ライフサイエンスコーパス: LCL

1 LCL and CAPE play a more important role than TCWV in det

2 LCL HiC data mapped intergenic EBNA2 sites to EBNA2 up-r

3 LCL hits were enriched for EBV-induced genes, including

4 LCL proliferation induces p16(INK4A) and p14(ARF)-mediat

5 LCL-derived iPSCs exhibited normal karyotype, expressed

6 LCLs from women with past PMD (n = 8) or control women (

7 We report the generation of iPSCs from 2 LCLs (LCL-iPSCs) via a feeder-free episomal method using

8 These highlighted 57 BL and 87 LCL genes uniquely important for their growth and surviv

9 rence from the intended of -0.18+0.35x7 (95% LCL, -1.91+1.22x38; 95% UCL, +0.75+1.09x145).

10 ative refractive error was -0.30+0.47x6 (95% LCL, -2.36+1.31x36; 95% UCL, +1.00+1.18x148) with a diff

11 th (multivariable-adjusted hazard ratio, (95%LCL) aHR(95%UCL) ), over follow-up through December 2018

12 ochondrial protective pathways and that AD-A LCLs are better able to activate these protective pathwa

13 better understand mitoplasticity in the AD-A LCLs we examined changes in mitochondrial function using

14 ncrease in mitochondrial respiration in AD-A LCLs.

15 y acute DMNQ exposure but this varied across LCL groups.

16 nvironmental exposures; another subset of AD LCLs demonstrated normal mitochondrial activity (AD-N).

17 Immediately after LCL establishment, EBV lytic genes were also expressed i

18 decline in mitochondrial respiration in all LCL groups.

19 Although LCLs internalized DEC-205-targeted antigens less efficie

20 detected in the exosomes from Raji cells and LCL.

21 o were also important for MYC expression and LCL growth.

22 MYC ESEs greatly reduced MYC expression and LCL growth.

23 25ESE reporter activity, MYC expression, and LCL growth.

24 ential for ESE activity, MYC expression, and LCL growth.IMPORTANCE SEs play critical roles in cancer

25 romosomes from human primary lymphocytes and LCL, showing that higher level distribution is not alter

26 rences in immunopathogenesis between MCL and LCL may result from an imbalance between prostaglandins

27 We compared results from paired WB and LCL DNA samples for 16 subjects, using LCLs of low passa

28 ecreased MYC or BCL2 expression and arrested LCL growth.

29 ASD LCLs exhibited a significantly greater change in these p

30 Compared to Sib LCLs, ASD LCLs exhibited significantly higher ATP-linked respirati

31 while multi-cell-type DARNS were enriched at LCL-specific DHS sites.

32 at, in contrast to the soil enzyme, the ATII-LCL mercuric reductase is functional in high salt, stabl

33 extremely demanding environment of the ATII-LCL.

34 enesis using a lymphoblastoid B cell line (B-LCL) and U3A cells.

35 ytes (PBLs) and a B lymphocytic cell line (B-LCL).

36 Mutant B-LCL and U3A cells also displayed reduced pSTAT4.

37 or the blocks present in marmoset PBLs and B-LCLs are different.

38 ontrast, the restriction factor present in B-LCLs blocks HIV-1 replication at a later step, after nuc

39 to escape the restriction in the marmoset B-LCLs.

40 otencies and effects were comparable between LCLs of two genetically unrelated individuals, providing

41 exhibited RNA half-life differences between LCLs at a false discovery rate (FDR) < 0.05, which accou

42 pression varied from ~1- to 400-fold between LCLs.

43 ifferences in gene expression levels between LCLs and B cells are of small magnitude, and that LCLs c

44 -ITD(+) AML drug resistance is attenuated by LCL-461, a mitochondria-targeted ceramide analog drug, i

45 These motif associations were confirmed by LCL RBPJ ChIP-seq finding 72% RBPJ occupancy and Encyclo

46 own of the MYC -428 and -525 ESE eRNA caused LCL growth arrest and reduced cell growth.

