1 th increasing concentrations of CcrA blocked
gel shift.
2 assayed for binding to recombinant POU5F1 by
gel shift.
3 resonance (SPR) and electrophoretic mobility
gel shift.
4 TosR binds to this region, affecting a
gel shift.
5 e and material that bound RT was isolated by
gel-shift.
6 s shown by chromatin immunoprecipitation and
gel shifts.
7 ferent conformational changes underlying the
gel shifts.
8 In vitro immunoprecipitation assays and
gel shift analyses have further demonstrated that purifi
9 In this report, near equilibrium binding and
gel shift analyses showed that A3G assembly and disassem
10 iatum by radioimmunoassay, Western blot, and
gel shift analyses, respectively.
11 Gel-shift analyses showed that both the native HIF-1alph
12 al and translational fusions, and performing
gel-shift analyses, we identified 40 genes in six operon
13 Gel shift analysis and chloramphenicol acetyl transferas
14 ike prior to receptor engagement, but trimer
gel shift analysis and slow kinetics of shedding induced
15 While
gel shift analysis confirmed NF-Y binding to both sites,
16 utations in the promoter region of pilA1 and
gel shift analysis demonstrated that both sigma(54) and
17 Electrophoretic
gel shift analysis demonstrated that HbrL binds the prom
18 Native polyacrylamide
gel shift analysis did suggest that Bap1 exhibits lectin
19 Luciferase assays and
gel shift analysis have identified a single motif upstre
20 Gel shift analysis identified MarT as a transcriptional
21 n, the principal AP-1 components detected by
gel shift analysis include c-jun, ATF-2, fos-B, fra-1, a
22 Electrophoretic mobility
gel shift analysis revealed that PapX binds to the flhD
23 Gel shift analysis revealed that the combination gene th
24 Gel shift analysis revealed that the purified MBP-SyrF,
25 Gel shift analysis showed that purified SarA protein bin
26 Glycosidase
gel shift analysis suggested that K(v)2.1, K(v)4.2, and
27 and SLVI, (SLV-VI) and (iii) demonstrate by
gel shift analysis that nsp1 purified from Escherichia c
28 Gel shift analysis with purified recombinant NikR verifi
29 FEN1 was later shown, by
gel shift analysis, to remove the wild type Dna2 from th
30 However, using
gel shift analysis, we demonstrate that IE86 efficiently
31 trometry, chromatin immunoprecipitation, and
gel shift analysis.
32 in the presence of TO901317 was confirmed by
gel shift analysis.
33 Gel-shift analysis demonstrates that glucocorticoid/andr
34 Gel-shift analysis showed that SDF1alpha enhances DNA bi
35 DNA damage, including BRCA1 and PARP2, with
gel-shift analysis showing that SOG1 can physically asso
36 Gel-shift analysis suggests that Spi-C, ectopically expr
37 We used
gel-shift analysis to refine the Sox2 region bound by Ar
38 An in vitro
gel-shift analysis was used to show that the mutation in
39 als as revealed by Western blot analysis and
Gel-shift analysis, respectively.
40 By
gel-shift analysis, the corresponding oligonucleotide pr
41 Using
gel-shift analysis, we found that the two major forms of
42 ce motif 5'-GTTGCA-3', were identified using
gel-shift analysis.
43 ts its cognate RNA aptamer, boxB, using both
gel shift and biolayer interferometry assays.
44 omoter using a luciferase reporter assay and
gel shift and ChIP studies.
45 Using
gel shift and chromatin immunoprecipitation (ChIP) assay
46 ced increases in Smad 1/5/8 levels; further,
gel shift and chromatin immunoprecipitation analyses dem
47 Gel shift and chromatin immunoprecipitation assays confi
48 Gel shift and chromatin immunoprecipitation assays confi
49 itical for the transcriptional activity, and
gel shift and chromatin immunoprecipitation assays confi
50 Gel shift and chromatin immunoprecipitation assays ident
51 Gel shift and chromatin immunoprecipitation assays revea
52 As confirmed by
gel shift and chromatin immunoprecipitation assays, ATRA
53 Gel shift and chromatin immunoprecipitation studies demo
54 However,
gel shift and competitive binding assays indicated that
55 Gel shift and DNase I footprinting assays confirmed the
56 Using
gel shift and DNase I footprinting assays, we found that
57 intergenic promoter region as determined by
gel shift and DNase I footprinting assays.
