ライフサイエンスコーパス: Jurkat cell

1 further understanding the cancer biology of Jurkat cells.

2 model membranes as well as to the surface of Jurkat cells.

3 ssociated apoptotic cell death in cocultured Jurkat cells.

4 R and only the mutant allele is expressed in Jurkat cells.

5 uring Fas ligand (FasL)-induced apoptosis in Jurkat cells.

6 s with SVGA-Tat cells or with HIV-1-infected Jurkat cells.

7 NA knockdown of the GAPDH gene in individual Jurkat cells.

8 time-dependent reduction of PI-3,4,5-P(3) in Jurkat cells.

9 ndependent mitochondrial permeabilization in Jurkat cells.

10 ing 4-HNE-induced, Fas-mediated apoptosis in Jurkat cells.

11 cells and Namalwa cells but not in U937 and Jurkat cells.

12 etected only in TCR-ligated Siva-1 knockdown Jurkat cells.

13 pressed TRPC1 in HEK293 cells and I(crac) in Jurkat cells.

14 LV-1-transformed lines and in Tax-expressing Jurkat cells.

15 full-length KIR and expressed them in human Jurkat cells.

16 + T cell clone and expressed this HCV TCR in Jurkat cells.

17 (BSO) was studied in NB4, U937, Namalwa, and Jurkat cells.

18 ogy phosphatase (SHP)-2 and class IA PI3K in Jurkat cells.

19 ne receptor 4 (CXCR4)-mediated chemotaxis of Jurkat cells.

20 stores IL-2 production by anthrax LT-treated Jurkat cells.

21 pression, and phagocytosis rate of apoptotic Jurkat cells.

22 d transactivation as compared with wild type Jurkat cells.

23 cin- and anti-CD3-induced IL-2 production in Jurkat cells.

24 opy screen to detect Ab binding to apoptotic Jurkat cells.

25 formed cells including U937, HL-60, THP, and Jurkat cells.

26 bited ratio-dependent cytotoxicity to Fas(+) Jurkat cells.

27 of HeLa cells and Fas ligand stimulation of Jurkat cells.

28 take during passive transfection in HeLa and Jurkat cells.

29 ptor (IL-1R)-related protein 2 (IL-1Rrp2) in Jurkat cells.

30 ts cell growth in autonomously proliferating Jurkat cells.

31 LCB1 protein expression, or SPT activity in Jurkat cells.

32 n kinetics displayed by Tax1/Jurkat and Tax2/Jurkat cells.

33 d NFATc2 in nuclear extracts from Hut102 and Jurkat cells.

34 nol, were evaluated for SHG effectiveness in Jurkat cells.

35 ol 13-acetate (PMA) and Ionomycin stimulated Jurkat cells.

36 ced abrogation of MAL-II and PNA epitopes in Jurkat cells.

37 cid-extracted histones from HeLa, MCF-7, and Jurkat cells.

38 s of VacA to cause functional alterations in Jurkat cells.

39 fied 96 glycoproteins with the Tn antigen in Jurkat cells.

40 iptional activity in transiently transfected Jurkat cells.

41 mplex isolated from the nucleus of activated Jurkat cells.

42 and non-CAAX predominant in U2OS, HeLa, and Jurkat cells.

43 In Jurkat cells, a density-dependent increase in cross-corr

44 ited anti-TCR-mediated CD69 up-regulation in Jurkat cells, a human T leukemic cell line.

45 epithelial cell lines (Beas-2B and A549) and Jurkat cells, a leukemia cell line derived from T lympho

46 As compared with Jurkat cells, a smaller PKC polypeptide and mRNA were ex

47 necessary for the induction of apoptosis in Jurkat cells, a T-cell leukemia line.

48 ing shRNA to knock down ADAM17 expression in Jurkat cells, a well-studied cell line in terms of the m

49 Overexpression of HRES-1/Rab4 in Jurkat cells abrogated HIV infection, gag p24 production

50 7 chemoattraction, whereas CXCR1-transfected Jurkat cells acquired responsiveness.

51 ents showed that epithelial ADAM-15-mediated Jurkat cell adhesion to Caco2-BBE cells enhances the mec

52 Jurkat cell adhesion to osteopontin was markedly enhance

53 gmentation were suppressed in MST1 knockdown Jurkat cells after etoposide treatment.

