ライフサイエンスコーパス: gel shift assay

1 nd a calcium-RGS3 interaction (observed in a gel-shift assay).

2 -1 binds to the ATF3 promoter as assessed by gel shift assay.

3 gion of the sarX promoter as demonstrated by gel shift assay.

4 esponding to the proximal VEGF promoter in a gel shift assay.

5 ally to the IL-2 ARE with high affinity in a gel shift assay.

6 with deltaEF1 for binding at these sites in gel shift assay.

7 nd activator protein 1 in polarized cells by gel shift assay.

8 ifted the mobility of CaM in a nondenaturing gel shift assay.

9 ement site using an electrophoretic mobility gel shift assay.

10 Ets-1 activity was analyzed using gel shift assay.

11 reviously identified T-box binding site in a gel shift assay.

12 dently confirmed by electrophoretic mobility gel shift assay.

13 BPbeta transcription factor bound to AABS by gel shift assay.

14 r factor-kappaB activities were evaluated by gel shift assay.

15 ction of the L-ferritin transcript in an RNA gel shift assay.

16 (Tyr) and tRNA acceptor stem models, using a gel shift assay.

17 ma/retinoid X receptor (RXR) alpha-dependent gel shift assay.

18 vity to Egr-1 consensus sites as assessed by gel shift assay.

19 ong with decreased RNA binding activity in a gel shift assay.

20 tivation was monitored using electrophoretic gel shift assay.

21 d the binding domain of enzyme, we have used gel shift assay.

22 re consistent with data from the traditional gel shift assay.

23 ce search algorithms and were analyzed using gel-shift assay.

24 DNA complexes at various temperatures by the gel-shift assay.

25 te mRNA were prepared and tested in the same gel-shift assay.

26 nd to 1 of the 3 NR motifs, named gtNR1 in a gel-shift assay.

27 4 protein could bind RNA as evidenced by the gel-shift assay.

28 identified regulatory elements was tested by gel shift assays.

29 uted protein was assayed for DNA affinity by gel shift assays.

30 on factor NF-Y binding were authenticated by gel shift assays.

31 heterodimer that displays rapid mobility in gel shift assays.

32 g strand increases RFX1 complex formation in gel shift assays.

33 mation of a faster migrating pets complex in gel shift assays.

34 s, respectively, as the source of protein in gel shift assays.

35 tional analysis in both yeast two-hybrid and gel shift assays.

36 that between mERalpha and a consensus ERE in gel shift assays.

37 binding protein (CREB) to the nucleus using gel shift assays.

38 TNFalpha ARE in cell-free cross-linking and gel shift assays.

39 c and in repR upstream region in PhiCD119 by gel shift assays.

40 o the sarZ promoter region, as determined by gel shift assays.

41 split ubiquitin yeast two-hybrid system and gel shift assays.

42 Binding to the promoters was confirmed by gel shift assays.

43 AP-1 and NF-kappaB activation was studied by gel-shift assays.

44 motif reduces binding 20-fold in competition gel-shift assays.

45 f DnaK protein to retard a dnaKp fragment in gel-shift assays.

46 r some of our predictions was obtained using gel-shift assays.

47 B activity, as determined using reporter and gel-shift assays.

48 tivity in DC nuclear protein was detected by gel shifting assay.

49 We demonstrate by a gel shift assay a strong and specific affinity of recomb

50 liL, and fleSR promoters was demonstrated by gel shift assay, along with experiments to conclusively

51 Gel shift assays also demonstrated that Sp1 interacted w

52 Electrophoretic mobility gel shift assay and immunohistochemistry for NF-kappaB i

53 Using native polyacrylamide gel shift assay and negative-stain EM, we found that the

54 nes as indicated by electrophoretic mobility gel shift assay and prevented the nuclear retention of p

55 Gel shift assay and Western blot analyses showed dose-de

56 Gel shift assays and affinity pull-down followed by mass

57 ability, and markedly reduced DNA binding in gel shift assays and as assessed by chromatin immunoprec

58 Gel shift assays and chromatin immunoprecipitation assay

59 Gel shift assays and chromatin immunoprecipitation exper

60 Gel shift assays and chromatin immunoprecipitation studi

61 Moreover, gel shift assays and cotransfection experiments showed t

62 of ResD to the ctaA promoter was examined by gel shift assays and DNase I footprinting assays.

