1 ng the mobility of a protein:CRCE 1 complex (
SuperShift).
2 hown by electrophoretic mobility shift assay
supershift.
3 nly the attP/attB combination could generate
supershifts.
4 A probe indicate that recombinant MBD3L1 can
supershift an MBD2-methylated DNA complex.
5 bination of mutational and anti-Met antibody
supershift analyses confirmed the binding properties of
6 Electrophoretic mobility shift and
supershift analyses demonstrated increased binding of c-
7 However,
supershift analyses demonstrated that the relative contr
8 d a single complex with the site at -89, and
supershift analyses implicated AP-2alpha and ERalpha, an
9 Supershift analyses implicated c-Jun homodimers binding
10 EMSA competition and
supershift analyses reveal the formation of multiple DNA
11 Supershift analyses revealed that oxLDL stimulates bindi
12 EMSAs and
supershift analyses revealed that the transcription fact
13 rophoretic mobility shift assays (EMSAs) and
supershift analyses were used to characterize the protei
14 Competition EMSAs and
supershift analyses with HsrA-enriched protein fractions
15 Gel shift and
supershift analyses with nuclear extracts prepared from
16 Gel shift and
supershift analyses, as well as ChIP, show binding of Ju
17 uclear extracts from hypoxic RAW cells, with
supershift analysis confirming activation of Egr-1, HIF-
18 Supershift analysis demonstrated that deltaEF1, a known
19 Gel mobility shift assay
supershift analysis demonstrated that the serum response
20 Supershift analysis detects the presence of Smads 1, 5,
21 DNase I footprinting, gel retardation and
supershift analysis identified a NF-kappa B site in the
22 Supershift analysis identified CREB1, JunB, c-Fos, Fra-1
23 Supershift analysis identified this binding activity as
24 of NF-kappaB complexes detected by EMSA and
supershift analysis in nuclear lysates derived from Bcl-
25 d NF-kappaB DNA-binding activity, whereas Ab
supershift analysis indicated that aspirin targeted prim
26 Supershift analysis indicated that the GABPalpha binding
27 Supershift analysis of EMSAs using crude extracts contai
28 ty of ZNF143 with AP-2alpha was supported by
supershift analysis of HeLa cells where AP-2 may act as
29 Fra-1 within the AP-1 DNA binding complex by
supershift analysis of nuclear extracts from oxysterol-t
30 actions could not be detected by anti-STAT5b
supershift analysis of PPARalpha-DNA complexes.
31 Supershift analysis revealed binding of c-Jun and c-Fos
32 A gel mobility
supershift analysis revealed interaction of the AP1 fact
33 A gel mobility
supershift analysis revealed interaction of the AP1 fact
34 DNA-protein binding assays and
supershift analysis revealed that c-Myc forms a complex
35 Supershift analysis revealed that the gel-shifted comple
36 Supershift analysis revealed that the major AP-1 complex
37 Gel mobility
supershift analysis revealed the binding of RARalpha and
38 Gel
supershift analysis showed that each of the NFAT binding
39 By
supershift analysis this element binds members of the ba
40 ysis of protein-DNA complexes, combined with
supershift analysis using different monoclonal antibodie
41 Standard gel shift and
supershift analysis using liver nuclear extracts establi
42 functional composition of the AP-1 complex,
supershift analysis was performed to characterize which
43 Supershift analysis with specific antibodies to USF-1 an
44 se substrates, co-purify with complex A, and
supershift analysis with specific antisera revealed that
45 Based on
supershift analysis, molecular weight estimation experim
46 By
supershift analysis, the first two elements bound NF-kap
47 hin the SOCS-1 promoter as shown by EMSA and
supershift analysis.
48 DNA complex as is evident by electrophoretic
supershift analysis.
49 F-kappaB activity, the findings confirmed by
supershift analysis.
50 was determined to be functional by EMSA and
supershift analysis.
