ライフサイエンスコーパス: K562 cell

1 nscription factors binding to this region in K562 cells.

2 rythroid or megakaryocyte differentiation of K562 cells.

3 tiprotein complex from human erythroleukemic K562 cells.

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

5 over BRD4-mediated cell-state transitions in K562 cells.

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

7 crophage colony-stimulating factor-secreting K562 cells.

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

9 age independence and facilitate apoptosis of K562 cells.

10 s assessed by perturbing their expression in K562 cells.

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

12 elevated level of gamma globin expression in K562 cells.

13 ments between human embryonic stem cells and K562 cells.

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

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

16 d differentiation caused by Sp1 knockdown in K562 cells.

17 U1 RNA was affinity purified from K562 cells.

18 imary skeletal muscle cells and erythroblast K562 cells.

19 o control acquisition of erythroid traits by K562 cells.

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

21 clear translocation after hemin treatment in K562 cells.

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

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

24 oid differentiation of human erythroleukemic K562 cells.

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

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

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

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

29 bin promoters, which are activated by HS2 in K562 cells.

30 nerated and coexpressed with bovine CD11a in K562 cells.

31 lters the expression of metabolic enzymes in K562 cells.

32 lphaLbeta2 or isolated I domain expressed on K562 cells.

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

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

35 and cytoplasmic compartments of transfected K562 cells.

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

37 tivated killer-mediated cytotoxicity against K562 cells.

38 HDR frequency; HDR frequency reached 86% in K562 cells.

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

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

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

42 omoter when transfected into human erythroid K562 cells.

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

44 sesses unique enhancer activity in erythroid K562 cells.

45 autonomous promoter activity genome-wide in K562 cells.

46 in chromatinized episomes in fetal/embryonic K562 cells.

47 uced cell cycle block and differentiation of K562 cells.

48 NA and protein levels compared with parental K562 cells.

49 ed resistance to etoposide in human leukemia K562 cells.

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

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

52 karyocytic differentiation in human leukemia K562 cells.

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

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

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

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

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

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

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

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

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

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

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

64 and machine learning was used to load single K562 cells amongst clusters based on their instantaneous

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

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

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

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

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

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

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 d Tuxedo-ch to analyze benchmark datasets of K562 cells and further characterize the genomic features

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

76 64 ENCODE ChIP-seq datasets from GM12878 and K562 cells and identified many novel protein-DNA interac

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 loss of PEL expression on ABCC4-CRISPR-Cas9 K562 cells and its overexpression in ABCC4-transfected c

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

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

82 In both human CML K562 cells and murine Ba/F3 cells expressing BCR-ABL1, l

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

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

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

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 V- Zif-VP64 and CMV-eGFP-S/MAR transfected a)K562 cells; b)murine beta-YAC bone marrow cells (BMC); c

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

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 Knockdown of CTCF in K562 cells caused loss of CTCF binding and transcription

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

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

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

119 1% and 2% homology directed repair in single K562 cells co-injected with a donor template along with

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

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 Stably transfected K562 cells could only tolerate very low level expression

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

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

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

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

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

131 10- to 1,000-fold increase of viral yield in K562 cells, dependent on the DENV serotype, was observed

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

133 med in vitro by demonstrating a reduction of K562 cell differentiation towards RBCs in the presence o

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 K562 cells expressing latent WT or constitutively activa

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

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

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

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

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

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

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

158 was detected by RNA immunoprecipitation with K562 cell extracts.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 ternalization of virions into human leukemia K562 cells in vitro, indicating their possible ability t

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

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

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

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

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

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

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

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

186 additionally shown in hematologic malignant K562 cells, indicating the generality of the observed EM

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

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

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

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

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

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

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

194 roliferation in the presence of the parental K562 cell line and cytokines was increased by adding ago

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

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

197 eas low expression of CD137L by the parental K562 cell line only supported the expansion by 2 x 10(3)

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

202 dentified among the 100 TFs expressed in the 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 lian ZIKV isolate in a FcgammaRII-expressing K562 cell line.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

222 K562 cells overexpressing constitutively active Fyn kina

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

242 K562 cells showed a reduced ability to differentiate to

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

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

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

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

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

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

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

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

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

252 We show in human K562 cells that the triplex is stable in vivo.

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

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

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

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

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

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

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

260 however, did not modulate the sensitivity of K562 cells to the intrinsic cytotoxicity of NK cells.

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

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

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

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

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

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

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

268 tire XIST gene, were homozygously deleted in K562 cells using the Cas9 nuclease and paired guide RNAs

269 those overexpressed in K/VP.5 compared with K562 cells; validation by quantitative polymerase chain

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

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

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

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

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

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

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

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

278 e screens for essential CTCF loop anchors in K562 cells were not single guide RNAs (sgRNAs) that disr

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

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

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

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

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

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

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

286 b increased TNT formation in both Kcl-22 and K562 cells, while nilotinib or IFNalpha increased TNTs i

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

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

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

290 Transfecting K562 cells with a reporter plasmid harboring the TOP2alp

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

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

293 1-6 were found to be active against leukemia K562 cells with IC50 in the nanomolar range (200-1100 nM

294 Transfection of K562 cells with miR-9-3p or miR-9-5p mimics led to decre

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

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

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

300 ckdown and deletion experiments performed in K562 cells, zebrafish, and mice demonstrate that loss of