ライフサイエンスコーパス: GC box

1 duced binding to the promoter or a consensus GC box.

2 tion of either the hMCP-1 GAS element or the GC box.

3 on, which includes a TATA-like element and a GC box.

4 d Egr-1, and enhanced the footprint over the GC box.

5 s indicated that it is indeed a nonconsensus GC box.

6 = 0.37 nM, at least as high as the consensus GC box.

7 three sites have a neighbouring Sp1-binding GC-box.

8 se repeats separated by 3 bp, followed by a "GC" box.

9 es and contains a TATA-box-like sequence and GC boxes.

10 nes are devoid of TATA boxes but are rich in GC boxes.

11 eviously been found to contain two consensus GC boxes.

12 cAMP response element motif flanked by three GC boxes.

13 r respiratory factor-1 (NRF-1) site, and two GC boxes.

14 includes a CpG island, and contains several GC boxes.

15 40 promoter/enhancer, which contains several GC boxes.

16 bited strong hypomethylation specifically at GC boxes.

17 1A expression is TATA-less and contains many GC boxes.

18 receptor elements, and a number of conserved GC boxes.

19 moter and the fibronectin promoter with four GC boxes.

20 , including potential TATA-boxes and several GC boxes.

21 recombinant GKLF bound to each of the three GC-boxes.

22 of the EGR-1 transcription factor to the two GC-boxes.

23 Computer analysis identified two GC boxes, GC box 1 and GC box 2, in the downstream region which we

24 Mutation of GC box 1 resulted in loss of Sp1 and Sp3 binding and an

25 box 2, additional mutations introduced into GC box 1 upstream of the CAAT box led to a large decreas

26 f the Sp family (Sp1 and Sp3) stably bind to GC box 1, but not to GC box 2.

27 f transcription factors Sp1, Sp2, and Sp3 to GC boxes 1 and 6, Sp1 and Sp2 to GC boxes 2 and 5, NF-Y

28 al analyses showed that in this short region GC boxes 1, 2, 5, and 6, a CCAAT box, an inverted CCAAT

29 r factor Yin Yang 1 (YY1) that overlaps with GC box 2 was also identified.

30 box and cap site identified two tracts of C (GC box 2) as the inhibitory sequences.

31 the H1t promoter was relieved by mutation of GC box 2, additional mutations introduced into GC box 1

32 be responsible for the inhibitory effect of GC box 2, and additional binding proteins (CTB-4 and CTB

33 alysis identified two GC boxes, GC box 1 and GC box 2, in the downstream region which were predicted

34 and Sp3) stably bind to GC box 1, but not to GC box 2.

35 and Sp3 to GC boxes 1 and 6, Sp1 and Sp2 to GC boxes 2 and 5, NF-Y to CCAAT boxes, and CREB, ATF1, a

36 In particular, three closely spaced GC-boxes 5' of the TATA box resemble the established bin

37 t; (d) modulated weakly by a positive-acting GC box (-568-GAGGCGGTGC) and strongly by a proximal GC/G

38 with the 69-bp fragment demonstrated that a GC box (-568/-559) and an E box (-523/-528), which inter

39 is of this region revealed (5' --> 3') a Sp1/GC box, a noncanonical cAMP-response element (CRE), a CC

40 This element contains a GC box, a putative binding site for transcription factor

41 located upstream of P1, contains a TATA box, GC boxes, a CCAAT box and GATA and ets consensus sequenc

42 quence has revealed an obvious TATA box, tow GC boxes, a putative GA response element, and several AC

43 Any change to the GC-box abolished replication, but changes to the other m

44 Mutations within this GC box abrogated the ability of p53 to activate transcri

45 Basal and GC-box activated transcription were compared by various

46 First, mutations in the GC boxes affected the 15-LOX2 promoter activity.

47 tains typical promoter elements, including a GC box, an initiator site, and consensus transcription f

48 , GC-rich promoters, including consensus Sp1/GC boxes, an initiator element, cAMP-responsive element-

49 idate proximal elements include the proximal GC box and a 43 bp region between a KpnI site (at -182)

50 In addition, there are a variant GC box and a variant AP1 site in the promoter region.

51 tivity by competing with Sp1 at the upstream GC box and also independently by binding the three downs

52 cription factor binding sequences (TATA box, GC box and CCAAT box), cAMP regulated sequences (CRE), s

53 ll line through both an upstream Sp1 binding GC box and downstream gastrin responsive elements.

54 0 contained two potential Sp1 binding sites (GC box and GT box) and one Ets binding site (EBS).