47 ESEs) are essential for lymphoblastoid cell (LCL) growth and survival.

48 mble the proliferating lymphoblastoid cells (LCLs) (latency III) that are generated after infection.

49 and reactivation from lymphoblastoid cells (LCLs) with type III latency.

50 agents and the proapoptotic chemotherapeutic LCL-161.

51 ncreases in ROS compared to both Sib and Con LCLs.

52 ncreased in both ASD and Sib compared to Con LCLs.

53 epletion of CBFbeta in an EBNA3C-conditional LCL confirmed the role of CBF in the regulation of EBNA3

54 to the IgH V-D-J region from the conditional LCL was used to formally show that SHM is activated by f

55 n either newly infected cells or conditional LCLs-by inactivating EBNA3A and EBNA3C.

56 the Seahorse XF96 analyzer in AD and Control LCLs after exposure to trichloroacetaldehyde hydrate (TC

57 ed the detrimental effect of TCAH in Control LCLs and resulted in a increase in mitochondrial respira

58 ally binds to hypo-methylated DNA in control LCLs, whereas the differential DNA methylation alters co

59 significantly higher in mutant than control LCLs, consistent with an abnormality of nuclear calcium

60 is study, lymphoblastoid cell line cultures (LCLs) from women with PMDD and asymptomatic controls wer

61 Our data indicate that DBA LCLs could be a useful model for molecular and pharmacol

62 not been fully characterized to what degree LCLs preserve the in vivo status of non-genetic biologic

63 ere indistinguishable from wild-type-derived LCLs in terms of steady-state EBV gene transcription.

64 ts had higher levels of serum AnxA1 than did LCL patients or control subjects.

65 e lymphoblastoid cell lines (LCLs), dividing LCLs established from the individuals homozygous for the

66 gous target cells and unloaded HLA-B8(+) EBV LCL target cells.

67 pression analysis and cDNA sequencing in EBV LCLs of individuals support the presence of a stable tru

68 irus-infected lymphoblastoid cell lines (EBV-LCL) were isolated based on their intercellular adhesive

69 J occupancy and Encyclopedia Of DNA Elements LCL ChIP-seq finding EBF, NFkappaB RELA, and PU.1 at 54%

70 ted mice at 9 d after the injection of empty LCL.

71 gle injection (10 mg/kg) of PLP-LCL or empty LCL as a control.

72 ongly affect cell gene expression and enable LCL growth.

73 ded the MYC and BCL2 oncogenes, which enable LCL proliferation and survival.

74 Using ENCODE LCL transcription factor ChIP-sequencing data, EBNA3C si

75 GWAS using a genomic data-enriched LCL model system, together with functional and mechanist

76 EBNA3B is not necessary to establish LCLs, but EBNA3A and EBNA3C are required to sustain prol

77 Newly established LCLs from both individuals demonstrated the same phenome

78 CD1d-expressing LCL elicited interferon gamma secretion and cytotoxicity

79 1-induced cFLIP was found to be critical for LCL defense against TNFalpha-mediated programmed cell de

80 criptional regulators that are essential for LCL establishment, proliferation, and survival.

81 percent of LCL genes that are essential for LCL growth and survival were differentially expressed.

82 Approximately 30% of genes essential for LCL growth were linked to EBV enhancers.

83 ription factor, RBPJ, which is essential for LCL growth.

84 monstrate that while Cp is not essential for LCL outgrowth in vitro, it enhances transformation effic

85 t CYTOR and NORAD lncRNAs were important for LCL growth.

86 tative trait loci (eQTL), mQTL detected from LCLs were enriched in associations for a broader range o

87 These results validate the use of DNA from LCLs of low passage number for exome sequencing.

88 rain neurons or patient-derived LRRK2 G2019S LCLs with the LRRK2 kinase inhibitor GNE-7915, either pr

89 y correlated with RSV-G expression in HapMap LCLs.

