ライフサイエンスコーパス: K562 cell

1 autonomous promoter activity genome-wide in K562 cells.

2 crophage colony-stimulating factor-secreting K562 cells.

3 own to be required for miR-15a expression in K562 cells.

4 age independence and facilitate apoptosis of K562 cells.

5 s assessed by perturbing their expression in K562 cells.

6 ndent cytotoxicity (CDC) was investigated in K562 cells.

7 t BCR-ABL activated STAT5 phosphorylation in K562 cells.

8 elevated level of gamma globin expression in K562 cells.

9 ments between human embryonic stem cells and K562 cells.

10 cytes or upon PMA-induced differentiation of K562 cells.

11 d not eliminate DENV-4-enhancing activity in K562 cells.

12 d differentiation caused by Sp1 knockdown in K562 cells.

13 U1 RNA was affinity purified from K562 cells.

14 imary skeletal muscle cells and erythroblast K562 cells.

15 ss 240 kb of the human alpha-globin locus in K562 cells.

16 clear translocation after hemin treatment in K562 cells.

17 of phosphorylated Akt in the BCRP-expressing K562 cells.

18 U1 and Y RNAs were affinity purified from K562 cells.

19 e increase in apoptosis of the KCL22 and the K562 cells.

20 including Cos-7, NIH3T3, HEK293, Jurkat and K562 cells.

21 e some distinct RNA targets and functions in K562 cells.

22 , up-regulate transcription of Galpha(i2) in K562 cells.

23 nerated and coexpressed with bovine CD11a in K562 cells.

24 lters the expression of metabolic enzymes in K562 cells.

25 lphaLbeta2 or isolated I domain expressed on K562 cells.

26 ndent increase in gamma-globin expression in K562 cells.

27 constructs containing the UIRR in wild-type K562 cells.

28 and cytoplasmic compartments of transfected K562 cells.

29 I (Pol2) ChIP-seq along with ENCODE data for K562 cells.

30 exerted synergistic apoptosis of MV4-11 and K562 cells.

31 tivated killer-mediated cytotoxicity against K562 cells.

32 a 5.5-kb globin gene model locus in vivo in K562 cells.

33 K562-R cells while having limited effects of K562 cells.

34 ox), augments Nox1 activity in reconstituted K562 cells.

35 omoter when transfected into human erythroid K562 cells.

36 nd USF2 crosslink to the beta-globin gene in K562 cells.

37 sesses unique enhancer activity in erythroid K562 cells.

38 in chromatinized episomes in fetal/embryonic K562 cells.

39 uced cell cycle block and differentiation of K562 cells.

40 C or [3H]uridine and the differentiation of K562 cells.

41 nophosphate kinase and for their toxicity to K562 cells.

42 nude mice as compared to vector transfected K562 cells.

43 -globin locus by using chIp-chip analysis of K562 cells.

44 otal levels of Ras, Rap1a, RhoA, and RhoB in K562 cells.

45 ted to phenylalanine and stably expressed on K562 cells.

46 karyocytic differentiation in human leukemia K562 cells.

47 s by NK cell-derived TRAIL was detectable in K562 cells.

48 d S-phase cell-cycle arrest and apoptosis in K562 cells.

49 nd CD44 fused to cyan fluorescent protein on K562 cells.

50 marrow homing/engraftment of Slug-expressing K562 cells.

51 nscription factors binding to this region in K562 cells.

52 rythroid or megakaryocyte differentiation of K562 cells.

53 tiprotein complex from human erythroleukemic K562 cells.

54 Seq in two different cell lines, GM12878 and K562 cells.

55 d identified more than 5000 binding sites in K562 cells.

56 and 3 in human chronic myelogenous leukemia (K562) cells.

57 In addition, forced expression of HPIP in K562 cells, a multipotent erythro-megakaryoblastic leuke

58 sion of inducible dominant negative c-Myb in K562 cells accelerated their exit from M phase.