55 AAT element disrupts binding to the adjacent GC box and partially reduces binding in the distal S/X/Y

56 s demonstrated that both the positive-acting GC box and the negative-acting GC/GT box were recognized

57 motifs such as a TATA-like box, AP-1 sites, GC boxes and a nuclear factor-kappaB binding domain.

58 ne TGFBR1 gene lacks a TATA box but contains GC boxes and CAAT boxes.

59 we found that several Sp1 sites (i.e., three GC boxes and one CACCC box) in the proximal promoter reg

60 contained multiple Sp sites, including four GC boxes and one CACCC box, which directed the highest l

61 important roles for Sp1/Sp3 binding to three GC boxes and one GT box and for binding of myeloid zinc

62 nsus sequences, but is GC rich with multiple GC boxes and other putative cis-regulatory elements.

63 AT box is not present, but there are several GC boxes and potential binding sites for numerous transc

64 e systematically dissected the role of these GC boxes and report that five bona fide Sp1-binding elem

65 ents necessary for its regulation, including GC boxes and Sp1-, AP1-, and AP2-binding sites.

66 In addition to six GC boxes and two GT boxes, a TTAAAA box is located at -2

67 When the GC-box and CRE/AP-1-like elements were mutated, a 60--90

68 We suggest that this GC-box and its binding factor are required for regulated

69 otein complexes involving a highly conserved GC-box and Sp1 or Sp3.

70 h harbors a putative TPA response element, a GC box, and an Ets-like binding site, was required for h

71 pecifically abolished NF-ODC1 binding to the GC box, and binding affinities of 12 different double-st

72 BSAP site, a SP1/Egr-1 site termed the CD19 GC box, and two novel sites named the AT box and PyG box

73 contains a consensus TATA box, two potential GC boxes, and a potential nuclear respiratory factor (NR

74 promoter activity critically depends on four GC boxes, and members of the Sp1 family appear to be inv

75 fied the relative contribution of individual GC boxes, and of the factors they bind, to the regulatio

76 am GC-rich DNA sequence, containing multiple GC boxes, and that transcription factor Sp1 [or related

77 e is not complete redundancy among the three GC boxes, and there is a hierarchy of importance with re

78 plasmid constructs containing CAAT-deleted, GC-box, and nonspecific oligomers in HL60/VCR transfecta

79 esting that cis elements such as the PyG and GC boxes are also necessary for high level CD19 promoter

80 We show that these GC boxes are binding sites for Sp-family transcription f

81 The individual GC boxes are functionally redundant with regard to Mig1-

82 Several consensus GC boxes are present within the sequence.

83 This study shows that all three GC boxes are required to maintain basal transcription an

84 Both E- and GC-boxes are crucial for v-Src-responsive and basal prom

85 proximal promoter contains a similar E- and GC-box arrangement.

86 Mechanistically, we identified two GC boxes as a key TNF response element in the CPI-17 pro

87 T or TATA-like elements but does contain two GC boxes as well as several putative transcription facto

88 ted by a negative region, and at least eight GC-boxes as determined by sequence homology.

89 Sp1 was shown to bind to a GC box at the 5' end of the C/EBP regulatory element in

90 nesis identifies enhanced Sp1 binding to two GC-boxes at -238/-231 and -118/-106 as the core mechanis

91 A typical TATA box (at -25 nt) and a GC box (at -65 nt) were identified in the promoter regio

92 oxes, we detect protein binding only to that GC-box (at position -64 and -55) closest to the transcri

93 in --377 bp promoter contains four clustered GC boxes between nucleotides --146 and --58 and an inver

94 Sp1, as well as Sp3, bound to four GC boxes between nucleotides -130 and -80 as observed by

95 Deletion of three Sp1 sites (GC box) between -376 and -268 or mutation of a CAGA box

96 ve contribution of the Sp family proteins to GC box binding and the transcriptional activity of these

97 classes of transcription factors related to GC box binding proteins (e.g. SP1 and SP7/Osterix) and E

98 domain which showed significant homology to GC box binding proteins BTEB2 and SP1.

99 f the MBP promoter that contains a conserved GC box binding sequence.

100 The GC box binding transcription factor Sp3 both activates a

101 /CCAAT element along with a lesser effect on GC box binding.

102 o -345 bp) in the SLC19A2 promoter and a SP1/GC-box binding site (-48 to -45 bp) in the SLC19A3 promo

103 ied the proposed technique on the PWM of the GC-box, binding site for Sp1.