90 We conclude that genetically diverse human LCLs enable identification of susceptibility genes (e.g.

91 l effects, preventing virus release in human LCLs and abrogating gp350 expression in 12-O-tetradecano

92 rvival, their presence was not detectable in LCL-iPSCs.

93 nes (PDEGs), which are up-regulated genes in LCL for a given class of drug response phenotype in trip

94 is, IFI16 colocalized with the EBV genome in LCL and Raji cell nuclei.

95 ChIP-seq of EBNA2 and RBPJ sites in LCL DNA found EBNA2 at 5,151 and RBPJ at 10,529 sites.

96 equencing identified >13,000 EBNA3C sites in LCL DNA.

97 known transcription factor binding sites in LCL GM12878 revealed substantial co-localization of EBNA

98 d IRF4, EBNA2, and SPI1 binding to 525ESE in LCLs.

99 ost of the original 49 samples but absent in LCLs, while multi-cell-type DARNS were enriched at LCL-s

100 FA treatment attenuated cAMP accumulation in LCLs.

101 5ESE and 428ESE) had very high activities in LCLs but not in EBV-negative BJAB cells.

102 GWA analyses in LCLs identified 198 mRNA expression probe sets, 12 SNP l

103 ffect the direction of methylation change in LCLs.

104 ence of EBNA3C, and (v) H2AX knocked down in LCLs led to enhanced expression of Bub1 and downregulati

105 As expected, CIITA was downregulated in LCLs.

106 re annotated, 78% as mQTL and 31% as eQTL in LCLs, which covered 37% of the investigated diseases/tra

107 ntidepressant action, these were examined in LCLs.

108 ment, EBV lytic genes were also expressed in LCLs, and ~4% of the LCLs express gp350.

109 Twelve proteins had detectable expression in LCLs and three, CCT8, MX1 and PWP2, showed elevated leve

110 Gal1 expression in LCLs was dependent on both activating protein 1 (AP-1) a

111 lyl cyclase (AC) and BDNF gene expression in LCLs.

112 tarabine treatment from 1.7- to 26.6-fold in LCLs.

113 latory elements was significantly greater in LCLs than in non-immune cells (P < 2.0e-05).

114 Candidate eQTL analyses in in LCLs in the Hutterites suggest that these rare non-codin

115 cal for BIM suppression and MYC induction in LCLs.

116 CT8, MX1 and PWP2, showed elevated levels in LCLs derived from patients with DS compared with control

117 Elimination of LMP2A in LCLs using a shLMP2A approach showed that the expression

118 previously reported that DNA methylation in LCLs is highly variable in a data set of ~27,000 CpG din

119 ose binding leads to histone modification in LCLs.

120 uced gene expression differences observed in LCLs may be influenced by their transformation, and thus

121 association (GWA) analyses were performed in LCLs using 1.3 million SNPs, 485k DNA methylation probes

122 f LMP1 expression from the ED-L1 promoter in LCLs already expressing LMP1.

123 we generated a comprehensive EBV regulome in LCLs.IMPORTANCE Epstein-Barr virus (EBV) immortalization

124 ndidate genes governing lytic replication in LCLs undergoing ER stress.

125 of the integrated 525ESE-driven reporter in LCLs.

126 properties as well as GPCR drug responses in LCLs, which are suspension cells.

127 aracterizing GPCR-mediated drug responses in LCLs.

128 e promoter (AP) and strong enhancer (SE)] in LCLs more than expected by chance [45.3-fold enrichment

129 stoid cell lines (LCLs), chromatin states in LCLs and MS-associated genomic regions.

130 st, inference based on functional studies in LCLs may be more limited to the cell lines.

131 uantitative PCR (ChIP-qPCR) indicate that in LCLs inhibition of CDKN2C (p18INK4c) and PRDM1 (BLIMP-1)

132 cture that underlies regulatory variation in LCLs can typically be generalized to primary B cells.

