1 ween nucleotides -130 and -80 as observed by
gel shift analysis.
2 y" and detection of a binding complex by RNA
gel shift analysis.
3 nstrated increased NF-kappa B DNA binding on
gel shift analysis.
4 pa B binding activity in nuclear extracts by
gel shift analysis.
5 the tgt/sec promoter, were also confirmed by
gel shift analysis.
6 DNA with comparable affinities, as shown by
gel shift analysis.
7 on were shown to bind to nuclear proteins by
gel shift analysis.
8 e of binding to this sequence as assessed by
gel shift analysis.
9 ha, IFN gamma, and IL-1 beta was assessed by
gel shift analysis.
10 ing to this sequence in vitro as assessed by
gel shift analysis.
11 in the presence of TO901317 was confirmed by
gel shift analysis.
12 stable binding in vitro, as demonstrated by
gel shift analysis.
13 n resonance spectroscopy and electrophoretic
gel shift analysis.
14 trometry, chromatin immunoprecipitation, and
gel shift analysis.
15 s TR alpha1 and TR beta1 was demonstrated by
gel-shift analysis.
16 rdation of the DNA fragment when assessed by
gel-shift analysis.
17 active IGS mutant ribozymes was evaluated by
gel-shift analysis.
18 their respective proteins was studied using
gel-shift analysis.
19 ce motif 5'-GTTGCA-3', were identified using
gel-shift analysis.
20 kappaB DNA binding activity as determined by
gel-shift analysis.
21 Gel shift analysis and chloramphenicol acetyl transferas
22 nding of NF-kB to the kB-site as assessed by
gel shift analysis and chromatin immunoprecipitation.
23 s was determined by electrophoretic mobility
gel shift analysis and co-purification assays.
24 Gel shift analysis and DNase I footprinting determined t
25 arget RNA motif for TIAR binding by both RNA
gel shift analysis and immunoprecipitation experiments.
26 Gel shift analysis and luciferase assays demonstrated th
27 Furthermore, by a combination of
gel shift analysis and site-directed mutagenesis, we hav
28 ike prior to receptor engagement, but trimer
gel shift analysis and slow kinetics of shedding induced
29 To study BCL3 function, we have used
gel shift analysis and tagged protein and tagged DNA cop
30 ate gene transcription was determined by the
gel shift analysis and transient transfection assays.
31 Gel-shift analysis and site-directed mutagenesis demonst
32 ind to cTnC, as shown by urea-polyacrylamide
gel-shift analysis and size exclusion chromatography.
33 en -300 and -60 bp; binding was confirmed by
gel shift analysis,
and tissue specificity was demonstra
34 mplex can be detected by affinity column and
gel-shift analysis,
and has a proteolytic signature whic
35 treated cells showed strong AP-1 activity by
gel-shift analysis,
and supershift analysis showed the A
36 FIJKLM promoter bound PmrA, as determined by
gel shift analysis,
as did a 40-bp region of the PmrA-Pm
37 In
gel shift analysis,
binding to CAR was observed only wit
38 ce of added deoxyribonucleotides, as seen by
gel-shift analysis,
but retain the ability to strand tra
39 Gel-shift analysis competition assays indicated that cat
40 While
gel shift analysis confirmed NF-Y binding to both sites,
41 Gel shift analysis confirmed the ability of the GLI1 pro
42 Gel-shift analysis confirmed that AP-1 DNA binding activ
43 tuents which bind to the repressor region by
gel shift analysis; (
d) demonstrate the translational re
44 Gel shift analysis demonstrated that a protein(s) within
45 Gel shift analysis demonstrated that ACM enhanced AP-1 b
46 utations in the promoter region of pilA1 and
gel shift analysis demonstrated that both sigma(54) and
47 Electrophoretic
gel shift analysis demonstrated that HbrL binds the prom
48 Gel shift analysis demonstrated that infection with EZ b