54 mediated elevated resistance to apoptosis in Jurkat cells after serum deprivation, Tax1 was unique in

55 ndothelial cells, was also anti-apoptotic in Jurkat cells against tumor necrosis factor and etoposide

56 ering RNA-mediated knockdown of PKC-theta in Jurkat cells also resulted in apoptosis upon TCR stimula

57 Jurkat cells also underwent apoptosis in a dose-dependen

58 y reduced cell cycle arrest and apoptosis in Jurkat cells and a reduction in the proinflammatory resp

59 sion of the regulatory MAT-IIbeta subunit in Jurkat cells and accordingly shifted the K(m L-Met) of t

60 pheral blood naive CD4(+) T cells as well as Jurkat cells and analyzed their effects on cellular beha

61 0% at 180 microM, and 80% inhibition between Jurkat cells and Caco-2 cells was seen at 90 microM.

62 ate this by reconstructing the cell cycle of Jurkat cells and disease progression in diabetic retinop

63 of H. pylori extracts and live H. pylori on Jurkat cells and freshly isolated human normal T lymphoc

64 nd mediated truncation of SCN5A mRNA in both Jurkat cells and human embryonic stem cell-derived cardi

65 xin binding and CdtB internalization in both Jurkat cells and human macrophages.

66 ased the mitogen-induced [Ca(2+)](i) rise in Jurkat cells and in activated T lymphocytes.

67 ent 5-azacytidine induced PLS3 expression in Jurkat cells and in vitro methylation of the cloned PLS3

68 y showed that Px44-TRAIL caused apoptosis of Jurkat cells and inhibited IFN-gamma production by activ

69 alpha induced extrinsic apoptosis in control Jurkat cells and necroptosis in FADD-deficient cells; tr

70 rther supported by experiments in which both Jurkat cells and normal human lymphocytes were protected

71 diated down-regulation of SOCS1 and SOCS3 in Jurkat cells and normal T cells enhanced the transcripti

72 In this study, using Jurkat cells and OT-I TCR transgenic primary murine CTLs

73 CSup, derived from both FasL-overexpressing Jurkat cells and PBMC, could induce cell death, the requ

74 eater in CypA-rich MT-2 and H9 cells than in Jurkat cells and peripheral blood mononuclear cells (PBM

75 IKKVII likewise reduced IL-22 induction in Jurkat cells and peripheral blood mononuclear cells.

76 ference-induced knockdown of Zap70 or Lck in Jurkat cells and peripheral blood T lymphocytes also res

77 eracts with Ro60 on the surface of apoptotic Jurkat cells and prevents binding of anti-Ro60 IgG.

78 We characterized in Jurkat cells and primary T lymphocytes a pathway depende

79 X-7081 binding to Hsp90 was characterized in Jurkat cells and RA synovial fibroblasts (RASFs).

80 ased the viability of MVA-infected THP-1 and Jurkat cells and reduced several biochemical hallmarks o

81 the maintenance of the leukemic phenotype in Jurkat cells and showed that TAL1 binding can be associa

82 4 were able to inhibit cell adhesion between Jurkat cells and SRBC nearly 50% at 180 microM, and 80%

83 to rescue signaling defects in LAT-deficient Jurkat cells and thymocyte development in LAT(-/-) mice.

84 status of the IFNgamma and IL4 promoters in Jurkat cells and two lung adenocarcinoma cell lines, and

85 he reactivity of these ATG preparations with Jurkat cells and with primary leukocytes.

86 a factor of 18 times stiffer than lymphoid (Jurkat) cells and six times stiffer than human neutrophi

87 S formation and phospholipid peroxidation in Jurkat cells, and either chemical interference with NADP

88 owth and survival of human leukemia U937 and Jurkat cells, and enhanced apoptosis and cleavage of Bcl

89 HEXIM2 is expressed in HeLa and Jurkat cells, and glycerol gradient analysis and immunop

90 AP coprecipitates with dynein from activated Jurkat cells, and loss of ADAP prevents MTOC translocati

91 al cell lines, including cholangiocarcinoma, Jurkat cells, and osteoclasts.