104 tion element-binding protein (BTEB), a small GC box-binding protein, as a T(3)-regulated gene in deve

105 also increased significantly by coexpressed GC box-binding proteins (Sp1, 3, or 4) in nonstimulated

106 Thus, our data show that the GC box-binding Sp proteins contribute to the regulation

107 mobility shift assays demonstrated that the GC box bound Sp-1 and Sp-3, although the level of bindin

108 Multiple Nix promoter GC boxes bound transcription factor Sp-1, and basal and

109 dvantage of the specific localization of the GC-boxes bound by SP4 transcription factors, I analyzed

110 rc-responsive element, which contains E- and GC-boxes bound by USF1 and Sp1/Sp3, respectively.

111 ses the level of Sp1 promoter binding to the GC box but does not change the level of Sp3 binding.

112 sites, including an E box, CAAT boxes, and a GC box, but this region lacks a TATA element.

113 and activates the FGF-BP promoter through a GC box by luciferase reporter, oligo pull down and chrom

114 ibition of Sp family factors binding to this GC box by mithramycin A led to a significant increase in

115 dence in vivo for inducible signaling to the GC box by this cytokine.

116 This GC-rich region constitutes a "GC box" capable both of binding members of the Sp family

117 These sites include four GC-boxes (CCCGCCC at -227, -68, -46 and GGGCGAG at -382)

118 e-rich 30 base-pair sequence, a mimic of the GC-box cis-element, bound threefold more tightly than an

119 structs having CCAAT or YY1 sites or certain GC boxes cloned upstream of the E2F1 minimal promoter di

120 tudies within this region revealed that four GC boxes conferred hyperacetylation-induced PKCdelta pro

121 moter contained an E box, a Y box, and three GC box consensus elements but lacked both TATA and CCAAT

122 omoter, which contains the X-box, E-box, and GC-box consensus motifs, is able to elicit substantial t

123 I found that the GC-box containing genes are significantly over-represent

124 Site-directed mutagenesis of a potential GC box core motif GCG in the -58/-56 region of the beta1

125 Enhanced binding of Sp1 to this GC box correlates with RA induction of KOR gene.

126 Mutations in two or more of the four GC boxes decreased promoter activity by >80%.

127 n similar cells from wild-type mice, and Hdc GC box-deficient mice failed to develop anaphylaxis.

128 sophils, brain cells, and stomach cells from GC box-deficient mice transcribed the Hdc gene much less

129 ith a reporter construct containing the -263 GC box demonstrated that Sp1 regulates transcription of

130 that 1) the E box is essential for both the GC box-dependent and -independent promoter activity of t

131 box, but it increases Sp1/Sp3 binding to the GC-box despite no change in their cellular protein abund

132 Disruption of the GC box did not affect fold induction by IFN-gamma but re

133 Mutation of the -263 GC box diminished the response of the promoter to Sp1 pr

134 The statistical parameters of GC-box distribution in promoter regions and in the human

135 ors Sp1, Sp3, and Sp4 constitute most of the GC box DNA binding activity in neurons.

136 single-point mutation was introduced to each GC box, EBS, and GT box in PFP9a20, at least 3-fold less

137 tation was introduced again to each proximal GC box, EBS, and GT box of PFP5a.

138 I footprinting revealed that three canonical GC boxes, either overlapping or tightly clustered within

139 Mutation of the core sequence of a putative GC box element located between nucleotides -101 and -99

140 perative interaction between the GAS and the GC box element.

141 pha) by decreasing Sp1 binding to a proximal GC box element.

142 mobility-shift assays identified a positive GC-box element (-107 to -95); Sp1 and Sp3, which bound t

143 that enhanced binding of Sp1 and Sp3 to two GC box elements in the rat Na,K-ATPase beta1 subunit gen

144 nucleotides spanning the proximal and distal GC box elements of the beta1 promoter showed enhanced bi

145 The data are interpreted to indicate that GC-box elements do not stimulate the rate constants for

146 Within exon 1 there are three GC-box elements that displayed distinct binding affinity

147 In vitro, two GC boxes formed protein-DNA complexes (GC-II and GC-III)

148 fic cis-elements have been implicated: three GC boxes (GC-I, GC-II and GC-III) and two nutrient-sensi

149 Computer analysis identified two GC boxes, GC box 1 and GC box 2, in the downstream regio

150 Luc-MCS-beta 72-167 was reduced when the two GC boxes immediately upstream from the PGRE were translo

151 s, gel shift mobility assays targeting three GC boxes immediately upstream of the main transcription

152 The distal GC box in the 5'-UPS of the alphaI(I) collagen gene may

153 UV activated JNK utilized a distal GC box in the 5'-UPS of the collagen gene to regulate ge

154 he repressor complex to a glucose-responsive GC box in the angiopoietin-2 promoter, resulting in incr

155 A second GC box in the P2 promoter also binds the Sp1 protein and

156 ed to be mediated through interaction with a GC box in the proximal portion of the promoter.

