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 RNA
gel shift analyses established that AUF1 (hnRNP D) binds
9 In vitro immunoprecipitation assays and
gel shift analyses have further demonstrated that purifi
10 In this report, near equilibrium binding and
gel shift analyses showed that A3G assembly and disassem
11 iatum by radioimmunoassay, Western blot, and
gel shift analyses, respectively.
12 Gel-shift analyses showed that both the native HIF-1alph
13 al and translational fusions, and performing
gel-shift analyses, we identified 40 genes in six operon
14 Gel shift analysis and chloramphenicol acetyl transferas
15 ike prior to receptor engagement, but trimer
gel shift analysis and slow kinetics of shedding induced
16 While
gel shift analysis confirmed NF-Y binding to both sites,
17 utations in the promoter region of pilA1 and
gel shift analysis demonstrated that both sigma(54) and
18 Electrophoretic
gel shift analysis demonstrated that HbrL binds the prom
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 By quantitative
gel shift analysis, we demonstrate that although the C t
31 However, using
gel shift analysis, we demonstrate that IE86 efficiently
32 trometry, chromatin immunoprecipitation, and
gel shift analysis.
33 in the presence of TO901317 was confirmed by
gel shift analysis.
34 Gel-shift analysis demonstrates that glucocorticoid/andr
35 Gel-shift analysis showed that SDF1alpha enhances DNA bi
36 DNA damage, including BRCA1 and PARP2, with
gel-shift analysis showing that SOG1 can physically asso
37 Gel-shift analysis suggests that Spi-C, ectopically expr
38 We used
gel-shift analysis to refine the Sox2 region bound by Ar
39 An in vitro
gel-shift analysis was used to show that the mutation in
40 als as revealed by Western blot analysis and
Gel-shift analysis, respectively.
41 By
gel-shift analysis, the corresponding oligonucleotide pr
42 Using
gel-shift analysis, we found that the two major forms of
43 ce motif 5'-GTTGCA-3', were identified using
gel-shift analysis.
44 Gel shift and ChIP experiments revealed a novel CTCF/BOR
45 omoter using a luciferase reporter assay and
gel shift and ChIP studies.
46 imaging, effects on DNA binding measured by
gel shift and chromatin immunoprecipitation (ChIP) assay
47 Using
gel shift and chromatin immunoprecipitation (ChIP) assay
48 ced increases in Smad 1/5/8 levels; further,
gel shift and chromatin immunoprecipitation analyses dem
49 Gel shift and chromatin immunoprecipitation assays confi
50 Gel shift and chromatin immunoprecipitation assays confi
51 itical for the transcriptional activity, and
gel shift and chromatin immunoprecipitation assays confi
52 pression at the protein and mRNA levels, and
gel shift and chromatin immunoprecipitation assays furth
53 Gel shift and chromatin immunoprecipitation assays ident
54 Gel shift and chromatin immunoprecipitation assays revea
55 As confirmed by
gel shift and chromatin immunoprecipitation assays, ATRA
56 Gel shift and chromatin immunoprecipitation studies demo
57 However,
gel shift and competitive binding assays indicated that
58 Using
gel shift and DNase I footprinting assays, we found that
59 intergenic promoter region as determined by
gel shift and DNase I footprinting assays.
60 Using
gel shift and enzymatic footprinting assays and atomic f
61 ing or the NCp7/RNA interaction monitored by
gel shift and fluorescence.
62 In this study, we show by
gel shift and footprint assays with the C-terminal DNA-b
63 The results from
gel shift and footprint studies demonstrate that tight b
64 This element bound HIF-1 in the
gel shift and in in-cell luciferase assays.
65 Using
gel shift and in vitro transcription assays we showed th
66 Gel shift and luciferase assays indicate that both varia
67 Gel shift and luciferase assays reveal a strong bias for
68 B-dependent transporter FhuA, as assessed by
gel shift and mass spectrometry assays.
69 Gel shift and mass spectrometry experiments confirmed th
70 n blot analysis, and NF-kappaB activation by
gel shift and reporter assays.
71 Using a previously reported in vitro mRNA
gel shift and stability assay, antibodies to the GR bloc
72 Gel shift and supershift analyses, as well as ChIP, show
73 DI RNA cis-replication signal, (ii) show by
gel shift and UV-cross-linking analyses that cellular pr
74 nding to the MKP1 gene promoter, as shown by
gel shifting and chromatin immunoprecipitation assays.
