1 TP to the tumor necrosis factor (TNF) ARE by
gel mobility shift analyses and fluorescence anisotropy
2 Gel mobility shift analyses of PICs and characterization
3 Gel mobility shift analyses with nuclear extracts from R
4 sion of a gltB::lacZ transcriptional fusion,
gel mobility shift analyses, and DNA footprinting assays
5 mation of UvrB-DNA complexes by quantitative
gel mobility shift analyses, and the rates of UvrABC inc
6 Using
gel mobility shift analyses, UV, circular dichroism and
7 Footprinting and electrophoretic
gel mobility shift analysis (EMSA) provide further evide
8 Gel mobility shift analysis confirmed that TCDD inductio
9 Gel mobility shift analysis demonstrated a sequence-spec
10 Gel mobility shift analysis demonstrated that binding to
11 Gel mobility shift analysis of protein-DNA complexes, co
12 Gel mobility shift analysis revealed that DnaC810 could
13 Electrophoretic
gel mobility shift analysis showed that a component in e
14 Gel mobility shift analysis showed that binding of the t
15 Gel mobility shift analysis showed the interaction of Sp
16 Gel mobility shift analysis suggests that the BRCT domai
17 Here, we used
gel mobility shift analysis to determine that CsrA binds
18 A new technique of high-pressure
gel mobility shift analysis was used to test the effects
19 Gel mobility shift analysis with purified AerR indicates
20 Using
gel mobility shift analysis, our data demonstrate that t
21 n method involving affinity bead-binding and
gel mobility shift analysis.
22 of LHR mRNA binding sequence, as examined by
gel mobility shift analysis.
23 ct methyl transfer reactions was assessed by
gel mobility-shift,
analytical ultracentrifugation, and
24 Gel mobility shift and (45)Ca(2)+ overlay assays demonst
25 Gel mobility shift and chromatin immunoprecipitation ass
26 Gel mobility shift and chromatin immunoprecipitation ass
27 Gel mobility shift and chromatin immunoprecipitation ass
28 ng to this GC-rich promoter as determined in
gel mobility shift and chromatin immunoprecipitation ass
29 th ACSL3-PPRE sequences were demonstrated by
gel mobility shift and chromatin immunoprecipitation ass
30 uced AP-2alpha binding using electrophoretic
gel mobility shift and chromatin immunoprecipitation ass
31 Gel mobility shift and chromatin immunoprecipitation ass
32 Gel mobility shift and DNA footprint analyses further in
33 Gel mobility shift and DNase I footprinting assays showe
34 Gel mobility shift and DNase I footprinting assays with
35 re confirmed to be direct targets of CodY by
gel mobility shift and DNase I footprinting assays.
36 Gel mobility shift and DNase I footprinting experiments
37 Gel mobility shift and DNase I protection assays reveale
38 solution avoiding the intrinsic problems of
gel mobility shift and filter binding assays while provi
39 By using
gel mobility shift and fluorescence anisotropy assays, w
40 Computer modelling,
gel mobility shift and footprint analyses identified two
41 Results from
gel mobility shift and footprint assays demonstrated tha
42 DNA affinity purification,
gel mobility shift and footprinting analyses revealed th
43 orresponding phosphodiester TFO, as shown by
gel mobility shift and footprinting assays.
44 Gel mobility shift and kinetic analyses indicate that th
45 The combined results of
gel mobility shift and KMnO(4) footprinting assays show
46 In this study, we used RNA
gel mobility shift and nitrocellulose filter-binding ass
47 ichia coli-expressed recombinant proteins in
gel mobility shift and Northwestern assays, we demonstra
48 antly stronger than previously determined by
gel mobility shift and polyacrylamide gel coelectophores
49 The smFRET results, complemented by
gel mobility shift and small angle x-ray scattering anal
50 Gel mobility shift and supershift assays demonstrated th
51 Gel mobility shift and supershift assays performed with
52 Gel mobility shift and supershift assays show that the n
53 icase proteins bind to RNA in vitro based on
gel mobility shift and surface plasmon resonance measure
54 th an altered conformation, as observed by a
gel mobility shift and the detection of two related prot
55 Gel mobility shift and toeprint analyses demonstrate tha
56 Furthermore, we demonstrate with
gel mobility shift and transient transfection assays tha
57 tion of Rab5 with DATFP-FPP, demonstrated by
gel mobility shift and Triton X-114 phase separation exp
58 Using
gel mobility shift and UV cross-linking assays, we ident
59 were subjected to CSR binding analysis using
gel mobility shift and UV cross-linking.