51 Band/
supershift and ChIP assays demonstrated binding of Nrf2
52 Both
supershift and ChIP assays revealed the presence of the
53 REB2 were identified by competition EMSA and
supershift and chromatin immunoprecipitation assays as c
54 Subsequent
supershift and chromatin immunoprecipitation assays conf
55 Electrophoretic mobility
supershift and chromatin immunoprecipitation assays demo
56 e in a sequence-specific manner confirmed by
supershift and chromatin immunoprecipitation assays, res
57 Using electrophoretic mobility
supershift and chromatin immunoprecipitation assays, we
58 Gel mobility
supershift and chromatin immunoprecipitation reveal that
59 Gel
supershift and DNase I protection assays identified DNA
60 Gel
supershift and dominant negative cotransfection experime
61 n S- but not N-type cells by electromobility
supershift and gene reporter assays.
62 extracts from primary human T cells based on
supershift and immunoprecipitation assays.
63 Supershift and microaffinity isolation assays were used
64 Supershift and mutational analyses confirmed the binding
65 Using
supershifts and an ORE.AP-1 probe, we find c-Fos and c-J
66 Subsequent antibody
supershifts and chromatin immunoprecipitations demonstra
67 Furthermore, we show by EMSA
supershifts and coimmunoprecipitation that C/EBPbeta and
68 Moreover, electrophoretic mobility shift,
supershift,
and chromatin immunoprecipitation analyses r
69 Gel shift,
supershift,
and chromatin immunoprecipitation assays con
70 Electrophoretic mobility shift,
supershift,
and chromatin immunoprecipitation assays sho
71 more, electrophoretic mobility shift assays,
supershift,
and cotransfection assays revealed that the
72 electrophoretic mobility shift assays using
supershifting antibodies, the SP1 motifs bound SP1 prote
73 ith the ATXN2 promoter by an electromobility
supershift assay and chromatin immunoprecipitation polym
74 Antibody
supershift assay confirmed the presence of MEF-2A in thi
75 Western blotting and a gel shift/
supershift assay demonstrated that endogenous CBF DNA bi
76 used for gel mobility shift assay (GMSA) and
supershift assay for activating protein (AP)-1 transcrip
77 Supershift assay indicated that the antibodies to p65, p
78 Electrophoretic mobility
supershift assay indicated that the JunB, JunD, and c-Fo
79 Supershift assay indicated that the two NF-kappa B subun
80 binding and transcriptional activities, and
supershift assay revealed that AP-1 composition was shif
81 footprinting, competition EMSA, and antibody
supershift assay showed that the IR0 is a binding site f
82 A
supershift assay using an antibody against the CRE-bindi
83 Electrophoretic mobility
supershift assay using an involucrin activator protein 1
84 Supershift assay with the purified SBP and anti-SLUG ant
85 n was confirmed via electrophoretic mobility
supershift assay, and analysis of the ICAM-1 promoter re
86 Gel shift,
supershift assay, and ChIP analysis demonstrated the spe
87 ectrophoretic mobility shift assay, antibody
supershift assay, and mutations of the Egr-1 binding sit
88 inity chromatography, mass spectrometry, and
supershift assay, human heterogeneous nuclear ribonucleo
89 e was sequence specific, as confirmed by the
supershift assay.
90 ement was tested by electrophoretic mobility
supershift assays and chromatin immunoprecipitation anal
91 Specificity of binding was established by
supershift assays and treatment with the Sp-1 inhibitor
92 ence; (c) electrophoretic mobility shift and
supershift assays confirm the specific binding of transc
93 Electrophoretic mobility shift and
supershift assays confirmed that this element binds spec
94 Biochemical fractionation and antibody
supershift assays demonstrate that the C/EBPbeta heterod
95 Electrophoretic mobility
supershift assays demonstrated binding of NRF-2 to the o
96 Chromatin immunoprecipitation and
supershift assays demonstrated that AP-1 blockade caused
97 Electrophoretic mobility shift and
supershift assays demonstrated that the binding activity
98 ectrophoretic mobility shift (EMSAs) and gel-
supershift assays demonstrated that the transcription fa
99 Gel mobility shift and
supershift assays demonstrated that this cis-acting elem
100 Gel
supershift assays demonstrated that thrombin induced bin
101 RNA gel mobility
supershift assays demonstrated that vinculin and far ups
102 Supershift assays further confirmed the presence of Sp1
103 EMSAs and
supershift assays identified complexes consisting of Fos
104 Antibody
supershift assays identified this protein as lung Kruppe
105 Competition and gel mobility
