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