92 onserved sequences have enhancer activity in Jurkat cells, and that many of the orthologous mouse seq

93 ished model of Fas/CD95-induced apoptosis in Jurkat cells, and to determine the mechanism by which CO

94 ed TALENs along with a targeting vector into Jurkat cells, and we confirmed the precise introduction

95 gnaling significantly reduced SW620-mediated Jurkat cell apoptosis.

96 As a proof of concept, Jurkat cells are enriched to high purity of viable cells

97 reduced in Zap70-negative and Zap70-inactive Jurkat cells as compared with wild-type cells.

98 NF-kappaB in an IL-1Rrp2-dependent manner in Jurkat cells as well as in multiple other human and mous

99 sis in both peripheral blood lymphocytes and Jurkat cells, as it is an essential pathway to control T

100 When added to Jurkat cells at 10 microM, this receptor enhanced uptake

101 99% of fluorescent- and magnetically-labeled Jurkat cells at reasonable throughputs (10(3) cells/min)

102 DNase I hypersensitive site distal to LTA in Jurkat cells based on reporter gene analysis, with evide

103 By using primary CD4(+) and Jurkat cell-based in vitro HIV-1 latency models, we obse

104 ssion of ADAM-15 in Caco2-BBE cells enhanced Jurkat cell binding, and overexpression of ADAM-15 in Ju

105 xpression of pro-IL-16 in pro-IL-16-negative Jurkat cells blocks cell cycle progression from G(0)/G(1

106 g RNA increases CD1D transcripts in K562 and Jurkat cells but there are different levels of surface C

107 NA, protein level, and activity were high in Jurkat cells but undetectable in Raji cells.

108 activation by NPI-0052 was seen in wild-type Jurkat cells, but was significantly lessened in Fas-asso

109 ficantly elevated cAMP was also triggered in Jurkat cells by adding exosomes with ATP but not by addi

110 1 tat into HeLa cells or infection of H9 and Jurkat cells by HIV-1 increased HRES-1/Rab4 protein leve

111 iated signaling was seen after engagement of Jurkat cells by perforin-deficient human cytotoxic lymph

112 Conversely, reconstitution of PTEN in Jurkat cells by using a tetracycline (Tet-on)-inducible

113 In Jurkat cells, calmodulin binds to Fas, the death recepto

114 the CD8alpha and CD8beta chains into CD8(-) Jurkat cell clones expressing cloned TCRs with known ant

115 the proviral integration position of latent Jurkat cell clones, we demonstrate that this drug combin

116 ed on lysates made from wild-type and mutant Jurkat cells cocultured with SK-RC-45 revealed caspase a

117 nt cytotoxicity toward human T-cell leukemia Jurkat cells compared with a panel of cancer cell lines

118 spectrometry of permethylated O-glycans from Jurkat cells confirmed the presence of significant amoun

119 o implementation of the proposed approach in Jurkat cells confirms a 63% reduction in tracking error

120 vation in vivo, we developed a population of Jurkat cells containing integrated, but transcriptionall

121 y active form of calcineurin in PKC-theta-/- Jurkat cells could readily overcome the above inhibition

122 TFF2 pretreatment of Jurkat cells decreased Ca2+ rise and chemotactic respons

123 Studies with Jurkat cells deficient in Lck and CD45 demonstrate that

124 erexpression of FLAG-tagged HOX5 proteins in Jurkat cells demonstrated HOX5 binding to the Gata3 locu

125 T cell receptor agonist antibody-stimulated Jurkat cells demonstrating a transient increase in NFAT-

126 uced CD69 up-regulation and NFAT activity in Jurkat cells, demonstrating that kinase activity is requ

127 1 inhibits HIV-1 replication in CD4-positive Jurkat cells, despite its capability of up-regulating CD

128 Similarly, depletion of TIP47 in Jurkat cells did not impair HIV-1 Env incorporation, vir

129 Usp12(-/-) Jurkat cells displayed defective NFkappaB, NFAT, and MAP

130 P/AMP was similarly absent in RIP1-deficient Jurkat cells during apoptotic responses to chemotherapeu

131 r HL60 cells, E(infinity) = 48 +/- 35 Pa for Jurkat cells, E(infinity) = 156 +/- 87 for neutrophils,

132 a cells and inhibition of IL-2 production by Jurkat cells, effects identical to those produced by the

133 Further, caspase-8-deficient Jurkat cells efficiently cleaved Bid and were sensitive

134 In stably XIAP-transfected Jurkat cells, embelin effectively overcomes the protecti

135 ll binding, and overexpression of ADAM-15 in Jurkat cells enhanced their aggregation.

