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1                                              EMSA also shows that positions 3 and 18 are important fo
2                                              EMSA analyses and data obtained from binding-site mutati
3                                              EMSA analyses identified two E-box motifs as the minimal
4                                              EMSA analyses showed that FGF2, but not VEGF, stimulated
5                                              EMSA analysis and reporter gene assays revealed that NFA
6                                              EMSA analysis confirmed binding of Sox18 to a canonical
7                                              EMSA analysis from Bryo-1-treated MonoMac6 cells showed
8                                              EMSA analysis using nuclear extracts from either A549 ce
9                                              EMSA analysis using nuclear extracts from IMCD cells sho
10                                              EMSA and ChIP assays demonstrate that the risk allele di
11                                              EMSA and ChIP assays further confirmed that upon P2Y2R a
12                                              EMSA and DNA-binding protein affinity purification analy
13                                              EMSA and FISH analyses suggest that these are genuine Su
14                                              EMSA and functional studies indicated two function-coope
15                                              EMSA and inhibitor studies show that HOSCN up-regulation
16                                              EMSA and missing contact point analysis revealed that FB
17                                              EMSA and supershift EMSA (with the use of specific antib
18                                              EMSA and supershift experiments indicated binding of USF
19                                              EMSA assays revealed that both binding sites are require
20                                              EMSA competition studies indicate that NF-Y binds with a
21                                              EMSA experiments showed increased HIF-1alpha binding to
22                                              EMSA results show that hRPA binds to a 58-mer that inclu
23                                              EMSA results showed that both cMYC and P53 bind to cis-o
24                                              EMSA revealed a concurrent decrease in consensus binding
25                                              EMSA revealed that 1,25(OH)(2)D(3) markedly inhibited nu
26                                              EMSA revealed that sulphite, a product of the reaction c
27                                              EMSA showed that hADAR2-D requires duplex RNA and is sen
28                                              EMSA showed the specific binding of Nanog to each of the
29                                              EMSA studies demonstrated that Sp1 bound to two putative
30                                              EMSA suggested that EAPP and R1 competed with Sp1 for bi
31                                              EMSA using this extract revealed formation of a C/EBPzet
32                                              EMSA, ChIP assay and real-time PCR analyses suggest CaWR
33                                              EMSA, ITC, and NMR studies show that PTB RRMs 1 and 2 bi
34                                              EMSA, luciferase reporter gene experiments, Western blot
35                                              EMSAs and DNase I footprinting showed that the [4Fe-4S]
36                                              EMSAs and supershift assays identified complexes consist
37                                              EMSAs indicated that rs8023462 and rs6495309 bind nuclea
38                                              EMSAs using a combination of mutational and anti-Met ant
39                                              EMSAs with splenic B cell extracts directly demonstrated
40                                              EMSAs, chromatin immunoprecipitation assays, and small i
41  of HIF as demonstrated by the following: 1) EMSA; 2) transfection studies with IL-8 promoter reporte
42 echanisms underlying the induction of IL-31, EMSAs, reporter gene assays, and small interfering RNA-b
43                                 Accordingly, EMSA experiments demonstrated that either the cold canon
44                                 In addition, EMSA demonstrated that Bryo-1-mediated induction of RANT
45                                Additionally, EMSAs and supershift assays showed that ER-alpha binds t
46 se binding sites did not significantly alter EMSA shifting patterns on longer templates but did on sh
47                                           An EMSA confirmed the p50/p50 and/or p65/p50 complex (s) bo
48 assay, chromatin immunoprecipitation, and an EMSA revealed that STAT3 activated caspase-3 However, ca
49 d by bioinformatic and biochemical analyses (EMSA and FBA), was further supported by TNT and promoter
50 electrophoretic gel mobility shift analysis (EMSA) provide further evidence for a direct interaction
51                        Promoter analysis and EMSA revealed that copper stimulates the Atox1 binding t
52                Luciferase reporter assay and EMSA data strongly suggest that ALMS1 transcription is r
53        Transcriptional activation assays and EMSA were used to confirm the yeast-one hybrid results.
54 l regions of these receptors, cell-based and EMSA studies have suggested that these molecules can reg
55 kappaB were measured by Western-blotting and EMSA; miRNAs were measured by q-PCR in the cerebellum.