59 identified mRNAs whose levels are altered in K562 cells acutely depleted of the two major alphaCP pro

60 fferentiation but inhibited proliferation of K562 cells, alone or upon C/EBPalpha activation.

61 rs, Weak Enhancers, or Repressed elements in K562 cells, along with other sequences predicted to be E

62 nts and intact alpha5beta1 On the surface of K562 cells, alpha5beta1 is 99.8% bent-closed.

63 C4-MAD triggered vigorous differentiation of K562 cells an order of magnitude more potently than tiaz

64 ronic myeloid leukemia blast crisis (CML-BC) K562 cells and acute leukemia MV4-11 cells with the acti

65 lated by inhibition of the BCR-ABL kinase in K562 cells and BaF3/BCR-ABL transfectants, suggesting a

66 of gp350 were incubated with CR2-expressing K562 cells and binding was assessed by flow cytometry.

67 s in CD34+ primary stem/progenitor cells and K562 cells and by mapping the previously known DNaseI hy

68 osis in STI571 (imatinib mesylate)-resistant K562 cells and CD34+ mononuclear cells obtained from a p

69 TfR2 have similar cellular localizations in K562 cells and coimmunoprecipitate to only a very limite

70 cted with human chronic myelogenous leukemia K562 cells and doxorubicin-resistant human chronic myelo

71 repeats impaired insulator activity in human K562 cells and Drosophila embryos.

72 ucleoprotein (mRNP) complex in both cultured K562 cells and erythroid-differentiated human CD34(+) ce

73 CTCF occupies these sites in both erythroid K562 cells and fibroblast 293T cells, the long-range int

74 ession of CD107a; and their capacity to lyse K562 cells and HIV-1-infected T cells.

75 64 ENCODE ChIP-seq datasets from GM12878 and K562 cells and identified many novel protein-DNA interac

76 71 + adaphostin induced more cytotoxicity in K562 cells and in CML CFU-G than either agent alone did.

77 Sox6-overexpression in K562 cells and in human primary ex vivo erythroid cultur

78 roid K562 cells, in plasmids integrated into K562 cells and in purified DNA used as template in in vi

79 or by inhibiting Bcr-Abl kinase activity in K562 cells and leukemic cells derived from CML patients.

80 nous TRAF4 and MEKK4 associate in both human K562 cells and mouse E10.5 embryos.

81 d previously gamma-globin gene inhibition in K562 cells and primary erythroid progenitors treated wit

82 d human fetal globin gene expression in both K562 cells and primary human adult erythroid progenitor

83 ukemia virus integrations in human HepG2 and K562 cells and subjected them to second-generation seque

84 n rabbit reticulocyte lysate and in cultured K562 cells and that casein kinase II is capable of quant

85 s of embryonic placental cells and erythroid K562 cells and transfected LTRs of recombinant GFP plasm

86 nd tubacin augmented the loss of survival of K562 cells and viability of primary acute myeloid leukem

87 ic DNA was highly active in Bcr-Abl-positive K562 cells and was activated when Bcr-Abl-negative cells

88 PTPROt expression was suppressed in K562 cells and was relieved upon treatment of the cells

89 gene assays in transiently transfected human K562 cells and/or after site-directed integration into m

90 ls, Human Immortalized Myelogenous Leukemia (K562) cells and hematopoietic stem cells (HSCs).

91 tion of arginase activity in human leukemic (K562) cells and sickle erythrocytes.