58 Using
gel shift and enzymatic footprinting assays and atomic f
59 ing or the NCp7/RNA interaction monitored by
gel shift and fluorescence.
60 In this study, we show by
gel shift and footprint assays with the C-terminal DNA-b
61 The results from
gel shift and footprint studies demonstrate that tight b
62 This element bound HIF-1 in the
gel shift and in in-cell luciferase assays.
63 Using
gel shift and in vitro transcription assays we showed th
64 Gel shift and luciferase assays indicate that both varia
65 Gel shift and luciferase assays reveal a strong bias for
66 B-dependent transporter FhuA, as assessed by
gel shift and mass spectrometry assays.
67 Gel shift and mass spectrometry experiments confirmed th
68 n blot analysis, and NF-kappaB activation by
gel shift and reporter assays.
69 Using a previously reported in vitro mRNA
gel shift and stability assay, antibodies to the GR bloc
70 Gel shift and supershift analyses, as well as ChIP, show
71 Using native
gel shift and surface plasmon resonance analyses, we det
72 DI RNA cis-replication signal, (ii) show by
gel shift and UV-cross-linking analyses that cellular pr
73 nding to the MKP1 gene promoter, as shown by
gel shifting and chromatin immunoprecipitation assays.
74 consensus sequence is supported by in vitro
gel shifts and by in vivo functional reporter gene studi
75 d exons could still bind Tra2beta protein by
gel shifts and functional splicing analyses.
76 om reverse transcription-PCR experiments and
gel-shift and binding assays demonstrated that MMC rapid
77 DNA binding experiments using
gel-shift and ChIP assays demonstrated a progressive red
78 Gel-shift and chromatin immunoprecipitation assays revea
79 ing promoter-reporter constructs, as well as
gel-shift and chromatin immunoprecipitation experiments
80 431 both in vitro and in vivo as revealed by
gel-shift and chromatin immunoprecipitation, respectivel
81 Gel-shift and fluorescence polarization assays showed th
82 d via bead binding, fluorescence anisotropy,
gel shift,
and analytical ultracentrifugation methods.
83 encing studies in combination with promoter,
gel shift,
and chromatin immunoprecipitation assays indi
84 Combined, luciferase,
gel shift,
and chromatin immunoprecipitation assays show
85 wn, coimmunoprecipitation, yeast two-hybrid,
gel shift,
and chromatin immunoprecipitation assays) to
86 In silico analysis,
gel shift,
and in vitro reporter assays were performed t
87 Chromatin immunoprecipitation,
gel shift,
and luciferase assays confirmed LEF1 occupanc
88 Transcription assays,
gel shifting,
and chromatin immunoprecipitation (ChIP) a
89 Transactivation,
gel-shift,
and chromatin immunoprecipitation assays indi
90 Promoter truncation, point mutation,
gel-shift,
and protein-DNA ELISA analysis showed that tr
91 all chaperone activities, as demonstrated by
gel shift annealing assays, decreasing in the order HIV-
92 Gel-shift annealing and sedimentation assays were used t
93 ve polyacrylamide gel electrophoresis (PAGE)
gel shifts as well as affinity pull-down assays implicat
94 hr421/Ser424), rpS6 (Ser235/236) and 4E-BP1 (
gel shift),
as well as deficits in total eEF2 accretion.
95 Using electrophoretic mobility
gel shift assay (EMSA)-based competition assays, the kl-
96 We demonstrate by a
gel shift assay a strong and specific affinity of recomb
97 Using native polyacrylamide
gel shift assay and negative-stain EM, we found that the
98 Gel shift assay and Western blot analyses showed dose-de
99 ost cases, as evidenced by our nondenaturing
gel shift assay data.
