ライフサイエンスコーパス: TTP

1 TTP expression was necessary for TGF-beta-dependent P-bo

2 TTP is an mRNA-destabilizing, RNA-binding protein that e

3 TTP is approximately 2-fold more frequent in women, and

4 TTP is specifically related to a severe deficiency in AD

5 TTP knockout mice exhibit a profound inflammatory syndro

6 TTP negatively regulates PD-L1 expression through AU-ric

7 TTP recurred in 6 pregnancies.

8 TTP targets AU-rich elements in the NLRP3 3'-untranslate

9 TTP was a more sensitive measure of bacterial burden tha

10 TTP was inversely correlated with vascular patency and v

11 TTP-bound mRNAs are targeted for destruction via recruit

12 Platelet transfusions were reported in 10.1% TTP, 7.1% HIT, and 25.8% ITP admissions.

13 presence of del(17p) compared with t(4;14) (TTP, 7.3 vs 2.8 months; duration of response, 8.3 vs 2.4

14 We conclude that the newly identified miR-9/TTP circuitry limits unscheduled accumulation of neurona

15 ter matching, the overall CR rate (P = .94), TTP (P = .83), and overall survival (P > .99) were not s

16 disorders, including hereditary and acquired TTP, in the presence of anti-ADAMTS13 autoantibodies.

17 ovides a risk factor for developing acquired TTP.

18 with immunosuppressive agents, for acquired TTP.

19 es in women who have recovered from acquired TTP are not well documented.

20 nset of microvascular thrombosis in acquired TTP and potentially other immune thrombotic disorders.

21 gies for the TMA findings including acquired TTP will allow for a more accurate diagnosis and prevent

22 ectomized for recurrent episodes of acquired TTP, the splenic B-cell response against ADAMTS13 was ch

23 ve CD4(+)T cells in the etiology of acquired TTP.

24 cTTP presents more frequently than acquired TTP during pregnancy and must be differentiated by ADAMT

25 Most patients with acquired TTP respond to a combination of plasma exchange and ritu

26 we randomly assigned patients with acquired TTP to subcutaneous caplacizumab (10 mg daily) or placeb

27 HLA-DRB1*03-positive subjects with acquired TTP.

28 in a DRB1*03-positive patient with acquired TTP.

29 Activated TTP-deficient neutrophils exhibited decreased apoptosis

30 The first-line therapy for acute TTP is based on daily therapeutic plasma exchange supply

31 Upfront treatment of acute TTP includes plasma exchange and corticosteroids.

32 not effective in resolving preexistent acute TTP signs in mice and baboons.

33 mab induced a faster resolution of the acute TTP episode than did placebo.

34 Additionally, TTP(min) can help identify highly aggressive WHO III ast

35 nvolvement of LARP4 as a target of TNF-alpha-TTP regulation provides a clue as to how its functional

36 Although TTP's effects on gene expression have been well studied

37 s of arterial thrombosis and mortality among TTP and HIT patients.

38 anine-DNA methyltransferase status, age, and TTP(min) remaining significant in the multivariate analy

39 for recruitment of the CCR4-NOT complex and TTP-directed decay of an mRNA containing an AU-rich elem

40 y of the transcriptomes of TTP-deficient and TTP-expressing macrophages upon short LPS stimulation su

41 nes over purines, whereas effectors dGTP and TTP select for substrates ADP and GDP, respectively.

42 WHO grade and TTP(min) reached a similar fit for the prognostic evalua

43 of feedback regulation in which RNase L and TTP target SRF mRNA and SRF-induced transcripts.

44 alysis revealed an enrichment of RNase L and TTP targets among SRF-regulated genes suggesting that th

45 ssociation between exonic SNP rs12422149 and TTP in patients treated with ADT was confirmed in univar

46 fractionated, the analytical sensitivity and TTP were superior when testing plasma.

47 contrast enhancement, initial treatment, and TTP(min) showed prognostic significance, with WHO grade,

48 en with a history of nonpregnancy-associated TTP: 18 subsequent pregnancies have been successfully ma

49 -3 in most patients with acquired autoimmune TTP at presentation (median, approximately 170 ng/mL; ra

50 Because TTP also represses IL-1beta expression, it is a dual inh

51 ere we show that a novel interaction between TTP and the CCR4-NOT subunit, CNOT9, is required for rec

52 od-oxygen-level-dependent time-to-peak (BOLD-TTP; a physiological measure of vascular dysfunction) we

53 those of the standard regimen based by both TTP and CFU/mL over 28 days of treatment.