92 ates of 10 to 25% in 293T cells, 13 to 8% in K562 cells, and 2 to 4% in induced pluripotent stem cell

93 rotein beta (CEBPB)-bound sites in HepG2 and K562 cells, and found that CEBPB-bound sites co-occurrin

94 fragment reduced reporter gene expression in K562 cells, and GATA-1 was shown to bind within this seq

95 ype or mutant forms of CR2 were expressed on K562 cells, and the ability of these CR2-expressing cell

96 as measured as the percentage of DV-infected K562 cells, and viral titer (infected K562 cell supernat

97 Short interfering RNA "knockdown" of NmU in K562 cells arrested cell growth.

98 With the use of pWizGFP plasmid and K562 cells as a model system, SFE showed better transgen

99 Here, we have used IR-induced apoptosis of K562 cells as a model to explore a role for IMP-3 in cel

100 icantly induced erythroid differentiation of K562 cells, as assessed by benzidine staining and quanti

101 rforin; their degranulation upon exposure to K562 cells, as indicated by cell surface expression of C

102 Indolequinones inhibited NQO2 activity in K562 cells at nanomolar concentrations that did not inhi

103 consisting of an alpha(5)beta(1) expressing K562 cell attached to the atomic force microscopy cantil

104 e effects of these agents on the survival of K562 cells, bcr/abl-transduced FDC-P1 cells, and myeloid

105 In contrast, K562 cells bearing randomly coupled sPSGL-1 or 2-GSP-6 t

106 ere that upon treatment with phorbol esters, K562 cells become adherent and permissive for parvovirus

107 In addition, K562 cells become visibly red after Sp1 knockdown.

108 also identified a new looping interaction in K562 cells between the beta-globin Locus Control Region

109 ription factor EKLF, which is not present in K562 cells but is required for beta-globin expression in

110 e blocked the LEF-induced differentiation of K562 cells but only restored the CTP pool.

111 s were validated by CRISPR/Cas9 knockdown in K562 cells, but simulations indicate that effect sizes n

112 eptor-dependent binding and iron donation to K562 cells, but with diminished receptor occupancy by th

113 oid differentiation of human erythroleukemia K562 cells by hemin simultaneously increases gamma-globi

114 Lysis of K562 cells by LN NK cells from acutely infected animals

115 expression of catalytically active PTPROt in K562 cells caused reduced proliferation, delayed transit

116 We generated HLAnull K562 cell clones that were engineered to express CD1d an

117 Human K562 cells co-express epsilon- and gamma-globin but not

118 1% and 2% homology directed repair in single K562 cells co-injected with a donor template along with

119 levels in Bcr-Abl-expressing cultured CML-BC K562 cells confers resistance to 17-AAG-induced apoptosi

120 cinia virus vector also induced apoptosis of K562 cells, consistent with earlier studies that demonst

121 However, due to limiting amounts of SEPT9, K562 cells contain both hexameric and octameric heterome

122 ereas rho- and beta(H)-mRNA was activated in K562 cells containing chicken chromosomes with deletions

123 ta(H)-globin gene expression was detected in K562 cells containing the chicken chromosome without del

124 K562 cells continuously flowing at a speed of up to 100

125 es of dominant-negative (DN) Jak2 expressing K562 cells correlated very well with the reduction of tu

126 Stably transfected K562 cells could only tolerate very low level expression

127 Inhibition of FLVCR in K562 cells decreases heme export, impairs their erythroi

128 n H gene fused to a luciferase reporter into K562 cells demonstrated that hemin activates ferritin H

129 Analysis of mRNP complexes in K562 cells demonstrates in vivo association of p21(WAF)

130 A CRISPRi screen for essential genes in K562 cells demonstrates that the large majority of sgRNA

131 experiments for 73 diverse RBPs in HepG2 and K562 cells, demonstrating that eCLIP enables large-scale

132 10- to 1,000-fold increase of viral yield in K562 cells, dependent on the DENV serotype, was observed

133 s of preillness plasma EA of DV infection in K562 cells did not correlate with the clinical severity

134 HPIP-expressing CD34(+) cells and decreased K562 cell differentiation.

135 ution levels of freeze-dried preparations of K562 cells diluted in HL60 cells was prepared.