133 icting valid sequence differences, including LCLs with putative mosaicism for the non-reference allel

134 is due to the combined effects of increasing LCL and decreasing TCWV.

135 EBNA1 depletion from latently infected LCLs results in the loss of cell proliferation and the l

136 B plasma detection or from latently infected LCLs.

137 and E gene products relative to WT-infected LCLs and lytic replication of the viral genome.

138 Incubation of the ZIIRmt-infected LCLs with the chemical inducer 12-O-tetradecanoyl-phorbo

139 d the same treatment of WT- or ZVmt-infected LCLs.

140 ions prevails in the lower convective layer (LCL) of the brine pool at Atlantis II (ATII) Deep in the

141 report the generation of iPSCs from 2 LCLs (LCL-iPSCs) via a feeder-free episomal method using a coc

142 g platform and performed the L. camara leaf (LCL) and root (LCR) de novo transcriptome analyses.

143 rated 72,877 and 513,985 unigenes from leaf (LCL) and root (LCR) respectively.

144 is causes localized cutaneous leishmaniasis (LCL) and mucocutaneous leishmaniasis (MCL).

145 ents with localized cutaneous leishmaniasis (LCL) or with controls from an area of endemicity.

146 can cause localized cutaneous leishmaniasis (LCL), which heals spontaneously, or mucosal leishmaniasi

147 (MCL) or localized cutaneous leishmaniasis (LCL).

148 ) and decreasing lifting condensation level (LCL) with elevation overwhelming the effects of decreasi

149 as -0.12+0.12x2 (95% lower confidence limit [LCL], -1.94+1.06x44; 95% upper confidence limit [UCL], +

150 derived from human lymphoblastoid cell line (LCL) culture media.

151 enes essential for lymphoblastoid cell line (LCL) growth and survival.

152 r immortal human B-lymphoblastoid cell line (LCL) growth.

153 r for EBV transformed lymphoblast cell line (LCL) growth.

154 tion of ESEs stops lymphoblastoid cell line (LCL) growth.

155 lyses of published lymphoblastoid cell line (LCL) Hi-C data and our 4C-seq experiments position EBV e

156 Lymphoblastoid cell line (LCL) is a common tool to study genetic disorders.

157 completely ablated lymphoblastoid cell line (LCL) outgrowth.

158 d DARNS from multiple lymphoblast cell line (LCL) samples.

159 ) and immortalized lymphoblastoid cell line (LCL).

160 S patient-derived lymphoblastoid cell lines (LCL) demonstrated increased mtDNA damage relative to age

161 a panel of human lymphoblastoid cell lines (LCL) to infer drug response networks (DRNs) that are res

162 V-infected cells, lymphoblastoid cell lines (LCL) were treated with AM580, a synthetic retinoic acid

163 ) of 5 ATM mutant lymphoblastoid cell lines (LCL), an ATM mutant MCL cell line, an ATM knockdown PGA

164 f MDV-transformed lymphoblastoid cell lines (LCL).

165 , and latency III lymphoblastoid cell lines (LCL).

166 on changes in 480 lymphoblastoid cell lines (LCLs) after in vitro simvastatin treatment, and identifi

167 even human HapMap lymphoblastoid cell lines (LCLs) and analyzed the effect of DNA sequence variation

168 s) in transformed lymphoblastoid cell lines (LCLs) and human embryonic stem cell (ES) lines, but were

169 ruba (YRI) HapMap lymphoblastoid cell lines (LCLs) and identified 12 cis and 160 trans protein level

170 EBV-transformed lymphoblastoid B-cell lines (LCLs) and primary PTLDs overexpress galectin-1 (Gal1), a

171 lysis in adipose, lymphoblastoid cell lines (LCLs) and skin.

