ライフサイエンスコーパス: PTD

1 PTD induced protein transduction into cells was assessed

2 PTD mediated delivery of a peptide inhibitor of the IL-1

3 PTD-DRBD-delivered siRNA induced rapid RNAi in a large p

4 PTD-HA-Bcl-xL was effective even when it was administere

5 PTD-mediated transfer through the cell membrane occurs t

6 PTD-OVA-transduced DC induced CTL in vivo in a Th cell-i

7 PTD-p65-P1 had no effect on TNF-induced AP-1 activation.

8 PTD-p65-P1 had no effect on TNF-induced inhibitory subun

9 PTD-p65-P1 suppressed NF-kappaB activation induced by li

10 PTDs usually consist of short stretches of basic amino a

11 Furthermore, the NTA(3)-PTD peptide was able to deliver functional Cre recombina

12 a pH-sensitive PTD delivery peptide (NTA(3)-PTD).

13 tion mutant rPdx1Delta protein, as well as a PTD-green fluorescent protein, were evaluated in vitro.

14 arious risk groups, and the probability of a PTD was calculated for each subject.

15 rate that inhibitors of IKK, in particular a PTD-NBD peptide, may be therapeutic in the treatment of

16 When fused to a PTD, direct addition of the DeltaFRD peptide conferred a

17 -537, respectively) that, when linked with a PTD derived from the third helix sequence of antennapedi

18 e and as a recombinant fusion protein with a PTD, derived from HIV-Tat.

19 ran sulfate glycosaminoglycans (GAGs) with a PTD.

20 In addition, PTD-containing rOVA was processed and presented by DC to

21 we used a secretory signal peptide to allow PTD-CRE fusion proteins to be exported from transfected

22 ing the siRNA's negative charge and allowing PTD-mediated cellular uptake.

23 s of mononuclear leukocyte (MNL) density and PTD.

24 etween perceived residential environment and PTD were found in the total sample.

25 ed with increased risk of pregnancy loss and PTD.

26 predict increased risk of pregnancy loss and PTD.

27 lood were associated with pregnancy loss and PTD.

28 able amount of ACh in both pair-fed (PF) and PTD rats, it did so to a greater extent in PF rats.

29 etion also prevented cervical remodeling and PTD in LPS-treated mice.

30 tion plays a role in cervical remodeling and PTD.

31 and cytokines) were compared among term and PTD subjects grouped by presence/absence of HCA and high

32 The NFkappaB inhibitor (TLCK and PTD-p65), or a specific CaMKII inhibitor (m-AIP), was us

33 eated a Bcl-xL fusion protein, designated as PTD-HA-Bcl-xL, which contains the protein transduction d

34 ern blotting, and substrate-cleavage assays, PTD-HA-Bcl-xL attenuated ischemia-induced caspase-3 acti

35 Traditionally, to assess PTD mediated protein delivery, PTD-fusion proteins have

36 Thus, abruption-associated PTD is initiated by functional progesterone withdrawal,

37 stochemical staining in abruption-associated PTD versus gestational-age matched control placentas, an

38 one pathway initiating abruption-associated PTD.

39 MNL-CMR-associated PTD showed higher CRP and corticotropin-releasing hormon

40 HCA-associated PTD showed higher CRP and cytokine levels.

41 An epidemiological association between PTD and various bacteria that are part of the vaginal mi

42 pectroscopy to study the interaction between PTD of the HIV-1 Tat protein (TAT-PTD; residues 47-60 of

43 t inverse associations were observed between PTD rates and perceptions of the following neighborhood

44 ively worsened and dialysis was initiated by PTD 160, followed by transplant nephrectomy on PTD 184.

45 Suppression of NF-kappaB by PTD-p65-P1 enhanced the apoptosis induced by TNF and che

46 minate the behavioral impairment produced by PTD.

47 Consequently, PTDs resemble small-molecule therapeutics in their lack

48 e the identification of the PARTING DANCERS (PTD) gene, as a gene with an elevated expression level i

49 ute rejection episode on posttransplant day (PTD) 6, that warranted treatment with OKT3.

