ライフサイエンスコーパス: ATG

1 ATG induced profound T-cell depletion followed by CD8(+)

2 ATG should be added to myeloblative and non-myeloblative

3 ATG treatment resulted in highly significant increases o

4 ATG-exposure measures were determined with a validated p

5 ATG-treated patients had 159 grade 3-4 adverse events, m

6 ATG/G-CSF therapy was associated with relative preservat

7 Radial growth of 18 Group 1 ATG mutants was significantly reduced compared to the wi

8 In the PBSC group (n = 139), ATG was associated with a lower CI of both grades III to

9 The 5'-ATG PAM is recognized in duplex form, from the minor gro

10 The 3-year probabilities of LFS after ATG-containing, alemtuzumab-containing, and T cell-reple

11 We studied the relationships among ATG exposure, IR, and clinical outcomes.

12 apsid-delta fusion protein and the use of an ATG-independent mechanism for translation initiation.

13 In multivariate regression analyses, ATG induction was the single most important variable ass

14 in sorting) 34, VPS15, BECN1 (Beclin 1), and ATG (autophagy-related) 14.

15 nal regulator SKN-1/Nrf1, ATG-18/WIPI1/2 and ATG-16.2/ATG16L exert their function through the DAF-16/

16 IR, BEC-1/BECN1/Beclin1, ATG-18/WIPI1/2, and ATG-16.2/ATG16L all promote cell-cycle progression and a

17 treated with busulfan, cyclophosphamide, and ATG.

18 Both daclizumab and ATG therapy resulted in a significant reduction in acute

19 conditioning with TBI 300 cGy, CY, FLU, and ATG.

20 31 (60%) patients died in the inolimomab and ATG arms, respectively.

21 h the increased light chain 3-II/I ratio and ATG-5 expression.

22 significant increases of both IgM (for anti-ATG and anti-Neu5Gc) and IgG (for anti-ATG, -Gal, and -N

23 anti-ATG and anti-Neu5Gc) and IgG (for anti-ATG, -Gal, and -Neu5Gc), peaking at 1 month and still de

24 ibited significantly elevated titers of anti-ATG (P = 0.043) and anti-Neu5Gc (P = 0.007) IgGs in late

25 treatment were then assessed for total anti-ATG, anti-Neu5Gc, and anti-Gal antibodies using ELISA as

26 the START study to decipher the various anti-ATG specificities developed by the patients in this stud

27 ped by the patients in this study: antitotal ATG, but also antigalactose-alpha1-3-galactose (Gal) and

28 d by conserved gene products, the autophagy (ATG) proteins.

29 Similar to DAF-2/IIR, BEC-1/BECN1/Beclin1, ATG-18/WIPI1/2, and ATG-16.2/ATG16L all promote cell-cyc

30 immune activation is the causal link between ATG and CVEs.

31 Both ATG and splice-blocking PEAR1 morpholinos enhanced throm

32 Upstream open reading frames initiated by ATG but not CTG mediated translational repression of the

33 Consistently, induction of TF PCA by ATG did not require maximal phosphatidylserine membrane

34 Induction of TF PCA by ATG was dependent on lipid raft integrity and complement

35 approximately 250 bp upstream of the coding ATG.

36 (protein synthesis is initiated at the codon ATG) of neutrophil elastase (ELANE) result in the produc

37 Combination ATG/G-CSF treatment tended to preserve beta cell functio

38 In conclusion, ATG associated with both immune activation and post-tran

39 n PB1-F2 plasmids lacking the well-conserved ATG start codon.

40 In contrast, ATG-7 functions in concert with the DAF-7/TGF-beta pathw

41 were randomized to ATG and pegylated G-CSF (ATG+G-CSF) (N = 17) or placebo (N = 8).

42 LT recipients received 3.75 mg/kg per day ATG from days 0 to 5 followed by rapamycin-based immunos

43 High-dose ATG followed by short-term rapamycin treatment failed to

44 protein (C-terminal PB1-F2) from downstream ATGs in PB1-F2 plasmids lacking the well-conserved ATG s

45 lar in all groups: no ATG, 71% +/- 8%; early ATG, 68% +/- 9%; and late ATG, 61% +/- 7%.