49 Gel shift analysis demonstrated that the DR-DS junction
50 Gel shift analysis demonstrated that the flanking nucleo
51 Gel shift analysis demonstrated that UreR bound to a 135
52 Gel-shift analysis demonstrated binding of PU.1 to this
53 Gel-shift analysis demonstrated that glucocorticoid rece
54 Electrophoretic
gel shift analysis demonstrates binding of specific DNA-
55 Moreover, competition
gel shift analysis demonstrates that dHAND and eHAND can
56 Gel shift analysis demonstrates that in addition to Sp1,
57 Gel-shift analysis demonstrates that glucocorticoid/andr
58 Gel shift analysis detected a factor that appears to bin
59 Gel shift analysis determined the presence of a correspo
60 Native polyacrylamide
gel shift analysis did suggest that Bap1 exhibits lectin
61 0 hypervariable region 1 (HVR1) clones using
gel shift analysis (
GSA), which allowed determination of
62 Luciferase assays and
gel shift analysis have identified a single motif upstre
63 Gel shift analysis identified a corresponding nuclear pr
64 Gel shift analysis identified four major DNA-protein com
65 Gel shift analysis identified Fra-1 as distinguishing mi
66 Gel shift analysis identified MarT as a transcriptional
67 Gel shift analysis in LNCaP and CWR22-Rv1 cells demonstr
68 By
gel-shift analysis,
in vitro synthesized ERF-1 comigrate
69 n, the principal AP-1 components detected by
gel shift analysis include c-jun, ATF-2, fos-B, fra-1, a
70 Immunoprecipitation studies and
gel shift analysis indicate that c-myb does not directly
71 Thus, functional and
gel shift analysis indicate that the 91 bp fragment cont
72 Gel shift analysis indicated enhanced binding of protein
73 Gel shift analysis indicated enhanced binding of Sp3 fro
74 Gel shift analysis indicated that a complex in neuroblas
75 Results from
gel shift analysis indicated that CHK regulates CXCR4 tr
76 Gel shift analysis indicated that each of these three si
77 Gel shift analysis indicated that HNF3beta present in is
78 Gel shift analysis indicated that NFI-B3 disrupts the fu
79 Gel shift analysis indicated that PPAR gamma, in the pre
80 Gel shift analysis indicates that this site binds IRF-1.
81 Gel-shift analysis indicates that one CTD destabilizes h
82 Competitive
gel-shift analysis indicates there is a small increase i
83 similar 2A10-reactive protein, detectable by
gel shift analysis of cellular p53 in complex with a spe
84 oP2, we have used quantitative footprint and
gel shift analysis of CRP and CytR binding to evaluate t
85 Electrophoretic mobility shift assay and
gel shift analysis of nuclear cell extracts confirmed th
86 Gel shift analysis of nuclear extract binding to an olig
87 Gel shift analysis of nuclear extracts from the ischemic
88 Gel shift analysis of protein binding from nuclear extra
89 Gel shift analysis of ssDBP revealed that its DNA bindin
90 Gel shift analysis of the putative PPARgamma site demons
91 Gel shift analysis of this 14-bp region confirms a hypox
92 By systematic mutagenesis and
gel shift analysis of this enhancer, we demonstrate that
93 Gel-shift analysis of nuclear extracts from hypoxic MPs
94 Gel-shift analysis of stage 6 embryonic chicken protein
95 Gel-shift analysis of the reconstituted products indicat
96 Gel-shift analysis of undifferentiated amoebae cell extr
97 Gel shift analysis performed with disrupted (open) virio
98 After modification of nuclear extract and
gel shift analysis procedures, Nkx2.8 was identified in
99 consensus GC box sequence as a competitor in
gel shift analysis reduced factor binding to the low K(+
100 als as revealed by Western blot analysis and
Gel-shift analysis,
respectively.