100 A leucine zipper swap:
gel shift assay demonstrates that C/EBPalpha zippers wit
101 emia homeobox 3 (TLX3) TF was confirmed with
gel shift assay experiments.
102 ycol derivatives (MPEG) was measured using a
gel shift assay of tryptic fragments.
103 Gel shift assay showed that Osx bound to the Satb2 promo
104 Gel shift assay showed that Osx bound to the VEGF promot
105 In parallel, a
gel shift assay showed that SuhB forms a tight complex w
106 Computer analysis and
gel shift assay showed that the -1132 and -879 region in
107 d ubiquitination, and allowed DNA-binding in
gel shift assay similar to wild-type Runx1.
108 Also the
gel shift assay suggested that NFkappaB p65 is responsib
109 The
gel shift assay supported the fact that there exists an
110 A
gel shift assay with a radiolabeled OARE module and nucl
111 enhancer that strongly bind C/EBPalpha in a
gel shift assay, and interaction with endogenous C/EBPal
112 Using the
gel shift assay, chemical probing and dimethyl sulfate (
113 In a
gel shift assay, gefitinib led to decreased retardation
114 Using an infrared
gel shift assay, we demonstrated the presence of potenti
115 Using a
gel shift assay, we identified a cytoplasmic RNA-binding
116 d DNA-protein binding assay and conventional
gel shift assay, we successfully identified a ZBTB20-bin
117 d the binding domain of enzyme, we have used
gel shift assay.
118 re consistent with data from the traditional
gel shift assay.
119 -1 binds to the ATF3 promoter as assessed by
gel shift assay.
120 gion of the sarX promoter as demonstrated by
gel shift assay.
121 esponding to the proximal VEGF promoter in a
gel shift assay.
122 The
gel-shift assay (EMSA) revealed that the recombinant Gly
123 Binding was evaluated by
gel-shift assay and affinity by frontal affinity chromat
124 dimensions were confirmed using a calibrated
gel-shift assay and atomic force microscopy, and their i
125 Gel-shift assay experiments confirmed that pioglitazone
126 overall results of transcript analysis, RNA
gel-shift assay, and transgenic expression, for the firs
127 e found that Fis-DNA binding, as assessed by
gel-shift assay, changed in accordance with our expectat
128 assay, chromatin immunoprecipitation assay,
gel-shift assay, coimmunoprecipitation, and western blot
129 In the
gel-shift assay, Glu1 mutants K81E and T82Y failed to bi
130 Using
gel-shift assay, we showed that AML1-ETO and AML1-MTG16
131 4 protein could bind RNA as evidenced by the
gel-shift assay.
132 binding activity by electrophoretic mobility
gel shift assays (EMSA) and mitochondrial damage by JC-1
133 Gel shift assays also demonstrated that Sp1 interacted w
134 Gel shift assays and affinity pull-down followed by mass
135 ability, and markedly reduced DNA binding in
gel shift assays and as assessed by chromatin immunoprec
136 Gel shift assays and chromatin immunoprecipitation assay
137 Gel shift assays and site-directed mutagenesis allowed t
138 site decreased both NFI binding affinity in
gel shift assays and stimulation of SV40 promoter activi
139 of NF-kappaB p50/p65 DNA-binding activity in
gel shift assays and the activity of an NF-kappaB-respon
140 binding to a kappaB oligonucleotide probe in
gel shift assays and to the MMP-9 promoter in chromatin
141 Gel shift assays and transfection with wild-type and mut
142 Gel shift assays and UV cross-linking experiments identi
143 Gel shift assays confirmed high affinity binding of CsrA
144 Gel shift assays confirmed that both V. cholerae FadR an
145 Chromatin immunoprecipitation and
gel shift assays confirmed that Kar4 binds to regulatory
146 Gel shift assays demonstrate clear binding between SRF a
147 Gel shift assays demonstrated nonspecific binding of pur
148 Gel shift assays demonstrated that MrpJ and another para
149 Gel shift assays demonstrated that NF-kappaB inhibits th
150 Electromobility
gel shift assays demonstrated the activation of chondroc
151 Promoter reporter and
gel shift assays determined that the AirR response regul
152 Nonetheless,
gel shift assays did not reveal direct binding between R