54 gene RS is independently prognostic for both TTP and 2-year OS in ER-positive/HER2-negative de novo s

55 that posttranscriptional gene regulation by TTP schedules the termination of the antimicrobial engag

56 tocytes, and tissue injury that characterize TTP.

57 olymer incorporating a Pt-porphyrin complex (TTP-Pt) into the backbone for efficient singlet to tripl

58 t is based on plasma infusion for congenital TTP, or plasma exchange, often in combination with immun

59 ro macrophage systems, we found constitutive TTP expression in late-stage tumor-associated macrophage

60 erum compared with heat-inactivated control, TTP, and normal serum.

61 lization patterns of lipid binding-defective TTP mutants highlight the importance of protein-lipid in

62 or Tnfaip3, in the absence of MK2-dependent TTP neutralization resulted in a strong reduction of the

63 a proposed mechanistic model that describes TTP-facilitated trafficking of alpha-tocopherol through

64 Knocking down TTP in primary macrophages leads to an increased inducti

65 Engagement of the DUSP1-TTP regulatory axis by PGE2 is likely to contribute to t

66 Early TTP(min) is associated with worse outcome in patients wi

67 ognosis of WHO III astrocytoma with an early TTP(min) of 12.5 min or less did not differ significantl

68 stitution of 2 amino acids of the endogenous TTP protein renders it constitutively active as an mRNA-

69 ell-established murine and baboon models for TTP.

70 cancer, RS was independently prognostic for TTP (hazard ratio, 1.40; 95% CI, 1.05 to 1.86; P = .02)

71 ing features contained predictive signal for TTP (concordance index = 0.658; P = .0006) and CLOVAR pr

72 nt, is a possible new treatment strategy for TTP, as it was demonstrated to reduce disulfide bonds in

73 ge is the most effective initial therapy for TTP to date.

74 We conclude that the TZF domains from TTP family members in these evolutionarily widely diverg

75 comes of pregnancies following recovery from TTP associated with acquired, severe ADAMTS13 deficiency

76 erformed deep RNA sequencing on spleens from TTP knockout mice that were also deficient in both TNF r

77 irs bound (CDP/dATP, UDP/dATP, ADP/dGTP, GDP/TTP) that reveal the conformational rearrangements respo

78 ocked, demonstrating that synthesis of [(3)H]TTP from [(3)H]TMP arose solely from the dephosphorysynt

79 udine to inhibit TK2, the synthesis of [(3)H]TTP from [(3)H]TMP was effectively blocked, demonstratin

80 hymidine or [(3)H]TMP as precursors of [(3)H]TTP in isolated intact or broken mitochondria from the r

81 ddition of [(3)H]TMP produced far less [(3)H]TTP than the amount observed with [(3)H]thymidine as the

82 Here, we focused on how TTP controls cytokine and chemokine production in the no

83 However, TTP also employs the same mechanism to inhibit the expre

84 However, TTP's effects on AU-rich mRNA stability were negligible

85 In rare cases, however, TTP begins as soon as childhood, with frequent inherited

86 Zfs1 with the equivalent domains from human TTP and the single family member proteins expressed in t

87 results suggest potential involvement of HuR/TTP RNA binding protein axis in regulation of inflammati

88 s to examine RNA binding protein (RNABP) HuR/TTP axis in endometriosis patients compared to menstrual

89 3 causes hereditary or acquired (idiopathic) TTP.

90 Importantly, TTP downregulation in this context is essential for prop

91 innovative drugs is still needed to improve TTP management.

92 rmore, MRD negativity significantly improved TTP of patients >75 years (HR, 4.8; P < .001), as well a

93 The change in TTP localization is specific to alpha-tocopherol and is

94 The endothelial dysfunction in TTP(-/-) mice was associated with increased levels of re

95 mouse LARP4 accumulated to higher levels in TTP gene knockout (KO) cells than in control cells.