63 Gel shift assays and end boundary experiments demonstrat

64 Gel shift assays and reporter gene studies with construc

65 induction by activated p53 was determined by gel shift assays and RNA silencing (small interfering RN

66 Gel shift assays and site-directed mutagenesis allowed t

67 Using gel shift assays and Six-specific antisera, we demonstra

68 site decreased both NFI binding affinity in gel shift assays and stimulation of SV40 promoter activi

69 Gel shift assays and supershift assays using an Olf-1-sp

70 of NF-kappaB p50/p65 DNA-binding activity in gel shift assays and the activity of an NF-kappaB-respon

71 binding to a kappaB oligonucleotide probe in gel shift assays and to the MMP-9 promoter in chromatin

72 Gel shift assays and transfection with wild-type and mut

73 Gel shift assays and UV cross-linking experiments identi

74 We used DNA binding (gel shift) assays and Western immunoblots to demonstrate

75 Binding was evaluated by gel-shift assay and affinity by frontal affinity chromat

76 dimensions were confirmed using a calibrated gel-shift assay and atomic force microscopy, and their i

77 s promoter DNA upon binding, as evidenced by gel-shift assays and by recent end-to-end fluorescence e

78 Gel-shift assays and chromatin immunoprecipitation as we

79 Extent of attenuation determined by native gel-shift assays and co-transcriptional assembly is corr

80 rring X and M13 ssDNAs (as judged by agarose gel-shift assays and electron microscopic analysis).

81 n levels measured by iron regulatory protein gel-shift assays and ferritin levels.

82 cally to its target sequence using both bulk gel-shift assays and single-molecule methods.

83 dT(n) oligomers (as judged by polyacrylamide gel-shift assays) and in its binding to the longer natur

84 enhancer that strongly bind C/EBPalpha in a gel shift assay, and interaction with endogenous C/EBPal

85 AP-1 transcription factors was determined by gel shift assay, and JNK, p38, and ERK1 and ERK2 activat

86 sus sequence specifically bound to C/EBPs in gel shift assays, and four of the five sites (-432, -340

87 w cytometry, immuno-fluorescence, arrays and gel shift assays, and show affinities as high as antibod

88 d heteronuclear NMR, circular dichroism, DNA gel-shift assay, and fluorescent methods were employed t

89 overall results of transcript analysis, RNA gel-shift assay, and transgenic expression, for the firs

90 judged by thermal melts, circular dichroism, gel-shift assays, and fluorescence quenching.

91 to AG cis-regulatory elements was tested by gel-shift assays, and putative BLR binding motifs were i

92 recipitation studies from nuclear fractions, gel-shift assays, and transient transfections with T cel

93 -containing RNA probes, as determined by RNA gel shift assays; AUF1p45 did not bind to the RNA probes

94 In gel shift assays, AvrXa7 bound double-stranded DNA with

95 associates with the ISRE oligonucleotide in gel shift assays, but is quickly replaced by IRF-1 follo

96 In gel-shift assays c-Myc bound to the E-box in the insulin

97 e found that Fis-DNA binding, as assessed by gel-shift assay, changed in accordance with our expectat

98 Using the gel shift assay, chemical probing and dimethyl sulfate (

99 assay, chromatin immunoprecipitation assay, gel-shift assay, coimmunoprecipitation, and western blot

