ライフサイエンスコーパス: EMSA

1 EMSA also shows that positions 3 and 18 are important fo

2 EMSA analyses and data obtained from binding-site mutati

3 EMSA analyses identified two E-box motifs as the minimal

4 EMSA analyses showed that FGF2, but not VEGF, stimulated

5 EMSA analysis and reporter gene assays revealed that NFA

6 EMSA analysis confirmed binding of Sox18 to a canonical

7 EMSA analysis from Bryo-1-treated MonoMac6 cells showed

8 EMSA analysis using nuclear extracts from either A549 ce

9 EMSA analysis using nuclear extracts from IMCD cells sho

10 EMSA and ChIP assays demonstrate that the risk allele di

11 EMSA and ChIP assays further confirmed that upon P2Y2R a

12 EMSA and DNA-binding protein affinity purification analy

13 EMSA and FISH analyses suggest that these are genuine Su

14 EMSA and functional studies indicated two function-coope

15 EMSA and inhibitor studies show that HOSCN up-regulation

16 EMSA and missing contact point analysis revealed that FB

17 EMSA and supershift EMSA (with the use of specific antib

18 EMSA and supershift experiments indicated binding of USF

19 EMSA assays revealed that both binding sites are require

20 EMSA competition studies indicate that NF-Y binds with a

21 EMSA experiments showed increased HIF-1alpha binding to

22 EMSA results show that hRPA binds to a 58-mer that inclu

23 EMSA results showed that altering "amyloid" or adjacent

24 EMSA results showed that both cMYC and P53 bind to cis-o

25 EMSA revealed a concurrent decrease in consensus binding

26 EMSA revealed that 1,25(OH)(2)D(3) markedly inhibited nu

27 EMSA revealed that sulphite, a product of the reaction c

28 EMSA showed that hADAR2-D requires duplex RNA and is sen

29 EMSA showed the specific binding of Nanog to each of the

30 EMSA studies demonstrated that Sp1 bound to two putative

31 EMSA suggested that EAPP and R1 competed with Sp1 for bi

32 EMSA using this extract revealed formation of a C/EBPzet

33 EMSA, ITC, and NMR studies show that PTB RRMs 1 and 2 bi

34 EMSA, luciferase reporter gene experiments, Western blot

35 EMSAs and DNase I footprinting showed that the [4Fe-4S]

36 EMSAs and supershift assays identified complexes consist

37 EMSAs indicated an increased binding activity with osmot

38 EMSAs indicated that rs8023462 and rs6495309 bind nuclea

39 EMSAs reveal that upstream stimulatory factor 1, Runx1,

40 EMSAs show binding of PU.1 to oligonucleotides derived f

41 EMSAs using a combination of mutational and anti-Met ant

42 EMSAs with splenic B cell extracts directly demonstrated

43 EMSAs, chromatin immunoprecipitation assays, and small i

44 EMSAs, chromatin immunoprecipitation, and Western blotti

45 of HIF as demonstrated by the following: 1) EMSA; 2) transfection studies with IL-8 promoter reporte

46 echanisms underlying the induction of IL-31, EMSAs, reporter gene assays, and small interfering RNA-b

47 Accordingly, EMSA experiments demonstrated that either the cold canon

48 In addition, EMSA demonstrated that Bryo-1-mediated induction of RANT

49 Additionally, EMSAs and supershift assays showed that ER-alpha binds t

50 se binding sites did not significantly alter EMSA shifting patterns on longer templates but did on sh

51 An EMSA confirmed the p50/p50 and/or p65/p50 complex (s) bo

52 assay, chromatin immunoprecipitation, and an EMSA revealed that STAT3 activated caspase-3 However, ca

53 d by bioinformatic and biochemical analyses (EMSA and FBA), was further supported by TNT and promoter

54 electrophoretic gel mobility shift analysis (EMSA) provide further evidence for a direct interaction

55 Promoter analysis and EMSA revealed that copper stimulates the Atox1 binding t

56 Luciferase reporter assay and EMSA data strongly suggest that ALMS1 transcription is r

57 a from luciferase transactivation assays and EMSA lead us to conclude that the binding of OCT-1 to th

58 Transcriptional activation assays and EMSA were used to confirm the yeast-one hybrid results.

59 l regions of these receptors, cell-based and EMSA studies have suggested that these molecules can reg

60 In addition, Western blot and EMSA experiments revealed that morphine withdrawal-induc

61 kappaB were measured by Western-blotting and EMSA; miRNAs were measured by q-PCR in the cerebellum.