136 In imatinib mesylate-resistant K562 cells displaying increased Bcr/Abl expression, bort

137 Overexpression of HLTF in K562 cells does not affect the endogenous levels of gamm

138 Finally, as studied in erythroid K562 cells, DYRK3 proved to effectively inhibit NFAT (nu

139 Conversely, K562 cells ectopically expressing Mcl-1 or Bcl-x(L) were

140 Enforced RUNX1 expression in K562 cells enhanced the induction of the megakaryocytic

141 Conversely, PTEN knockdown in K562 cells enhanced the response to t-BHQ.

142 Preillness plasma enhances DV infection of K562 cells even in the presence of detectable neutralizi

143 Furthermore, the QR2 knockdown K562 cells exhibit increased antioxidant and detoxificat

144 , E255K, and M351T), as well as IM-resistant K562 cells exhibiting Bcr/Abl-independent, Lyn-dependent

145 In K562 cells, exposure to LBH589 attenuated Bcr-Abl, p-AKT

146 Myeloid K562 cells express three SEPT9 isoforms, all of which ha

147 his process, we used transcript profiling in K562 cells expressing a dominant-negative Myb (MERT) pro

148 CR2 to EBV gp350; with regard to SCR1, both K562 cells expressing an S15P mutation and recombinant S

149 of CD86 (CD86Ig) bound to a magnetic bead or K562 cells expressing CD86, we demonstrated that ligatio

150 of mutationally activated G12 proteins into K562 cells expressing E-cadherin blocked cadherin-mediat

151 K562 cells expressing latent WT or constitutively activa

152 on of STI571 (i.e., 1-2 microM) in resistant K562 cells expressing marked increases in Bcr-Abl protei

153 s, 15-25 mum simvastatin reduced adhesion by K562 cells expressing recombinant CR3 and by primary hum

154 s and integrated the plasmids into erythroid K562 cells expressing the lac repressor protein.

155 ring peripheral blood mononuclear cells with K562 cells expressing the NK-stimulatory molecules 4-1BB

156 to inhibit [(3)H]MTX transport with RFC-null K562 cells expressing wt and K411A RFCs.

157 In HL-60/BCR-ABL and K562 cells (expressing p210(BCR-ABL)), abundant cytoplas

158 In K562 cells, expression of delta(358-452), delta(389-418)

159 I ELISA, and by IP assay using (35)S-labeled K562 cell extract.

160 was detected by RNA immunoprecipitation with K562 cell extracts.

161 as9 together with donor template into single K562 cells for targeting the human beta-globin gene.

162 Although ectopic survivin protected K562 cells from apoptosis induced by STI571, it did not

163 blicly available RNA-seq data in GM12878 and K562 cells from the ENCODE consortium and experimentally

164 We demonstrate that in human K562 cells geminin is associated with HOXA9 regulatory e

165 -presenting cells derived from IL-11Ralpha + K562 cells genetically modified to coexpress T-cell cost

166 r in phase 2 clinical trials, was studied in K562 cells, granulocyte-colony-stimulating factor-mobili

167 We find that phorbol ester (PE) treatment of K562 cells greatly stimulates promoters (T cell receptor

168 ted induction of gamma-globin also inhibited K562 cell growth by causing arrest in G1/S, apoptosis, a

169 Although K562 cells have been reported to be insensitive to TRAIL

170 e Bcr-abl oncogene expressing human leukemia K562 cells, HDAC6 can be co-immunoprecipitated with HSP9

171 equencing of endogenous peptides eluted from K562 cells (HLA class I null) made to express a single H

172 d C4-MAD were found to inhibit the growth of K562 cells (IC(50) = 0.7 microM and IC(50) = 0.1 microM,

173 ype II)] inhibited proliferation of leukemic K562 cells (IC50 = 1.1 microM) more potently than tiazof

174 Analysis of soluble proteins from a human K562 cells identified 5130 unique proteins, with approxi

175 etion analysis in 293T, BaF3, BaF3-p210, and K562 cells identified the region essential for basal tra

176 attenuated SAHA/STI571-mediated apoptosis in K562 cells, implicating disruption of the Raf/MEK/ERK ax

177 obin transcript levels in stably transfected K562 cells in a DNA-binding dependent fashion.