100 In vitro gel shift assays, competition assays, and immunoprecipit

101 Gel-shift assays confirm that PAX-FKHR bind to core enha

102 Gel shift assays confirmed high affinity binding of CsrA

103 Gel shift assays confirmed that both V. cholerae FadR an

104 Chromatin immunoprecipitation and gel shift assays confirmed that Kar4 binds to regulatory

105 Gel shift assays confirmed that the TBE1 site is capable

106 Gel shift assays confirmed the presence of a distal PB-r

107 Accordingly, gel-shift assays confirmed the binding of CLOCK and BMAL

108 Gel-shift assays confirmed the METTL16-MALAT1 ENE+A inte

109 Gel shift assays demonstrate clear binding between SRF a

110 Gel shift assays demonstrate that BTEB3 specifically bin

111 Results from gel shift assays demonstrate that several molecules of C

112 Gel-shift assays demonstrate BEL5/POTH1 binding specific

113 However, gel-shift assays demonstrate that a factor in C. remanei

114 ChIP, DNA-pull down, and gel-shift assays demonstrate their direct binding to the

115 A gel shift assay demonstrated that the expressed A. actin

116 Gel shift assay demonstrated the binding of Snail to the

117 Gel shift assays demonstrated nonspecific binding of pur

118 RNA-protein gel shift assays demonstrated that a specific cytoplasmi

119 fection studies and electrophoretic mobility gel shift assays demonstrated that GKLF repressed ODC pr

120 Gel shift assays demonstrated that Mafs bind to the MARE

121 Gel shift assays demonstrated that MrpJ and another para

122 Gel shift assays demonstrated that NF-kappaB inhibits th

123 Furthermore gel shift assays demonstrated that point mutations in th

124 Comparative gel shift assays demonstrated that RB69 RegA protein has

125 Electrophoretic mobility gel shift assays demonstrated that rMtsR specifically bi

126 Gel shift assays demonstrated that SarA binds to the fnb

127 Gel shift assays demonstrated that StBEL5 and POTH1 bind

128 Gel shift assays demonstrated that the betaGK and insuli

129 Gel shift assays demonstrated that the PGC-1alpha-respon

130 RNA gel shift assays demonstrated that this AURE bound an RN

131 Electromobility gel shift assays demonstrated the activation of chondroc

132 Gel shift assays demonstrated the existence of specific

133 Gel shift assays demonstrated the physical association b

134 Gel-shift assays demonstrated an increase in Sp1 binding

135 Gel-shift assays demonstrated direct binding of Sp1 to t

136 RNA from approximately 25 to 60 min, and RNA gel-shift assays demonstrated direct binding of Tat to T

137 Gel-shift assays demonstrated the HIV-1 PR is capable of

138 A leucine zipper swap:gel shift assay demonstrates that C/EBPalpha zippers wit

139 Promoter reporter and gel shift assays determined that the AirR response regul

140 Nonetheless, gel shift assays did not reveal direct binding between R

141 , real-time RT-PCR, transcriptional fusions, gel-shift assays, DNase I footprinting, and in vitro tra

142 an NDI hexaintercalator that was analyzed by gel-shift assays, DNase I footprinting, and UV-vis spect

143 Using electrophoretic mobility gel shift assay (EMSA)-based competition assays, the kl-

144 binding activity by electrophoretic mobility gel shift assays (EMSA) and mitochondrial damage by JC-1

145 positive control) to perform electromobility gel shift assays (EMSA) with a purified, baculovirus-syn

146 The gel-shift assay (EMSA) revealed that the recombinant Gly

147 CcpA binds to the ackA promoter region in gel shift assays even in the presence of mutations in th

148 emia homeobox 3 (TLX3) TF was confirmed with gel shift assay experiments.

149 Gel-shift assay experiments confirmed that pioglitazone

150 hemistry for LBP, liver enzyme analysis, and gel shift assay for NF-kappaB and AP-1 were performed.