60 Gel mobility shifts and DNase I footprints showed that N
61 RNA
gel mobility-shift and UV cross-linking assays indicated
62 Subsequent
gel-mobility shift and supershift experiments involving
63 mutants demonstrate normal calcium-dependent
gel-mobility shifts and changes in their near-UV CD spec
64 Gel-mobility-shift and mutagenesis studies revealed that
65 DNA loci in conjunction with DNA protection,
gel mobility shift,
and genetic experiments to test seve
66 th an altered conformation, as detected by a
gel mobility shift,
and is required for specific binding
67 Using cotransfection,
gel mobility shifts,
and DNase I footprinting, we have i
68 Electrophoretic
gel mobility shift assay (EMSA) revealed that the -1C-->
69 , 15, 30, or 60 minutes; lysed; and used for
gel mobility shift assay (GMSA) and supershift assay for
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 This site, as determined by
gel mobility shift assay and DNaseI footprinting, is loc
74 increase AP-1 binding in an electrophoretic
gel mobility shift assay and increase the expression of
75 We apply this approach to the
gel mobility shift assay and use it to modify a self-cle
76 Gel mobility shift assay demonstrated that c-Jun is the
77 ort RNA transcripts were studied using a new
gel mobility shift assay from which melting temperatures
78 A
gel mobility shift assay indicated that the UL5-UL52 sub
79 However, a
gel mobility shift assay indicates that MrpJ does not bi
80 Our electrophoretic
gel mobility shift assay results demonstrated that the c
81 Furthermore, a
gel mobility shift assay revealed that MMS was able to i
82 A
gel mobility shift assay revealed that nuclear proteins
83 Gel mobility shift assay showed that heat-shock factor (
84 combination with further development of the
gel mobility shift assay to allow simultaneous compariso
85 hromatography and a quantitative fluorescent
gel mobility shift assay to reveal an additional binding
86 in vitro modification with pure enzymes and
gel mobility shift assay to study the subject.
87 or neuregulin-1-heparin interactions using a
gel mobility shift assay together with an assay that mea
88 Gel mobility shift assay using a double stranded oligonu
89 A
gel mobility shift assay was used to examine the effect
90 AF-, AAF- and AP-DNA adducts, determined by
gel mobility shift assay, are 33 +/- 9, 8 +/- 2 and 23 +
91 ion was further confirmed by electrophoretic
gel mobility shift assay, chromatin immunoprecipitation,
92 alyses in reporter gene assays, as well as a
gel mobility shift assay, identified an LXR response ele
93 and normal adjacent tissue were analysed by
gel mobility shift assay, immunoblotting of nuclear extr
94 rse transcription PCR, Western blotting, and
gel mobility shift assay, respectively.
95 s has entailed the development of a modified
gel mobility shift assay, utilizing fluorescence end-tag
96 Using the
gel mobility shift assay, we demonstrated that an increa
97 Using a
gel mobility shift assay, we found that HBD2 bound to a
98 Using a
gel mobility shift assay, we show that MnmA binds to unm
99 Using a
gel mobility shift assay, we show that the displaced str
100 activated T cells-p300 complex to IRE in the
gel mobility shift assay.
101 mined by gel filtration chromatography and a
gel mobility shift assay.
102 and quantified using a native polyacrylamide
gel mobility shift assay.