62 te, deoxycholate, and chenodeoxycholate, and EMSA showed that deoxycholate is able to abolish the for

63 ChIP and EMSA results demonstrated binding of WT1 to the CDC73 pr

64 Chromatin immunoprecipitation (ChIP) and EMSA identified a ZBP-89-binding site in the proximal pr

65 f the CCR7 gene, using luciferase, ChIP, and EMSA.

66 Chromatin immunoprecipitation and EMSA experiments demonstrated that S-SOX5 associates wit

67 Using chromatin immunoprecipitation and EMSA, we found that STAT3 binds with low affinity to the

68 ermined by chromatin immunoprecipitation and EMSA.

69 Site-directed mutagenesis and EMSA were used to identify a YY1-binding site at +25 in

70 Further mutational and EMSA analysis helped identify a minimal 37-bp region tha

71 as confirmed by independent methods (PCR and EMSA).

72 Luciferase reporter and EMSA assays revealed that C/EBPepsilon binds to the regu

73 Deletion studies and EMSA revealed 2 elements in the MIF promoter that were r

74 Both ChIP assays with canine OB tissue and EMSA experiments with the human Th proximal promoter did

75 us studies, using transient transfection and EMSA experiments, implicated involvement of the transcri

76 ive vitamin D response elements (VDREs), and EMSA confirmed that the VDRE at -312 (a DR4-type VDRE) c

77 characterised by sedimentation velocity and EMSA using native and mutant promoter sequences.

78 sing molecular biological approaches such as EMSA, supershift EMSA, ChIP, re-ChIP, and promoter-repor

79 As EMSAs can be performed using partially purified or cell

80 myc IRES in filter binding assays as well as EMSAs.

81 Electrophoretic mobility shift assay (EMSA) analyses were performed to confirm the results of

82 Electrophoretic mobility shift assay (EMSA) analysis disclosed that SarR binds more avidly to

83 Electrophoretic mobility shift assay (EMSA) analysis of nuclear extracts prepared from ultravi

84 Electrophoretic mobility shift assay (EMSA) analysis showed that c-Jun and c-Fos bind to the A

85 med by electrophoretic mobility shift assay (EMSA) analysis, which also suggested that binding by the

86 ys and electrophoretic mobility shift assay (EMSA) analysis.

87 we use electrophoretic mobility shift assay (EMSA) and atomic force microscopy (AFM) to show that Ver

88 Using electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP), we found

89 Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation analysis demonst

90 of an electrophoretic mobility-shift assay (EMSA) and confocal microscopy.

91 by an electrophoretic mobility shift assay (EMSA) and DNase I protection.

92 Using electrophoretic mobility shift assay (EMSA) and isothermal titration calorimetry (ITC), we fou

93 ned by electrophoresis mobility shift assay (EMSA) and phosphorylation of c-Fos and activation of ERK

94 Electrophoresis mobility shift assay (EMSA) experiments showed that Hoechst33342 binds to H369

95 Electrophoretic mobility shift assay (EMSA) experiments using an IE62 fragment containing the

96 D) and electrophoretic mobility shift assay (EMSA) experiments were used to show that hRPA can bind a

97 es and electrophoretic mobility shift assay (EMSA) for our in vitro studies, we demonstrated that bot

98 Electrophoretic mobility shift assay (EMSA) further confirmed activated Stat-1 binding to the

99 he gel electrophoresis mobility shift assay (EMSA) is used to detect protein complexes with nucleic a

100 Electrophoretic mobility shift assay (EMSA) revealed that PMA induced binding of c-jun and GA-

101 The gel-shift assay (EMSA) revealed that the recombinant GlyR3 bound specific

102 Electrophoretic mobility shift assay (EMSA) showed distinct DNA-nuclear protein interaction in

103 Electrophoretic mobility shift assay (EMSA) showed that Mn exposure increased binding of IRP t

104 Electrophoretic mobility shift assay (EMSA) showed that PDGF-BB stimulated protein binding to

105 Electrophoresis mobility shift assay (EMSA) studies that demonstrate physical interactions bet

106 and an electrophoretic mobility shift assay (EMSA) suggested that SknR functions as a negative regula

107 ted an electrophoretic mobility shift assay (EMSA) to isolate genomic DNA fragments that bind the arc

108 formed electrophoretic mobility shift assay (EMSA) using wild-type sequence deriving from Cxcl2 gene

109 econd, electrophoretic mobility shift assay (EMSA) was used to demonstrate the direct binding of MYB4

110 s, and electrophoretic mobility shift assay (EMSA) was used to demonstrate transcription factor bindi

111 Electrophoretic mobility shift assay (EMSA) was used to identify SNPs that had the potential t

112 es for electrophoretic mobility shift assay (EMSA) with different fragments of the Abeta peptide.