46 or Utrecht were divided into 3 groups: early ATG (days -9 to -5; n = 33), late ATG (days -5 to 0; n =

47 group compared with 18% (P = .018) for early-ATG and 5% (P < .001) for late-ATG groups.

48 ed autophagy by phosphorylating an essential ATG protein, Beclin 1, at serine 90, and that this phosp

49 In our experience, ATG proved to be safe, effective, and contributed to sig

50 lear LacZ cassette is knocked into the first ATG codon of Prom1, we confirmed that Prom1 is expressed

51 uct but not with a version lacking the first ATG.

52 reas AHSCT from unrelated donors with FluMel/ATG conditioning led to a high rate of graft failure and

53 ributing factor of late graft loss following ATG induction and that anti-Neu5Gc antibodies increase o

54 afted patients presenting with SSD following ATG induction treatment.

55 h our results confirm the recommendation for ATG to be added after PBSC transplantation, no obvious b

56 These findings support a role for ATG induction, and caution against the use of sirolimus-

57 me to reveal numerous noncanonical roles for ATG proteins during viral infection.

58 itiation codon and rely on a second in-frame ATG codon to produce an enzymatically active isoform lac

59 ted by the significant bias against in-frame ATGs specifically found at the beginning of the correspo

60 s, mainly at positions -124 and -146 bp from ATG start site that create binding motifs for E-twenty s

61 ion of FOXO3a-target autophagy-related gene (ATG) expression.

62 Disabling core autophagy-related gene (ATG) products prevents autophagy, a process through whic

63 More generally, ATG associated with features of immune activation.

64 characterization of autophagy-related genes (ATGs) in the wheat pathogenic fungus Fusarium graminearu

65 n immunosuppression: antithymocyte globulin (ATG) (n=85) or basiliximab (n=29) and were followed up f

66 ents received rabbit antithymocyte globulin (ATG) as part of the conditioning regimen (ATG group), wh

67 ocyte depletion with antithymocyte globulin (ATG) can be complicated by systemic coagulation activati

68 Daclizumab and antithymocyte globulin (ATG) have been shown to reduce allograft rejection.

69 The impact of antithymocyte globulin (ATG) in the setting of a myeloablative conditioning tran

70 g patients receiving antithymocyte globulin (ATG) induction (aRR for AR, 1.16; 95% CI, 0.41-3.35, P=0

71 lantation (LT) using antithymocyte globulin (ATG) induction and rapamycin.

72 radiation (TLI) with antithymocyte globulin (ATG) is a unique regimen that prepares recipients for al

73 Antithymocyte globulin (ATG) is used as induction therapy after cardiac transpla

74 trials suggest that antithymocyte globulin (ATG) might be effective for reducing this autoimmune res

75 early, late, and no antithymocyte globulin (ATG) on immune reconstitution and outcome.

76 Low-dose antithymocyte globulin (ATG) plus pegylated granulocyte colony-stimulating facto

77 ting doses of rabbit antithymocyte globulin (ATG) to human peripheral blood mononuclear cells has bee

78 radiation (TBI), and antithymocyte globulin (ATG) with or without fludarabine (FLU), followed by T-ce

79 tions of four drugs: antithymocyte globulin (ATG), granulocyte-colony stimulating factor (G-CSF), a d

80 irradiation without antithymocyte globulin (ATG), whereas the relapse risk was similar in the group

81 uences of polyclonal antithymocyte globulin (ATG)-induced immune modifications, which include alterat

82 (n = 241) or without antithymocyte globulin (ATG; n = 491) following reduced-intensity conditioning r

83 irradiation (TLI) and anti-T-cell globulin (ATG), that donor long-term hematopoietic stem cell (LT-H

84 n of antihuman T-lymphocyte immune globulin (ATG) in a myeloablative conditioning regimen for patient

85 ination of low-dose anti-thymocyte globulin (ATG) and pegylated granulocyte CSF (G-CSF) would preserv

86 Pretreatment with anti-thymocyte globulin (ATG) decreases the occurrence of chronic graft-versus-ho

87 uction therapy with anti-thymocyte globulin (ATG) instead of anti-interleukin-2Ra monoclonal antibody

88 Usage and timing of anti-thymocyte globulin (ATG), introduced to the conditioning to prevent graft-ve

89 ng with FluMel plus anti-thymocyte globulin (ATG).