96 S13 antigen levels correlate with outcome in TTP with increased cardiac and neurological involvement

97 ied several conserved tryptophan residues in TTP that serve as major sites of interaction with two tr

98 f Tnf mRNA and other cytokine transcripts in TTP-deficient mice results in the development of a profo

99 Platelet transfusions in TTP were associated with higher odds of arterial thrombo

100 Increased TTP binding to the 3'UTR of feedback inhibitor mRNAs, su

101 This resulted in increased TTP protein expression in LPS-stimulated macrophages and

102 Although PP2A inhibition increases TTP mRNA expression, resultant TTP protein builds up in

103 The TNF-alpha-induced TTP pulse was followed by a transient decrease in LARP4

104 igatoxin-2 or recombinant murine VWF-induced TTP syndrome in mice despite a lack of plasma ADAMTS13 a

105 tor alpha (TNF-alpha), which rapidly induces TTP, robustly decreased LARP4 with a coincident time cou

106 The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable to that of tran

107 From the United Kingdom TTP registry, we undertook a prospective study investiga

108 e observed elevated mRNA expression of known TTP targets like tumor necrosis factor-alpha (TNF-alpha)

109 -regulated genes suggesting that the RNase L/TTP axis represents a viable target to inhibit SRF-drive

110 sed stability of the otherwise highly labile TTP mRNA.

111 Mice lacking TTP develop a severe, spontaneous inflammatory syndrome

112 adopt the beta-sandwich fold of phage lambda TTP.

113 However, local TTP appears to originate from collagen area fraction, as

114 es < 1.0 denote diminished fecundity (longer TTP).

115 embolization to provide significantly longer TTP than cTACE.

116 rvival was significantly associated with low TTP/HuR mRNA ratios and correlated with high levels of t

117 . albicans Zfs1 bound to the ideal mammalian TTP binding site with high affinity, and Zfs1 was associ

118 Median TTP and OS were 13.9 and 20.4 months, respectively, and

119 d >/=10(-5) vs >/=10(-4) (both with a median TTP of 15 months; 63% and 55% OS at 3 years, respectivel

120 stable oscillations of tumor burdens; median TTP is at least 27 months with reduced cumulative drug u

121 er in WHO IV than in WHO III gliomas; median TTP(min) was 12.5 min in both groups.

122 lization group had significant longer median TTP (>26 mo) than patients in the cTACE group (6.8 mo; P

123 At a median follow-up of 29 months, median TTP was 20 months (95% CI, 16 to 26 months), and median

124 nt benefit for MRD-negative patients (median TTP not reached, 70% OS at 3 years), and similar poorer

125 ng hereditary and acquired antibody-mediated TTP in murine models.

126 Moreover, TTP augmented mitotic cell-cycle arrest as demonstrated

127 nd by a non-MK2-phosphorylatable TTP mutant (TTP-AA) in 1 h LPS-stimulated macrophages and correlated

128 one with abundant collaterals showed neither TTP nor TSA time delay.

129 s without obvious MRA lesions showed neither TTP nor TSA time delay.

130 leotide incorporation, the first nucleotide (TTP) was incorporated at a fast rate (152 s(-1)), wherea

131 F-kappaB activation depends on lysine 105 of TTP, which we identified as the corresponding TRAF2 ubiq

132 stabilization of Mcl1 mRNA in the absence of TTP.

133 In the aorta of TTP(-/-) mice we observed elevated mRNA expression of kn

134 nalysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically associated wi

135 K2, whereas retained RNA-binding capacity of TTP-AA to 3'UTRs caused profound changes in the transcri

136 ndent protein kinase (PKA) in the control of TTP family activity in mRNA decay remains largely unknow

137 d that both the N- and C-terminal domains of TTP are involved in an interaction with CNOT9.

138 approach, we examined whether knock-down of TTP can play a functional role on other RNABPs that comp

139 ion in vitro However, the in vivo effects of TTP mutation are uniformly anti-inflammatory despite the

140 Instead, elimination of TTP caused excessive protein production of inflammatory

141 The first acute episode of TTP usually occurs during adulthood, with a predominant

142 The mutant form of TTP was constitutively degraded by the proteasome and th

143 A single allele encoding the mutant form of TTP was sufficient for enhanced mRNA degradation and und

144 Mice expressing only the mutant form of TTP were healthy and fertile, and their systemic inflamm

145 ation suggested an effective inactivation of TTP by MK2, whereas retained RNA-binding capacity of TTP

146 On the other hand, inactivation of TTP in non-neuronal cells leads to dramatic upregulation

147 S leads to phosphorylation and inhibition of TTP by the kinase MK2.

148 othesis that increasing endogenous levels of TTP in an intact animal might be beneficial in the treat

149 imulated macrophages and increased levels of TTP protein in mouse tissues.

150 ta suggest that increased systemic levels of TTP, secondary to increased stability of its mRNA throug

151 In light of TTP being a couple-dependent outcome, both partner and c

152 found that the intracellular localization of TTP in hepatocytes is dynamic and responds to the presen

153 ife and inflammatory output, because loss of TTP amplifies inflammation by increasing the stability o

154 placizumab show promise in the management of TTP.