113 in an electrophoretic mobility shift assay (EMSA), and a Mur binding site was identified in the -55

114 erase, electrophoretic mobility shift assay (EMSA), and ChIP analysis revealed that Sox9 represses Cc

115 ction, electrophoretic mobility shift assay (EMSA), and chromatin immunoprecipitation (ChIP).

116 ChIP), electrophoretic mobility shift assay (EMSA), and luciferase assays reveal that p53 binds and a

117 formed electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation (ChIP), promoter cl

118 Using electrophoretic mobility shift assay (EMSA), purified LsrR and CRP proteins were shown to bind

119 tro by electrophoretic mobility shift assay (EMSA), revealed that a 14-bp sequence (CGTATCATAAGTAA; t

120 Electrophoretic mobility shift assay (EMSA), supershift EMSA, Western blot analysis, and immun

121 sed by electrophoretic mobility shift assay (EMSA), the mutations did not disrupt mLANA's ability to

122 D) and electrophoretic mobility shift assay (EMSA), we have shown that the guanine-rich (G-rich) stra

123 zed by electrophoretic mobility shift assay (EMSA), with in vitro-translated proteins and radiolabele

124 ng electrophoretic mobility gel shift assay (EMSA)-based competition assays, the kl-TSS was found to

125 n vitro electophoretic mobility shift assay (EMSA).

126 ECs by electrophoretic mobility shift assay (EMSA).

127 ed via electrophoretic mobility shift assay (EMSA).

128 using electrophoretic mobility shift assay (EMSA).

129 by the electrophoretic mobility shift assay (EMSA).

130 ing an electrophoretic mobility shift assay (EMSA).

131 ted by electrophoretic mobility shift assay (EMSA).

132 In addition, reporter assay, EMSA, chromatin immunoprecipitation and RNA interference

133 Both electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays de

134 Electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays de

135 ed by electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation assays (ChIP).

136 y electrophoretic mobility gel shift assays (EMSA) and mitochondrial damage by JC-1 (5,5', 6,6'-tetra

137 Electrophoretic Mobility Shift Assays (EMSA) confirmed that the protein encoded by this allele

138 Electrophoretic mobility shift assays (EMSA) demonstrate that purified LasR protein binds direc

139 ) and electrophoretic mobility shift assays (EMSA) experiments showed that ER81 bound directly to a c

140 Electrophoretic mobility shift assays (EMSA) indicated that a cellular factor binds specificall

141 g and electrophoretic mobility shift assays (EMSA) using bovine retinal nuclear extract demonstrate t

142 Electrophoretic mobility shift assays (EMSA) with mutant AtSPL14 DNA-binding domain proteins in

143 ed to electrophoretic mobility shift assays (EMSA) with recombinant HP0166-His(6) or a mutated respon

144 says, electrophoretic mobility shift assays (EMSA), and RNA expression by RT-PCR were used to examine

145 sR in electrophoretic mobility shift assays (EMSA), we localized binding to a sequence with partial d

146 oying electrophoretic mobility shift assays (EMSA).

147 ed by electrophoretic mobility shift assays (EMSA).

148 ed by electrophoretic mobility shift assays (EMSA).

149 l and electrophoretic mobility shift assays (EMSA).

150 ion (ChIP) and electromobility shift assays (EMSA).

151 ed by electrophoretic mobility shift assays (EMSA).

