ライフサイエンスコーパス: ATL

1 ATL is classified into 4 distinct clinical diseases: acu

2 ATL is highly refractory to current therapies, making th

3 ATL is needed to not only form, but also maintain, the E

4 ATL is preceded by decades of chronic HTLV-1 infection,

5 ATL tethers and fuses tubules stabilized by the Rtns, an

6 ATLs harness the energy of GTP hydrolysis to initiate a

7 500 sera, ELISA using rLb6H detected all 219 ATL samples (sensitivity of 100.0%) with an overall spec

8 ues and finds effective local control across ATL subtypes.

9 t oncolytic activity against HTLV-1 actuated ATL cells.

10 Acute ATL is the most aggressive form, representing 60% of cas

11 40 substrate-binding domain in 8 of 32 acute ATL patients (25%).

12 ent complication and cause of death in acute ATL patients is the presence of lytic bone lesions and h

13 tive Notch1 signaling in patients with acute ATL.

14 Additional ATLs, including miltefosine and perifosine, also displac

15 xis provides new therapeutic targets against ATL and might explain genomic instability leading to the

16 ctor (HBZ) protein which is expressed in all ATL cases physically interacts with NRF-1 and inhibits t

17 oral lobectomy with amygdalohippocampectomy (ATL), but the utility of interictal epileptiform dischar

18 sformed T cell lines, MT-2, MT-4, SLB-1, and ATL-2.

19 tween HTLV-I asymptomatic carriers (ACs) and ATL and HAM/TSP patients.

20 cluding HTLV-I-seronegative donors, ACs, and ATL and HAM/TSP patients.

21 more, despite recent claims that both AG and ATL are semantic hubs, the two areas responded very diff

22 e DNA lesion search by highly motile ATL and ATL-UvrA complexes on DNA at the molecular level.

23 ly activated in HTLV-I-transformed cells and ATL cells, and activating STAT3 mutations were detected

24 o understand the link between HTLV-1 HBZ and ATL in infected individuals.

25 en they judged conceptual size, both LOC and ATL stimulation eradicated the otherwise robust effect.

26 disparate functional profiles of the LOC and ATL, providing the first evidence of a malleable network

27 onstrated increased fMRI activity in OFC and ATL at the onset of the odor cue itself, followed by res

28 nuclear cells (PBMCs) from ATL patients, and ATL patient sera contain higher concentrations of BDNF t

29 tudies indicated that HTLV-I-transformed and ATL cells, but not normal peripheral blood mononuclear c

30 break TRAIL resistance in HTLV-1-associated ATL by transcriptional down-regulation of c-FLIP, a key

31 So far, HTLV-1-associated ATL is incurable by presently known therapies.

32 nt of select patients with HTLV-I-associated ATL and HAM/TSP.

33 , sampled from three ocean basins (Atlantic [ATL]: n = 30, four species; Mediterranean (MED): n = 56,

34 s of dynamin-like GTPases known as atlastin (ATL).

35 ulum (ER) membranes is mediated by atlastin (ATL), which consists of an N-terminal cytosolic domain c

36 well as the membrane-fusing GTPase atlastin (ATL) and the lunapark protein (Lnp).

37 The dynamin-related GTPase atlastin (ATL) catalyzes membrane fusion of the endoplasmic reticu

38 fusion of tubules mediated by the atlastin (ATL) guanosine triphosphatase (GTPase).

39 nt on the guanosine triphosphatase atlastin (ATL).

40 triphosphatases (GTPases) called atlastins (ATLs), which are also required to maintain ER morphology

41 Here, we show that atlastins (ATLs), a subset of ER resident proteins involved in neur

42 e present the first structure of a bacterial ATL, from Vibrio parahaemolyticus (vpAtl).

43 Because ATL patients are unresponsive to chemotherapy, this mali

44 Maintenance requires a balance between ATL and Rtn, as too little ATL activity or too high Rtn4

45 odal semantic cognition, including bilateral ATL, inferior frontal gyrus, medial prefrontal cortex, a

46 is related to the patients' total, bilateral ATL atrophy.

47 NE assembly requires fusion by both ATL and ER-soluble N-ethyl-maleimide-sensitive factor ad

48 We show that both ATL proteins bind with high affinity to oligodeoxyribonu

49 was reduced by ATL, and engagement of ALX by ATL on both neutrophils and platelets was necessary to p

50 me of prokaryotic NER, to an alkyl lesion by ATL.