103 talled elongation complexes as measured in a
gel mobility shift assay.
104 ed ability to bind to the tcpA promoter in a
gel mobility shift assay.
105 defined RNA molecules was characterized by a
gel mobility shift assay.
106 th purified FadR protein was determined by a
gel mobility shift assay.
107 Similar results were obtained with a
gel mobility shift assay.
108 nd to the leader sense RNA, as determined by
gel mobility shift assay.
109 aracterized by site-directed mutagenesis and
gel mobility shift assay.
110 nd 77 +/- 6 Pm, respectively, as measured by
gel mobility shift assay.
111 nary complexes that could be visualized in a
gel mobility shift assay.
112 hBVR and nuclear extract containing hBVR in
gel mobility-shift assay bound to AP-1 sites in the ATF-
113 A
gel mobility-shift assay was used to demonstrate the bin
114 II of DsrA ncRNA (DsrA(DII)) and A(18) by a
gel-mobility shift assay, fluorescence anisotropy, and f
115 ffinity to DsrA(DII) by <or=2-fold using the
gel-mobility shift assay.
116 uorescence, CD spectroscopy, NMR, and native
gel mobility shift assays (GMSAs).
117 elated with previously reported values using
gel mobility shift assays and a similarly sized poly-dT.
118 Gel mobility shift assays and analysis of ROS3 immunopre
119 Gel mobility shift assays and aztR O/P-lacZ induction ex
120 relevance of this sequence was obtained from
gel mobility shift assays and by transfection of TCC mut
121 Furthermore, by using
gel mobility shift assays and chromatin immunoprecipitat
122 Gel mobility shift assays and co-immunoprecipitation exp
123 d by this focused set of genes, we performed
gel mobility shift assays and demonstrated that ChvI dir
124 ng in vivo transcriptional fusions, in vitro
gel mobility shift assays and DNase I footprinting assay
125 In vitro
gel mobility shift assays and DNase I footprinting exper
126 nsus site centered at position -162 by using
gel mobility shift assays and DNase I footprinting exper
127 pped within the cbbLS promoter by the use of
gel mobility shift assays and DNase I footprinting.
128 ation results were independently verified by
gel mobility shift assays and quantitative DNA footprint
129 he function of the heterodimer, we performed
gel mobility shift assays and showed that the A14/A43 he
130 Gel mobility shift assays and supershift assays with spe
131 Gel mobility shift assays and surface plasmon resonance
132 the activities of various ecdysteroids using
gel mobility shift assays and transfection assays in Sch
133 Here we compare the self-cleavage and
gel mobility shift assays applied to the DNA binding of
134 directly bind the hilA and hilC promoters in
gel mobility shift assays but not the flhD, fliA, hilD,
135 However,
gel mobility shift assays clearly show that other as yet
136 Gel mobility shift assays combined with DNase I footprin
137 transfected with a SOX9 cDNA (M12/SOX9), and
gel mobility shift assays confirmed binding of nuclear p
138 Gel mobility shift assays confirmed that CcrR directly b
139 mobility complex with DNA in electrophoretic
gel mobility shift assays corresponding to occupancy by
140 Gel mobility shift assays demonstrate that GATA-6 binds
141 Gel mobility shift assays demonstrate that the aptamers
142 Gel mobility shift assays demonstrated specific binding
143 Results from
gel mobility shift assays demonstrated that Hoxa10-1, Ho
144 Gel mobility shift assays demonstrated that purified TEF
145 Gel mobility shift assays demonstrated that the protein(
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 predictions were experimentally validated by
gel mobility shift assays for two NrtR family representa
149 Gel mobility shift assays further demonstrated that DDX1
150 Binding of tRNA by
gel mobility shift assays gives a dissociation constant
151 Gel mobility shift assays identified the upstream stimul