151 e replacement kinetics were measured using a gel-shift assay for 12, 14 and 16-nucleotide probes as a

152 ear extracts by the electrophoretic mobility gel shift assay from 3-day bile duct-ligated (BDL) mice

153 sults from chromatin immunoprecipitation and gel shift assays further confirmed the functional bindin

154 In gel shift assays FXR was also able to recruit DRIP205 in

155 In a gel shift assay, gefitinib led to decreased retardation

156 In the gel-shift assay, Glu1 mutants K81E and T82Y failed to bi

157 , methoxy-polyethylene glycol maleimide, and gel shift assay has been used.

158 The complex observed in gel shift assays has been resolved by second-dimension s

159 Gel shift assays identified a conserved non-canonical E-

160 Reporter and gel shift assays in Chinese hamster ovary cells show tha

161 romoters was demonstrated in transfection or gel shift assays in vitro.

162 Gel shift assays indicate that DN-p38 MAP kinase inhibit

163 Gel shift assays indicate that in isolation, nsp10 binds

164 In contrast, gel shift assays indicate that only Stat 1 binds to the

165 Gel-shift assays indicate the regulation of miR172 by mi

166 on and point mutation analysis, coupled with gel shift assays, indicate the presence of a 43-base pai

167 Further experiments with gel shift assay indicated that IGF-1 regulated the Sp1 s

168 Gel shift assays indicated that CREB/ATF-1 was the major

169 ibodies directed toward Myc and OCT-1 in the gel shift assays indicated that Myc and OCT-1 participat

170 Overexpression studies and gel shift assays indicated that Sp1 may serve as a trans

171 Gel shift assays indicated that the overexpression of ZU

172 Gel shift assays indicated that these DNA-binding sites

173 RNA gel shifts assays indicated that recombinant nucleolin (

174 A gel-shift assay indicated that the endogenous R1 protein

175 Gel-shift assays indicated that the transcription factor

176 antly recognized by anti-Sp1 and Sp3 sera in gel shift assays, indicating that the DSE was recognized

177 Employing gel shift assays, NF-kappaB, C/EBPbeta, and c-Jun were c

178 In gel-shift assays, NuMA-RARalpha bound to retinoic acid r

179 An RNA gel -shift assay of a 5' region of the mRNA that include

180 on of E2F binding activity seen in a nuclear gel shift assay of cultured smooth muscle cells was not

181 ycol derivatives (MPEG) was measured using a gel shift assay of tryptic fragments.

182 Gel shift assays of the agr P2, agr P3, protein A (spa),

183 Gel shift assays on CP2 mutants confirmed that the CP2 m

184 Purified VirR was used in DNA gel shift assays on target promoters and VirR : promoter

185 to bind DNA either in vitro, as assessed by gel shift assay, or in vivo, as shown by transactivation

186 Gel shift assays performed in the presence of core- and

187 Gel shift assays performed with mouse L-M, rabbit RK-13,

188 ling kinetics were studied systematically by gel-shift assays performed in the presence or absence of

