ライフサイエンスコーパス: ATG

1 ATG should be added to myeloblative and non-myeloblative

2 ATG treatment resulted in highly significant increases o

3 ATG-exposure measures were determined with a validated p

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

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

6 Subjects (N = 89) were randomized to 1) ATG and pegylated granulocyte colony-stimulating factor

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

8 ulocyte colony-stimulating factor (GCSF), 2) ATG alone, or 3) placebo.

9 In general, only 20 ATG genes are highly conserved, including most but not a

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

11 the autophagy proteins autophagy-related 7 (ATG) and light chain 3 (LC3).

12 After ATG induction, although absolute counts of CD4 and CD8 T

13 ) study, we compared T cell phenotypes after ATG or non-ATG induction.

14 small amounts of EBNA3A using an alternative ATG at residue 15.

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

16 nsitive" recognition sites combined with an "ATG-out" design.

17 in subjects treated with ATG (P = 0.011) and ATG/GCSF (P = 0.022) versus placebo.

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

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

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

21 (+)CD4(+) T cells following low-dose ATG and ATG/GCSF.

22 treated with busulfan, cyclophosphamide, and ATG.

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

24 31 (60%) patients died in the inolimomab and ATG arms, respectively.

25 phagosomes and that defects in transport and ATG-4.2-mediated maturation genetically interact to enha

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

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

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

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

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

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

32 Arctigenin (ATG) is a major component of Fructus Arctii, a tradition

33 or alternative initiation of translation at ATG-40, are the predominantly expressed p53 variants in

34 ode pathogens with 25 Arabidopsis autophagy (ATG) proteins.

35 Both MV and stretch first induce autophagy (ATG 5-12 [autophagy related 5-12] and LC3B-II [microtubu

36 requires the induction of several Autophagy (ATG) genes.

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

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

39 Enhanced PP2A activity by ATG reduces p65 NF-kappaB-mediated inflammatory response

40 nflammation are two key pathways affected by ATG treatment, and mass spectrometry analysis identified

41 CI, 0.62-3.24; P = 0.4) at 1-year post-KT by ATG dose.

42 acute rejection (AR) among KT recipients by ATG dose.

43 dependent autophagy still requires canonical ATG factors including FIP200.

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

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

46 divergence also was observed to several core ATG genes, such as highly divergent ATG8 paralogs in der

47 the lysosome in the absence of several core ATGs, including the LC3 lipidation machinery.

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

49 sed PD-1(+)CD4(+) T cells following low-dose ATG and ATG/GCSF.

50 re studies should determine whether low-dose ATG might prevent or delay the onset of type 1 diabetes.

51 Low-dose ATG partially preserved beta-cell function and reduced H

52 o reveal alternative isoforms and downstream ATG sites, which will aid users in avoiding the expressi

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

54 codon is inserted downstream from the first ATG and the open reading frame is disrupted by a 1-bp in

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

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

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

58 afted patients presenting with SSD following ATG induction treatment.

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

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

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

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

63 to probe the role of autophagy-related gene (ATG)14, a PI3KC3-C1-specific subunit implicated in targe

64 iptional control of autophagy-related genes (ATGs) in the intestinal epithelium.

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

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

67 Optimizing antithymocyte globulin (ATG) dosage is critical, particularly for high-risk kidn

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

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

70 combining PTCY with antithymocyte globulin (ATG) may help to reduce GVHD incidence.

71 arding concerns that antithymocyte globulin (ATG) might increase HCV-related complications.

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

73 onal induction using antithymocyte globulin (ATG) reduces rates of acute rejection in adult kidney tr

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

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

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

77 versus steroids plus antithymocyte globulin (ATG).

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

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

80 rated that low-dose anti-thymocyte globulin (ATG) (2.5 mg/kg) preserved beta-cell function and reduce

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

82 tation (AHSCT) with anti-thymocyte globulin (ATG) conditioning as treatment of active multiple sclero

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

84 The use of anti-thymocyte globulin (ATG) has represented the standard of care in graft-versu

85 rding concerns that anti-thymocyte globulin (ATG) might increase HCV-related complications.

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

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

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

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

90 gone thymoglobulin (antithymocyte globulins [ATG]) or basiliximab (BSX) therapy.