supershift assays identify upstream stimulatory factor (
106 Using bandshifts and
supershift assays in which permissive and non-permissive
107 tification of purified peptides and antibody
supershift assays indicate that PYR complex contains at
108 A-protein interaction at this same site, and
supershift assays indicate that the complex includes AP-
109 romoters, electrophoretic mobility shift and
supershift assays indicated NRF-1 binding to all ten pro
110 Competition EMSA and antibody
supershift assays indicated that ADAR1 KCS-l-binding pro
111 Electrophoresis mobility
supershift assays indicated that CRE-binding protein 1 (
112 Supershift assays indicated that cyclic AMP response ele
113 Competition and
supershift assays indicated that the nuclear protein bin
114 Gel mobility shift and
supershift assays performed with Rat1 nuclear extracts i
115 Electrophoretic mobility shift and
supershift assays reveal that p65 and p50 interact with
116 Electrophoretic mobility shift and
supershift assays revealed increased binding of the Sp1
117 Bandshift and
supershift assays revealed that Bach1 binds to the ARE a
118 Electrophoretic mobility shift assay
supershift assays revealed that HGF/SF treatment induced
119 Gel mobility shift and
supershift assays revealed that USF and NF1 have high bi
120 Gel mobility shift and
supershift assays show that the nuclear proteins binding
121 retic mobility shift assay experiments, (iv)
supershift assays show that this complex contains the VZ
122 However, band and
supershift assays showed a significant reduction in the
123 Supershift assays showed no effect of the anti-Sp1 antib
124 EMSA and
supershift assays showed that agonist anti-Fas (CH11) in
125 Additionally, EMSAs and
supershift assays showed that ER-alpha binds to the SNAT
126 Gel mobility and
supershift assays showed that LEDGF in the nuclear extra
127 Supershift assays showed that the transcription factors
128 Western blot analysis and
supershift assays showed that this cytosolic protein is
129 Electromobility shift assays (EMSAs) and
supershift assays showed that this element bound recombi
130 Electrophoretic mobility shift assay and
supershift assays showed that two members of the Sp fami
131 MvaT and MvaU were prepared and employed in
supershift assays to support these observations.
132 Gel shift assays and
supershift assays using an Olf-1-specific antibody demon
133 Gel
supershift assays using antibodies to the ATPase-helicas
134 Supershift assays using NF-kappaB protein-specific antib
135 Electrophoretic mobility shift assays and
supershift assays using recombinant oestrogen receptor a
136 ed and -untreated cells, in combination with
supershift assays using Sp1 antibodies, demonstrated tha
137 Gel shift and
supershift assays were used to identify NF-kappa B in nu
138 Gel shift and
supershift assays with anti-p65 and -p50 antibodies demo
139 rophoretic mobility shift assays (EMSAs) and
supershift assays with antibodies against members of the
140 Supershift assays with antibodies directed against known
141 Bandshift and
supershift assays with in vitro transcribed and translat
142 Supershift assays with keratinocyte nuclear extracts and
143 Electrophoretic mobility
supershift assays with nuclear extracts from beta-cell l
144 Gel mobility shift assays and
supershift assays with specific antibodies indicate that
145 Band and
supershift assays with the NQO1 gene ARE and nuclear pro
146 By using gel-shift and
supershift assays, a marked reduction in Nrf2/ARE bindin
147 Electrophoresis mobility shift assays,
supershift assays, and mutation studies demonstrated tha
148 Using EMSA,
supershift assays, and promoter pulldown assays, we demo
149 d CREB proteins, based on competitive EMSAs,
supershift assays, and Western blotting with an anti-CRE
150 analysis, electrophoretic mobility shift and
supershift assays, in vivo chromatin immunoprecipitation
151 analysis, electrophoretic mobility shift and
supershift assays, in vivo chromatin immunoprecipitation
152 In gel
supershift assays, the Sox family member Sox18 bound dir
153 Using antibody
supershift assays, we have identified these complexes as
154 Using specific antibodies in
supershift assays, we have shown that anti-E2F1 and 4 an
155 etic mobility shift assays (EMSAs), antibody
supershift assays, western blot analysis of partially pu
156 by electrophoretic mobility shift assay and
supershift assays.
157 STAT5 site, as determined by competition and
supershift assays.
158 ax-6, a conclusion that was confirmed by gel
supershift assays.
159 nding to the PAN promoter was confirmed with
supershift assays.