56 te, deoxycholate, and chenodeoxycholate, and EMSA showed that deoxycholate is able to abolish the for
57                                     ChIP and EMSA results demonstrated binding of WT1 to the CDC73 pr
58     Chromatin immunoprecipitation (ChIP) and EMSA identified a ZBP-89-binding site in the proximal pr
59 f the CCR7 gene, using luciferase, ChIP, and EMSA.
60            Chromatin immunoprecipitation and EMSA experiments demonstrated that S-SOX5 associates wit
61            Chromatin immunoprecipitation and EMSA revealed that STAT3 binds to the Wnt5a gene promote
62      Using chromatin immunoprecipitation and EMSA, we found that STAT3 binds with low affinity to the
63 ermined by chromatin immunoprecipitation and EMSA.
64                Site-directed mutagenesis and EMSA were used to identify a YY1-binding site at +25 in
65                       Further mutational and EMSA analysis helped identify a minimal 37-bp region tha
66 chromatin immunoprecipitation (ChIP)-PCR and EMSA were used to identify regulators of phase transitio
67 as confirmed by independent methods (PCR and EMSA).
68 -protein interaction analysis, ChIP-qPCR and EMSA were performed and suggested that HSI2 and HSL1 can
69                      Luciferase reporter and EMSA assays revealed that C/EBPepsilon binds to the regu
70                         Deletion studies and EMSA revealed 2 elements in the MIF promoter that were r
71   Both ChIP assays with canine OB tissue and EMSA experiments with the human Th proximal promoter did
72 us studies, using transient transfection and EMSA experiments, implicated involvement of the transcri
73 ive vitamin D response elements (VDREs), and EMSA confirmed that the VDRE at -312 (a DR4-type VDRE) c
74  characterised by sedimentation velocity and EMSA using native and mutant promoter sequences.
75 sing molecular biological approaches such as EMSA, supershift EMSA, ChIP, re-ChIP, and promoter-repor
76                                           As EMSAs can be performed using partially purified or cell
77 myc IRES in filter binding assays as well as EMSAs.
78        Electrophoretic mobility shift assay (EMSA) analyses were performed to confirm the results of
79        Electrophoretic mobility shift assay (EMSA) analysis disclosed that SarR binds more avidly to
80        Electrophoretic mobility shift assay (EMSA) analysis of nuclear extracts prepared from ultravi
81        Electrophoretic mobility shift assay (EMSA) analysis showed that c-Jun and c-Fos bind to the A
82 med by electrophoretic mobility shift assay (EMSA) analysis, which also suggested that binding by the
83 ys and electrophoretic mobility shift assay (EMSA) analysis.
84 we use electrophoretic mobility shift assay (EMSA) and atomic force microscopy (AFM) to show that Ver
85  Using electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP), we found
86        Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation analysis demonst
87  of an electrophoretic mobility-shift assay (EMSA) and confocal microscopy.
88  by an electrophoretic mobility shift assay (EMSA) and DNase I protection.