152 Gel mobility shift assays indicated that FlrC binds to a
153 However, in contrast to E. coli,
gel mobility shift assays indicated that neither E. coli
154 Up to five complex bands are observed in
gel mobility shift assays of HU binding to the 34 bp dup
155 zyme in Escherichia coli, as demonstrated by
gel mobility shift assays of ligand binding and peptide-
156 proviral DNA (env-DNA) were investigated by
gel mobility shift assays or by photo-cross-linking expe
157 ime course luciferase assays and time course
gel mobility shift assays reveal that the Smad3/4 comple
158 Gel mobility shift assays revealed binding of HBC cell n
159 In this study, electrophoretic
gel mobility shift assays revealed specific DNA-protein
160 Gel mobility shift assays revealed that LANA forms a com
161 Gel mobility shift assays revealed that mainly ATF2 boun
162 Electrophoretic
gel mobility shift assays revealed that the enzyme bound
163 In the present study,
gel mobility shift assays revealed the presence of A. ph
164 Specifically, the results of
gel mobility shift assays revealed the sloABC, sloR, com
165 Gel mobility shift assays show that AphA binds to a site
166 Gel mobility shift assays show that DICE forms B cell-sp
167 Gel mobility shift assays show that N-Myc binds specific
168 Gel mobility shift assays showed increased potential for
169 Gel mobility shift assays showed no binding of EcR-A/USP
170 Gel mobility shift assays showed that cellular proteins
171 Electrophoretic
gel mobility shift assays showed that operator binding b
172 Chromatin immunoprecipitation and
gel mobility shift assays showed that STAT-1 bound to an
173 Furthermore,
gel mobility shift assays showed that the resistant line
174 Gel mobility shift assays showed that this GC/TT substit
175 Gel mobility shift assays showed the specific binding of
176 Sequence analysis and
gel mobility shift assays suggest that the transcription
177 This suggestion was confirmed by
gel mobility shift assays that showed that DevA binds it
178 In a previous study, we used
gel mobility shift assays to determine that BreR binds a
179 Gel mobility shift assays using AR2 revealed a white pha
180 Gel mobility shift assays using HepG2 or rat hepatocyte
181 Gel mobility shift assays utilizing deoxyuridine modifie
182 Gel mobility shift assays validated the identity of the
183 equence database, lacZ reporter fusions, and
gel mobility shift assays were used to elucidate the reg
184 DNase I footprinting and
gel mobility shift assays were used to look for potentia
185 Gel mobility shift assays were used to measure the bindi
186 oter-reporter constructs and electrophoretic
gel mobility shift assays were utilized to examine COL1A
187 ound that it binds purified TBP and TFIIB in
gel mobility shift assays with cooperative enhancement o
188 ing to an estrogen responsive DNA element in
gel mobility shift assays with EC(50)s of about 0.1 micr
189 Gel mobility shift assays with maltose-binding protein (
190 s not exhibit DNA-binding activity in native
gel mobility shift assays with promoter regions of the p
191 Gel mobility shift assays with purified U1 snRNP and oli
192 plex by isothermal titration calorimetry and
gel mobility shift assays with rRNA and proteins from th
193 Gel mobility shift assays with the hRFC-B basal promoter
194 Gel mobility shift assays with the trcR promoter and Trc
195 series of overlapping trcR PCR fragments in
gel mobility shift assays with TrcR, an AT-rich region o
196 As determined using
gel mobility shift assays, 13 out of 14 negative complem
197 munofluorescence studies, live cell imaging,
gel mobility shift assays, and bimolecular fluorescence
198 Transient transfection,
gel mobility shift assays, and chromatin immunoprecipita
199 rized by using a promoter truncation series,
gel mobility shift assays, and DNase I footprinting.