90 ymocyte rabbit IgGs (antithymocyte globulin [ATG]) are popular immunosuppressive drugs used to preven

91 inical equivalent of antithymocyte globulin [ATG]) facilitates immune tolerance after bone marrow tra

92 oup was treated with antithymocyte globulin [ATG]).

93 Rabbit-generated antithymocyte globulins (ATGs), which target human T cells, are widely used as im

94 rrow Transplant registry, treated with horse ATG (hATG; lymphoglobulin) and cyclosporine.

95 ophagosomes recognize lipid droplets and how ATG proteins regulate membrane curvature for lipid dropl

96 However, ATGs can induce immune complex diseases, including serum

97 ssing and T cell pathogenicity, and identify ATG-dependent phagocytosis in DCs as a key regulator in

98 It is unknown if ATG induction is associated with decreased coronary plaq

99 C-peptide was not significantly different in ATG+G-CSF (0.49 nmol/L/min) versus placebo (0.29 nmol/L/

100 ) regulatory T cells (Treg) were elevated in ATG+G-CSF subjects at 6, 12, and 18 but not 24 months.

101 e cumulative incidence of CVEs was higher in ATG-treated patients (14.7% versus 8.2%; P=0.03).

102 A1c was lower in ATG/G-CSF-treated subjects at the 6-month study visit.

103 n associated significantly with CVEs only in ATG-treated patients (HR, 2.07; 95% CI, 1.16 to 3.70; P=

104 creased 1 year after transplantation only in ATG-treated patients.

105 cular events that distinguish how individual ATGs function promises to improve our understanding of t

106 d) PB1-F2, and PB1-F2 lacking the initiating ATG in mammalian and avian cells had no effect on cell a

107 me immediately at the translation initiating ATG of TSLP.

108 found an alternative translation initiation ATG codon in the +3 reading frame of human ATXN1 startin

109 d by study site) to receive either 6.5 mg/kg ATG or placebo over a course of four days.

110 a mutated PB1-F2 start codon (i.e., lacking ATG) was 1,000-fold more virulent for BALB/c mice than a

111 ups: early ATG (days -9 to -5; n = 33), late ATG (days -5 to 0; n = 48), and no ATG (n = 46).

112 71% +/- 8%; early ATG, 68% +/- 9%; and late ATG, 61% +/- 7%.

113 18) for early-ATG and 5% (P < .001) for late-ATG groups.

114 ul CD4(+) IR (HR, 0.26; P < .0001) and lower ATG exposure after CBT (HR, 1.005; P = .0071).

115 Here, we fully defined the maize (Zea mays) ATG system transcriptionally and characterized it geneti

116 Moreover, ATG initially "reprograms" CD4(+) T cells, but not monoc

117 roup) or standard GVHD prophylaxis alone (no ATG group).

118 33), late ATG (days -5 to 0; n = 48), and no ATG (n = 46).

119 ty of survival was similar in all groups: no ATG, 71% +/- 8%; early ATG, 68% +/- 9%; and late ATG, 61

120 compared with 16 (16%) of 97 who received no ATG (adjusted odds ratio 4.25 [95% CI 1.87-9.67]; p=0.00

121 in the ATG group vs 41 [42%] of 97 in the no ATG group).

122 ients to treatment (101 to ATG and 102 to no ATG).

123 re significantly higher (P < .001) in the no-ATG group at 1, 2, 3, 6, and 12 months post-UCBT.