155 hat understanding the molecular mechanism of TTP expression and its temporal regulation will guide fu

156 Experimental modulation of TTP or HuR expression led to changes in the mitosis ARE-

157 shown that the gain-of-function mutation of TTP impairs IL-10-mediated negative feedback control of

158 However, knowledge of the pathophysiology of TTP has inspired new ways to prevent early deaths by tar

159 The primary pathway of TTP synthesis in the heart requires thymidine salvage by

160 Perturbation of TTP function may therefore have mixed effects on inflamm

161 3MAF of >60% was an independent predictor of TTP in multivariable analysis (hazard ratio 0.22, 95% CI

162 h the exception of atypical presentations of TTP, which are treated with plasma exchange, anticoagula

163 Rapid recognition of TTP is crucial to initiate appropriate treatment.

164 Regulation of TTP family function through phosphorylation by p38 MAP k

165 In vivo, restoration of TTP expression enhances anti-tumor immunity dependent on

166 Taken together, our study uncovers a role of TTP as a suppressor of feedback inhibitors of inflammati

167 The balancing role of TTP comes at the cost of an increased risk of bacterial

168 Silencing of TTP in endometriotic and endometrial epithelial cells re

169 ompetitively bind to inflammatory targets of TTP in both endometriotic and endometrial epithelial cel

170 he close similarity of the transcriptomes of TTP-deficient and TTP-expressing macrophages upon short

171 a 136-base instability motif in the 3'UTR of TTP mRNA was deleted in the endogenous genetic locus.

172 Most studies on TTP center on the connection between mRNA half-life and

173 lium deficient in TGF-beta/Smad signaling or TTP expression showed attenuated P-body levels.

174 Median overall TTP was 11.1 months (95% CI: 8.8 months, 25.6 months) in

175 Manipulation of the p38alpha-TTP axis in macrophages has significant effects on the g

176 vity curves, including minimal time to peak (TTP(min)).

177 Time to peak (TTP) was employed to detect hypoperfusion.

178 e, wash-in rate, washout rate, time to peak (TTP), mean apparent diffusion coefficient (ADC), 10th pe

179 he time-intensity curve [AUC], time to peak [TTP], relative blood volume [rBV], relative blood flow [

180 e, we report the first evidence that a phage TTP, gp17.1 of siphophage SPP1, self-assembles into long

181 d-type TTP and by a non-MK2-phosphorylatable TTP mutant (TTP-AA) in 1 h LPS-stimulated macrophages an

182 between unphosphorylated and phosphorylated TTP is a critical determinant of the inflammatory respon

183 Mean placental TTP negatively correlated with fetal liver and brain vol

184 Mean placental TTP positively correlated with placental pathology.

185 Maps of oxygen Time-To-Plateau (TTP) were obtained in the placentas by voxel-wise fittin

186 nting (SSCC) on agar and time-to positivity (TTP) measurement in mycobacterial growth indicator tubes

187 alytical sensitivity and time to positivity (TTP) were compared, and a regression analysis was perfor

188 milliliter (CFU/mL) and time to positivity (TTP).

189 We compared culture time-to-positivity (TTP; a surrogate of bacterial load), MTB/RIF TB-specific

190 hich contains two highly conserved potential TTP binding sites, was significantly upregulated relativ

191 n imaging-based risk score system to predict TTP and CLOVAR profiles.

192 , 113 (72%) contained at least one predicted TTP family member binding site in their 3'UTR, compared

193 C was not effective in resolving preexisting TTP signs; thrombocytopenia, hemolytic anemia, and organ

194 of fecundity, measured as time to pregnancy (TTP).

195 ar elastic model with total tissue pressure (TTP) increasing above interstitial fluid pressure (IFP)

196 lity process, namely tape transfer printing (TTP), enabled by chemically induced dramatic modulation

197 sociations with time-to-disease progression (TTP) and HGSOC transcriptomic profiles (Classification o

198 inical variables, time to first progression (TTP), and 2-year overall survival (OS) were correlated w

199 t prognostic factor for time to progression (TTP) (hazard ratio [HR], 2.7; P = .007) and overall surv

200 We hypothesize time to progression (TTP) could be increased by integrating evolutionary dyna

201 vels, imaging response, time to progression (TTP), 90-day mortality, and survival.