136 model of leukemia, control shRNA-transduced Jurkat cells exhibited heightened engraftment, whereas c

137 Here we demonstrated that for Jurkat cells exposed to high concentrations of Cdt (>0.2

138 Jurkat cells express several members of the multidrug re

139 When Jurkat cells expressing a dominant negative form of NDE1

140 Live-cell imaging of Jurkat cells expressing green fluorescent protein-RBD, a

141 signaling, and cell proliferation in tet-off Jurkat cells expressing the GBV-C envelope glycoprotein

142 osphorylation, and cellular proliferation in Jurkat cells following activation through the TCR compar

143 We show that in 293T and Jurkat cells, forced expression of active NPM-ALK, but n

144 he ability of the Bcl-2 transgene to protect Jurkat cells from RelA degradation, caspase activation,

145 e also performed gene expression analysis on Jurkat cells, genetically engineered to express exogenou

146 luoromethyl ketone] and in caspase-resistant Jurkat cells (ICAD/double-mutated) that express a mutant

147 annose decreases cell surface sialylation in Jurkat cells in a dose-dependent manner up to 80%, quant

148 We show that Jurkat cells in culture rapidly modify the monocarbonato

149 ges ingested equivalent numbers of apoptotic Jurkat cells in the presence and absence of serum.

150 nx1-independent pathway for ATP release from Jurkat cells in the presence of benzyloxycarbonyl-VAD, a

151 stem used in this study was the viability of Jurkat cells in the presence of the agent Triton X-100).

152 soluble 6D VCAM-1 binding to alpha4beta1 on Jurkat cells (in 1 mM MnCl2) was 2 x 10(-9) M, compared

153 sexpression of wild-type or R620W Pep/Lyp in Jurkat cells, in the context of its binding partner Csk,

154 ysis, using WIP and WASP cotransfection into Jurkat cells, in which strong induction of NFAT reporter

155 nhibition of caspase 8 or FADD, which render Jurkat cells incapable of sphingolipid signaling and apo

156 However, Gb(3)-negative VT-resistant CHO/Jurkat cells incorporate adaGb(3) to become VT1/VT2-sens

157 o found that ADAM-15-mediated aggregation of Jurkat cells increases the expression of tumor necrosis

158 ells and Zap70 or Lck-deficient/Lck-inactive Jurkat cells, indicating an essential role of these kina

159 In this work, we demonstrate that Jurkat cells induced to die with actinomycin D suppresse

160 orced expression of p21(WAF1/CIP1) (i.e., in Jurkat cells inducibly expressing p21(WAF1/CIP1) under t

161 eplication was severely impaired in PSIP1-/- Jurkat cells infected at high multiplicity.

162 Here, we evaluated the immunopeptidome of Jurkat cells infected with the vaccine candidate MVA.HIV

163 Consistently, PTEN restoration in Jurkat cells inhibited t-BHQ-mediated expression of ferr

164 In Jurkat cells inhibition of proteasomal activity by MG132

165 ffects of CO, Fas/CD95-induced cell death in Jurkat cells is augmented by exposure to CO and that thi

166 We also found that in H9 lymphoma and Jurkat cells, knockdown of the predominant syndecan memb

167 Similarly, mutant Jurkat cells lacking FADD also show increased susceptibi

168 We demonstrate that 4-HNE exposure to Jurkat cells leads to the induction of both Fas and Daxx

169 dministration of 10(8) apoptotic or necrotic Jurkat cells led to the appearance of DNA in the plasma.

170 Correspondingly, i2 forms of VacA bound to Jurkat cells less avidly than did i1 forms of VacA.

171 -cell level by studying the interaction of a Jurkat cell line expressing a fluorescently labeled MTOC

172 In addition, an Lck-deficient Jurkat cell line that cannot efficiently activate ZAP 70

173 lood and in the nuclei of the T cell-derived Jurkat cell line.