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

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

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

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

95 5% CI, 65%-84%) and 68% (95% CI, 60%-78%) in ATG and BSX group, respectively, without significant dif

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

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

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

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

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

101 me immediately at the translation initiating ATG of TSLP.

102 is abolished via a mutation in the initiator ATG of the ORC5 gene.

103 show that these CIAO (cross-over insensitive ATG-out) vectors virtually eliminate leak expression.

104 ation of orf-I expression by mutation of its ATG initiation codon abolishes the infectivity of the mo

105 All or majority of the key ATG genes were lost in several fungal groups with unique

106 Here we systematically identified 41 known ATG genes in 331 species and analyzed their distribution

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

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

109 In adjusted and unadjusted models, ATG induction was associated with increased early event-

110 Moreover, ATG genes have diverse physiologically important roles i

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

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

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

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

115 onal transcription and repeat-associated non-ATG (RAN) have blurred these distinctions.

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

117 Repeat-associated non-ATG (RAN) translation is emerging as a driver of pathoge

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

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

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

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

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

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

124 NAs and six dipeptide repeat-associated, non-ATG (RAN) proteins, but their roles in disease are uncle

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

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

127 compared T cell phenotypes after ATG or non-ATG induction.

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

129 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

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

131 n frequency of naive T cells compared to non-ATG induction.

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

133 ith ATG versus placebo (P = 0.00005) but not ATG/GCSF versus placebo (P = 0.032).

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

135 d with steroids plus ATG, as the addition of ATG improves both response rates and graft survival.

136 e III rejection treated with the addition of ATG, and graft survival rates were significantly better

137 de II rejection treated with the addition of ATG.

138 Then, we studied the association of ATG (versus IL2RA) with KT outcomes (rejection, graft fa

139 Then, we studied the association of ATG (vs.

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

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

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

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

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

145 ther, independent losses and duplications of ATG genes have occurred throughout the fungal kingdom an

146 We examined the effects of ATG on the early clinical outcomes of alloimmune events

147 ironment that may compromise the efficacy of ATG therapy.

148 oantigens may improve safety and efficacy of ATG treatment.

149 conserved, the conservation and evolution of ATG genes at kingdom-wide remains to be conducted.

150 dge, this work presents the first example of ATG transcript regulation via 3' binding factors and exo

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

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

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

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

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

156 Moreover, majority of ATG genes had A-to-I RNA editing during sexual reproduct

157 ts demonstrate a renoprotective mechanism of ATG via PP2A activation and establish PP2A as a potentia

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

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

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

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

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

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

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

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

166 Here we demonstrate that ATG16L1 and other ATG proteins mediate protection against alpha-toxin thro

167 suppressive agents, superiority of PTCY over ATG was confirmed.

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

169 should usually be treated with steroids plus ATG, as the addition of ATG improves both response rates

170 ted with steroids alone versus steroids plus ATG.

171 ree patients were treated with steroids plus ATG.

172 rates of acute rejection in this population, ATG appears to be safe and reasonable for HCV+ recipient

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

174 ion in the cell body depends on the protease ATG-4.2, but not the related ATG-4.1, and that ATG-4.2 c

175 1B-light chain 3, autophagy-related protein (ATG)7, ATG2b, and autophagosome formation Unc-51 like ki

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

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

178 lls infused, significantly higher for PTCY + ATG patients.

179 ophenolate mofetyl + PTCY (n = 32) or PTCY + ATG (n = 26) as GVHD prophylaxis.

180 The results show that PTCY + ATG versus PTCY alone significantly limits the occurrenc

181 both types of transplant (PTCY versus PTCY + ATG) investigate their influence on patient outcomes.

182 h a slower T cell reconstitution with PTCY + ATG may limit GVHD occurrence, the quicker reconstitutio

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

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

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

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

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

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

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

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

191 Rabbit ATG appears to achieve excellent cost-effectiveness acce

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

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

194 arms included induction therapy with rabbit ATG, mycophenolate sodium, or mycophenolate mofetil and

195 in MS patients undergoing AHSCT with rabbit ATG.

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

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

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

199 HCV+ recipients were less likely to receive ATG than HCV- recipients (living donor, adjusted odds ra

200 HCV+ recipients were less likely to receive ATG than HCV- recipients (living donor, aOR=0.640.770.91

201 2-22.7), were included, of whom 82% received ATG.

