ライフサイエンスコーパス: gel mobility shift assay

1 activated T cells-p300 complex to IRE in the gel mobility shift assay.

2 talled elongation complexes as measured in a gel mobility shift assay.

3 mined by gel filtration chromatography and a gel mobility shift assay.

4 ed ability to bind to the tcpA promoter in a gel mobility shift assay.

5 and quantified using a native polyacrylamide gel mobility shift assay.

6 defined RNA molecules was characterized by a gel mobility shift assay.

7 aracterized by site-directed mutagenesis and gel mobility shift assay.

8 th purified FadR protein was determined by a gel mobility shift assay.

9 Similar results were obtained with a gel mobility shift assay.

10 nd to the leader sense RNA, as determined by gel mobility shift assay.

11 nd to be in the size range of 106-115 kDa by gel mobility shift assay.

12 NF-kappaB activity was determined using the gel mobility shift assay.

13 ream GRE functioned in cis and bound GR in a gel mobility shift assay.

14 c oligonucleotide substrates was analyzed by gel mobility shift assay.

15 fic binding to the gastrin CACC element in a gel mobility shift assay.

16 8 as indicated by a supershifted band in the gel mobility shift assay.

17 r protein-DNA complexes were identified by a gel mobility shift assay.

18 nd 77 +/- 6 Pm, respectively, as measured by gel mobility shift assay.

19 nary complexes that could be visualized in a gel mobility shift assay.

20 ffinity to DsrA(DII) by <or=2-fold using the gel-mobility shift assay.

21 cing the CbbR-cbbLS promoter interactions in gel mobility shift assays.

22 binding site, which we have verified here by gel mobility shift assays.

23 n using isothermal titration calorimetry and gel mobility shift assays.

24 xyl radical footprinting and electrophoretic gel mobility shift assays.

25 ipitation, DNA microarray hybridization, and gel mobility shift assays.

26 r by performing luciferase reporter gene and gel mobility shift assays.

27 DNA binding activities of wild type Pax9 in gel mobility shift assays.

28 P promoter at several sites as determined by gel mobility shift assays.

29 to have modified binding characteristics in gel mobility shift assays.

30 ed using recombinant proteins in competition gel mobility shift assays.

31 ding donors and acceptors, are determined in gel mobility shift assays.

32 ht ends of the transposon was compared using gel mobility shift assays.

33 r cisplatin-damaged DNA were investigated by gel mobility shift assays.

34 related hnRNP proteins reacted with CBF2 in gel mobility shift assays.

35 n of amyloid precursor protein (APP) mRNA in gel mobility shift assays.

36 nt plus poly(A) tail] were identified using gel mobility shift assays.

37 ifs bind specifically to p53, as assessed by gel mobility shift assays.

38 for in vitro binding to nucleic acids using gel mobility shift assays.

39 l as to the Tap-2 ISRE in vitro, as shown by gel mobility shift assays.

40 ite within their promoters, as determined by gel mobility shift assays.

41 following UV-catalyzed cross-linking and by gel mobility shift assays.

42 substrates using fluorescence anisotropy and gel mobility shift assays.

43 g of NRSF/REST to NRSE/RE-1 as determined by gel mobility shift assays.

44 from E. coli binds rsmB RNA as indicated by gel mobility shift assays.

45 ed with the SHFV 3'(-)209 RNA in competition gel mobility shift assays.

46 the COUP-TF.DNA binding complex detected in gel mobility shift assays.

47 nce was used with 3T3-L1 nuclear extracts in gel mobility shift assays.

48 2 x 10(-8) M and TGP1 can form supershift in gel mobility shift assays.

49 gions in the COL1A1 promoter was examined by gel mobility shift assays.

50 to EBNA2 and that they bind CBF1 and CBF2 in gel mobility shift assays.

51 in and DNA titration experiments analyzed by gel mobility shift assays.