50 Median LY30 was lower on post-trauma day (PTD)1 to PTD4 in patients with poor compared with good o

51 he pyrithiamine-induced thiamine deficiency (PTD) animal paradigm of WKS, our laboratory has demonstr

52 he pyrithiamine-induced thiamine deficiency (PTD) rat model of WKS, there are significant reductions

53 Pyrithiamine-induced thiamine deficiency (PTD) was used to produce a rodent model of Wernicke-Kors

54 a, pyrithiamine-induced thiamine deficiency (PTD), was used to investigate diencephalic-limbic intera

55 Preterm delivery (PTD) is the leading cause of infant morbidity and mortal

56 Preterm delivery (PTD) is the leading cause of infant mortality and morbid

57 ncluded stillbirths (SBs), preterm delivery (PTD), small for gestational age (SGA), and neonatal deat

58 ent may be associated with preterm delivery (PTD), though few studies exist.

59 e birth outcomes including preterm delivery (PTD), very preterm delivery (VPTD), and term low birth w

60 g pregnancy in relation to preterm delivery (PTD), we conducted a multicenter, member-based cohort st

61 on is frequently linked to preterm delivery (PTD).

62 mbranes (PPROM) as well as preterm delivery (PTD).

63 ted with increased risk of preterm delivery (PTD).

64 ated to pregnancy loss and preterm delivery (PTD).

65 tion linked to spontaneous preterm delivery (PTD).

66 thrombin generation elicit preterm delivery (PTD).

67 ly, to assess PTD mediated protein delivery, PTD-fusion proteins have been used as purified proteins.

68 n domain-double-stranded RNA-binding domain (PTD-DRBD) fusion protein.

69 A protein transduction domain (PTD) approach was used to accomplish this.

70 novel cationic peptide transduction domain (PTD) consisting of eight lysine residues (8K), we were a

71 A protein transduction domain (PTD) could efficiently transduce (approximately 90%) air

72 ch contains the protein transduction domain (PTD) derived from the human immunodeficiency TAT protein

73 ns fused with a protein transduction domain (PTD) freely traverse membrane barriers.

74 The TAT protein transduction domain (PTD) has been used to deliver a wide variety of biologic

75 ng release of a protein transduction domain (PTD) linked to the NF-kappaB inhibitor for translocation

76 sed an enhanced protein transduction domain (PTD) sequence to deliver HSP20 phosphopeptide analogs in

77 ls, possesses a protein transduction domain (PTD) that facilitates its entry into cells.

78 n which the HIV protein transduction domain (PTD) was fused to the N-terminus of p38.

79 ins the HIV TAT protein transduction domain (PTD) was readily engineered and purified, efficiently tr

80 iency virus TAT protein transduction domain (PTD), or cell-penetrating peptide, has previously been s

81 P), also termed protein transduction domain (PTD), to achieve effective intracellular protein or gene

82 The recent protein transduction domain (PTD)-mediated cell entry might solve the obstacle of eff

83 helical peptide protein transduction domain (PTD).

84 d by a cationic peptide transduction domain (PTD-5) without impairment of islet function.

85 (also termed as protein transduction domain; PTD).

86 referred to as protein transduction domains (PTDs) and are successfully used to transport heterologou

87 Protein transduction domains (PTDs) are powerful nongenetic tools that allow intracell

88 Protein transduction domains (PTDs) are versatile peptide sequences that facilitate ce

89 Protein-transduction domains (PTDs) have been shown to translocate into and through th

90 h limitations, protein transduction domains (PTDs) have been used as protein carriers, however they o

91 olecules using peptide transduction domains (PTDs) is an exciting technology with both experimental a

92 tides known as protein transduction domains (PTDs) provide a means to deliver molecules into mammalia

93 Peptide/Protein transduction domains (PTDs), also called cell-penetrating peptides (CPPs), can

94 Protein transduction domains (PTDs), both naturally occurring and synthetic, have been

95 Protein transduction domains (PTDs), such as the TAT PTD, have been shown to deliver a

96 omains, termed protein transduction domains (PTDs), which are able to penetrate cell membranes can be