124 acute GVHD (aGVHD; 31%) was found in the no-ATG group compared with 18% (P = .018) for early-ATG and

125 The no-ATG group received mycophenolate mofetile + cyclosporin

126 In the no-ATG group, significantly fewer viral reactivations (P =

127 idespread RNA foci and repeat-associated non-ATG (RAN) translated dipeptides, which were suppressed b

128 se sense and antisense repeat-associated non-ATG (RAN) translation proteins accumulate most abundantl

129 HD repeat-associated non-ATG (RAN) translation proteins also disrupted nucleocyto

130 eins (MBNL), undergoes repeat-associated non-ATG (RAN) translation, and potentially causes microRNA d

131 onal transcription and repeat-associated non-ATG (RAN) translation, have recently emerged from expans

132 NA biogenesis and (ii) repeat associated non-ATG (RAN) translation, in which repeating transcripts ar

133 lear foci or undergoes repeat-associated non-ATG (RAN) translation, producing "c9RAN proteins." Since

134 by a unique mechanism, repeat-associated non-ATG (RAN) translation.

135 chanism of translation-repeat-associated non-ATG (RAN) translation.

136 Repeat-associated non-ATG dependent translation gives rise to toxic dipeptide

137 uding the noncanonical repeat-associated non-ATG translation (RAN translation) into pathologic dipept

138 espite the presence of repeat-associated non-ATG translation (RAN) products.

139 leading to cytoplasmic repeat associated non-ATG translation and formation of potentially toxic dipep

140 rmed by unconventional repeat-associated non-ATG translation.

141 are translated through repeat-associated non-ATG-initiated translation.

142 proteins generated by repeat-associated, non-ATG translation.

143 y by the expanded RNA or dipeptides from non-ATG-initiated translation are responsible for the pathop

144 egimen (ATG group), whereas 579 did not (non-ATG group).

145 ntly higher in the ATG group than in the non-ATG group (36.6% vs. 16.8%, P=0.005).

146 val was similar in the ATG group and the non-ATG group (59.4% [95% CI, 47.8 to 69.2] and 64.6% [95% C

147 and 68.7% (95% CI, 58.4 to 80.7) in the non-ATG group (P<0.001).

148 G4C2) expansions undergo unconventional, non-ATG-dependent translation, generating toxic dipeptide re

149 gh the transcriptional regulator SKN-1/Nrf1, ATG-18/WIPI1/2 and ATG-16.2/ATG16L exert their function

150 Area under the curve (AUC) of ATG after infusion of the cord blood transplant predicte

151 Our findings suggest that a brief course of ATG does not result in preservation of beta-cell functio

152 Deletion of ATG genes or inhibition of vacuole protease activity com

153 graft loss was associated with lower dose of ATG during induction.

154 We gave a total dose of ATG of 4.5 mg/kg intravenously over 3 days (0.5 mg/kg 2

155 trials could determine whether the doses of ATG used in this trial are optimum, and could also provi

156 Individualized dosing of ATG to reach optimal exposure or, in selected patients,

157 Subanalyses suggest that the effect of ATG on CVEs is restricted to CMV-exposed patients.

158 ironment that may compromise the efficacy of ATG therapy.

159 oantigens may improve safety and efficacy of ATG treatment.

160 gs thus reveal an unconventional function of ATG proteins as cellular scaffolds in the regulation of

161 cellular cues that activate the function of ATG proteins during amino acid starvation are incomplete

162 ective analysis to investigate the impact of ATG in patients with acute myeloid leukemia or myelodysp

163 The inclusion of ATG resulted in a significantly lower rate of chronic GV

164 tivity is a prerequisite to the induction of ATG gene transcription and autophagy.

165 Pharmacological inhibition of ATG-dependent phagocytosis by the cardiac glycoside neri

166 We detected increased expression levels of ATG genes, and elevated autophagy activity, in cells lac

167 posure or, in selected patients, omission of ATG may contribute to improved outcomes in pediatric CBT

168 ter, open-label, randomized phase 3 study of ATG as part of a conditioning regimen.