101 In vitro
gel shift analysis revealed distinct and TPA-dependent b
102 Finally,
gel shift analysis revealed that coadministration of FP
103 Gel shift analysis revealed that oxidative suppression o
104 Electrophoretic mobility
gel shift analysis revealed that PapX binds to the flhD
105 Gel shift analysis revealed that the combination gene th
106 Gel shift analysis revealed that the purified MBP-SyrF,
107 Gel shift analysis revealed that these proteins bound to
108 DNase I foot-printing and
gel shift analysis revealed that this region can bind a
109 Gel-shift analysis revealed that four LIP- and LAP-conta
110 Gel-shift analysis revealed three different profile grou
111 Competition
gel shift analysis reveals that the P4 satellite phage a
112 Gel shift analysis showed specific and TPA-inducible pro
113 Gel shift analysis showed suppression of DMBA-induced NF
114 Finally,
gel shift analysis showed synergistic complex formation
115 Gel shift analysis showed that Ets and Sp1 family member
116 Gel shift analysis showed that mutations of Arg32 and As
117 Gel shift analysis showed that PPARalpha, either alone o
118 Gel shift analysis showed that purified calreticulin inh
119 Gel shift analysis showed that purified SarA protein bin
120 Furthermore,
gel shift analysis showed that TGF-beta1 did not prevent
121 Gel shift analysis showed that the amino acid insertions
122 Gel-shift analysis showed that SDF1alpha enhances DNA bi
123 Gel-shift analysis showed that the 22 bp D-TERM DNA form
124 Gel-shift analysis showed that the Lys(188) mutants boun
125 The CSD of yps was purified and
gel-shift analysis showed that this domain can interact
126 Gel-shift analysis showed that this GC-rich repressor el
127 DNA damage, including BRCA1 and PARP2, with
gel-shift analysis showing that SOG1 can physically asso
128 Gel shift analysis shows specific binding to this site i
129 Gel shift analysis shows that this sequence binds nuclea
130 Glycosidase
gel shift analysis suggested that K(v)2.1, K(v)4.2, and
131 Gel-shift analysis suggests that Spi-C, ectopically expr
132 nterstrand cross-link, we have shown through
gel shift analysis that both XPA and a minimal DNA bindi
133 and SLVI, (SLV-VI) and (iii) demonstrate by
gel shift analysis that nsp1 purified from Escherichia c
134 By
gel shift analysis,
the E2F element from the c-myb promo
135 By
gel-shift analysis,
the corresponding oligonucleotide pr
136 We used scanning force microscopy and
gel shift analysis to show that M.HhaI, a cytosine C-5 D
137 We used
gel-shift analysis to refine the Sox2 region bound by Ar
138 FEN1 was later shown, by
gel shift analysis,
to remove the wild type Dna2 from th
139 Results from
gel shift analysis using mutant Pur-alpha proteins indic
140 Gel shift analysis using nuclear extract prepared from H
141 Gel shift analysis using this potential binding site wit
142 Gel-shift analysis using a labeled PU.1 oligomer showed
143 abrogated 90% of the luciferase activity, 3)
gel-shift analysis using the binding sites showed activa
144 Gel shift analysis,
using extracts of B cells in latency
145 To identify the specific region involved,
gel shift analysis was performed.
146 An in vitro
gel-shift analysis was used to show that the mutation in
147 By
gel shift analysis we identified two strong SATB1 bindin
148 more, using promoter deletion constructs and
gel shift analysis,
we defined a functional NF-kappaB-bi
149 By quantitative
gel shift analysis,
we demonstrate that although the C t
150 However, using
gel shift analysis,
we demonstrate that IE86 efficiently
151 Using
gel shift analysis,
we demonstrate that stimulation by C
152 in vitro binding assays in combination with
gel shift analysis,
we demonstrated Ca(2+)-dependent for
153 Using the yeast three-hybrid screen and RNA
gel shift analysis,
we have found that the protein GLD-1
154 By
gel shift analysis,
we show that in mitogen-dependent no
155 Using
gel-shift analysis,
we found that the two major forms of
156 RAD51 small middle dotssDNA binding forms by
gel shift analysis,
which were distinct from a well defi
157 Gel shift analysis with (32)P-labeled Egr probe showed a
158 sion of a two-site reporter and the other on
gel shift analysis with crude E. coli extracts.
159 Finally,
gel shift analysis with end-blocked E2F-1 promoter seque
160 fied protein were analyzed by polyacrylamide
gel shift analysis with model oligonucleotides.
161 ce with the differences in AAV transduction,
gel shift analysis with nuclear extracts derived from th
162 Gel shift analysis with purified hexahistidine-tagged or
163 Gel shift analysis with purified recombinant NikR verifi