202 striking difference in time to progression (TTP), duration of response, and overall response rate (O

203 The primary outcome was time to progression (TTP), evaluated by intention-to-treat analysis.

204 condary end points were time to progression (TTP), response rate, and overall survival (OS) and were

205 edictor of response and time to progression (TTP).

206 nificantly longer time to tumor progression (TTP) (median 80 vs 31 months; P < .0001) and overall sur

207 e hepatic alpha-tocopherol transfer protein (TTP) preferentially selects dietary alpha-tocopherol and

208 ily by a helical array of tail tube protein (TTP) subunits.

209 cquired thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are appropriate

210 ediated thrombotic thrombocytopenic purpura (TTP) is a life-threatening disorder caused by antibodies

211 cquired thrombotic thrombocytopenic purpura (TTP) is a life-threatening disorder resulting from the d

212 Thrombotic thrombocytopenic purpura (TTP) is a microangiopathic disorder diagnosed by thrombo

213 Thrombotic thrombocytopenic purpura (TTP) is a rare and life-threatening thrombotic microangi

214 cquired thrombotic thrombocytopenic purpura (TTP) is caused by aggregation of platelets on ultralarge

215 cquired thrombotic thrombocytopenic purpura (TTP) is characterized by thrombocytopenia and microangio

216 cquired thrombotic thrombocytopenic purpura (TTP) is the consequence of a severe ADAMTS13 deficiency

217 ions of thrombotic thrombocytopenic purpura (TTP) or heparin-induced thrombocytopenia (HIT), and Trou

218 esis of thrombotic thrombocytopenic purpura (TTP) was a mystery for over half a century until the dis

219 odes of thrombotic thrombocytopenic purpura (TTP), but pregnancy outcomes in women who have recovered

220 ions in thrombotic thrombocytopenic purpura (TTP), heparin-induced thrombocytopenia (HIT) and immune

221 ecially thrombotic thrombocytopenic purpura (TTP), is difficult due to overlapping clinical manifesta

222 TP) and thrombotic thrombocytopenic purpura (TTP), respectively, illuminate the importance of conside

223 cquired thrombotic thrombocytopenic purpura (TTP), the persistence of severe ADAMTS13 deficiency (<10

224 cquired thrombotic thrombocytopenic purpura (TTP).

225 ndrome, thrombotic thrombocytopenic purpura (TTP).

226 oach to thrombotic thrombocytopenic purpura (TTP).

227 onsensus on the management of the refractory TTP patient.

228 ur management of the patient with refractory TTP, and discuss use of rituximab, increased plasma exch

229 py, is effective in preventing and resolving TTP signs, using well-established murine and baboon mode

230 ion increases TTP mRNA expression, resultant TTP protein builds up in the hyperphosphorylated inactiv

231 Our results suggest that RNABPs TTP and HuR are dysregulated in endometriotic lesions co

232 In the preoperative setting, TTP(min) can be a valuable noninvasive prognostic marker

233 exchange, was effective in preventing severe TTP signs in mice, but NAC was not effective in resolvin

234 on of NAC was effective in preventing severe TTP signs.

235 ex, particularly in t(4;14), given the short TTP, suggesting that patients were rescued at relapse wi

236 of chemotherapy was associated with shorter TTP.

237 ass (P = .0037) were associated with shorter TTP.

238 In doing so, TTP regulates body-wide levels of alpha-tocopherol.

239 uction of inflammatory mediators, suggesting TTP-dependent translational suppression of AU-rich mRNAs

240 The failure to synthesize TTP in broken mitochondria was not related to a loss of

241 We conclude that TTP mediates the cleavage of the 3' UTRs of stress respo

242 ing proteins in cancer, and demonstrate that TTP induces an antimitotic pathway that is diminished in

243 Here the authors show that TTP, encoded by Zfp36, degrades p28 to inhibit IL-27 pro

244 RNA coimmunoprecipitation showed that TTP specifically associated with LARP4 mRNA in vivo.

245 Our results suggest that TTP deficiency has profound effects on the splenic trans

246 results reveal new molecular details for the TTP-CNOT interaction that shape an emerging mechanism wh

247 val [CI], .22-.70) and a faster BER from the TTP model (OR, 0.71; 95% CI, .55-.94).

248 t on LARP4B or La protein or on LARP4 in the TTP KO cells.

249 neural lineage because of a decrease in the TTP protein expression mediated by the NS-enriched micro

250 ced nitric oxide inactivation by RONS in the TTP(-/-) animals.

251 excludes regulatory elements, including the TTP- and miRNA-223-binding sites.