153 sults from chromatin immunoprecipitation and
gel shift assays further confirmed the functional bindin
154 Gel shift assays identified a conserved non-canonical E-
155 Gel shift assays indicate that in isolation, nsp10 binds
156 Gel shift assays indicated that these DNA-binding sites
157 Gel shift assays on CP2 mutants confirmed that the CP2 m
158 Purified VirR was used in DNA
gel shift assays on target promoters and VirR : promoter
159 Gel shift assays performed in the presence of core- and
160 Gel shift assays revealed binding of HuR and TTP to rat
161 Gel shift assays revealed decreased protein binding to t
162 Gel shift assays revealed that CAR competes with HNF-4 f
163 Our
gel shift assays revealed that YhcR binds to the promote
164 Gel shift assays show binding of wBmxR1 to regions upstr
165 RNA
gel shift assays showed that a mutant SRSF2 derivative b
166 nditionally immortalized human podocytes and
gel shift assays showed that LMX1B recognizes AT-rich bi
167 Fluorescence anisotropy binding and
gel shift assays showed that the 3'BTE and 5'UTR RNAs ca
168 Gel shift assays showed that the region surrounding the
169 In contrast, competition experiments using
gel shift assays suggest that RAGE interaction with AGE
170 Gel shift assays suggest that XBP-1(S) binding occurs th
171 ence, chemical probing, optical melting, and
gel shift assays to characterize the structure of a seri
172 Gel shift assays using a bacterially expressed PUM2 RNA
173 Accordingly,
gel shift assays using both linear and circular DNA show
174 We performed
gel shift assays using nuclear extract from testes, brai
175 Gel shift assays using transfected myoblast nuclear extr
176 Importantly,
gel shift assays verified Tpx as a target in the intact
177 Electrophoretic mobility
gel shift assays were performed to determine the activat
178 Gel shift assays were performed with methylated or unmet
179 Gel shift assays were used to characterize bioY1_LL and
180 majority of the protease domain (H6.Gag.3h),
gel shift assays were used to monitor the annealing of t
181 Gel shift assays with model RNA substrates now show that
182 by chromatin immunoprecipitation in vivo and
gel shift assays with purified glutathione S-transferase
183 In vitro
gel shift assays, competition assays, and immunoprecipit
184 These data were confirmed in
gel shift assays, providing direct evidence that Pneumoc
185 Using electrophoretic mobility
gel shift assays, size-exclusion chromatography, and ele
186 egions of norB and tet38 was demonstrated by
gel shift assays, suggesting that MgrA was an indirect r
187 domain bind to a 55-bp AdMLP DNA fragment in
gel shift assays, suggesting that protein-DNA interactio
188 In the present studies, we found, by
gel shift assays, that PAX5-PML bound to a panel of PAX5
189 Moreover, using affinity chromatography and
gel shift assays, we demonstrate that caspase-7, but not
190 rough chromatin immunoprecipitation (IP) and
gel shift assays, we found that RORalpha in the form of
191 Using
gel shift assays, we have confirmed p16-NFkappaB and gig
192 (103P) does not bind to the speB promoter in
gel shift assays, which correlates with a lack of speB e
193 c and in repR upstream region in PhiCD119 by
gel shift assays.
194 o the sarZ promoter region, as determined by
gel shift assays.
195 split ubiquitin yeast two-hybrid system and
gel shift assays.
196 Binding to the promoters was confirmed by
gel shift assays.
197 identified regulatory elements was tested by
gel shift assays.
198 -containing RNA probes, as determined by RNA
gel shift assays; AUF1p45 did not bind to the RNA probes
199 s promoter DNA upon binding, as evidenced by
gel-shift assays and by recent end-to-end fluorescence e
200 Extent of attenuation determined by native
gel-shift assays and co-transcriptional assembly is corr
201 rring X and M13 ssDNAs (as judged by agarose
gel-shift assays and electron microscopic analysis).
202 cally to its target sequence using both bulk
gel-shift assays and single-molecule methods.