172 EBV-immortalized lymphoblastoid cell lines (LCLs) as a model, we found that the expression of major

173 pattern in human lymphoblastoid cell lines (LCLs) as well as identified specific differential DNA me

174 us immortalized lymphoblastoid B-cell lines (LCLs) can be generated from a minimal amount of blood an

175 ell lines such as lymphoblastoid cell lines (LCLs) could represent the ideal cellular model system.

176 ene expression in lymphoblastoid cell lines (LCLs) derived from 210 HapMap individuals, we identify c

177 ,540 CpG sites in lymphoblastoid cell lines (LCLs) derived from independent samples of European and A

178 model of PMD with lymphoblastoid cell lines (LCLs) derived from participants of a prior E2-WD clinica

179 EBV-transformed lymphoblastoid B cell lines (LCLs) derived from subjects with TERT promoter mutations

180 t that RP-mutated lymphoblastoid cell lines (LCLs) established from DBA patients show defective rRNA

181 Using lymphoblastoid cell lines (LCLs) established with EBV recombinants conditional for

182 How lymphoblastoid cell lines (LCLs) evolve from the infected lymphocytes is uncertain.

183 ng microarrays on lymphoblastoid cell lines (LCLs) from 413 cases and 446 controls.

184 histone marks in lymphoblastoid cell lines (LCLs) from 75 sequenced individuals with LCL-specific Hi

185 that a subset of lymphoblastoid cell lines (LCLs) from children with autistic disorder (AD) show mit

186 modifications in lymphoblastoid cell lines (LCLs) from human, chimpanzee and rhesus, and we identify

187 enomic regions in lymphoblastoid cell lines (LCLs) from humans, chimpanzees, and rhesus macaques, usi

188 ies involving 523 lymphoblastoid cell lines (LCLs) from individuals of European, African, Asian, and

189 use of banked human lymphoblast cell lines (LCLs) from normal and depressed subjects; the latter div

190 ein expression in lymphoblastoid cell lines (LCLs) from patients with DS and in brains from two mouse

191 Lymphoblastoid cell lines (LCLs) from some children with ASD exhibit increased oxid

192 ith HHV-6B, (iii) lymphoblastoid cell lines (LCLs) from subjects with inherited chromosomally integra

193 equence data from lymphoblastoid cell lines (LCLs) from the TwinsUK cohort, we identify a candidate s

194 h time in culture, lymphoblastic cell lines (LCLs) from two affected individuals in family UW-AP exhi

195 s into long-lived lymphoblastoid cell lines (LCLs) in vitro requires the collaborative effects of EBN

196 sly proliferating lymphoblastoid cell lines (LCLs) in vitro through manipulation of a number of major

197 ckdown of H2AX in lymphoblastoid cell lines (LCLs) led to the upregulation of the Bub1 oncoprotein an

198 BV) transformed lymphoblastoid B-cell lines (LCLs) not only express DEC-205 at similar levels to DCs,

199 latently infected lymphoblastoid cell lines (LCLs) partially via Toll-like receptor 2 triggering, as

200 (EBV) transformed lymphoblastoid cell lines (LCLs) provide a conveniently accessible and renewable re

201 B-lymphocytes to Lymphoblastoid Cell Lines (LCLs) requires four EBV nuclear antigen (EBNA) oncoprote

202 establishment of lymphoblastoid cell lines (LCLs) that can grow indefinitely in vitro EBV transforms

203 sly proliferating lymphoblastoid cell lines (LCLs) that carry EBV DNA as extra-chromosomal episomes,

204 e ZIIRmt-infected lymphoblastoid cell lines (LCLs) that did grow out exhibited a phenotype similar to

205 Lymphoblastoid cell lines (LCLs) were cocultured with autologous or allogeneic CD4(

206 an-derived HapMap lymphoblastoid cell lines (LCLs) were infected with RSV.