160 electrophoretic mobility shift and antibody
supershift assays.
161 genes, as shown in gel mobility and antibody
supershift assays.
162 tains the 8-bp SBE in gel mobility shift and
supershift assays.
163 specifically to AP-1 protein as verified by
supershift assays.
164 nt in late promoter-protein complexes in gel
supershift assays.
165 of electrophoretic mobility shift assays and
supershift assays.
166 4/-580 confirmed by electrophoretic mobility
supershift assays.
167 h bound to this motif, were also detected by
supershift assays.
168 Immunoelectrophoretic mobility shift (
supershift)
assays identified JunD, Fra1, and Fra2 as th
169 n their affinities for BAF, but all isoforms
supershifted BAF small middle dotDNA complexes.
170 und to the GBS in the mouse SP-A gene, and a
supershifted band was detected with a GATA-6-specific an
171 bind to the target C/EBPalpha sites or form
supershifted bands.
172 The addition of HMG-1
supershifts both complexes without altering the RAG prot
173 inding-proficient mutants were refractory to
supershift by BZ-1 monoclonal antibody (epitope amino ac
174 by electrophoresis mobility shift assays and
supershift by specific antibodies.
175 These complexes were not
supershifted by a monoclonal antibody that recognizes an
176 pitope in the C terminus; however, they were
supershifted by a monoclonal antibody that recognizes th
177 esponse element in the PHB promoter that are
supershifted by a STAT3 antibody.
178 t the nuclear protein bound to the motif was
supershifted by an anti-GATA-1 monoclonal antibody.
179 In EMSAs both complexes were
supershifted by an anti-HuR antibody, while Western blot
180 ecific for AML/CBFalpha and was specifically
supershifted by an antibody to AML3/CBFalpha1, placing f
181 nding to this IRF-1-binding motif, which was
supershifted by anti-IRF-1 antibody in electrophoretic m
182 y oligonucleotide-binding-site sequences and
supershifted by anti-Sp1 confirming the interaction.
183 s well as differences in their ability to be
supershifted by anti-Stat5 antibodies.
184 ound to the 25 bp probe (-872/-848) could be
supershifted by antibodies specific for JunD and Sp3 in
185 These DNA-protein complexes were
supershifted by antibody to VP16.
186 hifted by THP-1 cell nuclear extract and was
supershifted by antisera to Sp1 and Sp3.
187 extracts from HSV-2-infected cells which was
supershifted by c-Fos antibody and was not seen with ext
188 fic protein-oligonucleotide complex that was
supershifted by C/EBP alpha antibody, while a probe corr
189 omplexes formed by BeWo nuclear extracts are
supershifted by phosphoserine- and phosphothreonine- but
190 ore the retarded protein-DNA complex can be '
supershifted'
by anti-DnaK monoclonal antibody, demonstr
191 jun, which was further confirmed by antibody
supershift,
by immunoprecipitation with Southwestern blo
192 It was concluded that these
supershifted complexes contained the recombination synap
193 The linker DNA in the
supershifted complexes remains freely accessible to rest
194 ecombination products were isolated from the
supershifted complexes.
195 Antibody induced gel retardation
supershift confirmed the identification of the RNA-bindi
196 and mutant oligonucleotides and by antibody
supershifts,
contains the Sp1 transcription factor.
197 XRE is supported by electrophoretic mobility
supershift data and AHR/ARNT overexpression studies.
198 ophoretic mobility shift assays and antibody
supershifts detected the binding of cellular transcripti
199 Supershifts,
detected by anti-nuclear factor of activate
200 Using
supershift electrophoretic mobility shift analysis, we f
201 paB complexes are detected in ARP-1 cells by
supershift electrophoretic mobility shift assay (EMSA).
202 Competition and
supershift electrophoretic mobility shift assay did not
203 ion electrophoretic mobility shift assay and
supershift electrophoretic mobility shift assay with ant
204 Antibody
supershift electrophoretic mobility shift assays did not
205 tic mobility shift assay and competition and
supershift electrophoretic mobility shift assays.
206 ar factors and the ameloblastin OSE2 site by
supershift electrophoretic mobility shift assays.