97 ssion of the MLL partial tandem duplication (PTD) and the FLT3 internal tandem duplication (ITD) muta

98 n (ITD), and MLL partial tandem duplication (PTD) and uniformly treated on Cancer and Leukemia Group

99 The MLL-partial tandem duplication (PTD) associates with high-risk cytogenetically normal ac

100 g of an in-frame partial tandem duplication (PTD) of exons 5 through 11 in the absence of a partner g

101 fusions and MLL partial tandem duplications (PTD) may have mechanistically distinct contributions to

102 ly three genes for primary torsion dystonia (PTD), TOR1A (DYT1), THAP1 (DYT6) and CIZ1 (ref. 5), have

103 ly three genes for primary torsion dystonia (PTD), TOR1A (DYT1), THAP1 (DYT6) and CIZ1, have been ide

104 OR = 3.57, 95% CI: 2.53, 5.06) and for early PTD (</=35 weeks gestation) (OR = 2.87, 95% CI: 2.22, 3.

105 ), and some college (12-13 years) had excess PTD risks of 2.6% (95% confidence interval (CI): 2.4, 2.

106 bated with fluorescein isothiocyanate (FITC)-PTD or FITC-PTD-HSP20 peptides showed a diffuse peptide

107 luorescein isothiocyanate (FITC)-PTD or FITC-PTD-HSP20 peptides showed a diffuse peptide uptake.

108 develop predictive microbiologic models for PTD.

109 suggests that binding to HS is necessary for PTD internalization.

110 interval (CI): 1.3, 2.3) increased odds for PTD, 2.2% (95% CI: 1.0, 3.4) for VPTD, and 1.1% (95% CI:

111 n PTDs, is used to elucidate the pathway for PTD internalization.

112 The association was stronger for PTD due to premature rupture of membrane (OR = 3.57, 95%

113 he global probability of true damage (global PTD) for diagnosing glaucoma was assessed by sensitivity

114 At the global PTD cutoff point value of 2.0, the sensitivity was 85.9%

115 The AUC for the global PTD was 0.930 (95% confidence interval, 0.893-0.967) for

116 The global PTD was calculated as a sum of individual PTD values, ra

117 ith </=12 years of education also had higher PTD rates with higher social disorder (age-adjusted PR =

118 the FC recovered the rate of alternation in PTD rats as well as reduced arm-reentry perseverative er

119 Is would reduce the educational disparity in PTD.

120 veal a selective cholinergic dysfunction: In PTD-treated rats a significant loss of ChAT-immunopositi

121 ls in the RSC had no procognitive effects in PTD rats, but rather impaired alternation behavior in PF

122 nerated transferred DNA insertional lines in PTD showed that the mutants had reduced fertility.

123 efflux in the amygdala was not suppressed in PTD treated rats, relative to PF rats, prior to or durin

124 ring pregnancy was associated with increased PTD, SGA, and SB.

125 CMR, was associated with medically indicated PTD (odds ratio = 2.2, 95% confidence interval: 1.3, 3.6

126 al PTD was calculated as a sum of individual PTD values, ranging from 0% to 100% for all 31 visual lo

127 ied two mouse models of inflammation-induced PTD.

128 xytoluene (BHT) and the NF kappa B inhibitor PTD-p65 peptide inhibit NF kappa B activation and TNF al

129 gulatory properties of rPdx1 protein and its PTD-deletion mutant rPdx1Delta protein, as well as a PTD

130 ginine (R(9)), the most efficacious of known PTDs, is used to elucidate the pathway for PTD internali

131 te in the chorion of the membrane roll marks PTD pathways that are distinct from HCA and not entirely

132 ts with the MLL(PTD/WT) genotype express MLL PTD but not the MLL WT.

133 units, supporting opposing functions for MLL PTD and MLL WT whereby the MLL PTD contributes to the le

134 occurs in vivo and an etiologic role for MLL PTD gain of function in the genesis of AML.

