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 encodes a novel KNOTTED1-LIKE HOMEOBOX (KNOX) gene t

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

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

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

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

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

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

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

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

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

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

13 ScrR controls an adjacent PTS transporter (scrT), fructokinase (scrK) and second S

14 IB(Aga), EIIC(Aga), and EIID(Aga) of the Aga PTS are present, E. coli O157:H7 strains normally are ab

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

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

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 d cell wall proteases, efflux pumps, ABC and PTS transporters, and transcriptional regulators, as wel

21 controls, while the expression of AKR1B1 and PTS was significantly decreased in PD cases.

22 associated with a large burden of asthma and PTS symptoms 5 to 6 years after the September 11 WTC att

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

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

25 chiatric disorders with traumatic events and PTS symptoms was high, with the highest rates for anxiet

26 Main Outcome Measure Traumatic events and PTS were assessed from child and parent reports annually

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

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

29 eloping recurrent venous thromboembolism and PTS.

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

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

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

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

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

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

36 coding the components of the Vibrio cholerae PTS were coregulated with the vps genes, which are requi

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

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

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

40 ts with deep venous thrombosis still develop PTS.

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

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

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

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

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

46 fined the carbohydrate specificities of each PTS transporter.

47 ultimeric polyamine derivatives as efficient PTS ligands.

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

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

50 Few PTS symptoms or psychiatric disorders were observed for

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

52 Interestingly, five PTSs were always highly expressed regardless of the suga

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

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

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

56 8, 24, and 36 months, they were assessed for PTS manifestations according to the Villalta scale.

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

58 51 amino acids (CT51), which is required for PTS protein import.

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

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

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

62 The Gam PTS complex, in contrast, lacks EIIC(Gam), and consequen

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

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

65 d as ptsG based on homology with the glucose PTS in Bacillus subtilis.

66 at W1 only, and 9.5% (95% CI, 9.3%-9.8%) had PTS symptoms at W2 only.

67 Nearly 10% (9.6% [95% CI, 9.3%-9.8%]) had PTS symptoms at both surveys, 4.7% (95% CI, 4.5%-4.9%) h

68 t both surveys, 4.7% (95% CI, 4.5%-4.9%) had PTS symptoms at W1 only, and 9.5% (95% CI, 9.3%-9.8%) ha

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

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

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

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

73 are fairly common and do not often result in PTS symptoms, except after multiple traumas or a history

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

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

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

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

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

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

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

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

82 Many PTS components are repressed at the transcriptional leve

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

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

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

86 compromise with suboptimal activity for most PTS permeases.

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

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

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

90 Unlike Mif mutants, PTS mutants also were hyperbioluminescent.

91 S and a beta-sheet), and ALB/B49-54 (neither PTS nor a beta-sheet).

92 o beta-sheet), ALB/B29-34 (beta-sheet but no PTS), ALB/B36-41 (two PTS and a beta-sheet), and ALB/B49

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

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

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

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

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

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

99 g the HPr intermediate and the EI enzymes of PTS, or growth in the presence of glucose affect positiv

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

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

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

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

104 associated with a markedly decreased odds of PTS at 18 to 24 months compared with standard anticoagul

105 eta-sheet domain may require the presence of PTS elsewhere in the N-terminal region of apoB100.

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

107 ith placebo stockings, for the prevention of PTS.

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

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

110 safely and substantially reduce the risk of PTS in children with occlusive lower-extremity acute DVT

111 To further investigate the roles of PTS and beta-sheet domains in the translocation of apoB1

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

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

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

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

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

117 from the ubiquitination described for other PTS receptors.

118 nding and is thought to regulate the overall PTS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

135 eletion in the promoter of the PETROSELINUM (PTS) [3] gene upregulates the gene product in leaves and

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

137 However, the presence of predicted PTS regulatory domains (PRDs) within Mga suggests an int

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

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

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

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

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

143 I (GCH1), and 6-pyruvoyltetrahydrobiopterin (PTS), was also examined.

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

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

146 istory, 23.8% (95% CI, 23.4%-24.2%) reported PTS symptoms at either W1 (14.3%) or W2 (19.1%).

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

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

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

150 Severe PTS developed in 3 patients in each group.

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

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

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

154 of two common peroxisomal targeting signals (PTS).

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

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

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

158 Six PTSs were transcribed only if a specific sugar was prese

159 with 13.4% of those children developing some PTS symptoms.