51 ults indicate that fusion of ER membranes by ATL and interaction of ER with growing MT ends and dynei

52 in the lesion search mechanism, not only by ATL but also by AGT, thus opening opportunities for cont

53 e further characterize lesion recognition by ATL and directly visualize DNA lesion search by highly m

54 NPA formation in vitro, which was reduced by ATL, and engagement of ALX by ATL on both neutrophils an

55 We further show that Wnt5a secreted by ATL cells favors osteoclast differentiation and expressi

56 L and this may be used for finally capturing ATL.

57 Smoldering/chronic ATL cells produced IL-2 and IL-9 in 6-day ex vivo cultur

58 ere, we demonstrated that smoldering/chronic ATL peripheral blood mononuclear cells spontaneously pro

59 feration in patients with smoldering/chronic ATL that could be targeted for treatment.

60 cells from patients with smoldering/chronic ATL.

61 s, the arsenic/interferon combination clears ATL through degradation of its Tax driver, and this regi

62 utive patients with pathologically confirmed ATL treated with radiotherapy were reviewed.

63 ssion of WT FBXW7 in several patient-derived ATL lines demonstrated strong tumor-suppressor activity

64 potent oncolytic activity in patient-derived ATL transplanted into NSG mice and facilitated a signifi

65 ple worldwide, about 5% of whom will develop ATL.

66 n effective treatment in patients displaying ATL.

67 We found that two duplC-ATL genes underwent pseudogenization and that, in one ca

68 onary basis of a cluster of six genes, duplC-ATLs, which arose from segmental and tandem duplication

69 Most particles (n = 811) were fibres (ATL: 77.1% MED: 85.3% PAC: 64.8%) with blue and black be

70 5%) achieving an excellent outcome following ATL.

71 nhibitors may exert therapeutic benefits for ATL and HAM/TSP patients.

72 (1983-1991) assessed local radiotherapy for ATL.

73 y, there is no accepted curative therapy for ATL.

74 n of this pathway may improve treatments for ATL.

75 In lesser quantities were fragments (ATL: 22.9%: MED: 14.7% PAC: 20.2%) and microbeads (4.8%;

76 ients from ACs (odds ratio = 14.12) and from ATL patients (odds ratio = 7.00).

77 s at a true-positive rate of 85.42% and from ATL patients at a true-positive rate of 75.00%, and mode

78 However, in infected cells from ATL patients, the viral genome is frequently modified to

79 vivo spontaneous proliferation of PBMCs from ATL and HAM/TSP patients by 67.1% and 86.4%, respectivel

80 ipheral blood mononuclear cells (PBMCs) from ATL patients, and ATL patient sera contain higher concen

81 We then assessed rLb6H against sera from ATL patients infected with different species of Leishman

82 Functionally, ATL FBXW7 mutants lost their ability to interact with in

83 with alemtuzumab in a murine model of human ATL (MET-1).

84 tration predicts neural changes in the human ATL and task performance during semantic processing.

85 Our data identify ATLs as central hubs targeted by flaviviruses to establi

86 ither the C-terminal helix or the TMs impair ATL's ability to generate and maintain ER morphology in

87 fector, Pim1, is constitutively activated in ATL cells.

88 the combination of YM155 with alemtuzumab in ATL.

89 cterized non-conserved functional domains in ATL paralogues and show that the ATL interactome is prof

90 diesterase 1 (TDP1), a DNA repair enzyme, in ATL cells.

91 or cell proliferation and tumor formation in ATL-engrafted mice.

92 revent or reduce osteolytic lesions found in ATL patients and improve therapy outcome.

93 onsistent with the loss-of-function found in ATL patients, expression of WT FBXW7 in several patient-

94 ytic bone lesions and hypercalcemia found in ATL patients.

95 1 expression by inhibiting NRF-1 function in ATL cells.

96 sible for its tumor-suppressive functions in ATL cells.

97 ced and 264 repressed genes during growth in ATL compared to that in GM17 laboratory culture medium.

98 fold-greater cell densities during growth in ATL than the dairy-associated strain L. lactis IL1403.

