ライフサイエンスコーパス: Jurkat cell

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

2 iptional activity in transiently transfected Jurkat cells.

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

4 further understanding the cancer biology of Jurkat cells.

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

6 ssociated apoptotic cell death in cocultured Jurkat cells.

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

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

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

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

11 eraction, RPN2 Tyr-950, is phosphorylated in Jurkat cells.

12 d replication in low-CD4-expressing MDMs and Jurkat cells.

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

14 ndependent mitochondrial permeabilization in Jurkat cells.

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

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

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

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

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

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

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

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

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

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

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

26 d transactivation as compared with wild type Jurkat cells.

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

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

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

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

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

32 bility, which is replicated in DEF6-knockout Jurkat cells.

33 G2C(pos) NK cells stimulated with HLA-E(low) Jurkat cells.

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

35 mplex isolated from the nucleus of activated Jurkat cells.

36 rimary T cells, which were then expressed in Jurkat cells.

37 pression, and phagocytosis rate of apoptotic Jurkat cells.

38 take during passive transfection in HeLa and Jurkat cells.

39 ilar ICL delivery as the injection of intact Jurkat cells.

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

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

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

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

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

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

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

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

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

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

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

51 7 chemoattraction, whereas CXCR1-transfected Jurkat cells acquired responsiveness.

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

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

56 Jurkat cells also underwent apoptosis in a dose-dependen

57 Inversion of -31CBS in Jurkat cells alters chromatin accessibility, histone mod

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

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

65 HIV-1 entry and spread in low-CD4-expressing Jurkat cells and human monocyte-derived macrophages (MDM

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 localized with CD4 on the plasma membrane of Jurkat cells and MDMs and enhances CD4 internalization.

70 We found that knockdown of LY6E in Jurkat cells and MDMs increases HIV-1 infection, yet ove

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

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

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

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

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

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

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

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

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

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

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

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

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

84 4 were able to inhibit cell adhesion between Jurkat cells and SRBC nearly 50% at 180 microM, and 80%

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

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

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

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

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

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

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

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

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

94 as evaluated in human lung epithelial cells, Jurkat cells, and rat basophilic leukemia cells.

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

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

97 gnaling significantly reduced SW620-mediated Jurkat cell apoptosis.

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

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

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

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

102 99% of fluorescent- and magnetically-labeled Jurkat cells at reasonable throughputs (10(3) cells/min)

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

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

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

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

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

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

109 1 tat into HeLa cells or infection of H9 and Jurkat cells by HIV-1 increased HRES-1/Rab4 protein leve

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

111 of SERINC5 from the membrane of transfected Jurkat cells by these mutants was significantly reduced.

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 of caspase 3/7 were increased in HLA-E(high) Jurkat cells compared with HLA-E(low) Jurkat cells, cons

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

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

121 (high) Jurkat cells compared with HLA-E(low) Jurkat cells, consistent with higher rates of apoptosis

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

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

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

125 d leukemia, a single injection of 10 million Jurkat cells delivered DiD to ~15% of the tumor cells.

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

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

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

129 1 inhibits HIV-1 replication in CD4-positive Jurkat cells, despite its capability of up-regulating CD

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

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

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

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

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

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

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

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

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

139 Jurkat cells express several members of the multidrug re

140 When Jurkat cells expressing a dominant negative form of NDE1

141 om LAIR-1-sufficient and -deficient mice, 2) Jurkat cells expressing either LAIR-1 mutants or C-termi

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

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

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

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

146 RNA-sequencing of MALAT1-knockdown Jurkat cells further highlighted MALAT1 role in splicing

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

148 IV infection by transplanting "J-Lat" cells, Jurkat cells harboring a latent HIV provirus encoding an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 m(6)A levels were detected in total RNA from Jurkat cells infected by single-cycle HIV-1 pseudotyped

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

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

167 In Jurkat cells inhibition of proteasomal activity by MG132

168 V-1 infection, yet overexpression of LY6E in Jurkat cells inhibits HIV-1 entry and replication.

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

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

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

172 modulation of UBASH3A levels in unstimulated Jurkat cells leads to altered amounts of total cellular

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

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

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

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

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

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

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

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

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

182 11 proteins from 9 injections from a single Jurkat cell lysate sample consisting of 400 ng of total

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

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

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

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

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

188 Jurkat cells or activated lymphocytes were each killed b

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

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

191 Challenging miR-modulated Jurkat cells or primary CD4(+) T-cells with wild-type (W

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

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

194 ells and found that overexpression of CD4 in Jurkat cells overcomes the inhibitory effect of LY6E; co

195 3(OH)2D3 inhibited Il17 promoter activity in Jurkat cells overexpressing RORalpha or RORgamma.

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

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

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

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

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

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

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

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

204 2C(pos) NK cells stimulated with HLA-E(high) Jurkat cells released higher levels of Granzyme B compar

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

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

207 ion of microparticles produced in vitro from Jurkat cells resulted in a similar ICL delivery as the i

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

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

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

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

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

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

214 HIV-1 infection of CD4(+) primary T-cells or Jurkat cells significantly increases m(6)A levels of cel

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

234 1 also sensitizes Jurkat cells to cisplatin.

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

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

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

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

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

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

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

247 erase assay, we found that HBZ expression in Jurkat cells (used as effector cells) increases HTLV-1 i

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

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

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

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

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

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

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

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

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

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

258 First, in human Jurkat cells, we characterized the effect of zinc on pro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 ness of EXoO-Tn was benchmarked by analyzing Jurkat cells, where 947 Tn-glycosylation sites from 480

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

276 aken by CD30(+) Karpas 299 cells, but not by Jurkat cells which lack CD30.

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

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

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

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

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

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

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

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

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

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

287 Preincubation of Jurkat cells with a CD4 receptor-neutralizing antibody b

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

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

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

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

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

293 Cotreatment of Jurkat cells with marginally toxic concentrations of ada

294 Interestingly, treatment of Jurkat cells with recombinant gp120 of HIV-1 Env signifi

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

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

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

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

299 robeads with diameters from 1.5 to 10 um and Jurkat cells within a thin fluidic device using the comb

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