ライフサイエンスコーパス: lymphoblast

1 lation of adhesion and migration in autistic lymphoblasts.

2 (+) T cells on viral replication in CD4(+) T lymphoblasts.

3 tion and gene expression pattern in leukemic lymphoblasts.

4 ant activation of NOTCH1 signaling in T-cell lymphoblasts.

5 ein well above the levels found in wild-type lymphoblasts.

6 -ABL transcript in the absence of detectable lymphoblasts.

7 antibody construct targeting CD19 on B-cell lymphoblasts.

8 tatistically identified as methylated in ALL lymphoblasts.

9 nM) increased the viability and recovery of lymphoblasts.

10 in both mouse B-cell progenitors and human B lymphoblasts.

11 nopathy, hepatosplenomegaly, and circulating lymphoblasts.

12 cation in latency 1-infected Akata Burkitt B lymphoblasts.

13 PU.1, whereas the opposite is true in IM-9 B-lymphoblasts.

14 anslocation of Nrf2 and HO-1 expression in B-lymphoblasts.

15 ranosylguanine, is converted to ara-GTP in T lymphoblasts.

16 or Rac2 in the malignant precursor B-lineage lymphoblasts.

17 on of antiapoptotic Mcl-1 within replicating lymphoblasts.

18 script was overexpressed in LHON cybrids and lymphoblasts.

19 ential for the proliferation of EBV-infected lymphoblasts.

20 old higher than the average for EBV-positive lymphoblasts.

21 to amplify illegitimate RP1 transcripts from lymphoblasts.

22 regulated by endogenous DM levels in human B lymphoblasts.

23 relevant for steroid-mediated apoptosis in T-lymphoblasts.

24 fish transplanted with GFP-labeled leukemic lymphoblasts.

25 to CL in mitochondria of rat liver and human lymphoblasts.

26 e IFN gene signature in TREX1 mutant patient lymphoblasts.

27 in the mdx mouse model of DMD and human DMD lymphoblasts.

28 .1 and reduced SIPA1L3 expression in patient lymphoblasts.

29 tion of nucleus and cytoplasm of lymphocytes/lymphoblasts.

30 ized by the accumulation of undifferentiated lymphoblasts.

31 ents (2.6%), but none were contaminated with lymphoblasts.

32 lymphocytes than in normal, untransformed T lymphoblasts.

33 rine and 6-thioguanine when expressed in ALL lymphoblasts.

34 d from individuals with SRNS and transformed lymphoblasts.

35 igher in patient myoblasts, fibroblasts, and lymphoblasts.

36 th RACK1 in polarized SKW3 cells and human T lymphoblasts.

37 of mammalian cells including fibroblasts and lymphoblasts.

38 SCs as well as primary fibroblasts and human lymphoblasts.

39 After correcting the FANCA defect in EUFA867 lymphoblasts, a "clean" FA-M cell line was generated.

40 rmal FAK-Src signaling leads to defects in B-lymphoblast adhesion, migration, proliferation, and IgG

41 Northern blot analysis of lymphoblast and bladder RNA confirmed CNTNAP3 transcript

42 imens, and that they also preexist in normal lymphoblast and breast tissues.

43 s (TFs) in human-mouse erythroid progenitor, lymphoblast and embryonic stem-cell lines.

44 ferase-based reporter gene assays in human T lymphoblast and epithelial cell lines.

45 btain over 1,000 h of growth data from mouse lymphoblast and pro-B-cell lymphoid cell lines.

46 Furthermore, we observed both lymphoblasts and apoptotic lymphocytes in spleen late in

47 ed cell size distributions in populations of lymphoblasts and applied a mathematical analysis to calc

48 IgM ligation, characterized by a paucity of lymphoblasts and augmented apoptosis.

49 acteristic of late EBV replication in both B lymphoblasts and epithelial cells in immune-comprised pe

50 ented accuracy, the asymmetry of division in lymphoblasts and epithelial cells.