52 to the promoter regions of fruA and levD in gel mobility shift assays.

53 , was investigated by DNase I protection and gel mobility shift assays.

54 d for effective MAL-SRF complex formation in gel mobility shift assays.

55 293T cells, as measured by gene reporter and gel mobility shift assays.

56 This finding was confirmed by gel mobility shift assays.

57 inding site at +18 prevented HapR binding in gel mobility shift assays.

58 uman SHMT1 promoter by deletion analyses and gel mobility shift assays.

59 -binding sites of JMJ in the ANF enhancer by gel mobility shift assays.

60 f ESE-1 to bind to oligonucleotide probes in gel mobility shift assays.

61 te to bind DNA, a prediction confirmed using gel mobility shift assays.

62 directly bound only the proximal FixK box in gel mobility-shift assays.

63 surement), fluorescence, and electrophoretic gel mobility-shift assays.

64 re tightly than the DsrA.rpoS RNA complex in gel mobility-shift assays.

65 nse element (pTRE and nTRE, respectively) in gel-mobility shift assays.

66 to heparin resin nor to heparin fragments in gel-mobility shift assays.

67 As determined using gel mobility shift assays, 13 out of 14 negative complem

68 Using an electrophoretic gel mobility shift assay, [(35)S]SO(4)-labeled versican

69 in vitro DNase I footprinting analyses, and gel mobility shift assays, a beta-spectrin gene erythroi

70 activity were assessed by an electrophoretic gel mobility shift assay and a reporter gene luciferase

71 Using a gel mobility shift assay and analytical ultracentrifugat

72 the putative p53 recognition sequence using gel mobility shift assay and DNase I footprinting analys

73 Gel mobility shift assay and DNase I footprinting analys

74 binding to the E. coli DnaA protein using a gel mobility shift assay and DNase I footprinting.

75 This site, as determined by gel mobility shift assay and DNaseI footprinting, is loc

76 increase AP-1 binding in an electrophoretic gel mobility shift assay and increase the expression of

77 A gel mobility shift assay and protein-DNA cross-linking i

78 By electrophoretic gel mobility shift assay and supershift assay, the bindi

79 Gel mobility shift assay and supershifts with specific a

80 We apply this approach to the gel mobility shift assay and use it to modify a self-cle

81 traditional methods, such as filter binding, gel mobility shift assay and various fluorescence techni

82 elated with previously reported values using gel mobility shift assays and a similarly sized poly-dT.

83 Gel mobility shift assays and analysis of ROS3 immunopre

84 Gel mobility shift assays and aztR O/P-lacZ induction ex

85 relevance of this sequence was obtained from gel mobility shift assays and by transfection of TCC mut

86 Furthermore, by using gel mobility shift assays and chromatin immunoprecipitat

87 Gel mobility shift assays and co-immunoprecipitation exp

88 d by this focused set of genes, we performed gel mobility shift assays and demonstrated that ChvI dir

89 Gel mobility shift assays and DNase I footprinting analy

90 ng in vivo transcriptional fusions, in vitro gel mobility shift assays and DNase I footprinting assay

91 nsus site centered at position -162 by using gel mobility shift assays and DNase I footprinting exper

92 In vitro gel mobility shift assays and DNase I footprinting exper

93 Both gel mobility shift assays and DNase I footprinting revea

94 pped within the cbbLS promoter by the use of gel mobility shift assays and DNase I footprinting.

95 Gel mobility shift assays and methylation interference a

96 ation results were independently verified by gel mobility shift assays and quantitative DNA footprint

97 he function of the heterodimer, we performed gel mobility shift assays and showed that the A14/A43 he

98 CCCCC -64 region of the NOS-3 gene promoter, gel mobility shift assays and site-directed mutation ana

99 Gel mobility shift assays and supershift assays with spe

100 plex with mispaired bases was analyzed using gel mobility shift assays and surface plasmon resonance

101 Gel mobility shift assays and surface plasmon resonance

102 w magnesium concentrations, as determined by gel mobility shift assays and thermal dissociation profi

103 the activities of various ecdysteroids using gel mobility shift assays and transfection assays in Sch

104 Gel mobility shift assays and transient transfection ass

105 Gel mobility shift assays and transient transfection ass

106 Gel mobility shift assays and UV cross-linking experimen

107 on in vivo and nuclear proteins, we utilized gel mobility shift assays and UV-crosslinking studies.