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

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

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

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

206 HCV- KT recipients in 1999-2016 who received ATG or interleukin-2 receptor antagonist (IL2RA) for ind

207 HCV- KT recipients in 1999-2016 who received ATG or interleukin-2 receptor antagonist (IL2RA) for ind

208 In contrast, HCV+ recipients who received ATG were at lower risk of acute rejection compared to th

209 In contrast, HCV+ recipients who received ATG were at lower risk of acute rejection compared to th

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 TCY were matched with 179 patients receiving ATG.

213 ation of recipient HCV status with receiving ATG (versus IL2RA) using multilevel logistic regression.

214 ation of recipient HCV status with receiving ATG (vs.

215 In elderly recipients, ATG does not lead to poorer outcomes compared with BSX a

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

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

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

219 on the protease ATG-4.2, but not the related ATG-4.1, and that ATG-4.2 can cleave LGG-1/Atg8/GABARAP

220 autophagy mediated by the autophagy-related (ATG) Cys protease AtATG4a.

221 vered virtually all known autophagy-related (ATG) factors as well as previously uncharacterized facto

222 rmation requires multiple autophagy-related (ATG) factors.

223 558 genes, including the autophagy-related (ATG) gene MoATG4, was altered in MoHMT1 deletion mutants

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

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

226 scriptional regulation of autophagy-related (ATG) genes upon nutrient deprivation.

227 evolutionarily conserved autophagy-related (ATG) genes.

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

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

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

231 inds a specific subset of autophagy-related (ATG) transcripts and prevents their 3' to 5' degradation

232 rs, including the protein autophagy-related (ATG)-9A and the lipid, phosphatidylinositol-4-phosphate

233 graded by autophagy in an AUTOPHAGY-RELATED (ATG)5-dependent manner, and this degradation is promoted

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

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

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

237 n the induction protocol changed to a single ATG dose (3 mg/kg).

238 recipients without CMV prophylaxis, a single ATG dose decreased the risk of CMV infection without inc

239 or clinical and transplant factors, a single ATG dose was associated with a lower risk of CMV infecti

240 May 21, 2015) to determine whether a single ATG dose was safe and effective in patients without CMV

241 These results suggest a model for how some ATG genes bypass the general translational suppression t

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

243 G-4.2, but not the related ATG-4.1, and that ATG-4.2 can cleave LGG-1/Atg8/GABARAP from membranes.

244 These findings indicate that ATG proteins mediate a previously unknown form of defenc

245 Here we report that ATG administration is sufficient to attenuate proteinuri

246 Our studies revealed that ATG-4.2 is specifically necessary for the maturation and

247 Our findings suggest that ATG, as compared to IL2RA, may lower the risk of acute r

248 The ATG and PBSCs were the only variables that independently

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

250 ice exacerbates DKD injury and abrogates the ATG-mediated renoprotection.

251 two ascomycetes and deletion of FgATG11, the ATG gene with the most editing sites in Fusarium affecte

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

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

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

255 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

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

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

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

259 ere included in the BSX group and 179 in the ATG group with the average age of 71.0 and 70.5 years, r

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

261 tivation is dependent on the function of the ATG conjugation system, which mediates LC3 lipidation.

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

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

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

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

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

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

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

269 No deaths were attributable to ATG.

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

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

272 gradation by the exosome complex, leading to ATG mRNA stabilization and accumulation.

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

274 ein phosphatase 2 A (PP2A) as one of the top ATG-interacting proteins in renal cells.

275 ns shortly after the start codons of the two ATG mRNAs are necessary for their translational regulati

276 o study has compared the outcomes of PTCY vs ATG in 9/10 MMUD transplants.

277 However, whether ATG specifically provides renoprotection in DKD is not k

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

279 While ATG may improve delayed graft function, it may also be a

280 us reactivation (EBV-R) following AHSCT with ATG for severe autoimmune conditions is an underrecogniz

281 ogic parameters are drastically altered with ATG induction, long-term clinical benefits remain unclea

282 te GVHD was observed with PTCY compared with ATG.

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

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

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

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

287 reduced at 2 years in subjects treated with ATG (P = 0.011) and ATG/GCSF (P = 0.022) versus placebo.

288 ignificantly higher in subjects treated with ATG versus placebo (P = 0.00005) but not ATG/GCSF versus

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).