135 xpression (P < .001) and the presence of MLL PTD (P = .027) predicted worse CIR.

136 Reduction of MLL PTD expression induced MLL WT and reduced blast colony-f

137 MLL WT allele with the expression of the MLL PTD allele, along with the functional data presented her

138 The mechanism by which the MLL PTD contributes to aberrant hematopoiesis and/or leukemi

139 tions for MLL PTD and MLL WT whereby the MLL PTD contributes to the leukemic phenotype via a recessiv

140 Mll(PTD/WT) mice exhibit an alteration in the boundaries of

141 Mll(PTD/WT) mice overexpress Hoxa7, Hoxa9, and Hoxa10 in spl

142 Mll(PTD/WT):Flt3(ITD/WT) mice developed acute leukemia with

143 , mice with homozygous Flt3-ITD alleles, Mll(PTD/WT):Flt3(ITD/ITD), demonstrated a nearly 30-week red

144 The similarities between Mll(PTD/WT) and Mll(PTD/-) mice suggest that the Mll-PTD mutation can up-reg

145 The similarities between Mll(PTD/WT) and Mll(PTD/-) mice suggest that the Mll-PTD mut

146 ver cells (FLC) as baseline, we compared Mll(PTD/-) with Mll(PTD/WT) FLC and found both had increased

147 ortezomib, as a single agent, eradicates Mll(PTD/wt):Flt3(ITD/wt) AML in mouse and may represent a po

148 However, Mll(PTD/WT) HSPCs never develop leukemia in primary or recip

149 Silencing of MLL WT in MLL(PTD/WT) blasts was reversed by DNA methyltransferase (DN

150 )Sca1(+)Kit(+) (LSK)/SLAM(+) and LSK) in Mll(PTD/WT) mice are reduced in absolute number in steady st

151 In mice, a double knock-in (dKI) of Mll(PTD/wt) and Flt3(ITD/wt) mutations induces spontaneous A

152 rth unlike the normal life expectancy of Mll(PTD/WT), Mll(WT/-), and Mll(WT/WT) mice.

153 enitor cells (CFU-GM); in contrast, only Mll(PTD/WT) FLC had increased pluripotent hemopoietic progen

154 ile normal karyotype AML blasts with the MLL(PTD/WT) genotype express MLL PTD but not the MLL WT.

155 The Mll(PTD/WT)-derived phenotypic short-term (ST)-HSCs/multipot

156 These Mll(PTD/-) mice die at birth unlike the normal life expectan

157 as baseline, we compared Mll(PTD/-) with Mll(PTD/WT) FLC and found both had increased HoxA gene expre

158 MLL-PTD(+) patients who relapsed more often had other advers

159 M1 (P < .001), mutated CEBPA (P = .003), MLL-PTD (P = .009), absent FLT3-TKD (P = .005), and high ERG

160 ith previously reported studies, 9 (41%) MLL-PTD(+) patients continue in long-term first remission (C

161 Twenty-four (10.1%) patients harbored an MLL-PTD.

162 RUNX1-RUNX1T1, CBFB-MYH11, FLT3-ITD, and MLL-PTD, as well as mutations in NPM1, CEPBA, RUNX1, ASXL1,

163 us, we generated a mouse expressing both Mll-PTD and Flt3-ITD.

164 mpact of MLL partial tandem duplication (MLL-PTD) was evaluated in 238 adults aged 18 to 59 years wit

165 age leukemia partial tandem duplication (MLL-PTD), exhibits increased global DNA methylation versus A

166 ) is through partial tandem duplication (MLL-PTD); however, the mechanism by which MLL-PTD contribute

167 3-TKD), MLL partial tandem duplications (MLL-PTD), NPM1 and CEBPA mutations, and for the expression l

168 However, mice expressing either Mll-PTD or Flt3-ITD do not develop AML, suggesting that 2 mu

169 l death was observed in SMCT1-expressing MLL-PTD(+) AML cells treated with valproate.