51 Lymphoblasts and fibroblasts of FA patients have evidenc

52 ing phospho-specific antibodies with patient lymphoblasts and following ectopic expression of the mut

53 induced p100/NF-kappaB2 processing in human lymphoblasts and HEK293 cells.

54 RNA levels were highest in cultured patient lymphoblasts and lowest in postmortem central and periph

55 that: (1) UBE3A is imprinted in fibroblasts, lymphoblasts and neural-precursor cells; (2) allelic imp

56 t UTX escapes X-inactivation in female T-ALL lymphoblasts and normal T cells.

57 relevant interactions with HNF4alpha in both lymphoblasts and pancreatic beta-cells, including compou

58 Lymphoblasts and skeletal muscle expressing SCN5A also s

59 EBV-transformed but not mitogen-activated B lymphoblasts and that are also expressed in a range of B

60 FAK are significantly decreased in autistic lymphoblasts and that Src protein expression and the pho

61 throughput mass spectrometry, in both human lymphoblasts and their derived exosomes, revealing a cle

62 ere compared in CEM (T-lymphoblast), Raji (B-lymphoblast), and ML-1 (myeloid) cell lines.

63 sing exogenous RNF170 constructs and in ADSA lymphoblasts, and appears to result from enhanced RNF170

64 right ventricle, skeletal muscle, platelets, lymphoblasts, and fibroblasts from 19 children with BTHS

65 disrupting KLHDC8B function in HeLa cells, B lymphoblasts, and fibroblasts leads to significant incre

66 rol tissue specimens including normal brain, lymphoblasts, and fibroblasts, cortical tubers, and U87

67 f NPY messenger RNA in post-mortem brain and lymphoblasts, and levels of plasma NPY.

68 cells, Epstein-Barr virus (EBV)-transformed lymphoblasts, and many standard lymphoma cell lines prod

69 hibits mTOR complex 1 (mTORC1) activity in B lymphoblasts, and mTORC1-haploinsufficient B cells have

70 ysis on Epstein-Barr virus (EBV)-transformed lymphoblasts, and quantitative reverse-transcription pol

71 he mitotic spindle in control primary BMSCs, lymphoblasts, and skin fibroblasts and bound to purified

72 n primary bone marrow stromal cells (BMSCs), lymphoblasts, and skin fibroblasts, we show that SBDS st

73 Human resting T-lymphocytes, T-lymphoblasts, and the leukemic Jurkat T-cells all exhibi

74 detectable in lymph nodes, tonsil, cultured lymphoblasts, and the ovary.

75 ted in Trex1(-/-) mice, TREX1-V235fs patient lymphoblasts, and TREX1-V235fs knock-in mice.

76 at 2 lysosomal cysteine proteases present in lymphoblasts are able to degrade l-asparaginase.

77 w that the 3' ends of U6 snRNA in PN patient lymphoblasts are elongated and unexpectedly carry nontem

78 osomes isolated from juvenile Batten disease lymphoblasts are only defective for arginine transport.

79 rrant cell growth and proliferation in T-ALL lymphoblasts are sustained by activation of strong oncog

80 The lymphoblasts are very large and express a transcriptome

81 Using available data from HapMap and B lymphoblasts as a model system, we provide evidence at n

82 In this study, by using B lymphoblasts as a model, we tested whether integrin beta

83 ncreases of GCase activities of 90% in N370S lymphoblasts at 1 nM and 40% in L444P at 0.01 nM followi

84 ecombination between JCV and EBV occurs in B lymphoblasts at a sequence essential for JCV neurovirule

85 n expression was detected in fibroblasts and lymphoblasts at levels higher than those observed in the

86 hout morphologically identifiable persistent lymphoblasts at these times (P <.001 for both comparison

87 s were shared among osteosarcoma cybrids and lymphoblasts bearing LHON mutations.

88 EBV replication in latency I-infected Akata lymphoblasts, BHRF1 spliced 1.4-kb mRNA accumulated alon

89 nsformed cells, we show that compared with B lymphoblasts, BL cells express decreased levels of the c

90 Data for CNVs present in lymphoblasts but absent in fresh blood DNA suggest that

91 The killing of human leukemia lymphoblasts by NK cells depended on the expression of t

92 ificantly enhances the capture efficiency of lymphoblast CCRF-CEM cells over monovalent aptamers and

93 ial transcription factor for EBV transformed lymphoblast cell line (LCL) growth.

