

297 The primary outcome was PTS diagnosed at 6 months or later using Ginsberg's crit

298 One mechanism by which PTS promotes virulence gene expression appears to be by

299 ed loss of spouse or job was associated with PTS symptoms at W2.

300 eral recurrence was strongly associated with PTS.