203 Gel-shift assays confirm that PAX-FKHR bind to core enha
204 Accordingly,
gel-shift assays confirmed the binding of CLOCK and BMAL
205 Gel-shift assays confirmed the METTL16-MALAT1 ENE+A inte
206 Gel-shift assays demonstrate BEL5/POTH1 binding specific
207 ChIP, DNA-pull down, and
gel-shift assays demonstrate their direct binding to the
208 Gel-shift assays demonstrated direct binding of Sp1 to t
209 RNA from approximately 25 to 60 min, and RNA
gel-shift assays demonstrated direct binding of Tat to T
210 Gel-shift assays demonstrated the HIV-1 PR is capable of
211 Gel-shift assays indicate the regulation of miR172 by mi
212 ling kinetics were studied systematically by
gel-shift assays performed in the presence or absence of
213 Native
gel-shift assays revealed a shift in radiolabeled MALAT1
214 ChIP and
gel-shift assays revealed an interaction between a speci
215 Gel-shift assays show that the PV, similar to wild-type
216 Gel-shift assays show that upstream stimulatory factor (
217 Gel-shift assays sublocalized two cis-regulatory regions
218 Competitive
gel-shift assays suggested that protein binding depends
219 Sp3 at this GC box was confirmed by in vitro
gel-shift assays using either in vitro translated protei
220 DNase I footprinting and
gel-shift assays with human lung nuclear extract identif
221 dT(n) oligomers (as judged by polyacrylamide
gel-shift assays) and in its binding to the longer natur
222 judged by thermal melts, circular dichroism,
gel-shift assays, and fluorescence quenching.
223 , real-time RT-PCR, transcriptional fusions,
gel-shift assays, DNase I footprinting, and in vitro tra
224 an NDI hexaintercalator that was analyzed by
gel-shift assays, DNase I footprinting, and UV-vis spect
225 In
gel-shift assays, R1A-RARalpha was able to bind to a pan
226 our previous hypothesis, based on extensive
gel-shift assays, that TRBP preferentially binds to site
227 Using native
gel-shift assays, the relative stability of 16 different
228 Using ChIP and DNA
gel-shift assays, we demonstrate that PIF1 directly bind
229 Using
gel-shift assays, we show that recombinant GAPDH binds d
230 B activity, as determined using reporter and
gel-shift assays.
231 r some of our predictions was obtained using
gel-shift assays.
232 We used DNA binding (
gel shift)
assays and Western immunoblots to demonstrate
233 DNA
gel shift binding assays using norA and norB promoters s
234 ro study, which combined RNase footprinting,
gel shift binding assays, and processing assays, to inve
235 g a reporter assay with Escherichia coli and
gel shift binding assays, we also show that the B. burgd
236 ave differences in Rev multimerization using
gel shift binding assays.
237 Finally, dynamic light scattering and
gel shift binding experiments demonstrate that the ED in
238 Gel-shift binding assays confirm that N1 methylation int
239 site-specific chromatin immunopecipitations,
gel shifts,
BIOBASE data, and our model that accurately
240 Remarkably,
gel shift,
chemical cross-linking and gel filtration exp
241 and Pax6, but not NeuroD1, activated MafA in
gel shift,
chromatin immunoprecipitation (ChIP), and tra
242 l validations including luciferase reporter,
gel shift,
chromatin immunoprecipitation, and mRNA expre
243 Investigations using
gel-shift,
chromatin immunoprecipitation and functional
244 Competitive footprinting and
gel shift data demonstrate HlyU's higher affinity as com
245 Footprint and
gel shift data showed that whereas H-NS prevented bindin
246 tion constants (Kd values), determined using
gel shifts,
displayed no substantial differences, and we
247 Gel shift,
DNase I, and chemical cross-linking assays wi
248 Gel shift,
enzyme-linked immunosorbent, and chromatin im
249 has a direct effect on the vpsT promoter, as
gel shift experiments demonstrated that AphA binds to th
250 Gel shift experiments demonstrated that p65Nrf1 binds th
251 Gel shift experiments demonstrated that PapX binds direc
252 Gel shift experiments failed to show direct binding of S
253 Reporter gene assays and
gel shift experiments indicated that AP-1 transcription
254 Biotin-RNA pulldown, UV-crosslinking and
gel shift experiments indicated that MYF5 was capable of
255 Gel shift experiments show that binding of the FlhDC com
256 Gel shift experiments showed that A-ZIP53 can inhibit th
257 Gel shift experiments showed that TFB recruitment to the
258 DNA
gel shift experiments suggested that ppk expression migh
259 Fluorescent
gel shift experiments were used to quantify the binding
260 a combination of transcriptional profiling,
gel shift experiments, and the analysis of lacZ fusions.