94 We also generated DARNS from multiple lymphoblast cell line (LCL) samples.

95 glucocorticoid receptor (GR) in the human T-lymphoblast cell line CEM-C7.

96 RT-PCR analysis of a patient lymphoblast cell line confirmed abnormal splicing, leadi

97 A lymphoblast cell line derived from an MTS patient had de

98 serum sample was absorbed by a homozygous B-lymphoblast cell line of specific DQ typing, the eluted

99 rs, cancer cell lines and an EBV-transformed lymphoblast cell line over the Ig and TCR loci.

100 he stable diploid genome of the chicken DT40 lymphoblast cell line, an established DNA repair model s

101 ng B-lymphocyte (RBL) conversion to immortal lymphoblast cell lines (LCLs).

102 uction of wild-type IKBKAP transcripts in FD lymphoblast cell lines by improving exon inclusion.

103 cal analysis of WRN protein purified from TT lymphoblast cell lines confirmed that the R834C substitu

104 on of an in vitro model system consisting of lymphoblast cell lines derived from individuals with bot

105 n), and was also quantified by immunoblot in lymphoblast cell lines derived from schizophrenia and co

106 In lymphoblast cell lines derived from severe and mild form

107 Three lymphoblast cell lines derived from two DM1 patients tre

108 Furthermore, human lymphoblast cell lines endogenously expressing R264Q dis

109 Lymphoblast cell lines established from individuals with

110 and real-time quantitative RT-PCR in patient lymphoblast cell lines excluded a positional effect on t

111 mmunoprecipitation (MeDIP) array analysis on lymphoblast cell lines that revealed dispersed, rather t

112 ele at rs4355801, expression of TNFRSF11B in lymphoblast cell lines was halved (p=3.0x10(-6)).

113 s found between diagnostic groups, or in the lymphoblast cell lines, and no effect of rs7513662 genot

114 P2 and IRAK1 RNA levels were quantified from lymphoblast cell lines, and western blots were performed

115 Lysosomes isolated from lymphoblast cell lines, established from individuals wit

116 We also investigated allelic expression in lymphoblast cell lines.

117 re11 (MRE11(-/H129N)) chicken DT40 and human lymphoblast cell lines.

118 0.050) and protein expression (P = 0.025) in lymphoblast cell lines.

119 pts containing the p.R151X mutation in human lymphoblast cell lines.

120 otein levels and function in patient-derived lymphoblast cell lines.

121 by proteasome inhibitor MG132 in both human lymphoblast cells and MCF7 cells.

122 Patient lymphoblast cells carrying either SDHD-G12S or SDHD-H50R

123 osutinib decreases oxidative PTEN in patient lymphoblast cells carrying SDHD variants, but not in pat

124 nd protein levels decrease in fibroblast and lymphoblast cells derived from both normal controls and

125 n variation, we measured GSTM3 expression in lymphoblast cells from a human Centre d'Etude du Polymor

126 in species, including PSF, accumulate in the lymphoblast cells from the patients carrying pathogenic

127 ucible SCGB (IIS), because its expression in lymphoblast cells is augmented by IFN-gamma treatment.

128 addition, the net uptake of 5PTB into human lymphoblast cells is diminished relative to that of 5P2'

129 glucocorticoid receptor (hGR) 1A promoter in lymphoblast cells resides largely in two DNA elements (f

130 Furthermore, treatment of lymphoblast cells with IIS antisense phosphorothioate (S

131 es cannot reliably discriminate less than 5% lymphoblast cells.

132 ntrol hGR 1A promoter regulation in T- and B-lymphoblast cells.

133 ts was assessed in human MCF7 cells and TK-6 lymphoblast cells.

