戻る
「早戻しボタン」を押すと検索画面に戻ります。

今後説明を表示しない

[OK]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
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.

WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。
 
Page Top