108 ve EcREs to bind the EcR-B1-USP-1 complex in gel mobility shift assays and was responsible for the si

109 an oligonucleotide containing the 202-SBS in gel-mobility shift assays and to the 5'-regulatory regio

110 Using gel-mobility-shift assays and surface plasmon resonance

111 formation of three RNA-protein complexes by gel mobility shift assay, and UV-induced cross-linking d

112 munofluorescence studies, live cell imaging, gel mobility shift assays, and bimolecular fluorescence

113 Transient transfection, gel mobility shift assays, and chromatin immunoprecipita

114 rized by using a promoter truncation series, gel mobility shift assays, and DNase I footprinting.

115 ity isolation, DNA-binding site competition, gel mobility shift assays, and protein overexpression in

116 n analysis of the mouse Fas ligand promoter, gel mobility shift assays, and site-directed mutagenesis

117 Here we compare the self-cleavage and gel mobility shift assays applied to the DNA binding of

118 In gel mobility shift assays, approximately 70% of the gene

119 AF-, AAF- and AP-DNA adducts, determined by gel mobility shift assay, are 33 +/- 9, 8 +/- 2 and 23 +

120 In gel mobility shift assays, both active and inactive reco

121 hBVR and nuclear extract containing hBVR in gel mobility-shift assay bound to AP-1 sites in the ATF-

122 directly bind the hilA and hilC promoters in gel mobility shift assays but not the flhD, fliA, hilD,

123 box consensus DNA element in electrophoretic gel mobility shift assays, but only BjFur bound the irr

124 ion was further confirmed by electrophoretic gel mobility shift assay, chromatin immunoprecipitation,

125 However, gel mobility shift assays clearly show that other as yet

126 Gel mobility shift assays combined with DNase I footprin

127 transfected with a SOX9 cDNA (M12/SOX9), and gel mobility shift assays confirmed binding of nuclear p

128 Gel mobility shift assays confirmed that CcrR directly b

129 mobility complex with DNA in electrophoretic gel mobility shift assays corresponding to occupancy by

130 In gel mobility shift assays, COUP-TF bound as an apparent

131 ddition to real-time PCR and immunoblotting, gel mobility shift assays, coupled with specific antibod

132 Gel mobility shift assay data showed that GC-binding dru

133 Gel mobility shift assays demonstrate that GATA-6 binds

134 Gel mobility shift assays demonstrate that the aptamers

135 Gel mobility shift assays demonstrate that the human cSH

136 Gel mobility shift assays demonstrate that WT1 binds to

137 Electrophoretic gel mobility-shift assays demonstrate that the Tth ligas

138 Gel mobility shift assay demonstrated that c-Jun is the

139 Gel mobility shift assays demonstrated specific binding

140 Gel mobility shift assays demonstrated specific binding

141 Gel mobility shift assays demonstrated that CERIP intera

142 Results from gel mobility shift assays demonstrated that Hoxa10-1, Ho

143 Gel mobility shift assays demonstrated that purified TEF

144 Gel mobility shift assays demonstrated that the protein(

145 V 3'(-)209 RNA, and results from competition gel mobility shift assays demonstrated that these intera

146 Gel mobility shift assays demonstrated that tmRNA(Delta9

147 Results from filter binding and gel mobility shift assays demonstrated that TRAP binds s

148 Gel mobility shift assays demonstrated that U-rich RNA t

149 Gel mobility-shift assays demonstrated that assembly of

150 Gel mobility-shift assays demonstrated that specificity,

151 Gel-mobility shift assays demonstrated that the forkhead

152 equence GTCTG interfered with binding in the gel mobility shift assay, demonstrating that this pentan