174 LMP1 TES2 activated NF-kappaB in Jurkat cell lines harboring NEMO truncated at 372 (A45)

175 In both A45 and 2C Jurkat cell lines, LMP1 TES2-mediated NF-kappaB activati

176 In Jurkat cell lines, we demonstrate that expression of ITK

177 olytic gating of Panx1 channels in all three Jurkat cell lines.

178 11 proteins from 9 injections from a single Jurkat cell lysate sample consisting of 400 ng of total

179 functionality) to a tryptic digest of whole Jurkat cell lysate to estimate the depth of proteome cov

180 Furthermore, coimmunoprecipitation of Jurkat cell lysates revealed that c-Myb is associated wi

181 Immunoprecipitation of Jurkat cell lysates with Abs against both the regulatory

182 Here, we show that upon activation of Jurkat cells microtubules project from the MTOC to a rin

183 In Jurkat cells, MRP1 was largely localized to the plasma m

184 odomain antibody inhibited the attachment of Jurkat cells on Caco2-BBE monolayers.

185 PMA/ionomycin-induced CD69 up-regulation in Jurkat cells, on anti-IgM-mediated CD69 up-regulation in

186 Jurkat cells or activated lymphocytes were each killed b

187 Jurkat cells or activated T lymphocytes cultured with an

188 nant negative Orai1-E106A in either parental Jurkat cells or an unrelated human T cell line (CEM391)

189 modulation of Ca(2+) mobilization via CD2 on Jurkat cells or BCRs on blood B cells upon cross-linkage

190 Knockdown of NDE1 in Jurkat cells or primary mouse CTLs also inhibited MTOC t

191 Infection of CypA knockout Jurkat cells or treatment of Jurkat cells with cyclospor

192 3(OH)2D3 inhibited Il17 promoter activity in Jurkat cells overexpressing RORalpha or RORgamma.

193 In Jurkat cells, overexpression of c-Ets-1, c-Ets-2, or PU.

194 eatments dose-dependently impaired apoptotic Jurkat cell phagocytosis by primary rat or human AM, irr

195 Finally, reduction of Jurkat cell PI-3,4,5-P(3) synthesis using the PI3K inhib

196 For Jurkat cells, poly(I:C) and NO donors induced apoptosis

197 rated in several immune cell types including Jurkat cells, primary T cells and dendritic cells.

198 transcription factors in regulating HL-60 or Jurkat cell proliferation and differentiation compared w

199 ry domains are required for KLF2 to suppress Jurkat cell proliferation.

200 apoptosis because overexpression of RelA in Jurkat cells protects against cell death.

201 Jurkat cells released approximately 75-80% of their tota

202 Tetramer binding to HCV TCR-transduced Jurkat cells required CD8 expression, whereas antigen re

203 as 50- and 130-fold less active in HL-60 and Jurkat cells, respectively, confirming the importance of

204 nce-induced loss of ZAP 70 or Lck protein in Jurkat cells resulted in significant decrease in the RXR

205 ckdown of endogenous PKC-theta expression in Jurkat cells resulted in significant inhibition of TCR-i

206 or 4 in the presence of different numbers of Jurkat cells reveals that each cell is capable of modify

207 rmore, knockdown of GIMAP6 not only rendered Jurkat cells sensitive to apoptosis but also accelerated

208 in human neuroblastoma cells (SK-N-F1), but Jurkat cells show both diffuse and punctate cytoplasmic

209 domain with WC1 endodomains transfected into Jurkat cells showed that the tyrosine phosphorylation of

210 Consistent with these results, Jurkat cells stably expressing a p21(WAF1/CIP1) nuclear

211 FADD-deficient Jurkat cells stably expressing these FADD mutations did

212 To probe further the function of p57(Kip2), Jurkat cells stably transfected with a plasmid encoding

213 ed apoptosis using the human T-cell leukemic Jurkat cells stably transfected with or without shRNA ag

214 OPN3 down-regulation by siRNA knock-down in Jurkat cells suggested a possible role for OPN3 in modul

215 ranes are sufficient to induce cell death in Jurkat cells, suggesting that no active process or effec

216 by cocross-linking of CD3/TCR and CD4/WC1 in Jurkat cells, suggesting that the sustained membrane col