169 A phase II study of ATG+G-CSF in patients with new-onset type 1 diabetes is

170 egulated in neurons through the transport of ATG-9 by KIF1A/UNC-104 to regulate neurodevelopment.

171 n to arrest Type 1 Diabetes (START) trial of ATG therapy in new-onset type 1 diabetes.

172 DNA is inserted at position -517 upstream of ATG of the AtClpB-C gene.

173 ctively, our results suggest that the use of ATG could be detrimental, especially if given too close

174 blation and may help guide the future use of ATG in sensitized transplant recipients.

175 In multivariate analyses, the use of ATG was associated with decreased incidence of acute gra

176 ere, we define common processes dependent on ATGs, and discuss the challenges in mechanistically sepa

177 Daclizumab or ATG combined with a maintenance immunosuppressive regime

178 sed the safety and efficacy of daclizumab or ATG prophylaxis in combination with triple immunotherapy

179 ophylactic therapy with either daclizumab or ATG.

180 n patients receiving nonmyeloablative HCT or ATG in the conditioning regimen.

181 s compared with GAD autoantibody-negative or ATG-treated recipients.

182 autophagic process requiring ATG11 and other ATG components.

183 s) received IL2Mab and Group B (21 patients) ATG as induction immunosuppression.

184 In the ATG group, on 64 evaluable patients, ATG was discontinued 1 (n = 27), 2 (n = 20), or > 2 days

185 antagonist quercetin-3-rutinoside prevented ATG-mediated TF activation, and C5 complement activation

186 n rabbit ATG plus standard GVHD prophylaxis (ATG group) or standard GVHD prophylaxis alone (no ATG gr

187 of the integral membrane autophagy protein, ATG-9.

188 tophagy, however whether autophagy proteins (ATG) regulate cell signalling is unknown.

189 ion of conserved autophagy-related proteins (ATGs) that mediate bulk degradation of cytosolic materia

190 pients receiving antithymocyte globulins (R+/ATG).

191 Depletional antibodies (r-ATG and alemtuzumab) were more cost-effective across all

192 lemtuzumab, rabbit antithymocyte globulin (r-ATG), and interleukin-2 receptor-antagonist.

193 t regimens: rabbit antithymocyte globulin (r-ATG)/EVR (N = 85); basiliximab (BAS)/EVR (N = 102); BAS/

194 A higher proportion of patients in r-ATG/EVR showed subclinical WHAE (13% vs 7% vs 4%, P = 0.

195 In addition, only r-ATG was associated with graft survival benefit over no-i

196 Overall, depletional induction (preferably r-ATG) appears to offer the greatest benefits.

197 f developing clinical or subclinical WHAE (r-ATG/EVR vs BAS/MPS hazard ratio 1.30; BAS/EVR vs BAS/MPS

198 Rabbit ATG appears to achieve excellent cost-effectiveness acce

199 ins are also strongly immunogenic and rabbit ATG induces serum sickness disease in almost all patient

200 e assessed the safety and efficacy of rabbit ATG in preserving islet function in participants with re

201 method, to either pretransplantation rabbit ATG plus standard GVHD prophylaxis (ATG group) or standa

202 rse event]) versus those who did not receive ATG (two [no deaths]).

203 in a 1:1 ratio to receive ATG or not receive ATG, with stratification according to center and risk of

204 randomly assigned in a 1:1 ratio to receive ATG or not receive ATG, with stratification according to

205 2-22.7), were included, of whom 82% received ATG.

206 SSD(+) and SSD(-) patients that had received ATG induction treatment were then assessed for total ant

207 rformed on 25 subjects: 17 subjects received ATG (2.5 mg/kg intravenously) followed by pegylated G-CS

208 ntially more common in patients who received ATG (20 [one of whom died-the only death due to an adver

209 sion was attenuated in patients who received ATG by changes in maximal intimal area (1.0 +/- 1.2 vers

210 37 (37%) of 99 patients who received ATG were free from immunosuppressive treatment at 12 mon

211 Patients receiving ATG had a higher rate of first-year infection (P = 0.003

212 Furthermore, HIV-positive patients receiving ATG induction had a 2.6-fold lower risk of AR (aRR, 0.39

213 n (ATG) as part of the conditioning regimen (ATG group), whereas 579 did not (non-ATG group).