153 Electrophoretic gel mobility shift assay (EMSA) revealed that the -1C-->

154 II of DsrA ncRNA (DsrA(DII)) and A(18) by a gel-mobility shift assay, fluorescence anisotropy, and f

155 Gel mobility shift assays for factors binding to key ele

156 predictions were experimentally validated by gel mobility shift assays for two NrtR family representa

157 ort RNA transcripts were studied using a new gel mobility shift assay from which melting temperatures

158 Gel mobility shift assays further demonstrated that DDX1

159 Gel mobility shift assays further revealed that SF-1 can

160 ys and the formation of an ER.ERE complex in gel mobility shift assays, further indicating that the e

161 nfected Sf21 insect cells and the methods of gel mobility shift assays, gel filtration chromatography

162 Binding of tRNA by gel mobility shift assays gives a dissociation constant

163 , 15, 30, or 60 minutes; lysed; and used for gel mobility shift assay (GMSA) and supershift assay for

164 uorescence, CD spectroscopy, NMR, and native gel mobility shift assays (GMSAs).

165 In gel mobility shift assays, heterodimers of retinoic acid

166 Gel mobility shift assays identified the upstream stimul

167 alyses in reporter gene assays, as well as a gel mobility shift assay, identified an LXR response ele

168 ell lines, DNase I footprinting analyses and gel mobility shift assays, identified an AHSP gene eryth

169 and normal adjacent tissue were analysed by gel mobility shift assay, immunoblotting of nuclear extr

170 trations was determined using polyacrylamide gel mobility shift assays in the absence of dNTPs.

171 Gel mobility shift assays indicate that LPS induces NF-k

172 Nitrocellulose filter binding and gel mobility shift assays indicate that the PABP2.poly(A

173 Gel mobility shift assays indicate the presence of sever

174 A gel mobility shift assay indicated that a DNA fragment s

175 A gel mobility shift assay indicated that the UL5-UL52 sub

176 Gel mobility shift assays indicated that FlrC binds to a

177 However, in contrast to E. coli, gel mobility shift assays indicated that neither E. coli

178 Gel mobility shift assays indicated that the -94 to -101

179 However, a gel mobility shift assay indicates that MrpJ does not bi

180 Furthermore, we used gel mobility shift assays, methidiumpropyl-EDTA.Fe footp

181 tical gel filtration of native complexes and gel mobility shift assays of an maltose-binding protein-

182 Up to five complex bands are observed in gel mobility shift assays of HU binding to the 34 bp dup

183 zyme in Escherichia coli, as demonstrated by gel mobility shift assays of ligand binding and peptide-

184 In gel mobility shift assays, only the change of C(+7) to t

185 proviral DNA (env-DNA) were investigated by gel mobility shift assays or by photo-cross-linking expe

186 Gel mobility shift assays performed with an NRRE-1 probe

187 Based on gel mobility shift assays, phosphorylation does not appe

188 ption-PCR, Western blotting, electrophoretic gel mobility shift assays, promoter reporter, chromatin

189 However, in gel mobility shift assays pure EGR-1 or nuclear extracts

190 In gel-mobility shift assays, PutA47 was observed to bind c

191 rse transcription PCR, Western blotting, and gel mobility shift assay, respectively.