261 imolecular fluorescence complementation, and
gel shift experiments, we demonstrate a physical interac
262 Using in vivo RNA-protein crosslinking and
gel shift experiments, we reveal that yUtp23/hUTP23 make
263 genBA promoter region contains a cre box and
gel-shift experiments demonstrated that the operon is un
264 NMR chemical shift perturbations and
gel-shift experiments performed with CedA confirm that t
265 Gel-shift experiments show that CRX, OTX2, and RORbeta c
266 Gel-shift experiments show that mapped cis-elements are
267 Gel-shift experiments showed that both SUD-C and SUD-MC
268 Using DNase I footprinting and
gel-shift experiments, we identified two CodY-binding re
269 Various experimental approaches, including
gel shift,
fluorescence anisotropy, light scattering, an
270 Results from
gel shift,
footprint, toeprint and in vitro translation
271 Gel shift for TNFalpha-induced hiNOS NF-kappaB activatio
272 Using
gel shift,
glutathione S-transferase pull-down and cell-
273 TRPM2 N terminus was demonstrated utilizing
gel shift,
immunoprecipitation, biotinylated CaM overlay
274 CLK1 induces a unique
gel shift in SRSF1 that is not the result of enhanced Ar
275 serovar Typhimurium was characterized using
gel shift,
intrinsic tryptophan fluorescence, circular d
276 Native
gel shift mobility assays and isothermal titration calor
277 Gel-shift mobility assays demonstrated that BrrA bound t
278 d CcrB but not CcrA was shown to mediate the
gel shift of chromosomal target integration sequences (a
279 Using
gel shifts of microtubule-associated protein 1 light cha
280 Further results showed that H-NS
gel shifts other PhoP regulon promoters, indicating that
281 Electrophoretic mobility shift assay
gel shift patterns suggested that additional transcripti
282 s RNA molecules at multiple sites, producing
gel-shift patterns that suggest that each protein binds
283 te or bind to the AhR using a combination of
gel shift,
reporter gene, and competitive receptor bindi
284 Gel shift,
spectroscopic and yeast three-hybrid assays s
285 ndensation, as monitored by cGAMP formation,
gel shift,
spin-down, and turbidity assays, as well as t
286 of DNA binding is shown both in vitro, with
gel shift studies and DNA binding assays, and in vivo at
287 Chromatin immunoprecipitation and
gel shift studies indicated that SP1 interacted with the
288 Gel shift studies revealed that CsrA binds at two sites
289 Additional
gel shift studies with SarR and SarA suggest that these
290 Gel shift studies, including with recombinant protein, r
291 Gel-shift studies of M.RsrI binding to DNA suggested tha
292 btle but important differences from in vitro
gel-shift studies of Rop function are evident.
293 ally, a combination of promoter analyses and
gel-shift studies suggest that KLF15 can inhibit GATA4 a
294 A
gel shift study with monomeric ChxR supports that dimeri
295 Gel-shift,
super-shift and chromatin immunoprecipitation
296 Gel shift,
supershift, and chromatin immunoprecipitation
297 Gel shift/
supershift experiments and chromatin immunopre
298 e for the eIF4a3-SECIS interaction using RNA
gel shifts,
surface plasmon resonance and enzymatic foot
299 phorylation of multiple sites and promoted a
gel shift that was due in part to phosphorylation of Ser
300 Gel shifts using membrane fractions showed that AmpR bin