252 A member of the TTP family of proteins, TIS11d binds RNA with high speci

253 e used to build a pseudo-atomic model of the TTP tube.

254 In phages with a contractile tail, the TTP tube is surrounded by a sheath structure.

255 ized by the mitochondrial salvage enzymes to TTP in intact mitochondria.

256 , triclosan and triclorcarban in relation to TTP; chemical concentrations were modeled both continuou

257 Upon treatment with alpha-tocopherol, TTP- and alpha-tocopherol-containing vesicles translocat

258 Tristetraprolin (TTP) acts by binding to AU-rich elements in certain mRNA

259 Tristetraprolin (TTP) is an inducible zinc finger AU-rich RNA-binding pro

260 Tristetraprolin (TTP) is an inducible, tandem zinc-finger mRNA binding pr

261 Human antigen R (HuR) and Tristetraprolin (TTP) are RNA binding proteins that competitively bind to

262 ements (AREs) recognized by tristetraprolin (TTP/Zfp36), an RNA-binding protein previously implicated

263 wnstream of p38 MAPK, i.e., tristetraprolin (TTP).

264 e mRNA-destabilizing factor tristetraprolin (TTP) binds in a sequence-specific manner to the 3' untra

265 ound that overexpression of tristetraprolin (TTP), but not its RNA binding mutant or the other ARE-bi

266 ied the RNA-binding protein Tristetraprolin (TTP) as a negative regulator of NLRP3 in human macrophag

267 The zinc-finger protein tristetraprolin (TTP) binds to AU-rich elements present in the 3' untrans

268 mRNA-destabilizing protein tristetraprolin (TTP) is induced and extensively phosphorylated in respon

269 mRNA-destabilizing protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated in

270 of the ARE-binding protein tristetraprolin (TTP), which colocalized to P bodies.

271 ich element-binding protein tristetraprolin (TTP).

272 anti-inflammatory protein - tristetraprolin (TTP), a destabilizing RNA binding protein regulated at m

273 of the RNA-binding proteins tristetraprolin (TTP, ZFP36) and HuR (ELAVL1).

274 The RBP tristetraprolin (TTP/Zfp36) is a signal-induced phosphorylated anti-infla

275 Members of the tristetraprolin (TTP) family of CCCH tandem zinc finger proteins bind to

276 sac-specific member of the tristetraprolin (TTP) family of CCCH tandem zinc finger proteins.

277 Members of the tristetraprolin (TTP) family of proteins participate in the regulation of

278 TIS11b/BRF1) belongs to the tristetraprolin (TTP) family of zinc-finger proteins, which bind to mRNAs

279 this study, we identified tristetraproline (TTP) as a novel ERalpha-associated protein.

280 and highlights the importance of fine-tuned TTP activity-regulation by MK2 in order to control the p

281 ied numerous mRNA targets bound by wild-type TTP and by a non-MK2-phosphorylatable TTP mutant (TTP-AA

282 In refractory or unresponsive TTP, more intensive therapies including twice-daily plas

283 In the absence of the vitamin, TTP is localized to perinuclear vesicles that harbor CD7

284 ion that shape an emerging mechanism whereby TTP targets inflammatory mRNAs for deadenylation and dec

285 The mechanisms by which TTP facilitates alpha-tocopherol trafficking in hepatocy

286 with TMAs, including 9 with aHUS and 12 with TTP.

287 model of the 10th percentile of the ADC with TTP yielded accurate results in discriminating cancers w

288 model of the 10th percentile of the ADC with TTP yielded the highest AUC in both data sets.

289 For all patients, RS was associated with TTP (P = .01) and 2-year OS (P = .04).

290 tration, but not CA-125, was associated with TTP.

291 nivariate and multivariate associations with TTP and CLOVAR mesenchymal profile (worst prognosis).

292 with poor response and identified cases with TTP < 6 mo with 71% sensitivity (95% CI 42%-92%) and 88%

293 er one cycle of treatment were compared with TTP.

294 PBK, TOP2A) that negatively correlated with TTP/HuR mRNA ratios and was involved in the mitotic cell

295 There were 10 624 hospitalizations with TTP; 6332 with HIT and 79 980 with ITP.

296 ied CCR4-NOT subunits shown to interact with TTP.

297 phages and correlated their interaction with TTP to changes at the level of mRNA abundance and transl

298 trated the association of the ARE-mRNAs with TTP and HuR.

299 Also, long-term follow-up of patients with TTP is crucial to identify the occurrence of other autoi

300 e association of these genetic variants with TTP and OS in patients receiving ADT.