192 Our electrophoretic gel mobility shift assay results demonstrated that the c

193 Gel mobility shift assays reveal that a cT3Ralpha mutant

194 ime course luciferase assays and time course gel mobility shift assays reveal that the Smad3/4 comple

195 Furthermore, a gel mobility shift assay revealed that MMS was able to i

196 A gel mobility shift assay revealed that nuclear proteins

197 Gel mobility shift assays revealed binding of HBC cell n

198 In this study, electrophoretic gel mobility shift assays revealed specific DNA-protein

199 Gel mobility shift assays revealed that functional indep

200 Gel mobility shift assays revealed that LANA forms a com

201 Gel mobility shift assays revealed that mainly ATF2 boun

202 Gel mobility shift assays revealed that RNR can interact

203 Gel mobility shift assays revealed that the affinity of

204 Electrophoretic gel mobility shift assays revealed that the enzyme bound

205 In the present study, gel mobility shift assays revealed the presence of A. ph

206 Specifically, the results of gel mobility shift assays revealed the sloABC, sloR, com

207 Gel mobility-shift assay revealed that STAT3 and STAT6 a

208 Gel-mobility shift assays revealed very strong binding a

209 In gel mobility shift assays, rTGA2.1 binds to the rice RCH

210 Gel mobility shift assays show that AphA binds to a site

211 Gel mobility shift assays show that DICE forms B cell-sp

212 Gel mobility shift assays show that N-Myc binds specific

213 Native gel mobility-shift assays show that BS15 interacts speci

214 Gel mobility shift assay showed that 17beta-estradiol ha

215 Gel mobility shift assay showed that heat-shock factor (

216 Furthermore, a gel mobility shift assay showed that the purified transc

217 A gel mobility shift assay showed that transfected NRE TFD

218 Gel mobility shift assays showed increased potential for

219 Gel mobility shift assays showed no binding of EcR-A/USP

220 Gel mobility shift assays showed protein phosphorylation

221 Gel mobility shift assays showed that cellular proteins

222 Gel mobility shift assays showed that cellular proteins

223 Gel mobility shift assays showed that DNA binding is sev

224 Gel mobility shift assays showed that factor 2 formed st

225 Electrophoretic gel mobility shift assays showed that operator binding b

226 Gel mobility shift assays showed that RpbA-His(6) specif

227 Chromatin immunoprecipitation and gel mobility shift assays showed that STAT-1 bound to an

228 Furthermore, gel mobility shift assays showed that the resistant line

229 Gel mobility shift assays showed that this GC/TT substit

230 Gel mobility shift assays showed the specific binding of

231 Electrophoretic gel mobility shift assays showed two NF-kappaB proteins,

232 The gel-mobility shift assay showed that the peptide formed

233 Electrophoretic gel-mobility shift assays showed that differences in the

234 untranslated region of gerE mRNA in in vitro gel mobility shift assays, strongly suggesting that acon

235 Sequence analysis and gel mobility shift assays suggest that the transcription

236 In addition, gel mobility-shift assays suggest that YmgB may be a non

237 Gel mobility shift assays suggested that Sp1 binds const

238 Gel mobility shift assay supershift analysis demonstrate

239 This suggestion was confirmed by gel mobility shift assays that showed that DevA binds it

240 h in vitro dimethyl sulfate footprinting and gel mobility shift assays, that DnaA(L366K) in either nu

241 In gel mobility shift assays, the E65G and S66P enzymes wer

242 the promoter was E2-responsive; however, in gel mobility shift assays, the estrogen receptor alpha (

243 In gel mobility shift assays, the formation of a supershift

244 Using gel mobility shift assays, the liver-enriched protein GA

245 As shown by gel mobility shift assays, the rNSP2 multimers bound to

246 combination with further development of the gel mobility shift assay to allow simultaneous compariso

247 hromatography and a quantitative fluorescent gel mobility shift assay to reveal an additional binding

248 in vitro modification with pure enzymes and gel mobility shift assay to study the subject.