99 lant-inducible genes for L. lactis growth in ATL, xylose metabolism was targeted for gene knockout mu

100 (BIRC5) demonstrated a striking increase in ATL, and its expression was increased in patient ATL cel

101 Genes induced in ATL included those involved in the arginine deiminase pa

102 as a target for therapeutic intervention in ATL patients.

103 oth strains grew to similarly high levels in ATL, indicating redundancy in L. lactis carbohydrate met

104 However, the role of Tax loss in ATL response is disputed, and the molecular mechanisms d

105 tional burden in genes frequently mutated in ATL than did high-risk, age-matched HTLV-1 carriers who

106 Depletion of or mutations in ATL cause an unbranched ER morphology and hereditary spa

107 equency of constitutively activated Notch in ATL patients.

108 CD25(+)CD3(-) phenotype commonly observed in ATL.

109 and production of metabolic end products in ATL as measured by gas chromatography-time of flight mas

110 idence that BIRC5 plays an important role in ATL cell viability and provides important insight into A

111 ism underlying the downregulation of TDP1 in ATL cells remains elusive.

112 Ags were higher in HAM/TSP patients than in ATL patients.

113 nalysis to test whether activity patterns in ATLs carry information about conceptual object propertie

114 threonine (PEST) domain in T-ALLs, those in ATLs have, in addition, single-substitution mutations in

115 Interestingly, ATL cells overexpressed the osteolytic-associated genes-

116 iability and provides important insight into ATL genesis and potential targeted therapies.

117 inhibited STAT5 phosphorylation in isolated ATL T cells ex vivo.

118 i-HIV-1 drug, potently and selectively kills ATL cells.

119 o picture and voice naming in the human left ATL.

120 s placed directly on the surface of the left ATL in human subjects, we demonstrate nearly identical r

121 e dispositions are organized within the left ATL include both a single modality-independent (heteromo

122 is finding has led to the idea that the left ATL is a modality-independent convergence region for pro

123 ct electrophysiologic evidence that the left ATL is heteromodal for proper-name retrieval.

124 Specifically, the left ATL was positively activated for all semantic tasks, but

125 ) dispositions for proper naming in the left ATL.

126 American tegumentary leishmaniasis (ATL) (also known as cutaneous leishmaniasis [CL]) is cau

127 infection to lethal Adult T-cell Leukaemia (ATL); a progression that is more likely in Japanese men

128 he causative agent of adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical spastic p

129 etiological agent of adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical spastic p

130 Adult T-cell leukemia (ATL) and human T-cell lymphotropic virus type I (HTLV-I)

131 he etiologic agent of adult T-cell leukemia (ATL) and the neurological disorder HTLV-I-associated mye

132 entified a cluster of adult T-cell leukemia (ATL) cases in Japan, provided conclusive evidence that H

133 Adult T-cell leukemia (ATL) is a fatal malignancy caused by infection with the

134 Adult T cell leukemia (ATL) is a serious form of cancer with a high mortality r

135 Adult T-cell leukemia (ATL) is an aggressive malignancy of CD4(+)CD25(+) lympho

136 Adult T-cell leukemia (ATL) is an aggressive T-cell malignancy caused by human

137 eration of smoldering adult T cell leukemia (ATL) T cells.

138 Adult T-cell leukemia (ATL), a heterogeneous disease, can be divided into smold

139 in the development of adult T-cell leukemia (ATL), a T-cell malignancy caused by HTLV-1 infection.

140 I) is associated with adult T-cell leukemia (ATL), an aggressive lymphoproliferative disease with a d

141 -1) that recapitulate adult T-cell leukemia (ATL)-like leukemic symptoms and display HTLV-1-specific

142 etiological agent of adult T-cell leukemia (ATL).

143 he causative agent of adult T-cell leukemia (ATL).

144 f leukemia designated adult T-cell leukemia (ATL).

145 tic malignancy termed adult T cell leukemia (ATL).

146 etiological agent of adult T-cell leukemia (ATL).

147 iologically causal of adult T-cell leukemia (ATL).

148 al T-cell malignancy, adult T-cell leukemia (ATL).

149 this paper, we demonstrate that Sey1p, like ATLs, mediates homotypic ER fusion.