178 P gene expression was found to be induced in K562 cells in response to erythroid differentiation sign

179 tumor cells, but only slightly increased in K562 cells in response to IFN-alpha treatment.

180 activating immune synapses with 721.221 and K562 cells in which CD2, LFA-1 and actin were polarized

181 B1 phosphorylation mediated by the HDACIs in K562 cells, in conjunction with histone H4 hyperacetylat

182 hancer in the endogenous genome of erythroid K562 cells, in plasmids integrated into K562 cells and i

183 r and activator of transcription (STAT) 5 in K562 cells, including those ectopically expressing a con

184 Stable SAR expression in K562 cells increased gamma-globin mRNA expression and re

185 the other hand, forced expression of SK1 in K562 cells increased the ratio between total S1P/C18-cer

186 conjugation in protein ISGylation-defective K562 cells increases IFN-stimulated promoter activity.

187 onsiveness to IL-12 and IL-18, as well as to K562 cells, indicating that the NK cells were primed in

188 mediated "knockdown" of Hsp70 expression in K562 cells induced marked sensitivity to paclitaxel-indu

189 Enforced expression of miR-34a in K562 cells inhibits cell proliferation, induces cell-cyc

190 Overexpression of tescalcin in K562 cells initiates events of spontaneous megakaryocyti

191 mide ameliorates the leukemia progression in K562 cells inoculated nude mice.

192 on for CRD-BP in cell proliferation of human K562 cells, involving a possible IGF-II-dependent mechan

193 y to be direct, as the interaction occurs in K562 cells lacking functional adherens junctions and E-c

194 n GATA-3 with an NKG2A promoter construct in K562 cells led to enhanced promoter activity, and transf

195 In neutrophils and myeloid K562 cells, ligand ICAM-1 or activating Ab binding promo

196 d modulates the oxidative stress response in K562 cell line and primary erythroid progenitor cells.

197 Additional studies in the hematopoietic K562 cell line confirmed the ability of cHS4 insulator e

198 ference-mediated reduction of Hip within the K562 cell line rendered the cells more susceptible to NK

199 he obtained compounds against human leukemia K562 cell line was evaluated by flow cytometry in vitro.

200 ometry was conducted on the erythroleukaemic K562 cell line, expanding and terminally differentiating

201 In the human erythroleukemic K562 cell line, only one DNA region has been identified

202 lian ZIKV isolate in a FcgammaRII-expressing K562 cell line.

203 r levels of fetal hemoglobin than the native K562 cell line.

204 hotgun analyses of the human erythroleukemia K562 cell line.

205 oth cell-free systems and the human leukemia K562 cell line.

206 differentiation of a human erythroleukemia (K562) cell line and show that LEF induces a dose- and ti

207 poisomerase II cleavage complexes in CEM and K562 cell lines was investigated using an in vivo comple

208 In addition, we treated K562 cell lines with nicotinamide and kaempferol to inhi

209 rogenitors and myeloid leukemic blasts (KG1, K562 cell lines, and primary patient blasts) to differen

210 romoters, within and between the GM12878 and K562 cell lines, and related their modification status w

211 ues from 2.5 to 6.5 nM against the L1210 and K562 cell lines.

212 y disrupt MR1 expression in A459, THP-1, and K562 cell lines.

213 se inhibitor p27(Kip1) in both the KCL22 and K562 cell lines.

214 e more potent than vinorelbine on HCT116 and K562 cell lines.

215 tegy combining comprehensive two-dimensional K562/cell membrane chromatographic system and in silico

216 Clones of K562 cells (MNDA-null) that expressed ectopic MNDA prote

217 s) that expanded in cultures stimulated with K562 cells modified to express the high-affinity Fc rece

218 ells from chronically infected animals lysed K562 cells more efficiently than LN NK cells from uninfe

219 LTR-HS5-epsilonp-GFP plasmid integrated into K562 cells, mutation of the CCAAT motif in the LTR enhan

220 pecific binding complex containing GATA-1 in K562 cell nuclear extracts.