89  Using electrophoretic mobility shift assay (EMSA) and isothermal titration calorimetry (ITC), we fou
90 ned by electrophoresis mobility shift assay (EMSA) and phosphorylation of c-Fos and activation of ERK
91        Electrophoresis mobility shift assay (EMSA) experiments showed that Hoechst33342 binds to H369
92        Electrophoretic mobility shift assay (EMSA) experiments using an IE62 fragment containing the
93 D) and electrophoretic mobility shift assay (EMSA) experiments were used to show that hRPA can bind a
94 es and electrophoretic mobility shift assay (EMSA) for our in vitro studies, we demonstrated that bot
95 he gel electrophoresis mobility shift assay (EMSA) is used to detect protein complexes with nucleic a
96        Electrophoretic mobility shift assay (EMSA) revealed that PMA induced binding of c-jun and GA-
97                         The gel-shift assay (EMSA) revealed that the recombinant GlyR3 bound specific
98        Electrophoretic mobility shift assay (EMSA) showed that Mn exposure increased binding of IRP t
99        Electrophoretic mobility shift assay (EMSA) showed that PDGF-BB stimulated protein binding to
100        Electrophoresis mobility shift assay (EMSA) studies that demonstrate physical interactions bet
101 and an electrophoretic mobility shift assay (EMSA) suggested that SknR functions as a negative regula
102 ted an electrophoretic mobility shift assay (EMSA) to isolate genomic DNA fragments that bind the arc
103 formed electrophoretic mobility shift assay (EMSA) using wild-type sequence deriving from Cxcl2 gene
104 econd, electrophoretic mobility shift assay (EMSA) was used to demonstrate the direct binding of MYB4
105 s, and electrophoretic mobility shift assay (EMSA) was used to demonstrate transcription factor bindi
106        Electrophoretic mobility shift assay (EMSA) was used to identify SNPs that had the potential t
107 es for electrophoretic mobility shift assay (EMSA) with different fragments of the Abeta peptide.
108  in an electrophoretic mobility shift assay (EMSA), and a Mur binding site was identified in the -55
109 erase, electrophoretic mobility shift assay (EMSA), and ChIP analysis revealed that Sox9 represses Cc
110 ction, electrophoretic mobility shift assay (EMSA), and chromatin immunoprecipitation (ChIP).
111 ChIP), electrophoretic mobility shift assay (EMSA), and luciferase assays reveal that p53 binds and a
112 formed electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation (ChIP), promoter cl
113  Using electrophoretic mobility shift assay (EMSA), purified LsrR and CRP proteins were shown to bind
114 tro by electrophoretic mobility shift assay (EMSA), revealed that a 14-bp sequence (CGTATCATAAGTAA; t
115        Electrophoretic mobility shift assay (EMSA), supershift EMSA, Western blot analysis, and immun
116 sed by electrophoretic mobility shift assay (EMSA), the mutations did not disrupt mLANA's ability to
117 D) and electrophoretic mobility shift assay (EMSA), we have shown that the guanine-rich (G-rich) stra
118 zed by electrophoretic mobility shift assay (EMSA), with in vitro-translated proteins and radiolabele
119 ng electrophoretic mobility gel shift assay (EMSA)-based competition assays, the kl-TSS was found to
120 ), and Electrophoretic Mobility Shift Assay (EMSA).
121 ted by electrophoretic mobility shift assay (EMSA).
122 n vitro electophoretic mobility shift assay (EMSA).
123 ECs by electrophoretic mobility shift assay (EMSA).
124 ed via electrophoretic mobility shift assay (EMSA).
125  using electrophoretic mobility shift assay (EMSA).
126 by the electrophoretic mobility shift assay (EMSA).
127 ing an electrophoretic mobility shift assay (EMSA).
128                 In addition, reporter assay, EMSA, chromatin immunoprecipitation and RNA interference
129       Electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays de
130  Both electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays de
131 ed by electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation assays (ChIP).