150 Alkyltransferase-like (ATL) proteins in Schizosaccharomyces pombe (Atl1) and Th

151 alyses uncover that the CD and AT-hook-like (ATL) motif of Cbx7 constitute a functional DNA-binding u

152 pid edelfosine, a prototype antitumor lipid (ATL), kills yeast cells and selectively kills several ca

153 is metabolized to aspirin-triggered lipoxin (ATL), 15-epi-lipoxin A4.

154 t increased levels of ASA-triggered lipoxin (ATL; 15-epi-lipoxin A4), and blocking the lipoxin A4 rec

155 a balance between ATL and Rtn, as too little ATL activity or too high Rtn4a concentrations cause ER f

156 crucial role for the anterior temporal lobe (ATL) in semantic processing.

157 udies that the human anterior temporal lobe (ATL) is a semantic representational hub.

158 The anterior temporal lobe (ATL) makes a critical contribution to semantic cognition

159 regions, such as the anterior temporal lobe (ATL) or angular gyrus (AG).

160 ng indicate that the anterior temporal lobe (ATL) plays a crucial and necessary role in conceptualiza

161 s to the anterior part of the temporal lobe (ATL) remains to be clarified.

162 we asked whether the anterior temporal lobe (ATL) serves as a hub for a distributed neural circuit th

163 x (OFC) and the left anterior temporal lobe (ATL) was observed in response to words when preceded by

164 t perception, or the anterior temporal lobe (ATL), a "hub" of supramodal conceptual processing.

165 depends on the left anterior temporal lobe (ATL), where lesions can be associated with impaired nami

166 on subregions of the anterior temporal lobe (ATL).

167 r a craniotomy, Anterior Temporal Lobectomy (ATL), or a less invasive method of Selective Laser Amygd

168 The anterior temporal lobes (ATL) have become a key brain region of interest in cogni

169 ritical role of the anterior temporal lobes (ATLs) in object knowledge, fMRI studies using univariate

170 d adult T-cell leukemia and T-cell lymphoma (ATL) are aggressive diseases with poor prognoses, limite

171 elopment of adult T-cell leukaemia/lymphoma (ATL), an aggressive blood cancer, and HAM/TSP, a progres

172 notherapy in adult T-cell leukemia-lymphoma (ATL) patients.

173 xpression in adult T-cell leukemia-lymphoma (ATL).

174 d success in adult T cell leukemia/lymphoma (ATL) and in multiple sclerosis.

175 ction causes adult T-cell leukemia/lymphoma (ATL) and is associated with a variety of lymphocyte-medi

176 tive disease adult T-cell leukemia/lymphoma (ATL) and the neurodegenerative disorder tropical spastic

177 In adult T-cell leukemia/lymphoma (ATL) cell lines and patient T cells, hbz is often the on

178 )-associated adult T cell leukemia/lymphoma (ATL) cells as a model system.

179 Adult T-cell leukemia/lymphoma (ATL) is an aggressive and fatal disease.

180 Adult T cell leukemia/lymphoma (ATL) is an aggressive cancer of CD4/CD25(+) T lymphocyte

181 Adult T-cell leukemia/lymphoma (ATL) is an aggressive hematological malignancy caused by

182 Adult T-cell leukemia/lymphoma (ATL) is etiologically linked to infection with the human

183 1-associated adult T-cell leukemia/lymphoma (ATL) typically has survivals measured in months with che

184 formation in adult T-cell leukemia/lymphoma (ATL), a highly aggressive chemotherapy-resistant maligna

185 ive agent of adult T-cell leukemia/lymphoma (ATL), a malignancy of CD4(+) T cells whose etiology is t

186 es including adult T-cell leukemia/lymphoma (ATL).

187 HAM/TSP), or adult T cell leukemia/lymphoma (ATL).

188 an Arabidopsis thaliana leaf tissue lysate (ATL).

189 nnel, as well as, influenza virions and MDCK-ATL cells infected with influenza viruses of multiple se

190 visualize DNA lesion search by highly motile ATL and ATL-UvrA complexes on DNA at the molecular level

191 icant clinical activity in Tax-driven murine ATL or human patients.

192 ating mutations in Notch in more than 30% of ATL patients.

193 is significantly decreased in the absence of ATL proteins.

194 HTLV-1 infection is the etiological agent of ATL and, unfortunately, most patients succumb to the dis

195 ncoprotein, selectively induces apoptosis of ATL cell lines and has significant clinical activity in

196 driver mutations can be detected in cases of ATL years before the onset of symptoms.