170 vival (P=0.001 for FLT3-ITD, P=0.009 for MLL-PTD, P=0.05 for ASXL1, and P=0.006 for PHF6); CEBPA and

171 As in human MLL-PTD and/or the FLT3-ITD AML, mouse blasts exhibited norm

172 In MLL-PTD(+) cell lines having SLC5A8 promoter hypermethylatio

173 estigate ASXL1, CBL, IDH1/2, JAK2, KRAS, MLL-PTD, NPM1, NRAS, TP53, SRSF2, SF3B1, SETBP1, U2AF1 at mu

174 The partial tandem duplication of MLL (MLL-PTD) is found in 5% to 10% of patients with acute myeloi

175 ITD), partial tandem duplication in MLL (MLL-PTD), and mutations in ASXL1 and PHF6 were associated wi

176 Within the majority of MLL-PTD AML is a mechanism in which DNA hypermethylation sil

177 ertain the underlying pathogenic role of MLL-PTD in the clonal evolution of human leukemia, which sho

178 tem/progenitor cell (HSPC) phenotypes of Mll-PTD knock-in mice.

179 we demonstrate, for the first time, that Mll-PTD contributes to leukemogenesis as a gain-of-function

180 Thus, the Mll-PTD aberrantly alters HSPCs, enhances self-renewal, caus

181 therefore generated mice expressing the Mll-PTD in the absence of Mll-WT.

182 WT) and Mll(PTD/-) mice suggest that the Mll-PTD mutation can up-regulate target genes in a dominant,

183 types suggest that in select tissues the Mll-PTD requires cooperation with the Mll-WT in the genesis

184 Thirteen MLL-PTD(+) patients relapsed within 1.4 years of achieving C

185 normal cytogenetics, decreased Mll-WT-to-Mll-PTD ratio, loss of the Flt3-WT allele, and increased tot

186 OS at 3 years: 44.2%); (4) unfavorable: MLL-PTD and/or RUNX1 mutation and/or ASXL1 mutation (n = 203

187 LL-PTD); however, the mechanism by which MLL-PTD contributes to MDS and AML development and maintenan

188 ITD) is observed in 25% of patients with MLL-PTD AML.

189 ation silences a TSG that, together with MLL-PTD, can contribute further to aberrant chromatin remode

190 -prognosis group of CN-AML patients with MLL-PTD.

191 R) compared with 83% of patients without MLL-PTD (P=.39).

192 This novel PTD-based protein therapy offers a promising way to trea

193 sured in the hippocampus and the amygdala of PTD-treated and pair-fed (PF) control rats while they we

194 ractive target for the biological pH drop of PTD-mediated macropinocytotic delivery.

195 The efficiency of PTD-mediated transduction was influenced by the cell typ

196 Efficient entry of PTD-NY-ESO-1 into dendritic cells, confirmed by microsco

197 The etiology of PTD is largely unknown but is believed to be complex, en

198 Furthermore, intraperitoneal injection of PTD-HA-Bcl-xL into mice resulted in robust protein trans

199 ART from before pregnancy had higher odds of PTD (adjusted odds ratio [AOR], 1.2; 95% confidence inte

200 dovudine) was associated with higher odds of PTD (AOR, 1.4; 95% CI, 1.2, 1.8), SGA (AOR, 1.5; 95% CI,

201 e of F5 gene variants in the pathogenesis of PTD, and demonstrate the utility of high-throughput geno

202 associated with more than double the risk of PTD (odds ratio (OR) = 2.23, 95% confidence interval (CI

203 The present study revealed increased risk of PTD associated with genital herpes infection if left unt

204 regnancy was associated with a lower risk of PTD compared with not being treated, and the PTD risk wa

205 t of genital herpes infection on the risk of PTD.