221 paB GFP reporter, and their conjugation with K562 cells or ligation of NKp30 ligation resulted in rap

222 BCR-ABL-expressing murine Ba/F3 cells, human K562 cells or primary tissue samples from CML patients,

223 K562 cells overexpressing constitutively active Fyn kina

224 ential proteomic analysis on human erythroid K562 cells overexpressing Sox6.

225 Compared with K562 cells, overexpressing NGAL in K562 led to a higher

226 However, in p53-null K562 cells, phorbol esters induce miR-34a expression ind

227 both in SAR-expressing cells and HU-treated K562 cells, phosphatidylinositol 3 (PI3) kinase and phos

228 Screening of K562 cells producing recombinant ALL1/AF4 or ALL1/AF9 fu

229 epresses cyclin A1 expression, thus blocking K562 cell proliferation.

230 l experiments revealed that STI571-resistant K562 cells remained sensitive to adaphostin.

231 ble mediators of acquired STI571 resistance, K562 cells resistant to 5 microM STI571 (K562-R) were cl

232 ar effects were observed in LAMA84 cells and K562 cells resistant to STI571, as well as in CD34(+) ce

233 Knockdown of GATA-1 expression in K562 cells resulted in a approximately 4-fold decrease i

234 Introduction of the mutant coiled coil into K562 cells resulted in decreased phosphorylation of Bcr-

235 SF3B1 knockdown experiments in K562 cells resulted in down-regulation of U2-type intron

236 ptor expression was effectively removed from K562 cells, resulting in the development of a distinct n

237 Although their interaction with K562 cells results in effective target cell killing, the

238 Furthermore, studies with K562 cells reveal that disruption of the interaction wit

239 Transcriptional profiling of DZNep-treated K562 cells revealed marked up-regulation of SLC4A1 and E

240 Our analysis of PRO-seq data for K562 cells reveals dramatic transcriptional effects soon

241 Moreover, in K562 cells, RNA interference-mediated downregulation of

242 In K562 cells SATB1 family protein forms a complex with CRE

243 progenitors in vitro and remained active in K562 cells selected for imatinib mesylate resistance.

244 K562 cells showed a reduced ability to differentiate to

245 Experiments in K562 cells showed that simvastatin increased KLF2 mRNA a

246 f cell death (Bim) with short hairpin RNA in K562 cells significantly diminished sorafenib lethality,

247 Stable knockdown of NCOR1 in K562 cells slowed growth and significantly repressed gen

248 consequences of elevating the Gab2 level in K562 cells, stable cell lines for doxycycline-inducible

249 In K562 cells stably expressing transfected alpha(v)beta(3)

250 body-coated target cells (p = .029) and with K562 cell stimulation (p = .029).

251 uced erythroid-related genes, as observed in K562 cells, suggesting that DZNep induces erythroid diff

252 fected K562 cells, and viral titer (infected K562 cell supernatants) was measured in preillness plasm

253 tion in Bcr-abl-transduced Mo7e cells, or in K562 cells that endogenously express Bcr-abl, by transfe

254 tment to the globin locus in human erythroid K562 cells that express the embryonic epsilon-globin gen

255 In addition, we generated stable K562 cells that expressed an inducible Per2 gene.

256 ces for proliferation and differentiation of K562 cells, the effects of C/EBPalpha appear to involve

257 nsfected LTRs of recombinant GFP plasmids in K562 cells, the U3 enhancer activates synthesis of RNAs

258 Here we showed that in erythroid K562 cells these DNA motifs bound the following three tr

259 hermore, loss of the organizational loops in K562 cells through reduction of CTCF with shRNA results

260 ar sphingolipid content, thereby sensitizing K562 cells to apoptosis.