207 EMSA and
supershift EMSA (with the use of specific antibodies aga
208 Supershift EMSA and Western blot studies identified JunD
209 The
supershift EMSA confirmed that ZEB1, demonstrated to be
210 Supershift EMSA identified c-Jun, Fra-2, and c-Fos in AP
211 y, multiplexed-competitor-EMSA (MC-EMSA) and
supershift EMSA identified FOXA2 to rs327T, and CREB-bin
212 Competitive and
supershift EMSA identified the participation of GATA4, a
213 olecular biological approaches such as EMSA,
supershift EMSA, ChIP, re-ChIP, and promoter-reporter ge
214 Electrophoretic mobility shift assay (EMSA),
supershift EMSA, Western blot analysis, and immunocytoch
215 Combined with the data from the
supershift EMSAs, it appears that Sp1 is the transcripti
216 Gel shift/
supershift experiments and chromatin immunoprecipitation
217 Both mutation analysis and
supershift experiments demonstrated that androgen recept
218 Supershift experiments demonstrated that HSF1 was the tr
219 Supershift experiments demonstrated that the shifted pro
220 Electrophoretic mobility shift and
supershift experiments identified a Sp1 binding site in
221 Furthermore, gel mobility
supershift experiments identified Irr as a component of
222 Furthermore, gel mobility
supershift experiments identified Irr as the binding pro
223 ugh oligonucleotide competition and antibody
supershift experiments in electrophoretic mobility shift
224 the GPIX Ets site was identified in antibody
supershift experiments in nuclear extracts derived from
225 EMSA and
supershift experiments indicated binding of USF-1/-2 to
226 Antibody
supershift experiments indicated that the factor(s) is n
227 Subsequent gel-mobility shift and
supershift experiments involving the CTCCGCGC site in th
228 factor-1 (HIF-1) was shown by gel-shift and
supershift experiments that showed HIF-1alpha and HIF-1b
229 ctrophoretic mobility shift assay (EMSA) and
supershift experiments using an anti-Cbfa1 antibody.
230 In
supershift experiments using specific Abs, we showed tha
231 pose tissue; and 2) electrophoretic mobility
supershift experiments with specific antibodies indicate
232 Supershift experiments with specific antisera detected o
233 In antibody
supershift experiments, anti-p50 antibody supershifted t
234 t assays, including competition and antibody
supershift experiments, demonstrated binding of GATA-1,
235 r was specific, as judged by competition and
supershift experiments.
236 by electrophoretic mobility shift assay and
supershift experiments.
237 d antisera specific for Sp1 and Sp3 provided
supershifts for the former.
238 Using a
supershift gel mobility assay, we found evidence for sim
239 Western blot analysis and RNA
supershift identified Musashi 1 (Msi1) as the binding pr
240 Furthermore, we observed
supershift in mobility when DRE and NF-kappaB probes wer
241 A
supershift in the mobility of the DNA-protein complex wa
242 tivity in rhR4-treated cells, with increased
supershift in the presence of antibodies to JunB, JunD,
243 iver and olfactory mucosa, all of which were
supershifted in the presence of an anti-NF1 antibody.
244 in-induced CgA gene transcription, and pCREB
supershifts indicated Ser-133 as the active CREB moiety
245 RFX1 antiserum
supershifted MIE1-protein complexes.
246 s was confirmed by electrophoretic shift and
supershift mobility assays.
247 Interestingly, anti-CmHNF-4 serum caused a
supershift not only with nuclear extracts of scN-adapted
248 oprecipitated cross-linked p55 and induced a
supershift of a p55-containing complex formed in HeLa nu
249 Supershift of stimulated NK cells and fluorescence micro
250 -bound RXRalpha homodimers was proved by the
supershift of the complex when incubated with PELP1-spec
251 P) family members were performed to test for
supershifting of complexes by specific antibodies.
252 antibodies, but not preimmune serum, induce
supershifts of GST-Cdc6 and DNA complexes in these assay
253 because anti-AUF1 antibodies were capable of
supershifting or immunoprecipitating cyclin D1 mRNA-prot
254 TR4-DR3VDRE or TR4-DR4T3RE showed a distinct
supershifted pattern, and proteolytic analysis further d
255 promote MMP expression and a combination of
supershift,
RNA interference and overexpression experime
256 and naked DNA, as evidenced by formation of
supershifted species on native agarose gels.