206 d versatile biological vehicles, a series of PTD-inspired polyoxanorbornene-based synthetic mimics wi

207 TD risk group with the highest percentage of PTDs had an AUC of 0.91 (CI, 0.79 to 1).

208 D 160, followed by transplant nephrectomy on PTD 184.

209 A biopsy performed on PTD 154 to evaluate a rise in creatinine revealed polyom

210 To date, reports of genetic studies on PTD are sparse.

211 Comparing ranibizumab 0.5 mg versus sham or PTD treatment, respectively: 39.9% versus 29.1% and 10.9

212 Application of TLCK or PTD-p65 inhibited the glutamate-induced BDNF expression

213 e IKK inhibitor transduction fusion peptide (PTD-5-NBD) in situ to mouse islets resulted in improved

214 egy to effectively yet safely deliver potent PTD-modified protein toxins to the tumor.

215 or C5aR in the cervical changes that precede PTD.

216 It may be possible to predict PTD by using microbiologic risk factors measured once th

217 inhibited the release of MMP-9 and prevented PTD.

218 The model for the previous PTD risk group with the highest percentage of PTDs had a

219 ated a cell-permeable wild-type p38 protein (PTD-p38WT) in which the HIV protein transduction domain

220 teraction of TAT PTD and other arginine-rich PTDs with the cell membrane, perhaps aiding their transl

221 on to previously characterized arginine-rich PTDs, including TAT, lysine homopolymers were able to me

222 Transduction of arginine/lysine-rich PTDs occurred at 4 degrees C and following depletion of

223 al HIV was significantly associated with SB, PTD, SGA, and NND.

224 rate a novel approach to efficiently secrete PTD-containing protein domains, overcoming previous limi

225 These data illustrate that some secreted PTD proteins may be useful reagents to improve protein d

226 of this study was to develop a pH-sensitive PTD delivery peptide (NTA(3)-PTD).

227 Several PTDs were tested including the prototypic TAT, different

228 nfidence interval: 1.3, 3.6) and spontaneous PTD (odds ratio = 2.5, 95% confidence interval: 1.7, 3.7

229 from the cell surface completely ablated TAT PTD-mediated transduction.

230 induction of macropinocytotic uptake by TAT PTD.

231 We produced an HIV Tat PTD domain fusion protein (Tat-GR(554-777)) that potenti

232 Surprisingly, however, TAT PTD-mediated induction of macropinocytosis and cellular

233 Using labeled TAT PTD peptides and fusion proteins, in addition to TAT PTD

234 en proposed to aid in the interaction of TAT PTD and other arginine-rich PTDs with the cell membrane,

235 negative charge on the cell surface that TAT PTD binds avidly.

236 cidic glycans form a pool of charge that TAT PTD binds on the cell surface, but this binding is indep

237 The TAT PTD enters cells by a lipid raft-dependent macropinocyto

238 Because of the TAT PTD's strong cell-surface binding, early assumptions reg

239 transduction domains (PTDs), such as the TAT PTD, have been shown to deliver a wide variety of cargo

240 ides and fusion proteins, in addition to TAT PTD-Cre recombination-based phenotypic assays, we show t

241 TAT-PTD did not cause dissipation of membrane potential (165

242 By conjugating EEDs to a TAT-PTD/CPP spilt-GFP peptide complementation assay, we were

243 using a TAT-peptide transduction domain (TAT-PTD) to the minimal modular elements of GIV that are nec

244 parameter, which may regulate binding of TAT-PTD to the membrane.

245 on between PTD of the HIV-1 Tat protein (TAT-PTD; residues 47-60 of Tat, fluorescently labeled with t

246 pyrene-PG) in the membrane revealed that TAT-PTD preferentially bound to the membrane in the liquid s

247 The TAT-PTD tryptophan exhibited a decrease in fluorescence inte

248 polyethylene glycol (PEG) units from the TAT-PTD-cargo significantly enhanced cytoplasmic delivery in

249 When TAT-PTD was bound to lipid vesicles labeled with 1-(4-trimet

250 H was observed upon the interaction with TAT-PTD, indicating no significant disruption or perturbatio

251 inal, a proteasome inhibitor, confirmed that PTD-NY-ESO-1 entered dendritic cells by protein transduc

252 Recent data indicate that PTD-mediated transduction occurs via fluid-phase macropi

253 These findings indicate that PTD-p38WT is a novel and useful tool for unraveling the

254 uence similarity raises the possibility that PTD may present a previously unknown function conserved

255 studies with vesicular markers confirm that PTDs are internalized by endocytosis rather than by cros

256 The PTD rates of women with lower education may be significa

257 The PTD treatment increased progenitor cell proliferation an

258 PTD compared with not being treated, and the PTD risk was similar to that observed in the unexposed c

259 t IPIs will yield no important change in the PTD disparity by maternal educational level.