189 These data were confirmed in gel shift assays, providing direct evidence that Pneumoc

190 In gel-shift assays, R1A-RARalpha was able to bind to a pan

191 By electrophoretic mobility gel shift assay, recombinant GKLF and nuclear extracts f

192 A gel shift assay revealed induction of NF-KB by TNF-alpha

193 Gel shift assays revealed binding of HuR and TTP to rat

194 Gel shift assays revealed decreased protein binding to t

195 Gel shift assays revealed higher activation of nuclear f

196 Gel shift assays revealed that CAR competes with HNF-4 f

197 Our gel shift assays revealed that YhcR binds to the promote

198 Native gel-shift assays revealed a shift in radiolabeled MALAT1

199 ChIP and gel-shift assays revealed an interaction between a speci

200 Gel shift assays show binding of wBmxR1 to regions upstr

201 RNA gel shift assays show that GLD-1 binds the predicted sit

202 However, gel shift assays show that PPARgamma does not bind to th

203 Gel shift assays show that Smad6, but not Smad7, interac

204 Gel-shift assays show that ATL binds to short single- or

205 Gel-shift assays show that Rok binds directly to a DNA f

206 Gel-shift assays show that the PV, similar to wild-type

207 Gel-shift assays show that upstream stimulatory factor (

208 Gel shift assay showed constitutive NRF binding to the h

209 Gel shift assay showed that AdCMV transduction induced D

210 NF) kappaB-luciferase and an electromobility gel shift assay showed that DHT suppressed NFkappaB acti

211 Gel shift assay showed that NF-kappaB DNA-binding activi

212 Gel shift assay showed that Osx bound to the Satb2 promo

213 Gel shift assay showed that Osx bound to the VEGF promot

214 In parallel, a gel shift assay showed that SuhB forms a tight complex w

215 Computer analysis and gel shift assay showed that the -1132 and -879 region in

216 Gel shift assays showed binding of Ikaros to a sequence

217 RNA gel shift assays showed that a mutant SRSF2 derivative b

218 Gel shift assays showed that CAAT/enhancing binding prot

219 he pS2 ERE in chromatin immunoprecipitation, gel shift assays showed that estrogen-hERalpha binds wit

220 nditionally immortalized human podocytes and gel shift assays showed that LMX1B recognizes AT-rich bi

221 Gel shift assays showed that NT2 bound a specific sequen

222 Gel shift assays showed that the region surrounding the

223 Luciferase and gel shift assays showed that transcription factors Sp1 a

224 Gel-shift assays showed that CAR-RE binds CAR and pregna

225 syl)ates itself and Ku70/80 but not WRN, and gel-shift assays showed that poly-(ADP-ribosyl)ation of

226 d ubiquitination, and allowed DNA-binding in gel shift assay similar to wild-type Runx1.

227 Using electrophoretic mobility gel shift assays, size-exclusion chromatography, and ele

228 l expression, promoter data base mining, and gel shift assays; Slug and calpain 6 were identified as

229 Gel-shift assays sublocalized two cis-regulatory regions

230 Super gel shift assays suggest that both the AP2-binding oligo

231 However, gel shift assays suggest that p53 competes with other tr

232 In contrast, competition experiments using gel shift assays suggest that RAGE interaction with AGE

233 Gel shift assays suggest that XBP-1(S) binding occurs th

234 Also the gel shift assay suggested that NFkappaB p65 is responsib

235 Finally, gel shift assays suggested that p53 competes with Sp1 pr

236 Competitive gel-shift assays suggested that protein binding depends

237 egions of norB and tet38 was demonstrated by gel shift assays, suggesting that MgrA was an indirect r

238 domain bind to a 55-bp AdMLP DNA fragment in gel shift assays, suggesting that protein-DNA interactio

239 The gel shift assay supported the fact that there exists an

240 in Staphylococcus aureus and demonstrated by gel shift assay that the corynebacterial repressor DtxR

241 Using a gel-shift assay that adds a polyethylene glycol-conjugat

242 We demonstrated by in vitro gel-shift assays that binding interactions of the human

243 In the present studies, we found, by gel shift assays, that PAX5-PML bound to a panel of PAX5

244 our previous hypothesis, based on extensive gel-shift assays, that TRBP preferentially binds to site

245 In a gel shift assay, the HER3-ECD self-associates into a uni

246 In gel shift assays, the glutathione S-transferase-Smad3 fu

247 no difference in total Sp factor binding in gel shift assays, thus excluding a role for an unknown a

248 29-nucleotide (nt) element was determined by gel shift assay to be sufficient for maximal binding of

249 Here we developed a gel shift assay to study BAF DNA binding, and analyzed 1

250 ence, chemical probing, optical melting, and gel shift assays to characterize the structure of a seri

251 hat OccR is dimeric in solution, and we used gel shift assays to show that OccR is tetrameric when bo