132       Electrophoretic Mobility Shift Assays (EMSA) confirmed that the protein encoded by this allele
133       Electrophoretic mobility shift assays (EMSA) demonstrate that purified LasR protein binds direc
134 ) and electrophoretic mobility shift assays (EMSA) experiments showed that ER81 bound directly to a c
135       Electrophoretic mobility shift assays (EMSA) indicated that a cellular factor binds specificall
136 r and electrophoretic mobility shift assays (EMSA) showed that POU3F2 induces TRIM8 expression by bin
137 s work, we use electromobility shift assays (EMSA) to show that mutations in the NRE and RRM1 affect
138 g and electrophoretic mobility shift assays (EMSA) using bovine retinal nuclear extract demonstrate t
139       Electrophoretic mobility shift assays (EMSA) with mutant AtSPL14 DNA-binding domain proteins in
140 ed to electrophoretic mobility shift assays (EMSA) with recombinant HP0166-His(6) or a mutated respon
141 says, electrophoretic mobility shift assays (EMSA), and RNA expression by RT-PCR were used to examine
142 sR in electrophoretic mobility shift assays (EMSA), we localized binding to a sequence with partial d
143 oying electrophoretic mobility shift assays (EMSA).
144 ed by electrophoretic mobility shift assays (EMSA).
145 ed by electrophoretic mobility shift assays (EMSA).
146 l and electrophoretic mobility shift assays (EMSA).
147 ed by electrophoretic mobility shift assays (EMSA).
148                Electromobility shift assays (EMSAs) and competition EMSAs demonstrated binding of pro
149 ormed electrophoretic mobility shift assays (EMSAs) and demonstrate that nucleotide substitutions wit
150 ally, electrophoretic mobility shift assays (EMSAs) and DNase I footprinting were used to confirm a b
151       Electrophoretic mobility shift assays (EMSAs) are commonly used to analyze nucleic acid-protein
152       Electrophoretic mobility shift assays (EMSAs) confirmed a destabilizing effect of fructose-1,6-
153       Electrophoretic mobility shift assays (EMSAs) confirmed binding of Rep to off-target RBSs.
154 , and electrophoretic mobility shift assays (EMSAs) confirmed compromised affinities of MepR F27L and
155 ntly, electrophoretic mobility shift assays (EMSAs) determined that a recombinant MucR protein binds
156 ghput electrophoretic mobility shift assays (EMSAs) for identification and characterization of molecu
157       Electrophoretic mobility shift assays (EMSAs) identified positive DNA-protein interaction at th
158       Electrophoretic mobility shift assays (EMSAs) identified sequence-specific nuclear protein bind
159 inity electrophoretic mobility shift assays (EMSAs) in a high-throughput format suitable for small vo
160  PTE, electrophoretic mobility shift assays (EMSAs) indicated that eukaryotic translation initiation
161       Electrophoretic mobility shift assays (EMSAs) revealed that the overexpressed and purified OhrR
162       Electrophoretic mobility shift assays (EMSAs) revealed three classes of GATA3 mutations: those
163 s and electrophoretic mobility shift assays (EMSAs) showed that TC-EC contact mediated p38 phosphoryl
164 s and electrophoretic mobility shift assays (EMSAs) to elucidate a mechanism for EutR gene regulation
165 vitro electrophoretic mobility shift assays (EMSAs) using synthetic DNA substrates and purified RPA d
166       Electrophoretic mobility shift assays (EMSAs) were performed to investigate whether nuclear pro
167       Electrophoretic mobility shift assays (EMSAs) were used to prove that H. ducreyi CpxR interacte
168 ed by electrophoretic mobility shift assays (EMSAs) with Jurkat T-cell nuclear extracts.
169 ed by electrophoretic mobility shift assays (EMSAs) with the purified NmoR protein.
170 teps, electrophoretic mobility shift assays (EMSAs), and mass spectrometry analyses of proteins bound
171 luded electrophoretic mobility shift assays (EMSAs), filter binding assays (FBAs), coupled in vitro t
172 using electrophoretic mobility shift assays (EMSAs), the IHFalpha-IHFbeta protein complex was shown t
173 is in electrophoresis mobility shift assays (EMSAs), we demonstrated that the c-AMP-responsive elemen
174 g and electrophoretic mobility shift assays (EMSAs).