217 Overexpression of LEF-1 in K562 or Jurkat cells suppresses CD1D promoter activity and downr

218 hen infected with an ADP-deleted adenovirus, Jurkat cells survived and maintained viral DNA for great

219 Further, we observed that in Siva-1 knockout Jurkat cells, TCR-mediated activation of the canonical a

220 er gave a much higher luciferase activity in Jurkat cells than in K562 cells, whereas it was in rever

221 extrinsic pathways, we assessed apoptosis in Jurkat cells that are deficient in caspase 8 or Fas-asso

222 Jurkat cells that constitutively express Tax1 and Tax2 (

223 om) activate Ca2+ signaling in lymphoblastic Jurkat cells that could be abrogated by receptor desensi

224 Jurkat cells that did not express Syk (JCaM1, JCaM1/lck)

225 In Jurkat cells that had been knocked down for GIMAP6, trea

226 containing -4S isoforms are transfected into Jurkat cells that produce, but do not depend on IL-2 for

227 spase-3 or -8 were treated with lysates from Jurkat cells that were stimulated with staurosporine and

228 During etoposide-induced apoptosis in Jurkat cells, the cleavage of MST1 directly corresponded

229 nes were not required for WC1 endocytosis in Jurkat cells, the pan-protein kinase C inhibitor Go6983

230 e the ability of CdtB to induce G2 arrest in Jurkat cells; these effects were dependent upon protein

231 Fas-associated death domain protein-negative Jurkat cells, though apoptosis induced by purified gangl

232 n an increased sensitivity of the transduced Jurkat cell to generate cytokines when stimulated throug

233 1 also sensitizes Jurkat cells to cisplatin.

234 Exposure of Jurkat cells to CO resulted in augmentation in Fas/CD95-

235 erformed affinity purification of Orai1 from Jurkat cells to identify partner of STIM1 (POST), a 10-t

236 Exposure of apoptotic Jurkat cells to transgenic parasites demonstrated interf

237 as-associated death domain protein-deficient Jurkat cells, to assess whether the death ligands and ga

238 FOXO3a and its target genes was observed in Jurkat cells transduced by Tat alone.

239 Conversely, primary human T cells and Jurkat cells transfected with Siglec-5 become less respo

240 nduced apoptosis and has a minimal effect in Jurkat cells transfected with vector control.

241 mulation because IL-2 is released by beta(-) Jurkat cells transfected with Vgamma2Vdelta2 TCRs.

242 In EBV(-) Jurkat cells, transfection of miR-BART20-5p and miR-BART

243 Expression of this near-monoclonal TCR in a Jurkat cell-transfection system validated fine DYS speci

244 ative ERK dephosphorylation in extracts from Jurkat cells treated in suspension, as compared with adh

245 In KB 3-1 or Jurkat cells treated with cytotoxic agents or C6-ceramid

246 of DNA was assessed in BALB/c mice receiving Jurkat cells treated with etoposide or ethanol.

247 TL cell lines that lack Tax expression or in Jurkat cells treated with phorbol 12-myristate 13-acetat

248 efficiently by cell-to-cell contact between Jurkat cells under conditions where tetherin restricted

249 GSH release in Jurkat cells undergoing apoptosis was inhibited by the o

250 E8 can detect activated LFA-1 on both JY and Jurkat cells using flow cytometry and parallel plate adh

251 ified in lysates from pervanadate-stimulated Jurkat cells using PTPN22-D195A/C227S, an optimized subs

252 ide (NO) production in single T-lymphocytes (Jurkat cells) using a fluorescent marker, 4-amino-5-meth

253 We have recently characterized a new Jurkat cell variant, named H123, where IFNalpha stimulat

254 ne extracellular nucleotide pools in control Jurkat cells versus Jurkat lines that lack the Fas-assoc

255 ed in tert-butylhydroquinone (t-BHQ)-treated Jurkat cells via an ARE, and it was due to PTEN deficien

256 ependent apoptosis in procaspase 8-deficient Jurkat cells via the activation of ASK1, JNK, and caspas

257 -activated lymphocytes and on caspase-8(-/-) Jurkat cells was extremely low.