207 (VDR) binding in lymphoblastoid cell lines (LCLs), chromatin states in LCLs and MS-associated genomi

208 rast to wild-type lymphoblastoid cell lines (LCLs), dividing LCLs established from the individuals ho

209 -seq performed on lymphoblastoid cell lines (LCLs), expressing epitope-tagged EBNA3A, EBNA3B or EBNA3

210 Human lymphoblastoid cell lines (LCLs), generated through Epstein-Barr Virus (EBV) transf

211 lytic-permissive lymphoblastoid cell lines (LCLs), pulse exposure to the chemical ER-stress inducer

212 In GS-derived lymphoblastoid cell lines (LCLs), the proportion of ITPR1-positive cells using immu

213 (EBV)-transformed lymphoblastoid cell lines (LCLs), we identified four EBV oncoproteins and five EBV-

214 sly proliferating lymphoblastoid cell lines (LCLs), which represent an experimental model for EBV-ass

215 mary B cells into lymphoblastoid cell lines (LCLs).

216 c study using 266 lymphoblastoid cell lines (LCLs).

217 oteins, in Yoruba lymphoblastoid cell lines (LCLs).

218 (NPC) cells, and lymphoblastoid cell lines (LCLs).

219 the outgrowth of lymphoblastoid cell lines (LCLs).

220 ry B cells and in lymphoblastoid cell lines (LCLs).

221 cupancy in Yoruba lymphoblastoid cell lines (LCLs).

222 roliferation into lymphoblastoid cell lines (LCLs).

223 ansformation into lymphoblastoid cell lines (LCLs).

224 nversion to immortal lymphoblast cell lines (LCLs).

225 transformation to lymphoblastoid cell lines (LCLs).

226 ely proliferating lymphoblastoid cell lines (LCLs).

227 cent B cells into lymphoblastoid cell lines (LCLs).

228 screens in BL and lymphoblastoid cell lines (LCLs).

229 ene expression in lymphoblastoid cell lines (LCLs).

230 ll-studied Yoruba lymphoblastoid cell lines (LCLs); 14 of these lines were further differentiated int

231 ortalization into lymphoblastoid cell lines (LCLs); this latency program is controlled by the EBNA2 v

232 f treatment with long-circulating liposomes (LCL) containing prednisolone phosphate (PLP-LCL) in a mo

233 tiating B cell proliferation and maintaining LCL growth.

234 lation maintained in ambient CO2 (400 muatm, LCL, pHT : 8.02) for 1860 generations.

235 DMNQ did not affect AD-N LCLs, while it neutralized the detrimental effect of TCA

236 rting with the 3D genome organization map of LCL, we constructed a comprehensive EBV regulome encompa

237 Ninety-four percent of LCL genes that are essential for LCL growth and survival

238 Reanalyses of LCL global run-on sequencing (Gro-seq) data found abunda

239 ion on LCL, and restored iNKT recognition of LCL.

240 ype III latency, leading to the outgrowth of LCLs.

241 ns resulted in an increased proliferation of LCLs and demonstrated positive selection over time.

242 ed mitochondrial bioenergetics in 10 sets of LCLs from children with ASD, Sibs, and unrelated/unaffec

243 new insights into the epigenetic systems of LCLs and suggests that more specifically designed experi

244 t growth and survival phenotype from that of LCLs.

245 ken together, the results support the use of LCLs for the study of statin effects on cholesterol meta

246 ormation of B cells reduce the usefulness of LCLs as a surrogate model for primary tissues.

247 ry profiles, further enhances the utility of LCLs as a model system.

248 The major surface carbohydrates detected on LCL and MCL promastigotes were alpha-Man, alpha-Glc, and

249 licating these pathways in EBNA3C effects on LCL growth or survival.

250 promoter region, induced CD1d expression on LCL, and restored iNKT recognition of LCL.

251 genes were more highly expressed than other LCL genes.

252 Significantly, although the parental LCLs express viral EBNA-1 and other Epstein-Barr virus l

253 244 levels were also observed in the patient LCLs.

254 ed with a single injection (10 mg/kg) of PLP-LCL or empty LCL as a control.