249 In a previous study, we used gel mobility shift assays to determine that BreR binds a

250 The C-terminal domain was shown by gel mobility-shift assay to have approximately 8-fold lo

251 or neuregulin-1-heparin interactions using a gel mobility shift assay together with an assay that mea

252 In gel mobility shift assays, TR2 competes with P19 nuclear

253 f the bent-L pathway was characterized using gel mobility shift assays, two-dimensional gel analysis,

254 Gel mobility shift assay using a double stranded oligonu

255 Gel mobility shift assays using AR2 revealed a white pha

256 Gel mobility shift assays using HepG2 or rat hepatocyte

257 proteins were evaluated by quantitative RNA gel mobility shift assays using lysed cell supernatants.

258 roperties of protein-DNA complexes formed in gel mobility shift assays using uninfected and HSV-1-inf

259 Electrophoretic gel mobility shift assays using whole liver cell extract

260 ivation of these defense genes, we performed gel-mobility shift assays using nuclear extracts from Nt

261 Gel mobility shift assays utilizing deoxyuridine modifie

262 s has entailed the development of a modified gel mobility shift assay, utilizing fluorescence end-tag

263 Gel mobility shift assays, UV-cross-linking experiments,

264 Gel mobility shift assays validated the identity of the

265 In gel mobility shift assays, VPA-induced binding of nuclea

266 A gel mobility shift assay was developed to examine recogn

267 A gel mobility shift assay was used to examine the effect

268 A gel mobility-shift assay was used to demonstrate the bin

269 Using the gel mobility shift assay, we demonstrated that an increa

270 By gel mobility shift assay, we demonstrated that strain Be

271 Using a gel mobility shift assay, we found that HBD2 bound to a

272 nant catalytic subunit as the substrate in a gel mobility shift assay, we have identified an activity

273 Using a gel mobility shift assay, we show that MnmA binds to unm

274 Using a gel mobility shift assay, we show that the displaced str

275 By using an electrophoretic gel mobility shift assay, we showed that AaEcR.AaUSP exh

276 Using gel mobility shift assays, we demonstrate that the intri

277 bination of promoter mutational analysis and gel mobility shift assays, we have identified a binding

278 Using gel mobility shift assays, we have shown that an EWG dim

279 Using various regions of VIPR-RP in gel mobility shift assays, we show that the amino acid s

280 Further, using gel mobility shift assays, we were able to show the indu

281 sing a combination of DNase I footprints and gel mobility shifts assays, we showed that when NAC(WT)

282 Helix-coil transition curves and a gel mobility shift assay were used to characterize the i

283 ulatory elements within the COL1A1 promoter, gel mobility shift assays were performed with nuclear ex

284 equence database, lacZ reporter fusions, and gel mobility shift assays were used to elucidate the reg

285 DNase I footprinting and gel mobility shift assays were used to look for potentia

286 Gel mobility shift assays were used to measure the bindi

287 oter-reporter constructs and electrophoretic gel mobility shift assays were utilized to examine COL1A

288 R with the misR promoter was demonstrated by gel mobility shift assays, where MisR approximately P ex

289 ping H-NS/ToxT binding sites was observed in gel mobility shift assays, where ToxT was found to displ

290 nsensus sequence, Southwestern analysis, and gel mobility shift assays with antibodies identify MAZ a

291 Electrophoretic gel mobility shift assays with cell extracts prepared fr

292 ound that it binds purified TBP and TFIIB in gel mobility shift assays with cooperative enhancement o

293 ing to an estrogen responsive DNA element in gel mobility shift assays with EC(50)s of about 0.1 micr

294 Gel mobility shift assays with maltose-binding protein (

295 s not exhibit DNA-binding activity in native gel mobility shift assays with promoter regions of the p

296 Gel mobility shift assays with purified U1 snRNP and oli

297 plex by isothermal titration calorimetry and gel mobility shift assays with rRNA and proteins from th

298 Gel mobility shift assays with the hRFC-B basal promoter

299 Gel mobility shift assays with the trcR promoter and Trc

300 series of overlapping trcR PCR fragments in gel mobility shift assays with TrcR, an AT-rich region o