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 In silico analysis,
gel shift,
and in vitro reporter assays were performed t
86 Chromatin immunoprecipitation,
gel shift,
and luciferase assays confirmed LEF1 occupanc
87 Transcription assays,
gel shifting,
and chromatin immunoprecipitation (ChIP) a
88 Transactivation,
gel-shift,
and chromatin immunoprecipitation assays indi
89 Promoter truncation, point mutation,
gel-shift,
and protein-DNA ELISA analysis showed that tr
90 all chaperone activities, as demonstrated by
gel shift annealing assays, decreasing in the order HIV-
91 Gel-shift annealing and sedimentation assays were used t
92 ve polyacrylamide gel electrophoresis (PAGE)
gel shifts as well as affinity pull-down assays implicat
93 hr421/Ser424), rpS6 (Ser235/236) and 4E-BP1 (
gel shift),
as well as deficits in total eEF2 accretion.
94 Using electrophoretic mobility
gel shift assay (EMSA)-based competition assays, the kl-
95 We demonstrate by a
gel shift assay a strong and specific affinity of recomb
96 Using native polyacrylamide
gel shift assay and negative-stain EM, we found that the
97 Gel shift assay and Western blot analyses showed dose-de
98 A leucine zipper swap:
gel shift assay demonstrates that C/EBPalpha zippers wit
99 emia homeobox 3 (TLX3) TF was confirmed with
gel shift assay experiments.
100 ycol derivatives (MPEG) was measured using a
gel shift assay of tryptic fragments.
101 Gel shift assay showed that Osx bound to the Satb2 promo
102 Gel shift assay showed that Osx bound to the VEGF promot
103 In parallel, a
gel shift assay showed that SuhB forms a tight complex w
104 Computer analysis and
gel shift assay showed that the -1132 and -879 region in
105 d ubiquitination, and allowed DNA-binding in
gel shift assay similar to wild-type Runx1.
106 Also the
gel shift assay suggested that NFkappaB p65 is responsib
107 The
gel shift assay supported the fact that there exists an
108 enhancer that strongly bind C/EBPalpha in a
gel shift assay, and interaction with endogenous C/EBPal
109 Using the
gel shift assay, chemical probing and dimethyl sulfate (
110 In a
gel shift assay, gefitinib led to decreased retardation
111 to bind DNA either in vitro, as assessed by
gel shift assay, or in vivo, as shown by transactivation
112 Using a
gel shift assay, we identified a cytoplasmic RNA-binding
113 d DNA-protein binding assay and conventional
gel shift assay, we successfully identified a ZBTB20-bin
114 d the binding domain of enzyme, we have used
gel shift assay.
115 re consistent with data from the traditional
gel shift assay.
116 -1 binds to the ATF3 promoter as assessed by
gel shift assay.
117 gion of the sarX promoter as demonstrated by
gel shift assay.
118 esponding to the proximal VEGF promoter in a
gel shift assay.
119 ally to the IL-2 ARE with high affinity in a
gel shift assay.
120 with deltaEF1 for binding at these sites in
gel shift assay.
121 nd activator protein 1 in polarized cells by
gel shift assay.
122 tivity in DC nuclear protein was detected by
gel shifting assay.
123 The
gel-shift assay (EMSA) revealed that the recombinant Gly
124 Binding was evaluated by
gel-shift assay and affinity by frontal affinity chromat
125 dimensions were confirmed using a calibrated
gel-shift assay and atomic force microscopy, and their i
126 Gel-shift assay experiments confirmed that pioglitazone
127 A
gel-shift assay indicated that the endogenous R1 protein
128 overall results of transcript analysis, RNA
gel-shift assay, and transgenic expression, for the firs
129 e found that Fis-DNA binding, as assessed by
gel-shift assay, changed in accordance with our expectat
130 assay, chromatin immunoprecipitation assay,
gel-shift assay, coimmunoprecipitation, and western blot
131 In the
gel-shift assay, Glu1 mutants K81E and T82Y failed to bi
132 Using
gel-shift assay, we showed that AML1-ETO and AML1-MTG16
133 4 protein could bind RNA as evidenced by the
gel-shift assay.