152 Electromobility shift assays (EMSAs) and competition EMSAs demonstrated binding of pro

153 ormed electrophoretic mobility shift assays (EMSAs) and demonstrate that nucleotide substitutions wit

154 ally, electrophoretic mobility shift assays (EMSAs) and DNase I footprinting were used to confirm a b

155 Electrophoretic mobility shift assays (EMSAs) are commonly used to analyze nucleic acid-protein

156 Electrophoretic mobility shift assays (EMSAs) confirmed a destabilizing effect of fructose-1,6-

157 Electrophoretic mobility shift assays (EMSAs) confirmed binding of Rep to off-target RBSs.

158 , and electrophoretic mobility shift assays (EMSAs) confirmed compromised affinities of MepR F27L and

159 ntly, electrophoretic mobility shift assays (EMSAs) determined that a recombinant MucR protein binds

160 ghput electrophoretic mobility shift assays (EMSAs) for identification and characterization of molecu

161 Electrophoretic mobility shift assays (EMSAs) identified positive DNA-protein interaction at th

162 Electrophoretic mobility shift assays (EMSAs) identified sequence-specific nuclear protein bind

163 inity electrophoretic mobility shift assays (EMSAs) in a high-throughput format suitable for small vo

164 Electrophoretic mobility shift assays (EMSAs) revealed that the overexpressed and purified OhrR

165 Electrophoretic mobility shift assays (EMSAs) revealed three classes of GATA3 mutations: those

166 s and electrophoretic mobility shift assays (EMSAs) showed that TC-EC contact mediated p38 phosphoryl

167 s and electrophoretic mobility shift assays (EMSAs) to elucidate a mechanism for EutR gene regulation

168 vitro electrophoretic mobility shift assays (EMSAs) using synthetic DNA substrates and purified RPA d

169 Electrophoretic mobility shift assays (EMSAs) were performed to investigate whether nuclear pro

170 Electrophoretic mobility shift assays (EMSAs) were used to prove that H. ducreyi CpxR interacte

171 ed by electrophoretic mobility shift assays (EMSAs) with Jurkat T-cell nuclear extracts.

172 ed by electrophoretic mobility shift assays (EMSAs) with the purified NmoR protein.

173 teps, electrophoretic mobility shift assays (EMSAs), and mass spectrometry analyses of proteins bound

174 luded electrophoretic mobility shift assays (EMSAs), filter binding assays (FBAs), coupled in vitro t

175 using electrophoretic mobility shift assays (EMSAs), the IHFalpha-IHFbeta protein complex was shown t

176 is in electrophoresis mobility shift assays (EMSAs), we demonstrated that the c-AMP-responsive elemen

177 g and electrophoretic mobility shift assays (EMSAs).

178 experiments (quantitative PCR, Western blot, EMSA) or genome-wide assays (RNA-sequencing, ChIP-sequen

179 Studies using Western blotting, EMSA, and functional analysis indicated that the selecti

180 ectively, the results from Western blotting, EMSAs, and DNA footprinting reactions lead to the conclu

181 beta to the C/EBPbeta motif was confirmed by EMSA and ChIP analyses.

182 these regulatory elements were confirmed by EMSA and the chromatin immunoprecipitation approach, res

183 ind the hZip1 core promoter was confirmed by EMSA, GelSupershift and ChIP assays.

184 activity by HA(6) treatment, as confirmed by EMSA.

185 We demonstrate by EMSA that nitration of p53 by ONOO(-) (300 x 10(-6) M) a

186 in this 245 bp 5' region was demonstrated by EMSA and supershift with anti-NFAT antibodies.

187 to HREs in FLAP promoter as demonstrated by EMSA with nuclear extracts.

188 th the GAS promoter was also demonstrated by EMSA.

189 he binding of enzymes to DNA was detected by EMSA, steady-state, and stopped-flow fluorimetry.

190 e DNA binding activity of c-Jun, detected by EMSA.

191 ncreases in nuclear NF-kappaB as detected by EMSA.

192 oth in vitro as and in vivo as determined by EMSA and chromatin immunoprecipitation, respectively.

193 pressed gene transcription, as determined by EMSA and luciferase assays.

194 IgG IC-induced lung injury, as determined by EMSA.

195 patch maintained the ability to bind DNA by EMSA.

196 he putative Mur box was further evaluated by EMSA employing oligonucleotides in which the consensus n

197 re detailed mutagenesis analysis followed by EMSA and ChIP identified Sp1 sites in positions -668/-65

198 REB1 alone or with UNG2 or OGG1, followed by EMSA.

199 binding site on Dspp promoter were found by EMSA.

200 of Casp1, was determined to be functional by EMSA and supershift analysis.

201 detectable tRNA(Pyl) binding as measured by EMSA, but not catalytic activity.

202 were examined in ischemic cerebral tissue by EMSA and Western blots.

203 inding sites were biochemically validated by EMSA-FRET analysis and validated in vivo by ChIP-seq dat

204 t1 protein to these elements was verified by EMSA and ChIP.