252 Gel shift assays using a bacterially expressed PUM2 RNA

253 igh levels of E12 and ITF2b transcripts, and gel shift assays using A7R5 and NIH3T3 nuclear extracts

254 Gel shift assays using anti-TFII-I antibody show that TF

255 Accordingly, gel shift assays using both linear and circular DNA show

256 Gel shift assays using lens nuclear extracts demonstrate

257 Competition experiments in gel shift assays using mutated oligonucleotides showed t

258 We performed gel shift assays using nuclear extract from testes, brai

259 Gel shift assays using nuclear extracts of U-251MG cells

260 Gel shift assays using plant nuclear extracts or purifie

261 Gel shift assays using transfected myoblast nuclear extr

262 REB activity was increased by HG and GlcN on gel-shift assays using (32)P-CRE oligonucleotides.

263 Sp3 at this GC box was confirmed by in vitro gel-shift assays using either in vitro translated protei

264 tiple DNA-binding complexes were detected in gel-shift assays using the CYP1A2 NF-1-like element and

265 Importantly, gel shift assays verified Tpx as a target in the intact

266 In gel shift assays, very low levels of Sp1/Sp3 DNA-protein

267 A gel shift assay was optimized to detect several general

268 ternary complex dissociation as monitored by gel shift assay was prevented if both ends of the hetero

269 Increased Sp1/Sp3 binding in gel shift assays was observed upon treatment of HT1080 n

270 A gel-shift assay was used here to examine the binding of

271 ysis, enzyme-linked immunosorbent assay, and gel shift assay, we demonstrate that EGCG treatment of t

272 Using a gel shift assay, we identified a cytoplasmic RNA-binding

273 d DNA-protein binding assay and conventional gel shift assay, we successfully identified a ZBTB20-bin

274 Using mutated binding sites in competitive gel shift assays, we analyzed the nucleotides in the TAA

275 Finally, using gel shift assays, we demonstrate that Ku recruits WRN to

276 Using RNA gel shift assays, we found that LPS treatment increased

277 Using gel shift assays, we have confirmed p16-NFkappaB and gig

278 In cotransfection and gel shift assays, we show that EGR-1-binding sites are l

279 Using gel-shift assay, we showed that AML1-ETO and AML1-MTG16

280 Using ChIP and DNA gel-shift assays, we demonstrate that PIF1 directly bind

281 Using gel-shift assays, we show that recombinant GAPDH binds d

282 Using gel-shift assays, we showed that p53 binds to its putati

283 Gel shift assays were performed to assess NF-kappaB bind

284 Electrophoretic mobility gel shift assays were performed to determine the activat

285 Gel shift assays were performed with methylated or unmet

286 specificity of RNA binding, quantitative RNA gel shift assays were performed with synthetic RNAs corr

287 Gel shift assays were used to characterize bioY1_LL and

288 majority of the protease domain (H6.Gag.3h), gel shift assays were used to monitor the annealing of t

289 on, chromatin immunoprecipitation assay, and gel-shift assays were performed to show that HOXA5 can d

290 (103P) does not bind to the speB promoter in gel shift assays, which correlates with a lack of speB e

291 Gel shift assay with DC nuclear extracts confirmed speci

292 Gel shift assays with a (32)P-labeled leptin promoter -1

293 ed AML-1 (recently renamed RUNX1) binding in gel shift assays with a mutant oligonucleotide, whereas

294 Gel shift assays with model RNA substrates now show that

295 Gel shift assays with nuclear extracts from PE cells ind

296 activating transcription factor pathway, and gel shift assays with nuclear extracts.

297 by chromatin immunoprecipitation in vivo and gel shift assays with purified glutathione S-transferase

298 Gel shift assays with recombinant Smad1 and Smad4 demons

299 Gel shift assays with short DNA fragments demonstrated t

300 DNase I footprinting and gel-shift assays with human lung nuclear extract identif