175                By employing reporter assays, EMSA, inhibition studies, bisulphite sequencing, ChIP-Se
176 experiments (quantitative PCR, Western blot, EMSA) or genome-wide assays (RNA-sequencing, ChIP-sequen
177              Studies using Western blotting, EMSA, and functional analysis indicated that the selecti
178 ectively, the results from Western blotting, EMSAs, and DNA footprinting reactions lead to the conclu
179 beta to the C/EBPbeta motif was confirmed by EMSA and ChIP analyses.
180  these regulatory elements were confirmed by EMSA and the chromatin immunoprecipitation approach, res
181 ind the hZip1 core promoter was confirmed by EMSA, GelSupershift and ChIP assays.
182                            We demonstrate by EMSA that nitration of p53 by ONOO(-) (300 x 10(-6) M) a
183 in this 245 bp 5' region was demonstrated by EMSA and supershift with anti-NFAT antibodies.
184  to HREs in FLAP promoter as demonstrated by EMSA with nuclear extracts.
185 th the GAS promoter was also demonstrated by EMSA.
186 he binding of enzymes to DNA was detected by EMSA, steady-state, and stopped-flow fluorimetry.
187 e DNA binding activity of c-Jun, detected by EMSA.
188 ncreases in nuclear NF-kappaB as detected by EMSA.
189 oth in vitro as and in vivo as determined by EMSA and chromatin immunoprecipitation, respectively.
190 pressed gene transcription, as determined by EMSA and luciferase assays.
191 IgG IC-induced lung injury, as determined by EMSA.
192  patch maintained the ability to bind DNA by EMSA.
193 he putative Mur box was further evaluated by EMSA employing oligonucleotides in which the consensus n
194 re detailed mutagenesis analysis followed by EMSA and ChIP identified Sp1 sites in positions -668/-65
195 REB1 alone or with UNG2 or OGG1, followed by EMSA.
196  binding site on Dspp promoter were found by EMSA.
197 of Casp1, was determined to be functional by EMSA and supershift analysis.
198  detectable tRNA(Pyl) binding as measured by EMSA, but not catalytic activity.
199 were examined in ischemic cerebral tissue by EMSA and Western blots.
200 inding sites were biochemically validated by EMSA-FRET analysis and validated in vivo by ChIP-seq dat
201 t1 protein to these elements was verified by EMSA and ChIP.
202 ite that binds Foxc1a and Foxc1b in vitro by EMSA and in vivo using ChIP.
203 nts in the EBF1 promoter was demonstrated by EMSAs and chromatin immunoprecipitation analysis, sugges
204 tes within the Gpr49 gene locus, and show by EMSAs that GATA-6 can bind to these sites in vitro.
205 ficity of binding ascertained by competition EMSA.
206                                  Competition EMSAs and supershift analyses with HsrA-enriched protein
207 obility shift assays (EMSAs) and competition EMSAs demonstrated binding of protein(s) in the cultured
208         DNase I footprinting and competitive EMSA showed the binding site to be an 18-bp palindromic
209                          Rather, competitive EMSA using known binding sequences for the orphan nuclea
210              Finally, multiplexed-competitor-EMSA (MC-EMSA) and supershift EMSA identified FOXA2 to r
211 AG) separation lanes supports 384 concurrent EMSAs in 30 s using a single power source.
212 l strips acts as a chassis for 96 concurrent EMSAs.
213 er and synthetic RARE luciferase constructs, EMSA, and ChIP assays.
214 on of HP0166 in binding (including a control EMSA with in-vitro-phosphorylated HP0166-His(6)).
215                                     Detailed EMSA studies were used to confirm binding at these sites
216  preparations of MsvR demonstrated different EMSA binding patterns and regions of protection on the i
217 g to chromaffin cell nuclear proteins during EMSA, binding of endogenous c-FOS on ChIP, and different
218                                           EC-EMSA should be useful for further investigation of facto
219 lex electrophoretic mobility shift assay (EC-EMSA).