258 o the CD154 transcript, cytoplasm from human Jurkat cells was fractionated over a sucrose gradient an

259 In Jurkat cells we find multiple, distinct PDE-regulated ph

260 Following chemical mutagenesis of Jurkat cells we isolated mutants that are selectively re

261 By employing FADD-deficient Jurkat cells, we demonstrate that DR5 and c-FLIP(L) inte

262 ifically, by using normal and CypA-deficient Jurkat cells, we demonstrate that the presence of CypA i

263 Second, using Jurkat cells, we demonstrated specific interaction of ye

264 In further analysis of Jurkat cells, we detect and separate a subpopulation of

265 ased on the reactivity of the TCR-transduced Jurkat cells, we have identified a TCR that transfers an

266 Applying this technique to human Jurkat cells, we identified antisense transcription at 2

267 stituted medium during anti-Fas treatment of Jurkat cells, we observed cellular swelling, a property

268 oscopy and patch-clamp recording from single Jurkat cells, we show that STIM1 puncta form several sec

269 ly transfected mouse TOSO (mTOSO)-expressing Jurkat cells, we show that TOSO protects cells from Fas/

270 Lck-lacking Jurkat cells were also found to show markedly reduced GR

271 Parental and transfected EL4 and Jurkat cells were evaluated for adhesion, migration, and

272 By contrast, SOC and the CRAC current in Jurkat cells were inhibited by knockdown of Orai1 but we

273 Fas-associated death domain (FADD)-deficient Jurkat cells were resistant to Fas-mediated apoptosis ye

274 By comparison, Apaf-1-deficient Jurkat cells were sensitive to anti-Fas, exhibiting Bid

275 IOBA-NHC and Jurkat cells were stimulated with IFNgamma, TNFalpha, al

276 In contrast, when human lymphoma U937 and Jurkat cells were treated with Pc 4-PDT, staurosporine (

277 using Fas ligand (FasL)-induced apoptosis in Jurkat cells where changes in [GSH](i) can be analyzed b

278 Anthrax LT cleaves and inactivates MAPKKs in Jurkat cells, whereas not affecting proximal or parallel

279 +)](ne/er) due to applied Ca(2+) was seen in Jurkat cells, which entirely lack NCX.

280 Overexpression of SUMO or PIAS in Jurkat cells, which express high levels of endogenous SA

281 in T-cell acute lymphoblast leukemia (T-ALL) Jurkat cells, which is accompanied by elevating promoter

282 g from patients with HOX11+ T-ALL to that of Jurkat cells, which originated from a distinct subtype o

283 evels of ADP mRNA and protein were higher in Jurkat cells, which proceed with a lytic infection.

284 ment suppressed IL-2 production by activated Jurkat cells, which was partially attenuated when pretre

285 initiate apoptosis in transformed HL-60 and Jurkat cells while sparing their progenitors.

286 ression is sufficient to induce apoptosis in Jurkat cells, while its expression protects epithelial H

287 tly reduced ability to trigger cell death in Jurkat cells, while the corresponding double mutant was

288 PS externalization in actively metabolizing Jurkat cells with 7-ns pulses produces transmembrane pot

289 FcR, and coligation of FcmuR and Fas/CD95 on Jurkat cells with agonistic IgM anti-Fas mAb was shown t

290 hymocytes had no effect, whereas pretreating Jurkat cells with anti-annexin I or removing annexin I w

291 The interactions of Jurkat cells with cisplatin, cis-[Pt(15NH3)2Cl2]1, are s

292 f CypA knockout Jurkat cells or treatment of Jurkat cells with cyclosporine A eliminated the Vif-sens

293 al growth factor (EGF) receptor expressed in Jurkat cells with immobilized EGF was detected and quant

294 Cotreatment of Jurkat cells with marginally toxic concentrations of ada

295 Treatment of Jurkat cells with phorbol 12-myristate 13-acetate (PMA),

296 RelA overexpression endows Jurkat cells with resistance to GD3-mediated apoptosis,

297 Interestingly, transfection of Jurkat cells with siRNA directed against IKKalpha impair

298 Though Jurkat cells with transgenic overexpression of Bcl-2 or

299 eir in vitro cytotoxicities against a set of Jurkat cells with varied levels of Bcl-2 and Bcl-XL prot

300 In Jurkat cells, ZAP-70 is ubiquitinated at several sites t