134 cells prefer to bind to collagen, while PBT lymphoblasts choose fibronectin when presented with a co

135 Shafer ensemble) are employed for lymphocyte/lymphoblast classification.

136 ietic stem cells, leukemic cell lines, and B lymphoblasts compared with other tissues or cells.

137 into blood, we simulated leukemia cases with lymphoblast concentrations ranging from 1 to 30% of tota

138 bited near-normal levels of GALE activity in lymphoblasts, consistent with a diagnosis of peripheral

139 The overexpression of FAK in autistic lymphoblasts countered the adhesion and migration defect

140 Lymphoblasts deficient in DNA repair (derived from a xer

141 Studies here using human B lymphoblasts demonstrate the importance of HSP90alpha an

142 Second, lymphoblasts demonstrating the most severe reduction in

143 In lymphoblasts derived from an FA-C patient, overexpressio

144 f72 mRNA levels were quantified in brain and lymphoblasts derived from FTLD and ALS/FTLD patients and

145 When tested using lymphoblasts derived from patients with GD homozygous fo

146 tected a low level of LMAN1-MCFD2 complex in lymphoblasts derived from patients with missense mutatio

147 nd regulation of apoptosis and senescence in lymphoblasts derived from the cases.

148 istic explanation for previous findings that lymphoblasts derived from these patients exhibit subtle

149 ps of a complete hydatidiform mole and three lymphoblast-derived cell lines, and we validated the app

150 ic deletion in SLC38A10, three CNVs found in lymphoblast-derived DNA but not present in whole-blood d

151 eatment reduced the hyperexcitability in the lymphoblast-derived LR group but not in the NR group, st

152 e magnetic needle enhanced the percentage of lymphoblasts detectable by light microscopy by 10-fold i

153 compensated for CD22 deficiency by restoring lymphoblast development, proliferation, c-Myc and CUL1 e

154 ct of stroma in selecting Imatinib-resistant lymphoblasts did not require direct cell-cell contact.

155 normal myoblasts, myotubes, fibroblasts and lymphoblasts, does not vary significantly throughout the

156 In lymphoblasts, EBNALP and EBNA2 did not stably associate.

157 of the latent membrane protein 1 promoter in lymphoblasts; EBNALP could coactivate with a deficient m

158 ass I MHC molecules on the cell surface of B lymphoblasts enhances their recognition by mouse and hum

159 r for p53-dependent AICD because susceptible lymphoblasts expressed significantly elevated levels of

160 In FANCD2-deficient lymphoblasts, FANCD2 is essential to suppress endogenous

161 satisfy the enhanced demands of transformed lymphoblasts for iron.

162 Cultured lymphoblasts from 10 individuals with BRCA1 mutations an

163 cell acute lymphoblastic leukemia (BCP-ALL), lymphoblasts from 111 patients with BCP-ALL were assayed

164 e, we analyzed gene expression of diagnostic lymphoblasts from 189 children with ALL and compared the

165 MM was markedly deficient in fibroblasts and lymphoblasts from 23 patients with CDG-Ia (range 0-15.3%

166 samples, we interrogated gene expression in lymphoblasts from 244 families with discordant siblings

167 , we compared genome-wide gene expression of lymphoblasts from 270 patients with newly diagnosed chil

168 med on genomic DNA extracted from diagnostic lymphoblasts from 47 children with T-ALL treated on Chil

169 acid and sphingosine were added to cultured lymphoblasts from a Farber disease patient in the presen

170 er MyD88 knockdown after UVR, in contrast to lymphoblasts from a healthy control.

171 Lymphoblasts from adult patients with precursor B ALL we

172 Using B lymphoblasts from affected individuals of the Egyptian a

173 did not protect MDA-MB468 breast cells or B-lymphoblasts from apoptosis.