220 ing hit through orthogonal methods employing EMSA, STD-NMR, and MST methodologies.
221                                 Experimental EMSA results demonstrate that methylation of the CpG in
222                                    Following EMSA, denaturing gel electrophoresis is implemented to p
223 r SRY and YY1, with similar consequences for EMSA, endogenous factor binding, and responses to exogen
224 n-RNA complex without catalytic turnover for EMSA and ribonuclease footprinting analyses.
225                                 Furthermore, EMSA analysis demonstrated that STAT1 binds to the MD-2
226                                 Furthermore, EMSA and luciferase reporter assays demonstrated that KL
227                                 Furthermore, EMSAs demonstrated that the attachment of CREB binding p
228         The free-standing polyacrylamide gel EMSAs yielded reliable quantification of molecular bindi
229 ppaB proteins was similar between genotypes, EMSAs under nonreducing conditions showed increased DNA
230 ences to bind ATF4 and ATF3 using immunoblot-EMSA and confirmed ATF4, ATF3, and CCAAT/enhancer-bindin
231  showed phosphorylation-dependent binding in EMSA with HP0166-D52N-His(6).
232  of activator protein-1 response elements in EMSA.
233 to the lst promoter at multiple locations in EMSA and ChIP assays respectively.
234 r binding to the ICP27 N-terminal peptide in EMSA experiments.
235 sulfitobacterium hafniense bind tRNA(Pyl) in EMSA with apparent K(d) values of 0.12 and 0.13 muM, res
236 gh Z does not bind directly to the TNFR1p in EMSA studies, chromatin immunoprecipitation studies indi
237                                           In EMSAs, DUX4 specifically interacted with a 30-bp sequenc
238                               Interestingly, EMSA analyses demonstrate that the AP-1 site binds to c-
239     Finally, multiplexed-competitor-EMSA (MC-EMSA) and supershift EMSA identified FOXA2 to rs327T, an
240    Sample is dispensed onto the microfluidic EMSA card by acoustic droplet ejection (ADE), which redu
241 min) or even microchannel based microfluidic EMSAs ( approximately 0.3 data/min).
242 olin inhibited IL-6 production in microglia, EMSAs were performed to establish the effects of luteoli
243 though original data were available for most EMSA and immunoblot experiments, those corresponding to
244  conjunction with site-directed mutagenesis, EMSA, and reporter assays indicated that Ser(P)-193 is r
245                           Using mutagenesis, EMSA, and cotransfection assays, we identified two redun
246                                        Next, EMSA, immunoblots, and transient cotransfection studies
247                              On the basis of EMSA and ChIP assays, TNF-alpha treatment increases bind
248 atory sites, which allowed the generation of EMSA probes that bound NFs specific to BAFF-R-expressing
249                                   Results of EMSA and ChIP assays confirmed that LYAR bound to a DNA
250                    Interestingly, the use of EMSAs also indicated that H. ducreyi CpxR did not bind t
251 tions failed to bind target DNA sequences on EMSA and confocal microscopy; however, they did not inhi
252  rs11573156 C >G there were no luciferase or EMSA allelic differences seen.
253                                 We performed EMSAs to examine EutR activation of the LEE.
254                         The powerful 96-plex EMSAs increased the throughput to approximately 10 data/
255 trated by mutation analysis of the promoter, EMSA, and ChIP.
256 ssays after UV cross-linking and RNA-protein EMSA demonstrated that P311 binds directly to TGF-beta 5
257 iments, those corresponding to the published EMSA data of Supplementary Fig.
258 sion during pregnancy and lactation in rats, EMSAs demonstrate an elevated binding of pregnant and la
259 oustic droplet ejection (ADE), which reduces EMSA variability compared to sample dispensing using man
260 to the N terminus of truncated PylS regained EMSA-detectable tRNA(Pyl) binding.