134 binding activity by electrophoretic mobility
gel shift assays (EMSA) and mitochondrial damage by JC-1
135 Gel shift assays also demonstrated that Sp1 interacted w
136 Gel shift assays and affinity pull-down followed by mass
137 ability, and markedly reduced DNA binding in
gel shift assays and as assessed by chromatin immunoprec
138 Gel shift assays and chromatin immunoprecipitation assay
139 Gel shift assays and chromatin immunoprecipitation exper
140 Gel shift assays and site-directed mutagenesis allowed t
141 site decreased both NFI binding affinity in
gel shift assays and stimulation of SV40 promoter activi
142 of NF-kappaB p50/p65 DNA-binding activity in
gel shift assays and the activity of an NF-kappaB-respon
143 binding to a kappaB oligonucleotide probe in
gel shift assays and to the MMP-9 promoter in chromatin
144 Gel shift assays and transfection with wild-type and mut
145 Gel shift assays and UV cross-linking experiments identi
146 Gel shift assays confirmed high affinity binding of CsrA
147 Gel shift assays confirmed that both V. cholerae FadR an
148 Chromatin immunoprecipitation and
gel shift assays confirmed that Kar4 binds to regulatory
149 Gel shift assays demonstrate clear binding between SRF a
150 Gel shift assays demonstrated nonspecific binding of pur
151 Gel shift assays demonstrated that MrpJ and another para
152 Gel shift assays demonstrated that NF-kappaB inhibits th
153 Electromobility
gel shift assays demonstrated the activation of chondroc
154 Promoter reporter and
gel shift assays determined that the AirR response regul
155 Nonetheless,
gel shift assays did not reveal direct binding between R
156 sults from chromatin immunoprecipitation and
gel shift assays further confirmed the functional bindin
157 Gel shift assays identified a conserved non-canonical E-
158 Gel shift assays indicate that in isolation, nsp10 binds
159 Gel shift assays indicated that these DNA-binding sites
160 Gel shift assays on CP2 mutants confirmed that the CP2 m
161 Purified VirR was used in DNA
gel shift assays on target promoters and VirR : promoter
162 Gel shift assays performed in the presence of core- and
163 Gel shift assays revealed binding of HuR and TTP to rat
164 Gel shift assays revealed decreased protein binding to t
165 Gel shift assays revealed that CAR competes with HNF-4 f
166 Our
gel shift assays revealed that YhcR binds to the promote
167 Gel shift assays show binding of wBmxR1 to regions upstr
168 RNA
gel shift assays show that GLD-1 binds the predicted sit
169 RNA
gel shift assays showed that a mutant SRSF2 derivative b
170 nditionally immortalized human podocytes and
gel shift assays showed that LMX1B recognizes AT-rich bi
171 Gel shift assays showed that the region surrounding the
172 In contrast, competition experiments using
gel shift assays suggest that RAGE interaction with AGE
173 Gel shift assays suggest that XBP-1(S) binding occurs th
174 ence, chemical probing, optical melting, and
gel shift assays to characterize the structure of a seri
175 Gel shift assays using a bacterially expressed PUM2 RNA
176 Accordingly,
gel shift assays using both linear and circular DNA show
177 We performed
gel shift assays using nuclear extract from testes, brai
178 Gel shift assays using transfected myoblast nuclear extr
179 Importantly,
gel shift assays verified Tpx as a target in the intact
180 Electrophoretic mobility
gel shift assays were performed to determine the activat
181 Gel shift assays were performed with methylated or unmet
182 Gel shift assays were used to characterize bioY1_LL and
183 majority of the protease domain (H6.Gag.3h),
gel shift assays were used to monitor the annealing of t
184 Gel shift assays with model RNA substrates now show that
185 by chromatin immunoprecipitation in vivo and
gel shift assays with purified glutathione S-transferase
186 In vitro
gel shift assays, competition assays, and immunoprecipit
187 These data were confirmed in
gel shift assays, providing direct evidence that Pneumoc
188 Using electrophoretic mobility
gel shift assays, size-exclusion chromatography, and ele
189 egions of norB and tet38 was demonstrated by
gel shift assays, suggesting that MgrA was an indirect r
190 domain bind to a 55-bp AdMLP DNA fragment in
gel shift assays, suggesting that protein-DNA interactio
191 In the present studies, we found, by
gel shift assays, that PAX5-PML bound to a panel of PAX5
192 Using
gel shift assays, we have confirmed p16-NFkappaB and gig
193 (103P) does not bind to the speB promoter in
gel shift assays, which correlates with a lack of speB e
194 c and in repR upstream region in PhiCD119 by
gel shift assays.
195 o the sarZ promoter region, as determined by
gel shift assays.