174 We also found that lymphoblasts from autistic subjects exhibit significantl

175 Lymphoblasts from children with T-ALL should be evaluate

176 ein, and that RNASEL activity was reduced in lymphoblasts from heterozyogous individuals compared wit

177 AR1A expression were studied in PPNAD and in lymphoblasts from patients bearing PRKAR1A-mut.

178 Transacylase activity was decreased in lymphoblasts from patients with Barth syndrome (tafazzin

179 Lymphoblasts from patients with Fanconi anemia (FA) expr

180 liver and Epstein-Barr virus-immortalized B lymphoblasts from patients with polycystic liver disease

181 The presence of mutant RP1 mRNA in lymphoblasts from patients with RP1 disease implies that

182 pe and mutant RP1 mRNA were both detected in lymphoblasts from patients with RP1 disease.

183 revealed two mRNA transcripts of FAM136A in lymphoblasts from patients, which were confirmed by immu

184 a broad range of ALL cell lines and primary lymphoblasts from pediatric T-ALL and pre-B ALL patients

185 We observed that primary BMSCs and lymphoblasts from SDS patients exhibited an increased in

186 Treatment of primary BMSCs and lymphoblasts from SDS patients with nocodazole, a microt

187 Lymphoblasts from subjects homozygous for the -207G alle

188 Furthermore, lymphoblasts from the patient carrying a SYNE1 splice-si

189 SCL, LYL1, LMO1, and LMO2 can be detected in lymphoblasts from up to 80% of patients with acute T-cel

190 include studies of minimal residual disease, lymphoblast genetics (including genetic profiling studie

191 nduce remission in 3 of the 4 patients whose lymphoblasts harbored PTEN deletions at the time of diag

192 hia coli, Saccharomyces cerevisiae and mouse lymphoblasts, heavier cells grew faster than lighter cel

193 d even for patients with a low percentage of lymphoblasts (ie, 1%-4%) at either day 15 (5-year EFS =

194 th higher expression of DISC1Delta7Delta8 in lymphoblasts in an independent sample.

195 e repressive influences of Bcl-6, dividing B lymphoblasts in inflamed tissues should display heighten

196 e the expansion of latently infected CD27+ B lymphoblasts in the peripheral blood.

197 w that treatment of Barth syndrome patients' lymphoblasts in tissue culture with the iPLA(2) inhibito

198 gies that specifically target EBV-infected B lymphoblasts in vivo.

199 eIF2 alpha was also detected in EBV-infected lymphoblasts, in which high levels of LMP1 correlated wi

200 on were similar in Vav1(-/-) and wild-type T lymphoblasts, indicating that defective FOXO1 phosphoryl

201 1 that affects protein expression in human B lymphoblasts influenced several brain measures related t

202 In human B lymphoblasts, inhibition of the peptide transporter asso

203 tworks implicated in transforming the normal lymphoblast into immortalized lymphoblastoid cells.

204 the Ca(2+) mobilization defect seen in ADSA lymphoblasts is apparently not due to aberrant IP3 recep

205 ze single nucleotide polymorphisms (SNPs) in lymphoblasts isolated from children with acute lymphobla

206 uggest that inhibitors of Mer may potentiate lymphoblast killing when used in combination with chemot

207 ion of the TAL1 target genes in T-cell acute lymphoblast leukemia (T-ALL) Jurkat cells, which is acco

208 The immobilization of B-lymphoblast-like Burkitt's lymphoma Raji cells on the qu

209 els with CNV of the syntenic 7qF3 region and lymphoblast lines from 34 members of 7 multiplex ASD-aff

210 Two T-lymphoblast lines, CEM-C7 and Jurkat, contain high level

211 (WT:MU) IKBKAP transcript in EBV-transformed lymphoblast lines, primary fibroblasts, freshly collecte

212 II-matched LCLs but not mitogen-activated B lymphoblasts, many (1) do not map to any known EBV antig

213 We further demonstrate in this lymphoblast model that the gene-dosage directed increase

214 Northern analyses of lymphoblast mRNAs from 2 patients and reverse-transcribe

215 cribed polymerase chain reaction (RT-PCR) of lymphoblast mRNAs from all 3 patients revealed multiple

216 In human lymphoblasts, NRG1-mediated phosphatidyl-inositol,3,4,5

217 stably expressing NPM1c+; and (iii) primary lymphoblasts of NPM1c+ AML patients.