214 Enhanced expression of TOR-regulated ATG genes in TOR-RNAi roots suggested that TOR plays a r

215 tment nor RNAi against autophagy regulators (ATGs) promote cell death.

216 tes, and homologs of many autophagy-related (ATG) genes have been found in Arabidopsis thaliana.

217 ations in any of the core autophagy-related (ATG) genes have been reported in human patients to date.

218 ion and repression of the autophagy-related (ATG) genes is one crucial aspect of autophagy regulation

219 Autophagy-related (ATG) proteins have increasingly demonstrated functions o

220 , mediated by a number of autophagy-related (ATG) proteins, plays an important role in the bulk degra

221 ed actions of a series of autophagy-related (ATG) proteins.

222 uitin-like protein (ublp) autophagy-related (ATG)12 is a component of the ATG12 approximately ATG5-AT

223 therapy with Thymoglobulin, ATG-Fresenius S (ATG-F), and a control group without induction therapy.

224 nt discoveries are revealing that these same ATGs orchestrate processes that are related to, and yet

225 Mutagenesis of a conserved second ATG enhanced the plastidic localization of PGD1 and PGD3

226 ve regulator of the transcription of several ATG genes and a repressor of autophagy induction.

227 t type 1 diabetes is ongoing and may support ATG+G-CSF as a prevention strategy in high-risk subjects

228 destined to rise in the UK, we believe that ATG is a valid option to continue optimizing outcomes of

229 We found that ATG activated tissue factor procoagulant activity (TF PC

230 Cox regression analysis revealed that ATG use was an independent risk factor for CVEs (hazard

231 We showed that ATG-mediated TF activation required complement activatio

232 The ATG and PBSCs were the only variables that independently

233 The ATG had no impact on overall survival, disease-free surv

234 median follow-up time was 3.5 years for the ATG group and 5 years for the alemtuzumab and T cell-rep

235 y separated the Thymoglobulin group from the ATG-F group, while the control group had a similar profi

236 is (>/= 20%) occurred less frequently in the ATG arm (4.3% versus 26.3; P = 0.003).

237 in the inolimomab arm and 51 patients in the ATG arm.

238 he inolimomab and 11 patients (21.5%) in the ATG arms, with a hazard ratio of 0.874 (P = .28).

239 nfidence interval [CI], 22.1 to 46.7) in the ATG group and 68.7% (95% CI, 58.4 to 80.7) in the non-AT

240 ear relapse-free survival was similar in the ATG group and the non-ATG group (59.4% [95% CI, 47.8 to

241 in the primary endpoint: participants in the ATG group had a mean change in C-peptide area under the

242 All except one participant in the ATG group had both cytokine release syndrome and serum s

243 Patients in the ATG group received a mean dose of 4.98 mg/kg +/- 7.9 mg/

244 l at 2 years was significantly higher in the ATG group than in the non-ATG group (36.6% vs. 16.8%, P=

245 tment groups (34 [34%] of 99 patients in the ATG group vs 41 [42%] of 97 in the no ATG group).

246 In the ATG group, on 64 evaluable patients, ATG was discontinue

247 Acute T cell depletion occurred in the ATG group, with slow reconstitution over 12 months.

248 CI 0.04-0.87) was significantly lower in the ATG group.

249 In the ATG-induced group, there was a significant lower rate of

250 , and it has shown remarkable savings in the ATG-induced group.

251 infection begins at -127 bp upstream of the ATG codon and ends +188 bp downstream of the stop codon,

252 Loss of any of the ATG genes, except FgATG17, prevented the fungus from cau

253 on start site 519 base pairs upstream of the ATG initiation sequence, adding 173 N-terminal amino aci

254 t an unbiased RNA interference screen of the ATG proteome to reveal numerous noncanonical roles for A

255 nsertions in the region just upstream of the ATG start codon in the LAP varities, which might be the

256 of a TOC1 transposon 113 bp upstream of the ATG start codon of a putative omega-3 desaturase (CrFAD7

257 carrying uORFs or starting downstream of the ATG START codon.