196 split ubiquitin yeast two-hybrid system and
gel shift assays.
197 Binding to the promoters was confirmed by
gel shift assays.
198 identified regulatory elements was tested by
gel shift assays.
199 -containing RNA probes, as determined by RNA
gel shift assays; AUF1p45 did not bind to the RNA probes
200 s promoter DNA upon binding, as evidenced by
gel-shift assays and by recent end-to-end fluorescence e
201 Extent of attenuation determined by native
gel-shift assays and co-transcriptional assembly is corr
202 rring X and M13 ssDNAs (as judged by agarose
gel-shift assays and electron microscopic analysis).
203 cally to its target sequence using both bulk
gel-shift assays and single-molecule methods.
204 Gel-shift assays confirm that PAX-FKHR bind to core enha
205 Accordingly,
gel-shift assays confirmed the binding of CLOCK and BMAL
206 Gel-shift assays confirmed the METTL16-MALAT1 ENE+A inte
207 Gel-shift assays demonstrate BEL5/POTH1 binding specific
208 ChIP, DNA-pull down, and
gel-shift assays demonstrate their direct binding to the
209 Gel-shift assays demonstrated direct binding of Sp1 to t
210 RNA from approximately 25 to 60 min, and RNA
gel-shift assays demonstrated direct binding of Tat to T
211 Gel-shift assays demonstrated the HIV-1 PR is capable of
212 Gel-shift assays indicate the regulation of miR172 by mi
213 ling kinetics were studied systematically by
gel-shift assays performed in the presence or absence of
214 Native
gel-shift assays revealed a shift in radiolabeled MALAT1
215 ChIP and
gel-shift assays revealed an interaction between a speci
216 Gel-shift assays show that the PV, similar to wild-type
217 Gel-shift assays show that upstream stimulatory factor (
218 Gel-shift assays sublocalized two cis-regulatory regions
219 Competitive
gel-shift assays suggested that protein binding depends
220 Sp3 at this GC box was confirmed by in vitro
gel-shift assays using either in vitro translated protei
221 DNase I footprinting and
gel-shift assays with human lung nuclear extract identif
222 dT(n) oligomers (as judged by polyacrylamide
gel-shift assays) and in its binding to the longer natur
223 judged by thermal melts, circular dichroism,
gel-shift assays, and fluorescence quenching.
224 , real-time RT-PCR, transcriptional fusions,
gel-shift assays, DNase I footprinting, and in vitro tra
225 an NDI hexaintercalator that was analyzed by
gel-shift assays, DNase I footprinting, and UV-vis spect
226 In
gel-shift assays, R1A-RARalpha was able to bind to a pan
227 our previous hypothesis, based on extensive
gel-shift assays, that TRBP preferentially binds to site
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 In this report,
gel shift experiments were conducted to investigate the
260 Fluorescent
gel shift experiments were used to quantify the binding
261 a combination of transcriptional profiling,
gel shift experiments, and the analysis of lacZ fusions.
262 imolecular fluorescence complementation, and
gel shift experiments, we demonstrate a physical interac
263 Using in vivo RNA-protein crosslinking and
gel shift experiments, we reveal that yUtp23/hUTP23 make
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 of DNA binding is shown both in vitro, with
gel shift studies and DNA binding assays, and in vivo at
286 Gel shift studies revealed that CsrA binds at two sites
287 Additional
gel shift studies with SarR and SarA suggest that these
288 Gel shift studies, including with recombinant protein, r
289 Gel-shift studies of M.RsrI binding to DNA suggested tha
290 btle but important differences from in vitro
gel-shift studies of Rop function are evident.
291 ally, a combination of promoter analyses and
gel-shift studies suggest that KLF15 can inhibit GATA4 a
292 A
gel shift study with monomeric ChxR supports that dimeri
293 Gel-shift,
super-shift and chromatin immunoprecipitation
294 Gel shift,
supershift assay, and ChIP analysis demonstra
295 Gel shift,
supershift, and chromatin immunoprecipitation
296 Gel shift/
supershift experiments and chromatin immunopre
297 e for the eIF4a3-SECIS interaction using RNA
gel shifts,
surface plasmon resonance and enzymatic foot
298 phorylation of multiple sites and promoted a
gel shift that was due in part to phosphorylation of Ser
299 Gel shifts using membrane fractions showed that AmpR bin
300 Using in vitro RNA
gel shifts,
we have demonstrated that the CCAAT enhancer