218 Here, we show that lymphoblasts of women with BRCA1 mutations who had been

219 the expression profile of X-linked genes in lymphoblasts of XLMR males.

220 egion/Abelson murine leukemia (Bcr/Abl) P190 lymphoblasts on stroma and made them resistant to the FT

221 ulation of cell and viral gene expression in lymphoblasts only when the interaction is unstable; dele

222 ese hamster ovary effecter cells and human B lymphoblasts or epithelial cells by using a virus-free c

223 The percentage of mitotic lymphoblasts or PBMCs bearing p53 centrosomal localizati

224 amino acids stably associated with EBNA2 in lymphoblasts or with EBNA2 acidic activating domain from

225 alysis of doxorubicin exposed, related human lymphoblasts, p53 wild-type (WT) Tk6, and p53 mutant WTK

226 t pediatric cancer, and the peripheral blood lymphoblast percentage is an important index for ALL dia

227 In ADSA lymphoblasts, platelet-activating factor-induced Ca(2+)

228 ssion in response to glucocorticoids, CEM-C7 lymphoblasts possess three mechanisms ensuring high gluc

229 The ability to capture ALL lymphoblasts present in blood at low concentrations prov

230 RDC2, and genetic correction of FA-A or FA-C lymphoblasts prevented NPMc ubiquitination.

231 wed that IRF-4 inhibits growth of BCR/ABL+ B lymphoblasts primarily through negative regulation of ce

232 inhibits effector/memory peripheral blood T lymphoblast proliferation and IL-2 production, the inten

233 egulated proteasome activity in PHTS-derived lymphoblasts, Pten knock-in mice and cell lines expressi

234 the effects of ara-G were compared in CEM (T-lymphoblast), Raji (B-lymphoblast), and ML-1 (myeloid) c

235 parameters: (1) GALE activity in transformed lymphoblasts, representing a "nonperipheral" tissue, (2)

236 NA-mediated knockdown in duplication patient lymphoblasts restores MeCP2 to normal levels.

237 th phenylbutyrate of control fibroblasts and lymphoblasts resulted in an increase in the residual enz

238 those cells may arise when infected CD4(+) T lymphoblasts return to resting state.

239 42A cells with the GHR-expressing human IM-9 lymphoblasts revealed similar enrichment of GHR in the l

240 the same patient (lymphocyte, fibroblast and lymphoblast) revealed that only transformed cells contai

241 We used our XCA to survey lymphoblast RNA samples from 43 unrelated XLMR males and

242 catalytic activity and expression of IDE in lymphoblast samples from 12 affected and unaffected memb

243 Lymphoblast samples were drawn from 53 individuals with

244 iological effects seen in some primary human lymphoblast samples.

245 efects obtained from a 68-year-old man whose lymphoblasts showed no evidence of Fanconi anemia.

246 GJ response data of patient-derived cultured lymphoblasts, showing that protein aggregation is an imp

247 in the human T-cell acute leukemia Jurkat, B lymphoblast SKW 6.4, and acute myelogenous leukemia HL-6

248 the transcripts reported to be expressed in lymphoblast-somatic cell hybrids are not expressed in fi

249 Using lymphoblasts spiked into blood, we simulated leukemia ca

250 pared to those in SMARD1, and fibroblast and lymphoblast studies indicate that the IGHMBP2 protein le

251 lasmic alpha-GalA mRNA in normal and patient lymphoblasts suggested that mRNA degradation did not res

252 is critical for Epstein-Barr virus-infected lymphoblast survival.