255 (LCL) containing prednisolone phosphate (PLP-LCL) in a mouse model of arthritis.

256 Treatment of CIA with PLP-LCL significantly suppressed joint swelling.

257 ols only, and decreased by estradiol in PMDD LCLs.

258 C/E(Z) genes was decreased in untreated PMDD LCLs with MTF2, PHF19 and SIRT1 all significantly decrea

259 To assess this possibility, we prepared LCLs and purified B-cells from the same donors, and comp

260 ctionally, overexpression of EphA4 prevented LCLs from proliferation.

261 , EBV super-enhancer-targeted IRF2 protected LCLs against Blimp1-mediated tumor suppression.

262 Notably, however, rare LCLs could be established following infection with Cp-de

263 the looping at the CDKN2A/B loci and reduced LCL growth.

264 Thus, reprogramming LCLs could offer an unlimited source for patient-specifi

265 radiosensitive lymphoblastoid cell lines (RS-LCLs) derived from patients with undiagnosed diseases.

266 which were significantly enriched in the RS-LCLs compared to the reference.

267 For rs1203633, LCLs with AA genotype were more sensitive to cytarabine-

268 ing an extra expression data set of the same LCLs.

269 Compared to Con, both ASD and Sib LCLs exhibited significantly higher proton leak respirat

270 Compared to Sib LCLs, ASD LCLs exhibited significantly higher ATP-linked

271 We found that LCL DARNS were enriched at DHS sites present in most of

272 and B cells are of small magnitude, and that LCLs can often recapitulate the naturally occurring gene

273 These findings demonstrate that LCLs from women with PMDD manifest a cellular difference

274 However, it is possible that LCLs have a substantially higher rate of mutation than W

275 derived from the microbial community in the LCL, and here we describe a gene for a novel mercuric re

276 NAc, although observed on the surface of the LCL strain during the late stationary growth phase was h

277 Pathway analysis of the LCL transcriptome revealed, among others, over-expressio

278 % of gene expression differences between the LCLs of humans, chimpanzees, and rhesus macaques may be

279 n the promoters of genes up-regulated in the LCLs compared with the B-cells, and could be involved in

280 were also expressed in LCLs, and ~4% of the LCLs express gp350.

281 ed uniquely from early proliferation through LCL outgrowth.

282 ncRNAs) regulated by EBV also contributed to LCL growth and survival.

283 this biosensor technology can be applied to LCLs, despite their suspension cell nature, in order to

284 ithelial cells, B cells, and EBV-transformed LCLs, (ii) EBNA3C binds with wild-type H2AX but not with

285 ed Gal1 protein abundance in EBV-transformed LCLs.

286 nd six independent replicates of transformed LCLs derived from each sample.

287 Our data indicate that while this is true, LCL-level LMP1 expression and NF-kappaB activity are not

288 meostasis, distinguishes ASD from unaffected LCLs.

289 gulated gene silencing complex) in untreated LCLs from women with PMDD, with more than half of these

290 In untreated LCLs, our results overall suggest a divergence between m

291 We have previously used LCLs to examine the cellular effects of genetic variants

292 Using LCLs conditional for EBNA3A or EBNA3C activity, we demon

293 B and LCL DNA samples for 16 subjects, using LCLs of low passage number (<5).

294 bnormalities, we sought to determine whether LCLs from Sibs share ASD-associated mitochondrial abnorm

295 es (LCLs) from 75 sequenced individuals with LCL-specific Hi-C and ChIA-PET-based chromatin contact m

296 L. braziliensis isolates from patients with LCL or MCL.

297 t of AnxA1 levels in sera from patients with LCL or ML revealed that ML patients had higher levels of

298 rowth phase promastigotes from patients with LCL, compared with those from patients with MCL, and bot

299 ts with DCL than in those from patients with LCL.

300 Studies performed with LCLs can help to identify novel biomarkers that might co