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 formation serves as a model for lymphomagenesis, and

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

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

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

6 LCL-derived iPSCs exhibited normal karyotype, expressed

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

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

11 ncrease in mitochondrial respiration in AD-A LCLs.

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

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

14 decline in mitochondrial respiration in all LCL groups.

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

16 detected in the exosomes from Raji cells and LCL.

17 MYC ESEs greatly reduced MYC expression and LCL growth.

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

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

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

21 in synergy to kill EBV-positive BL cells and LCLs.

22 n serves as a model for lymphomagenesis, and LCLs are phenotypically similar to EBV-positive diffuse

23 ecreased MYC or BCL2 expression and arrested LCL growth.

24 ASD LCLs exhibited a significantly greater change in these p

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

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

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

28 extremely demanding environment of the ATII-LCL.

29 These results suggest that the autism LCLs exhibit a reduced glutathione reserve capacity in b

30 potential to a greater extent in the autism LCLs, although GSH/GSSG and ATP concentrations were simi

31 both cytosol and mitochondria in the autism LCLs.

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

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

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

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

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

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

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

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

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

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

42 ion specifically inhibits the growth of both LCLs and the DLBCL cell line IBL-1.

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

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

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

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

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

48 Lymphoblastoid cells (LCLs) derived from autistic children and unaffected cont

49 n than EBV-transformed lymphoblastoid cells (LCLs) or EBV-negative BL cells.

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

51 agents and the proapoptotic chemotherapeutic LCL-161.

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

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

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

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

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

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

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

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

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

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

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

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

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

65 ystem for studying the pathways that dictate LCL survival and regulate EBV transformation.

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

67 re RNA abundances in each of three different LCLs that conditionally express EBNA3C fused to a 4-OH-T

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

69 st three RNAs were assayed for each EBNA3CHT LCL under nonpermissive conditions, permissive condition

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

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

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

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

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

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

76 ongly affect cell gene expression and enable LCL growth.

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

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

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

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

81 pathway may have in controlling established LCL growth and EBV-mediated transformation of primary B

82 Newly established LCLs from both individuals demonstrated the same phenome

83 ule Nutlin-3 led to apoptosis of established LCLs and suppressed EBV-mediated transformation of prima

84 CD1d-expressing LCL elicited interferon gamma secretion and cytotoxicity

85 1-induced cFLIP was found to be critical for LCL defense against TNFalpha-mediated programmed cell de

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

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

88 g domain) and 733 to 909 to be essential for LCL growth, aa 728 to 732 and 910 to 992 to be important

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

90 associate with p53 and is also essential for LCL growth.

91 51 to 400 and 851 to 900 were essential for LCL growth; aa 447 to 544, 701 to 750, 801 to 850, and 9

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

93 Moreover, all mutants null for LCL growth had fewer S+G(2)/M-phase cells at 14 days, co

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

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

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

97 for the growth of both laboratory-generated LCLs and naturally occurring DLBCLs and suggest that tar

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

99 ina platforms were assayed for all 277 human LCLs.

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

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

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

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

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

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

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

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

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

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

110 ffect the direction of methylation change in LCLs.

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

112 As expected, CIITA was downregulated in LCLs.

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

114 shows that approximately 70% of cis-eQTLs in LCLs are shared with skin, as compared with the naive es

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

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

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

118 To identify EBNA3C-regulated genes in LCLs, microarrays were used to measure RNA abundances in

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

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

121 cal for BIM suppression and MYC induction in LCLs.

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

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

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

125 iR-155 is the most highly expressed miRNA in LCLs and that the selective inhibition of miR-155 functi

126 ose binding leads to histone modification in LCLs.

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

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

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

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

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

132 aracterizing GPCR-mediated drug responses in LCLs.

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

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

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

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

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

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

139 ligand and its CXCR4 receptor and increased LCL migration.

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

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

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

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

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

145 ergized with NF-kappaB inhibition in killing LCLs.

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

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

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

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

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

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

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

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

154 published panel of lymphoblastoid cell line (LCL) eQTLs.

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

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

157 irus-transformed B-lymphoblastoid cell line (LCL) in vitro, can be used to target EBV-positive malign

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

159 completely ablated lymphoblastoid cell line (LCL) outgrowth.

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

161 ) and immortalized lymphoblastoid cell line (LCL).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 es converted into lymphoblastoid cell lines (LCLs) by an Epstein-Barr virus that expresses a conditio

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

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

179 ely proliferating lymphoblastoid cell lines (LCLs) depends on the concerted activities of a subset of

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

181 ,540 CpG sites in lymphoblastoid cell lines (LCLs) derived from independent samples of European and A

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 the outgrowth of lymphoblastoid cell lines (LCLs).

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

217 cupancy in Yoruba lymphoblastoid cell lines (LCLs).

218 roliferation into lymphoblastoid cell lines (LCLs).

219 ansformation into lymphoblastoid cell lines (LCLs).

220 nversion to immortal lymphoblast cell lines (LCLs).

221 transformation to lymphoblastoid cell lines (LCLs).

222 ely proliferating lymphoblastoid cell lines (LCLs).

223 lly defined human lymphoblastoid cell lines (LCLs).

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

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

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

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

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

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

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

231 tiating B cell proliferation and maintaining LCL growth.

232 nd 851 to 900 were necessary for maintaining LCL growth, but not RBP-Jkappa interaction, and likely m

233 such cultures recognize HLA class II-matched LCLs but not mitogen-activated B lymphoblasts, many (1)

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

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

239 Tubacin induced apoptosis of LCLs, which was inhibited by pretreatment with a pancasp

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 Since LCLs retain wild-type p53, it was of interest to determi

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

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

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

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

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

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

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

279 % of gene expression differences between the LCLs of humans, chimpanzees, and rhesus macaques may be

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

281 ed uniquely from early proliferation through LCL outgrowth.

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

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

284 ed Gal1 protein abundance in EBV-transformed LCLs.

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

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

287 meostasis, distinguishes ASD from unaffected LCLs.

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

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

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

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

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

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

294 tion, suggesting a unique mechanism by which LCLs survive in the presence of a primed p53 pathway.

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