200 ity isolation, DNA-binding site competition,
gel mobility shift assays, and protein overexpression in
201 In
gel mobility shift assays, both active and inactive reco
202 box consensus DNA element in electrophoretic
gel mobility shift assays, but only BjFur bound the irr
203 ddition to real-time PCR and immunoblotting,
gel mobility shift assays, coupled with specific antibod
204 ys and the formation of an ER.ERE complex in
gel mobility shift assays, further indicating that the e
205 nfected Sf21 insect cells and the methods of
gel mobility shift assays, gel filtration chromatography
206 ell lines, DNase I footprinting analyses and
gel mobility shift assays, identified an AHSP gene eryth
207 Furthermore, we used
gel mobility shift assays, methidiumpropyl-EDTA.Fe footp
208 In
gel mobility shift assays, only the change of C(+7) to t
209 Based on
gel mobility shift assays, phosphorylation does not appe
210 ption-PCR, Western blotting, electrophoretic
gel mobility shift assays, promoter reporter, chromatin
211 In
gel mobility shift assays, rTGA2.1 binds to the rice RCH
212 untranslated region of gerE mRNA in in vitro
gel mobility shift assays, strongly suggesting that acon
213 h in vitro dimethyl sulfate footprinting and
gel mobility shift assays, that DnaA(L366K) in either nu
214 In
gel mobility shift assays, the E65G and S66P enzymes wer
215 In
gel mobility shift assays, the formation of a supershift
216 Using
gel mobility shift assays, the liver-enriched protein GA
217 In
gel mobility shift assays, TR2 competes with P19 nuclear
218 In
gel mobility shift assays, VPA-induced binding of nuclea
219 bination of promoter mutational analysis and
gel mobility shift assays, we have identified a binding
220 Using
gel mobility shift assays, we have shown that an EWG dim
221 Further, using
gel mobility shift assays, we were able to show the indu
222 R with the misR promoter was demonstrated by
gel mobility shift assays, where MisR approximately P ex
223 ping H-NS/ToxT binding sites was observed in
gel mobility shift assays, where ToxT was found to displ
224 293T cells, as measured by gene reporter and
gel mobility shift assays.
225 This finding was confirmed by
gel mobility shift assays.
226 inding site at +18 prevented HapR binding in
gel mobility shift assays.
227 uman SHMT1 promoter by deletion analyses and
gel mobility shift assays.
228 -binding sites of JMJ in the ANF enhancer by
gel mobility shift assays.
229 f ESE-1 to bind to oligonucleotide probes in
gel mobility shift assays.
230 te to bind DNA, a prediction confirmed using
gel mobility shift assays.
231 binding site, which we have verified here by
gel mobility shift assays.
232 n using isothermal titration calorimetry and
gel mobility shift assays.
233 xyl radical footprinting and electrophoretic
gel mobility shift assays.
234 ipitation, DNA microarray hybridization, and
gel mobility shift assays.
235 r by performing luciferase reporter gene and
gel mobility shift assays.
236 cing the CbbR-cbbLS promoter interactions in
gel mobility shift assays.
237 DNA binding activities of wild type Pax9 in
gel mobility shift assays.
238 P promoter at several sites as determined by
gel mobility shift assays.
239 to have modified binding characteristics in
gel mobility shift assays.
240 ed using recombinant proteins in competition
gel mobility shift assays.
241 ding donors and acceptors, are determined in
gel mobility shift assays.
242 ht ends of the transposon was compared using
gel mobility shift assays.
243 r cisplatin-damaged DNA were investigated by
gel mobility shift assays.
244 related hnRNP proteins reacted with CBF2 in
gel mobility shift assays.
245 n of amyloid precursor protein (APP) mRNA in
gel mobility shift assays.
246 nt plus poly(A) tail] were identified using
gel mobility shift assays.
247 ite within their promoters, as determined by
gel mobility shift assays.
248 substrates using fluorescence anisotropy and
gel mobility shift assays.
249 to the promoter regions of fruA and levD in
gel mobility shift assays.
250 , was investigated by DNase I protection and
gel mobility shift assays.
251 d for effective MAL-SRF complex formation in
gel mobility shift assays.