205 Oct-2 with all three sites both in vitro by EMSA and in vivo by chromatin immunoprecipitation assay.

206 ite that binds Foxc1a and Foxc1b in vitro by EMSA and in vivo using ChIP.

207 nts in the EBF1 promoter was demonstrated by EMSAs and chromatin immunoprecipitation analysis, sugges

208 tes within the Gpr49 gene locus, and show by EMSAs that GATA-6 can bind to these sites in vitro.

209 ficity of binding ascertained by competition EMSA.

210 Competition EMSAs and supershift analyses with HsrA-enriched protein

211 obility shift assays (EMSAs) and competition EMSAs demonstrated binding of protein(s) in the cultured

212 DNase I footprinting and competitive EMSA showed the binding site to be an 18-bp palindromic

213 Rather, competitive EMSA using known binding sequences for the orphan nuclea

214 Finally, multiplexed-competitor-EMSA (MC-EMSA) and supershift EMSA identified FOXA2 to r

215 AG) separation lanes supports 384 concurrent EMSAs in 30 s using a single power source.

216 l strips acts as a chassis for 96 concurrent EMSAs.

217 er and synthetic RARE luciferase constructs, EMSA, and ChIP assays.

218 on of HP0166 in binding (including a control EMSA with in-vitro-phosphorylated HP0166-His(6)).

219 Detailed EMSA studies were used to confirm binding at these sites

220 preparations of MsvR demonstrated different EMSA binding patterns and regions of protection on the i

221 g to chromaffin cell nuclear proteins during EMSA, binding of endogenous c-FOS on ChIP, and different

222 EC-EMSA should be useful for further investigation of facto

223 lex electrophoretic mobility shift assay (EC-EMSA).

224 Experimental EMSA results demonstrate that methylation of the CpG in

225 Following EMSA, denaturing gel electrophoresis is implemented to p

226 r SRY and YY1, with similar consequences for EMSA, endogenous factor binding, and responses to exogen

227 n-RNA complex without catalytic turnover for EMSA and ribonuclease footprinting analyses.

228 Furthermore, EMSA analysis demonstrated that STAT1 binds to the MD-2

229 Furthermore, EMSA and luciferase reporter assays demonstrated that KL

230 Furthermore, EMSAs demonstrated that the attachment of CREB binding p

231 The free-standing polyacrylamide gel EMSAs yielded reliable quantification of molecular bindi

232 ppaB proteins was similar between genotypes, EMSAs under nonreducing conditions showed increased DNA

233 ences to bind ATF4 and ATF3 using immunoblot-EMSA and confirmed ATF4, ATF3, and CCAAT/enhancer-bindin

234 showed phosphorylation-dependent binding in EMSA with HP0166-D52N-His(6).

235 of activator protein-1 response elements in EMSA.

236 to the lst promoter at multiple locations in EMSA and ChIP assays respectively.

237 r binding to the ICP27 N-terminal peptide in EMSA experiments.

238 sulfitobacterium hafniense bind tRNA(Pyl) in EMSA with apparent K(d) values of 0.12 and 0.13 muM, res

239 gh Z does not bind directly to the TNFR1p in EMSA studies, chromatin immunoprecipitation studies indi

240 In EMSAs, DUX4 specifically interacted with a 30-bp sequenc

241 tive cis element-trans factor interaction in EMSAs.

242 Interestingly, EMSA analyses demonstrate that the AP-1 site binds to c-

243 Finally, multiplexed-competitor-EMSA (MC-EMSA) and supershift EMSA identified FOXA2 to rs327T, an

244 Sample is dispensed onto the microfluidic EMSA card by acoustic droplet ejection (ADE), which redu

245 min) or even microchannel based microfluidic EMSAs ( approximately 0.3 data/min).

246 olin inhibited IL-6 production in microglia, EMSAs were performed to establish the effects of luteoli

247 conjunction with site-directed mutagenesis, EMSA, and reporter assays indicated that Ser(P)-193 is r

248 Using mutagenesis, EMSA, and cotransfection assays, we identified two redun

249 Next, EMSA, immunoblots, and transient cotransfection studies

250 On the basis of EMSA and ChIP assays, TNF-alpha treatment increases bind

251 atory sites, which allowed the generation of EMSA probes that bound NFs specific to BAFF-R-expressing

252 Results of EMSA and ChIP assays confirmed that LYAR bound to a DNA

253 Interestingly, the use of EMSAs also indicated that H. ducreyi CpxR did not bind t

254 tions failed to bind target DNA sequences on EMSA and confocal microscopy; however, they did not inhi

255 rs11573156 C >G there were no luciferase or EMSA allelic differences seen.