257 A
supershifted species was formed in the presence of McrC
258 Antibody
supershift studies and chromatin immunoprecipitation ass
259 Gel
supershift studies confirm sequence-specific DNA binding
260 ing cyclins A and B1, as anti-HuR antibodies
supershifted such RNA-protein complexes.
261 el mobility shift assays, the formation of a
supershifted ternary complex demonstrated that Mor and H
262 Using anti-TTP Abs, we showed by
supershift that this inducible activity contained TTP.
263 ve shown that anti-E2F1 and 4 antibodies can
supershift the A2-protein complexes, whereas anti-E2F2 a
264 site, and an anti-NF-Y antibody was able to
supershift the bound band.
265 antibodies targeted to the N terminus of p53
supershift the complex bands.
266 activity and that antibodies to Ikaros also
supershift the complex.
267 Consistently, anti-Gfi-1 antibody is able to
supershift the H369W-protein complex on the EMSA gel.
268 Antibodies against SUMO-1
supershift the HSF1 DNA-binding complex, and modificatio
269 d anti-human Sp1 (but not Sp2, Sp3, nor Sp4)
supershifted the B2:element 2 complex.
270 dy supershift experiments, anti-p50 antibody
supershifted the C1q-induced NFkappaB complex, whereas a
271 Anti-Sox9 antibodies
supershifted the complex of the 60-bp segment with recom
272 g sites, and the addition of Foxa2 antiserum
supershifted the complex.
273 cted against NF-IA, C/EBPalpha, or C/EBPbeta
supershifted the corresponding protein-DNA complexes, in
274 the -155/-131 DNA; antisera to LBP proteins
supershifted the LBP-9.DNA complex and inhibited formati
275 say, only the N-terminal monoclonal antibody
supershifted the mitochondrial DNA end-binding complex.
276 N- and C-terminal Ku80 monoclonal antibodies
supershifted the nuclear DNA end-binding complex on an e
277 n antibody to C/EBPbeta, but not C/EBPalpha,
supershifted the nuclear protein complex associated with
278 alpha nor retinoid X receptor beta antibody
supershifted the protein-DNA complex.
279 migrating GATA complex, and antiserum to Sp1
supershifted the slowest migrating Sp1 complex.
280 ein complexes, as antibodies recognizing HuR
supershifted these complexes and revealed HuR-immunoreac
281 e-specific mechanism, and anti-IK antibodies
supershifted this complex.
282 nst C/EBPbeta (but not other C/EBP proteins)
supershifts this complex, and Western blotting of affini
283 Additionally, antibody to ATM kinase
supershifts TonEBP/OREBP bound to its cognate ORE/TonE D
284 ing binding activity in nuclear extracts was
supershifted using a YY1-specific antibody.
285 inished in lysate depleted of METTL16, and a
supershift was detected after adding anti-METTL16 antibo
286 A2 and PDX-1 was found in NIT-1 cells, and a
supershift was observed for both BETA2 and PDX-1.
287 45 bp 5' region was demonstrated by EMSA and
supershift with anti-NFAT antibodies.
288 oligonucleotide probe and by demonstrating a
supershift with the antibody against the E2F4 and E2F5 p
289 The protein-DNA binding complex could be
supershifted with an antibody directed against FOXA1.
290 and the specific protein-DNA complexes were
supershifted with anti-beta-catenin or anti-Tcf-4 antibo
291 in electrophoretic mobility shift assays was
supershifted with anti-Fos and anti-Jun antibodies.
292 nt or Sp1-binding site oligonucleotides, and
supershifted with anti-p53 antibodies.
293 The NF-kappaB complex was
supershifted with anti-p65 antibodies, but not with anti
294 and 3) the complex was specific and could be
supershifted with antibodies against the p50 or p65 NF-k
295 The GATA complex was
supershifted with antibodies to GATA-2, but not GATA-3 o
296 h NIH 3T3 nuclear extracts and B2 probe were
supershifted with antibody against COUP-TF, identifying
297 r extracts from emphysematous lung which was
supershifted with antibody to Egr-1.
298 lex with the collagen sequence that was also
supershifted with the RFX1 antibody.
299 1 M NaCl), affinity-purified telomerase was '
supershifted'
with an anti-dyskerin antibody, however th
300 ear proteins and competition specificity (or
supershifts)
with oligonucleotides and antibodies.