197 The dependence of ATL cells to Pim1 activity was demonstrated using 2 Pim1

198 e intervention to prevent the development of ATL.

199 duals, 2 to 10 years before the diagnosis of ATL.

200 routine use in the serological diagnosis of ATL.

201 c domain but rather mediate the formation of ATL oligomers.

202 ing that this process is a major hallmark of ATL cytotoxicity in yeast.

203 Aspirin also increased the levels of ATL in the lungs of LPS-treated wild-type C57Bl6 mice (v

204 r critical roles in a conserved mechanism of ATL binding to alkylated DNA.

205 In this study, we used a mouse model of ATL and restored expression of the microRNA, miR-124a, t

206 nical testing of AZD1208 in a mouse model of ATL resulted in significant prevention of tumor growth i

207 umor formation in a xenograft mouse model of ATL.

208 ed to improvement in treatment or outcome of ATL.

209 n, T-cell proliferation, and pathogenesis of ATL in HTLV-1-infected individuals.

210 lay an important role in the pathogenesis of ATL.

211 c instability leading to the pathogenesis of ATL.

212 sidered for symptomatic local progression of ATL.

213 ty characterized by reduced proliferation of ATL cells.

214 r there would be autonomous proliferation of ATL leukemic cells, we purified leukemic cells from pati

215 These results reinforce the relevance of ATL in semantic memory, as well as its amodal organizati

216 erently, with results supporting the role of ATL, but not AG, in semantic representation.

217 clinical manifestations, different stages of ATL have different molecular signatures.

218 monomeric pre- and post-hydrolysis states of ATL.

219 ients with smoldering or chronic subtypes of ATL, or from those with HAM/TSP whose PBMCs are associat

220 ) T-cell immunophenotype similar to those of ATL cells, suggesting that HBZ protein has important rol

221 Clinical treatment of ATL patients with Zenapax or bortezomib decreased BIRC5

222 ovel therapeutic target for the treatment of ATL.

223 Cytotoxicity of ATLs is mainly dependent on the changes they induce in p

224 of wild-type or mutant ATL1 or depletion of ATLs alters ER morphology and affects store-operated cal

225 pting its repair by human AGT, a hallmark of ATLs.

226 e further evidence for the conserved role of ATLs in this primordial mechanism of DNA repair.

227 Based on the high similarity of ATLs and the DNA-interacting domain of AGTs, our results

228 nic/interferon-treated HTLV-1 transformed or ATL cells, Tax is recruited onto NBs and undergoes PML-d

229 Hence, the fingerprint of Tax is all over ATL and this may be used for finally capturing ATL.

230 sis by applying rTMS to normal participants: ATL stimulation generates a category-general impairment

231 and its expression was increased in patient ATL cells resistant to the anti-CD52 monoclonal antibody

232 while ATL can be measured in tissue, plasma ATL is not a biomarker of vascular COX-2 expression.

233 -2-knockout mice to establish whether plasma ATL could be used as a biomarker of vascular COX-2 in vi

234 Here we determine Schizosaccharomyces pombe ATL structures without and with damaged DNA containing t

235 mutations were detected in 25.5% of primary ATL patients.

236 Golgi fraction isolated from IL-2-producing ATL cells, we detected by Western blot phosphorylated Ja

237 Alkyltransferase-like proteins (ATLs) are a novel class of DNA repair proteins related t

238 Alkyltransferase-like proteins (ATLs) share functional motifs with the cancer chemothera

239 dditionally, alkyltransferase-like proteins (ATLs), which are structurally similar to AGTs, have been

240 Screen analysis confirmed non-redundant ATL functions and identified a specific role for ATL3, a

241 sk, age-matched HTLV-1 carriers who remained ATL-free after a median of 10 years of follow-up.

242 hy as well as to the balance of left > right ATL atrophy.

243 Disinhibition is related to right ATL and orbitofrontal atrophy, and face recognition to r

244 ontal atrophy, and face recognition to right ATL volumes.

245 nctional connectivity between left and right ATLs in patients with chronic aphasic stroke has been il

246 nthetic regenerated cellulosic fibres (SRCF; ATL: 63.2%: MED: 5.8% PAC: 68.9%).

247 ated with better outcomes following standard ATL in magnetic resonance imaging-negative TLE.