261 d that LA1 enhanced binding of CD11b/CD18 on K562 cells to ICAM-1 via the formation of long membrane

262 Exposing Indo-1-labeled K562 cells to NmU induced an intracellular Ca(++) flux c

263 each with a unique epitope tag, in RFC-null K562 cells to restore transport activity.

264 errin and was competent as an iron donor for K562 cells to which it bound in saturable fashion inhibi

265 n of cAMP, we used Chinese hamster ovary and K562 cells transfected to express CR3 and examined the s

266 nd 1 were characterized by using a series of K562 cells transfected with various mutant alpha3 integr

267 K562 cells treated with paraformaldehyde or methyl-beta-

268 phosphorylated at a basal level in untreated K562 cells; treatment of the K562 cells with PE results

269 ed the 2.8-kb PDGF-B mRNA in erythroleukemia K562 cells upon 12-O-tetradecanoylphorbol-13-acetate-ind

270 e mitochondrial proteome in Notch1-activated K562 cells using a comparative proteomics approach.

271 reduced the expression of TAL1 in erythroid K562 cells using lentiviral short hairpin RNA, compromis

272 ly inhibited the growth of Ba/F3-Bcr-Abl and K562 cells via impaired cell cycle entry and increased a

273 HPIP overexpression in both CD34(+) and K562 cells was associated with increased activation of t

274 CD44 on leukocytes and transfected K562 cells was cross-linked within a 1.14-nm spacer.

275 at the induction of FOXO3a activity in naive K562 cells was sufficient to enhance PI3K/Akt activity a

276 Using K562 cells, we have studied valproic acid-induced transc

277 dependent differentiation of erythroleukemia K562 cells, we observed effects that indicated that the

278 eIF4G isoforms from human K562 cells were cleaved with recombinant Coxsackievirus

279 Jurkat and K562 cells were examined under normal cell culture condi

280 tance to imatinib-induced apoptosis in human K562 cells were examined.

281 Both Enhancer and Weak Enhancer sequences in K562 cells were more active than negative controls, alth

282 reased DNA repair capacity was observed when K562 cells were transfected with nuclear-targeted MGMT (

283 ll-like receptor and interlukin signaling in K562 cells when compared with normal myeloid CD33+ cells

284 the M. tuberculosis Ag Mtb8.4 protein, into K562 cells when covalently linked to the respective Ags.

285 luciferase activity in Jurkat cells than in K562 cells, whereas it was in reverse for the region cov

286 AHSP promoter was transactivated by EKLF in K562 cells, which lack EKLF.

287 This effect was not seen in the transduced K562 cells, which may be due to the DNA hypomethylation

288 ly, the probe revealed no CD38 expression in K562 cells, which was previously reported to have solely

289 e number of genes and the differentiation of K562 cells, while the ectopic expression of this CTCF pa

290 Cotreatment of K562 cells with 250 nM imatinib mesylate and 2.0 micro M

291 ransient or stable transfection of LAMA84 or K562 cells with a constitutively active Lyn (Y508F), but

292 A single-color transcriptional analysis of K562 cells with a series of calibration controls (spiked

293 xample, compound 14j inhibited the growth of K562 cells with an EC(50) value of 1.7 muM and showed K(

294 1-6 were found to be active against leukemia K562 cells with IC50 in the nanomolar range (200-1100 nM

295 el in untreated K562 cells; treatment of the K562 cells with PE results in increased phosphorylation

296 K562 cells with QR2 expression suppressed by RNAi showed

297 Incubation of K562 cells with SB203580, SB203580-iodo, or SB202474, an

298 Treatment of K562 cells with the Hsp90 inhibitor, geldanamycin, cause

299 Incubation of both OCIM2 and K562 cells with WP1066 activated caspase-3, induced clea

300 ion of p53 binding protein 1 (53BP1) foci in K562 cells within 1 h of exposure, which is indicative o