256 We performed EMSAs to examine EutR activation of the LEE.

257 The powerful 96-plex EMSAs increased the throughput to approximately 10 data/

258 trated by mutation analysis of the promoter, EMSA, and ChIP.

259 ssays after UV cross-linking and RNA-protein EMSA demonstrated that P311 binds directly to TGF-beta 5

260 sion during pregnancy and lactation in rats, EMSAs demonstrate an elevated binding of pregnant and la

261 oustic droplet ejection (ADE), which reduces EMSA variability compared to sample dispensing using man

262 to the N terminus of truncated PylS regained EMSA-detectable tRNA(Pyl) binding.

263 In optimizing the riboswitch EMSAs on the free-standing polyacrylamide gel array, thr

264 ncing with HIF-1alpha small interfering RNA, EMSA, and chromatin immunoprecipitation analysis.

265 A electrophoretic mobility shift assays (RNA-EMSA) were used to confirm the RIP results and demonstra

266 RNA-EMSAs show that PfSR1 preferentially binds RNA molecules

267 Electrophoretic mobility shift (EMSA) and chromatin immunoprecipitation (ChIP) assays de

268 Electrophoretic mobility shift (EMSA) and chromatin immunoprecipitation (ChIP) assays de

269 (FA) and electrophoretic gel mobility shift (EMSA) assays, the interactions between HPNikR and the ta

270 Electrophoretic mobility shift (EMSAs) and gel-supershift assays demonstrated that the t

271 Focusing on the Sp-1 site, EMSA, super-shift and ChIP analysis was performed that e

272 more efficient than either conventional slab EMSAs ( approximately 0.01 data/min) or even microchanne

273 to 30.6), p = 1.22x10(-)(3)(5), and stronger EMSA binding of a nuclear protein compared to the T-alle

274 including: subcellular localization studies, EMSAs and luciferase-reporter assays, were undertaken an

275 EMSA and supershift EMSA (with the use of specific antibodies against NF-Y s

276 xed-competitor-EMSA (MC-EMSA) and supershift EMSA identified FOXA2 to rs327T, and CREB-binding protei

277 Competitive and supershift EMSA identified the participation of GATA4, another GATA

278 etic mobility shift assay (EMSA), supershift EMSA, Western blot analysis, and immunocytochemistry wer

279 ological approaches such as EMSA, supershift EMSA, ChIP, re-ChIP, and promoter-reporter gene assays,

280 The supershift EMSA confirmed that ZEB1, demonstrated to be present in

281 Supporting EMSA studies with a series of DeltaC truncated versions

282 A ternary complexes were not observed in the EMSA experiments, cross-linking experiments showed that

283 supershift the H369W-protein complex on the EMSA gel.

284 start site of TLR10 was established through EMSA and chromatin immunoprecipitation.

285 The high-throughput EMSAs was employed to assess binding of the Vc2 cyclic-d

286 addition of an anti-SAP155 antibody (Ab) to EMSA decreasing the mobility of a protein:CRCE 1 complex

287 nding sites within the Lbr promoter and used EMSAs and luciferase assays to show that Lbr is transcri

288 Using EMSA (electrophoretic mobility shift assay), ChIP (chrom

289 Using EMSA analysis, NsrR::FLAG was shown to interact with pre

290 Using EMSA, supershift assays, and promoter pulldown assays, w

291 Using EMSA, we demonstrate that the AHR-ARNT heterodimer binds

292 Using EMSA, we found that apigenin does not alter NF-kappaB-DN

293 d its binding specificity was analyzed using EMSA and SELEX.

294 flanking the TSS cluster were analyzed using EMSAs to identify discrete DNA-binding factors in primar

295 ite in TACE promoter and demonstrated, using EMSAs and chromatin immunoprecipitation assays, that AP-

296 Utilizing EMSA or ChIP assays, we found that both p50 and p65 NF-k

297 for these protein-protein interactions; (v) EMSA titrations revealed that while tri-complex formatio

298 of the CsoR regulon was confirmed in vitro (EMSA) and in vivo (RNA-seq), which highlighted that next

299 ides are required for transcription in vivo; EMSA-binding assays confirm that several of these nucleo

300 CD spectral changes in combination with EMSA titrations suggest that one hRPA heterotrimer is su