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

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

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

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

27 nd to 1 of the 3 NR motifs, named gtNR1 in a 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 c and in repR upstream region in PhiCD119 by gel shift assays.

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

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

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

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

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

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

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

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

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

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

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

50 Gel shift assays also demonstrated that Sp1 interacted w

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

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

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

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

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

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

57 Gel shift assays and chromatin immunoprecipitation assay

58 Gel shift assays and chromatin immunoprecipitation exper

59 Gel shift assays and chromatin immunoprecipitation studi

60 Moreover, gel shift assays and cotransfection experiments showed t

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

62 Gel shift assays and end boundary experiments demonstrat

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

64 Gel shift assays and site-directed mutagenesis allowed t

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

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

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

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

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

70 Gel shift assays and UV cross-linking experiments identi

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

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

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

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

75 Gel-shift assays and chromatin immunoprecipitation as we

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 Gel shift assays confirmed high affinity binding of CsrA

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

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

102 Gel shift assays confirmed that the TBE1 site is capable

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

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

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

106 ost cases, as evidenced by our nondenaturing gel shift assay data.

107 Gel shift assays demonstrate clear binding between SRF a

108 Gel shift assays demonstrate that BTEB3 specifically bin

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

110 Gel-shift assays demonstrate BEL5/POTH1 binding specific

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

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

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

114 Gel shift assay demonstrated the binding of Snail to the

115 Gel shift assays demonstrated nonspecific binding of pur

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

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

118 Gel shift assays demonstrated that Mafs bind to the MARE

119 Gel shift assays demonstrated that MrpJ and another para

120 Gel shift assays demonstrated that NF-kappaB inhibits th

121 Furthermore gel shift assays demonstrated that point mutations in th

122 Comparative gel shift assays demonstrated that RB69 RegA protein has

123 Electrophoretic mobility gel shift assays demonstrated that rMtsR specifically bi

124 Gel shift assays demonstrated that StBEL5 and POTH1 bind

125 Gel shift assays demonstrated that the betaGK and insuli

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

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

128 Electromobility gel shift assays demonstrated the activation of chondroc

129 Gel shift assays demonstrated the existence of specific

130 Gel shift assays demonstrated the physical association b

131 Gel-shift assays demonstrated an increase in Sp1 binding

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 Gel-shift assay experiments confirmed that pioglitazone

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

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

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

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

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

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

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

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

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

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

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

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

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

160 Gel shift assays indicate that in isolation, nsp10 binds

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

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

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

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

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

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

167 Gel shift assays indicated that the overexpression of ZU

168 Gel shift assays indicated that these DNA-binding sites

169 RNA gel shifts assays indicated that recombinant nucleolin (

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

171 Gel-shift assays indicated that the transcription factor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 Gel shift assays revealed decreased protein binding to t

191 Gel shift assays revealed higher activation of nuclear f

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

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

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

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

196 Gel shift assays show binding of wBmxR1 to regions upstr

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

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

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

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

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

202 Gel-shift assays show that upstream stimulatory factor (

203 Gel shift assay showed constitutive NRF binding to the h

204 Gel shift assay showed that AdCMV transduction induced D

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

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

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

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

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

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

211 Gel shift assays showed binding of Ikaros to a sequence

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

213 Gel shift assays showed that CAAT/enhancing binding prot

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

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

216 Gel shift assays showed that NT2 bound a specific sequen

217 Fluorescence anisotropy binding and gel shift assays showed that the 3'BTE and 5'UTR RNAs ca

218 Gel shift assays showed that the region surrounding the

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

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

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

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

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

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

225 Gel-shift assays sublocalized two cis-regulatory regions

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

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

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

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

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

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

232 Competitive gel-shift assays suggested that protein binding depends

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

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

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

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

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

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

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

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

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

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

243 Using native gel-shift assays, the relative stability of 16 different

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

245 29-nucleotide (nt) element was determined by gel shift assay to be sufficient for maximal binding of

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

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

248 Gel shift assays using a bacterially expressed PUM2 RNA

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

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

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

252 Gel shift assays using lens nuclear extracts demonstrate

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

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

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

256 Gel shift assays using plant nuclear extracts or purifie

257 Gel shift assays using transfected myoblast nuclear extr

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

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

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

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

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

263 A gel shift assay was optimized to detect several general

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

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

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

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

268 Using an infrared gel shift assay, we demonstrated the presence of potenti

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

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

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

272 Moreover, using affinity chromatography and gel shift assays, we demonstrate that caspase-7, but not

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

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

275 rough chromatin immunoprecipitation (IP) and gel shift assays, we found that RORalpha in the form of

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

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

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

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

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

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

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

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

284 Gel shift assays were performed with methylated or unmet

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

286 Gel shift assays were used to characterize bioY1_LL and

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

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

289 (103P) does not bind to the speB promoter in gel shift assays, which correlates with a lack of speB e

290 A gel shift assay with a radiolabeled OARE module and nucl

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