258 main (LBD) motif within 1 kb upstream of the ATG start codon.

259 y to a segment (-196 to -162 relative to the ATG start codon) of the AAO3 promoter.

260 s-host disease (GVHD) prophylaxis, while the ATG groups received cyclosporin A + prednisone.

261 ions in the inolimomab arm compared with the ATG arm.

262 Usage of this ATG can be preferentially down-regulated by directed ant

263 after induction therapy with Thymoglobulin, ATG-Fresenius S (ATG-F), and a control group without ind

264 TLI/ATG resulted in profound lymphoablation but endogenous h

265 TLI/ATG treated wild-type recipients had increased proportio

266 ynamics of donor hematopoiesis following TLI/ATG, and the effect of Treg on HSC activity.

267 rovide preclinical support for trials of TLI/ATG/alkylator regimens for MHC-mismatched BMT for hemogl

268 at Treg influence donor engraftment post-TLI/ATG by increasing HSC cell cycling, thereby promoting th

269 d 203 eligible patients to treatment (101 to ATG and 102 to no ATG).

270 d 154 individuals, randomly allocating 38 to ATG and 20 to placebo.

271 No deaths were attributable to ATG.

272 ication H3K9ac is added at promoter close to ATG and coding sequence of HvS40 after onset of senescen

273 can be achieved by reducing the exposure to ATG after CBT.

274 es (duration 4-24 months) were randomized to ATG and pegylated G-CSF (ATG+G-CSF) (N = 17) or placebo

275 ective single-center study to assess whether ATG associates with an increased incidence of atheroscle

276 r studies should precisely determine whether ATG-induced immune activation is the causal link between

277 We did a study to test whether ATG provides patient benefit, particularly in reducing t

278 We also tested whether ATG use induces a proatherogenic immune status.

279 e interaction of ERK cascade components with ATG proteins in the cytosol and nucleus.

280 al and relapse-free survival was higher with ATG.

281 and contrasted between patients induced with ATG and those who were not.

282 Patients induced with ATG were more sensitized (54.3% versus 14.3%).

283 renal transplant recipients, induction with ATG is associated with a reduction in the occurrence of

284 ERK2 interacts with ATG proteins via its substrate-binding domains.

285 rt of 889 first kidney graft recipients with ATG induction (86 with SSD [SSD(+)] and 803 without SSD

286 Induction therapy with ATG is associated with reduced first-year coronary plaqu

287 athway during immunosuppressive therapy with ATG may have broader implications for vascular thrombosi

288 did not complete the induction therapy with ATG, and three of 10 required adaptation of maintenance

289 Subjects treated with ATG+G-CSF demonstrated reduced CD4(+) T cells and CD4(+)

290 D was higher in URD without ATG and URD with ATG (P < .0001).

291 without ATG (P = .001), as well as URD with ATG (P = .01), relative to haploidentical transplants.

292 etween URD without ATG (P = .21) or URD with ATG (P = .16), relative to haploidentical transplants.

293 aploidentical, URD without ATG, and URD with ATG groups, respectively (P = .07).

294 aploidentical, URD without ATG, and URD with ATG groups, respectively (P = .44).

295 geneic transplantation than the rate without ATG.

296 III-IV acute GVHD was higher in URD without ATG (P = .001), as well as URD with ATG (P = .01), relat

297 g no survival difference between URD without ATG (P = .21) or URD with ATG (P = .16), relative to hap

298 sk of chronic GVHD was higher in URD without ATG and URD with ATG (P < .0001).

299 , and 36% in the haploidentical, URD without ATG, and URD with ATG groups, respectively (P = .07).

300 , and 17% in the haploidentical, URD without ATG, and URD with ATG groups, respectively (P = .44).