253 ional process transforms ETV6-RUNX1-positive lymphoblasts, targeting the promoters, enhancers and fir

254 ere found to be more effective for capturing lymphoblasts than commonly used, ALL-specific antibodies

255 roma selects Imatinib-resistant Bcr/Abl P190 lymphoblasts that are less dependent on Bcr/Abl tyrosine

256 ng B cells with EBV results in activation to lymphoblasts that are phenotypically similar to those ge

257 on occurs in HL-60 leukemic cells and Raji B lymphoblasts that express high levels of c-Myc and have

258 We demonstrate in peripheral blood T cell lymphoblasts that immediate early phosphotyrosine signal

259 evious reports, we demonstrated in patients' lymphoblasts that the mutation does not influence overal

260 The lymphoblasts that were resistant to this FTI were also m

261 at in three different clones of EBV-infected lymphoblasts the levels of expression of LMP1 in individ

262 We show that in human lymphoblasts, the silencing of one allele is incomplete.

263 at are over-expressed by resistant leukaemia lymphoblasts, thereby impairing drug activity and pharma

264 interactions is enhanced in dystonia patient lymphoblasts, thereby leading to intensified PKR activat

265 Unlike the lymphoblasts, this myeloid leukemia cell line (UoC-M1) w

266 As compared to normal lymphoblasts, those from an affected patient showed sign

267 ells (SAECs), macrophages (THP-1 cells), and lymphoblasts (TK6 cells)--were exposed to PEPs at a wide

268 ased the sensitivity of BCR-ABL1-transformed lymphoblasts to ABL1 kinase inhibitors.

269 d-type transcript and enzyme activity in CEP lymphoblasts to approximately 10% and 15% of normal, res

270 " tissue, (2) metabolic sensitivity of those lymphoblasts to galactose challenge in culture, and (3)

271 similarities between normal and malignant T lymphoblasts to screen a small molecule library for acti

272 ciated with a greater propensity of leukemic lymphoblasts to undergo apoptosis.

273 s a critical Notch target gene that mediates lymphoblast transformation and disease progression via i

274 t only contributed approximately 0.2% of the lymphoblast URO-synthase activity.

275 hat isolates and enumerates peripheral blood lymphoblasts using affinity separations.

276 The WT:MU ratio in cultured lymphoblasts varied with growth phase but not with serum

277 The spermine/spermidine ratio in lymphoblasts was 0.53, significantly reduced compared wi

278 (P = .031); EFS for patients with > or = 5% lymphoblasts was 51.9% +/- 18.0% (P = .009).

279 ensitivity in FSHD and control myoblasts and lymphoblasts was as follows: a non-genic D4Z4-adjacent s

280 AFF- and APRIL-promoted viability of cycling lymphoblasts was associated with sustained expression of

281 pression of C9orf72 transcripts in brain and lymphoblasts was found in sporadic FTLD and ALS/FTLD pat

282 TRPV4 protein on western blotting of patient lymphoblasts was no different to control.

283 In latency III-infected lymphoblasts, we have also identified a stable 1.3-kb RN

284 Using patients' lymphoblasts, we show here that indeed WT SOD1 is modifi

285 The lymphoblasts were composed of a CD4/CD8 double-positive

286 The lymphoblasts were examined by flow cytometry and immunoh

287 Of note, primary lymphoblasts were hypersensitive to gamma-secretase inhi

288 Their lymphoblasts were hypersensitive to MMC and MMC-induced

289 CCRF-CEM lymphoblasts were isolated in the chip with 82-97% purit

290 Lymphoblasts were isolated using monoclonal antibodies f

291 cts on the LMP1 promoter in transfected BJAB lymphoblasts were similar to EBNA2.

292 ap in the transcriptomes of the two types of lymphoblasts when compared to the original resting B cel

293 3 have been detected in latency III-infected lymphoblasts, where they are encoded within EBNA transcr

294 errant transcripts in both wild-type and CEP lymphoblasts, whereas BPS mutation reduced the wild-type

295 duces CLA expression by HSV-2-responsive CD4 lymphoblasts, while their reintroduction restores this p

296 30 patients (12.6%) had leukaemic lymphoblasts with an ETP-related gene-expression signatu

297 Among 113 children with newly diagnosed ALL, lymphoblasts with the TEL-AML1 translocation had signifi

298 Leukemic lymphoblasts within different immunophenotypic populatio

299 /F3 cells and primary BCR-ABL1-transformed B lymphoblasts without affecting cell survival.

300 um redistribution, and apoptosis in Jurkat T-lymphoblasts, without causing immediately apparent physi