248 ric patients with TLE who underwent standard ATL between January 1, 1990, and October 15, 2010, were

249 d MRS investigation showed that the stronger ATL BOLD response induced by the semantic task, the lowe

250 viduals developed acute and lymphoma subtype ATL.

251 t connectivity is identified in the superior ATL, which is connected to auditory and language areas.

252 s to restore the fusion activity of tailless ATL.

253 ile still allowing VSV to effectively target ATL cells.

254 We conclude that ATL regulates neutrophil-platelet aggregation and that p

255 Here we demonstrate that ATL-derived or HTLV-1-transformed cells are dependent on

256 Our study demonstrated that ATL cells do not express high levels of beta-catenin but

257 ling Wnt gene expression, we discovered that ATL patient leukemia cells shifted expression toward the

258 combined with structural results reveal that ATLs sculpt alkylated DNA to create a genetic and struct

259 inactive, strong evidence has suggested that ATLs target alkyl lesions to the nucleotide excision rep

260 The ATL includes several different cortical areas, namely, t

261 They reveal that (i) the ATL is an important element of the ventral semantic path

262 iduals with higher GABA concentration in the ATL showed better semantic performance and stronger BOLD

263 Multiple sensory modalities converge in the ATL.

264 and resting-state GABA concentrations in the ATL.

265 hanism underlying semantic processing in the ATL.

266 lacing retrograde tracer injections into the ATL: the temporal polar (n = 3), perirhinal (areas 35 an

267 r performance and reacted with 100.0% of the ATL and 89.4% of the VL samples.

268 However, the functional connectivity of the ATL and the functional network underlying semantic cogni

269 In addition, subregions of the ATL have distinct functional properties and thus the pot

270 However, the neurochemical nature of the ATL in the semantic processing remains unclear.

271 l to the neurobiological contribution of the ATL to semantic cognition.

272 valuate the consequences that lesions on the ATL have on the neurocognitive network supporting semant

273 Recent structural studies on the ATL soluble domain reveal two dimeric conformers propose

274 ave primarily implicated regions outside the ATL.

275 domains in ATL paralogues and show that the ATL interactome is profoundly reprogrammed following den

276 Together, our results suggest that the ATL is a central hub for representing and retrieving per

277 e and connectivity analyses suggest that the ATL stores abstract person identity representations.

278 igm designed to ensure signal throughout the ATL.

279 reflecting typical object size), whereas the ATL contributes to this computation when the context req

280 We studied the LPFC connections with the ATL by placing retrograde tracer injections into the ATL

281 in contrast, the dLPFC connections with the ATL were weak.

282 ces (MFC) showed dense connectivity with the ATL, namely, A13 with the temporopolar and perirhinal co

283 ers (MED: 61.2%; PAC: 3.4%), thermoplastics (ATL: 36.8%: MED: 20.7% PAC: 27.7%) and synthetic regener

284 Despite this, ATL was unchanged in plasma after LPS and aspirin.

285 Thus, ATL and AG do not share a common interest in semantic ta

286 substitutions cluster in regions adjacent to ATL's catalytic site, but the consequences for the GTPas

287 est that activated Notch may be important to ATL pathogenesis and reveal Notch1 as a target for thera

288 d by LOC stimulation but stayed resilient to ATL stimulation.

289 p and its homologues function analogously to ATLs in mediating ER fusion.

290 erbal production ability is related to total ATL atrophy as well as to the balance of left > right AT

291 -9/IL-15)-dependent manner, while acute-type ATL peripheral blood mononuclear cells did not prolifera

292 ipants, 12 underwent SLAH while 10 underwent ATL.

293 In the resting-state analysis, the ventral ATL (vATL) and anterior middle temporal gyrus (MTG) were

294 When ATL function is compromised, the morphology of the endop

295 We suggest a model in which ATL-mediated fusion counteracts the instability of free

296 study is the first to demonstrate that while ATL can be measured in tissue, plasma ATL is not a bioma

297 While ATLs are per se catalytically inactive, strong evidence

298 reversed ASA protection, and treatment with ATL in both LPS and TRALI models protected from ALI.

299 rred at much lower levels in the Golgi of WT ATL cells.

300 oliferation of IL-2-dependent wild-type (WT) ATL cells but not cells transfected with IL-2, suggestin