260 the observed hippocampal dysfunction in the PTD model and human WKS.

261 pocampal application of physostigmine in the PTD model likely increased activation of the extended li

262 linergic septohippocampal dysfunction in the PTD model.

263 nificantly enhanced alternation rates in the PTD-treated rats.

264 In contrast, rOVA lacking the PTD did not enter the DC MHC class I presentation pathwa

265 fficiently as native OVA or rOVA lacking the PTD.

266 ffect was seen using molecules devoid of the PTD and NF-kappaB inhibitory domains.

267 first necessary step must be binding of the PTD peptide to the surface of the lipid membrane.

268 utinin protein (HA2) helps the escape of the PTD-cargo from macropinocytosomes and therefore signific

269 face, but this binding is independent of the PTD-mediated transduction mechanism and the induction of

270 observed between the cationic charge on the PTD and the extent of secretion.

271 jury and provide the first evidence that the PTD can be used to efficiently transduce a biologically

272 These and other data indicate that the PTD-mediated delivery of molecules into live mammalian c

273 This suggests that the PTD-phosphoHSP20 peptide alone is sufficient to inhibit

274 Linkage to the PTD was not, however, required to suppress the binding o

275 Poor secretion was found when the PTD charge was greater than +5.

276 This PTD domain also enhanced gene expression after plasmid d

277 Thus, PTD-DRBD-mediated siRNA delivery allows efficient gene s

278 Thus, PTD-mediated DeltaFRD fragment delivery may provide a th

279 Thus, PTD-NY-ESO-1 accesses the cytoplasm by protein transduct

280 s, and the cervical remodeling that leads to PTD.

281 on scores were higher in PF rats relative to PTD-treated rats.

282 function of region (FC, RSC) and treatment (PTD, pair-fed [PF]).

283 sses the structure of the most commonly used PTDs and how their ability to transduce membranes is use

284 results demonstrate the feasibility of using PTD-mediated delivery to transiently modify islets in si

285 stigation was conducted to determine whether PTD treatment altered hippocampal neurogenesis in a stag

286 important first step in the process by which PTDs and their cargo traverse the plasma membrane.

287 phocytes specific for NY-ESO-1(157-165) with PTD-NY-ESO-1 compared with NY-ESO-1 control protein (44%

288 panics) gene haplotypes were associated with PTD in specific ethnic groups but not at global signific

289 nd physical environment were associated with PTD rates among postpartum African-American women (n = 1

290 identified as being causally associated with PTD, suggesting a multifactorial etiology.

291 and solid waste all had an association with PTD and VPTD.

292 Screening of GNAL in 39 families with PTD identified 6 additional new mutations in this gene.

293 Using exome sequencing in two families with PTD, we identified a new causative gene, GNAL, with a no

294 -ESO-1-specific T lymphocytes generated with PTD-NY-ESO-1 secreted IFN-gamma indicative of a Tc1-type

295 ficant association of F5 gene haplotype with PTD was revealed and remained significant after Bonferro

296 e polymorphisms with PTD in 300 mothers with PTD and 458 mothers with term deliveries at the Boston M

297 of 426 single-nucleotide polymorphisms with PTD in 300 mothers with PTD and 458 mothers with term de

298 maternal hypertension during pregnancy with PTD, SGA, and SB.

299 Treatment with PTD-p38WT significantly promoted the random migration of

300 inically apparent OVA-expressing tumors with PTD-OVA-transduced DC resulted in tumor regression in so