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

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

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

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

164 ion of the cel regulon, but loss of specific PTS permeases alleviated repression of cel genes in the

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

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

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

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

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

170 serial clinical evaluation and standardized PTS outcome assessments conducted in uniform fashion.

171 f potential trauma and posttraumatic stress (PTS) in a longitudinal community sample of children.

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

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

174 dent in strains containing an intact sucrose PTS.

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

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

177 llar catalysis using the designer surfactant PTS.

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

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

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

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

182 children, including postthrombotic syndrome (PTS), have recently been identified.

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

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

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

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

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

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

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

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

191 osphoenolpyruvate-phosphotransferase system (PTS) and ATP-binding cassette (ABC) transporters.

192 vate:carbohydrate phosphotransferase system (PTS) and other catabolic enzymes responsible for transpo

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

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

195 osphoenolpyruvate phosphotransferase system (PTS) enzymes.

196 ive for the sugar phosphotransferase system (PTS) exhibited a magnesium-independent phenotype similar

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

198 for an incomplete phosphotransferase system (PTS) have been found in the genome of S. meliloti.

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

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

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

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

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

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

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

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

207 component of the phosphotransferase system (PTS) of gram-positive bacteria and regulates catabolite

208 yruvate-dependent phosphotransferase system (PTS) operon.

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

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

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

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

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

214 dentified the GAS phosphotransferase system (PTS) responsible for non-MalE maltose/maltotriose transp

215 apparent fructose phosphotransferase system (PTS) sugar transporter.

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

217 osphoenolpyruvate phosphotransferase system (PTS), a multicomponent sugar transport system that phosp

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

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

220 ncodes a putative phosphotransferase system (PTS).

221 of the bacterial phosphotransferase system (PTS).

222 yruvate-dependent phosphotransferase system (PTS).

223 ate: carbohydrate phosphotransferase system (PTS).

224 vate:carbohydrate phosphotransferase system (PTS).

225 osphoenolpyruvate phosphotransferase system (PTS).

226 of the bacterial phosphoryl transfer system (PTS).

227 hosphoenolpyruvate:sugar transferase system (PTS).

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

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

230 ruvate-dependent phosphotransferase systems (PTS).

231 large family of phosphotransferase systems (PTSs).

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

233 d two-hybrid competition assays to show that PTS represses KNOX1 protein interactions with BIP, as we

234 The results revealed that PTSs were responsible for transport of monosaccharides,

235 The PTS is initiated by the binding of phosphoenolpyruvate (

236 The PTS locus was widespread in isolates from hospital outbr

237 The PTS modulates virulence gene expression by regulating ex

238 The PTS symptoms were predicted by previous exposure to mult

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

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

241 As the PTS is highly conserved among bacteria, the enzyme I reg

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

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

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

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

246 cts additional phosphorylation of HPr by the PTS enzyme EI at a conserved histidine residue.

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

248 model whereby phosphorylation of Mga by the PTS phosphorelay might link growth and sugar utilization

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

250 vailability and positively controlled by the PTS.

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

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

253 In this work, we identify the PTS components required for transport of glucose and inv

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

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

256 In the PTS, phosphoryl groups are transferred from phosphoenolp

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

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

259 In Escherichia coli, components of the PTS fulfill many regulatory roles, including regulation

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

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

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

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

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

265 in agaF, which encodes EIIA(Aga/Gam) of the PTS, changes a conserved glycine residue to serine (Gly9

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

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

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

269 cid similarity to Enzyme IIB proteins of the PTS.

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

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

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

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

274 tion/dephosphorylation of its substrate, the PTS protein HPr, at a conserved serine residue.

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

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

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

278 equired for transport of glucose through the PTS include enzyme I, histidine protein, enzyme IIA(Glc)

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

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

281 Compared to the PTSs, the ABC transporters showed higher transcription u

282 This PTS is encoded by an open reading frame (M5005_spy1692)

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

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

285 Three PTSs were repressed under all conditions tested.

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

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

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

289 oB chimeric cDNA constructs: ALB/B12-17 (two PTS but no beta-sheet), ALB/B29-34 (beta-sheet but no PT

290 -34 (beta-sheet but no PTS), ALB/B36-41 (two PTS and a beta-sheet), and ALB/B49-54 (neither PTS nor a

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

292 alyses suggested the presence in AtxA of two PTS (phosphenolpyruvate : sugar phosphotransferase syste

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

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

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

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

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

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

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

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

301 eral recurrence was strongly associated with PTS.

302 olved (in 97% of shoulders) in patients with PTS.