252 sing a combination of DNase I footprints and
gel mobility shifts assays, we showed that when NAC(WT)
253 Electrophoretic
gel mobility-shift assays demonstrate that the Tth ligas
254 Gel mobility-shift assays demonstrated that assembly of
255 Gel mobility-shift assays demonstrated that specificity,
256 Native
gel mobility-shift assays show that BS15 interacts speci
257 In addition,
gel mobility-shift assays suggest that YmgB may be a non
258 re tightly than the DsrA.rpoS RNA complex in
gel mobility-shift assays.
259 directly bound only the proximal FixK box in
gel mobility-shift assays.
260 surement), fluorescence, and electrophoretic
gel mobility-shift assays.
261 an oligonucleotide containing the 202-SBS in
gel-mobility shift assays and to the 5'-regulatory regio
262 Gel-mobility shift assays demonstrated that the forkhead
263 Gel-mobility shift assays revealed very strong binding a
264 Electrophoretic
gel-mobility shift assays showed that differences in the
265 ivation of these defense genes, we performed
gel-mobility shift assays using nuclear extracts from Nt
266 In
gel-mobility shift assays, PutA47 was observed to bind c
267 nse element (pTRE and nTRE, respectively) in
gel-mobility shift assays.
268 to heparin resin nor to heparin fragments in
gel-mobility shift assays.
269 Using
gel-mobility-shift assays and surface plasmon resonance
270 Analysis of the mutant proteins by
gel mobility shift,
beta-galactosidase and polyacrylamid
271 DNA sequence analysis,
gel mobility shifting,
chromatin immunoprecipitation, an
272 Relative IC(50) values from
gel mobility shift competition assays showed that the -7
273 The
gel mobility shift data plus in vivo expression data ind
274 rescence anisotropy (FA) and electrophoretic
gel mobility shift (
EMSA) assays, the interactions betwe
275 d antiparallel types of G-quadruplexes using
gel mobility shift experiments and a helicase assay.
276 for purified HlyU were discovered using DNA
gel mobility shift experiments and DNase protection assa
277 Gel mobility shift experiments indicate that TMPyP3 spec
278 Gel mobility shift experiments indicated no effect of AM
279 Rather, fluorescence polarization and
gel mobility shift experiments reveal that pX interacts
280 ,25(OH)2D3 to the -133 to -74 bp region, and
gel mobility shift experiments revealed that 1,25(OH)2D3
281 ore, both in vivo foot-printing and in vitro
gel mobility shift experiments revealed that hedamycin b
282 In vitro
gel mobility shift experiments show that Cph2 directly b
283 rA binding to tnrA and glnRA promoter DNA in
gel mobility shift experiments showed that TnrA bound wi
284 n transfected into HeLa carcinoma cells, and
gel mobility shift experiments with HeLa nuclear extract
285 roteins bound the two wild-type operators in
gel mobility shift experiments, but the mutated operator
286 discrete complex in vitro, as illustrated by
gel mobility shift experiments, direct isolation of the
287 In
gel mobility shift experiments, TRalpha, retinoid X rece
288 -4 and +14 that specifically bound EGR-1 in
gel mobility shift experiments.
289 Gel mobility-shift experiments demonstrated sequence-spe
290 Gel-mobility-shift experiments to characterize the inter
291 und to form complex with GAD(65) as shown by
gel mobility shift in non-denaturing gradient gel electr
292 both reconstituted transcription assays and
gel mobility shifts in order to investigate the biochemi
293 Gel mobility shift results showed that CsrA binds specif
294 Using
gel mobility shift RNase T1 protection assays and second
295 Chromatin immunoprecipitation and
gel mobility shift studies demonstrated the existence of
296 Gel mobility shift studies show that this complex contai
297 cterially expressed protein and native KCBP,
gel-mobility shift studies, and ATPase assays with the K
298 atural product yohimbine was found (based on
gel mobility shifts)
to block cleavage of the internal l
299 )) was analyzed by transport measurement and
gel mobility shifts upon oxidation with Cu (II)-(1,10-ph
300 Using
gel mobility shift,
we demonstrated a direct interaction