261            1e, and the independent replicate EMSA data of Supplementary Figs 6e, 8b, 8c and 8d, are u
262                 In optimizing the riboswitch EMSAs on the free-standing polyacrylamide gel array, thr
263 ncing with HIF-1alpha small interfering RNA, EMSA, and chromatin immunoprecipitation analysis.
264 A electrophoretic mobility shift assays (RNA-EMSA) were used to confirm the RIP results and demonstra
265                                          RNA-EMSAs show that PfSR1 preferentially binds RNA molecules
266              Electrophoretic mobility shift (EMSA) and chromatin immunoprecipitation (ChIP) assays de
267              Electrophoretic mobility shift (EMSA) and chromatin immunoprecipitation (ChIP) assays de
268 (FA) and electrophoretic gel mobility shift (EMSA) assays, the interactions between HPNikR and the ta
269              Electrophoretic mobility shift (EMSAs) and gel-supershift assays demonstrated that the t
270                   Focusing on the Sp-1 site, EMSA, super-shift and ChIP analysis was performed that e
271 more efficient than either conventional slab EMSAs ( approximately 0.01 data/min) or even microchanne
272 to 30.6), p = 1.22x10(-)(3)(5), and stronger EMSA binding of a nuclear protein compared to the T-alle
273 including: subcellular localization studies, EMSAs and luciferase-reporter assays, were undertaken an
274                          EMSA and supershift EMSA (with the use of specific antibodies against NF-Y s
275 xed-competitor-EMSA (MC-EMSA) and supershift EMSA identified FOXA2 to rs327T, and CREB-binding protei
276                   Competitive and supershift EMSA identified the participation of GATA4, another GATA
277 etic mobility shift assay (EMSA), supershift EMSA, Western blot analysis, and immunocytochemistry wer
278 ological approaches such as EMSA, supershift EMSA, ChIP, re-ChIP, and promoter-reporter gene assays,
279                               The supershift EMSA confirmed that ZEB1, demonstrated to be present in
280                                   Supporting EMSA studies with a series of DeltaC truncated versions
281 A ternary complexes were not observed in the EMSA experiments, cross-linking experiments showed that
282  supershift the H369W-protein complex on the EMSA gel.
283  start site of TLR10 was established through EMSA and chromatin immunoprecipitation.
284                          The high-throughput EMSAs was employed to assess binding of the Vc2 cyclic-d
285  addition of an anti-SAP155 antibody (Ab) to EMSA decreasing the mobility of a protein:CRCE 1 complex
286 nding sites within the Lbr promoter and used EMSAs and luciferase assays to show that Lbr is transcri
287                                        Using EMSA (electrophoretic mobility shift assay), ChIP (chrom
288                                        Using EMSA analysis, NsrR::FLAG was shown to interact with pre
289                                        Using EMSA, supershift assays, and promoter pulldown assays, w
290                                        Using EMSA, we demonstrate that the AHR-ARNT heterodimer binds
291                                        Using EMSA, we found that apigenin does not alter NF-kappaB-DN
292 d its binding specificity was analyzed using EMSA and SELEX.
293 were later confirmed experimentally by using EMSA.
294 flanking the TSS cluster were analyzed using EMSAs to identify discrete DNA-binding factors in primar
295 ite in TACE promoter and demonstrated, using EMSAs and chromatin immunoprecipitation assays, that AP-
296                                    Utilizing EMSA or ChIP assays, we found that both p50 and p65 NF-k
297  for these protein-protein interactions; (v) EMSA titrations revealed that while tri-complex formatio
298  of the CsoR regulon was confirmed in vitro (EMSA) and in vivo (RNA-seq), which highlighted that next
299 ides are required for transcription in vivo; EMSA-binding assays confirm that several of these nucleo
300      CD spectral changes in combination with EMSA titrations suggest that one hRPA heterotrimer is su

 
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