157 A GC box in the proximal promoter of the ornithine decarbo

158 compound that interferes with Sp1 binding to GC boxes in DNA.

159 s accomplished by periodic repression of the GC boxes in G1 phase.

160 ng KLF6(WT) demonstrated KLF6(WT) binding to GC boxes in promoters of Colalpha1 (I), Colalpha2 (I), a

161 NF, competed with Sp1 for the binding to the GC boxes in the CPI-17 promoter, and repressed CPI-17 tr

162 r to the different anatomy of the individual GC boxes in the mouse and human proximal promoters.

163 largely prevented by mutations of the tandem GC boxes in the promoter.

164 reveals differential methylation of proximal GC boxes in the two cell lines examined.

165 Sp5/8 bind directly to GC boxes in Wnt target gene enhancers and to adjacent, o

166 es decreased binding to a glucose-responsive GC-box in the angiopoietin-2 (Ang-2) promoter, resulting

167 any other schizophrenia-risk genes via these GC-boxes in the pathogenesis of schizophrenia.

168 tions of one or both of the first and second GC-boxes in the promoter resulted in diminished transact

169 , I analyzed the relative abundance of these GC-boxes in the proximal promoter regions of schizophren

170 ase-resistant chromatin does not require the GC boxes, indicating that other cis-acting elements can

171 nding with mithramycin A, or deletion of the GC boxes, inhibited COL1A2 activation by Smad3, suggesti

172 p containing an ETS-binding site (EBS) and a GC box is essential for both basal and PMA-inducible SPR

173 iated repression, however, only the upstream GC box is essential for high level expression of SUC2.

174 These findings indicate that the tandem GC box is necessary, but not sufficient, for LPS-mediate

175 wn that the central, GC-rich palindrome (the GC-box) is the most important motif for protein binding.

176 tions of the C-rich element that disrupted a GC box located on the inverse strand eliminated PMA resp

177 cated the TSA response is mediated through a GC box located on the RII promoter, which was previously

178 e N1, coinciding with reduced Sp1 binding to GC boxes located within nucleosome N2 and recruitment of

179 We have discovered a functional role for two GC-boxes located in the proximal promoter of the ABCA2 g

180 to the GC-rich motifs, a CACCC box and three GC boxes, located within the Tesc proximal promoter.

181 Our data also suggest that the GC-box-mediated, human-specific mechanism for TERT repre

182 ically to a DNA oligonucleotide containing a GC box motif.

183 oactivation of the Sp1 proteins bound to the GC-box motif footprinted in vivo in pachytene spermatocy

184 cytes identified a single footprint over the GC-box motif.

185 n nuclease sensitivity between wild-type and GC box mutant promoters was not evident in tup1- cells.

186 oter in derepressed cells was reduced in the GC box mutant promoters, particularly in the vicinity of

187 ors was abolished in gel shift studies using GC box mutants.

188 aled a number of such motifs, including Sp1 (GC box), NF-kappaB, and MyoD (E-box).

189 ), glucocorticoid responsive element (GRE), "GC" box, nuclear factor (NF)-kappaB, signal transducer a

190 Mutation of any single GC box of the two located at -40 to -57 did not affect a

191 ngly, site-specific mutations that abolished GC-box or GAS-element function produced clearly disparat

192 -464 to -27) confirmed the importance of two GC-boxes (positions -317 to -309 and -213 to -206) and t

193 yde response element was located in a distal GC box, previously described as the UV response element,

194 construct activity, while a mutation of the GC box reduced it modestly, and a PyG box mutation reduc

195 Whereas mutations in the GC box reduced the promoter activity by 50%, mutations i

196 Mediator complex constitutively occupies the GC box region but not the TRE, serving as a nexus for di

197 tigen to the helically in-phase sites in the GC box region induces DNA bending in the opposite direct

198 n-phase T-antigen binding sites exist in the GC box region located immediately downstream of the AT t

199 Binding of Egr-1 to the GC box region of the mPGES-1 promoter was enhanced by tr

200 ductive effect of TNF-alpha localized to the GC box region of the mPGES-1 promoter.

201 tivity of pluramycin at sequences within the GC box region that are known not to bind T-antigen.

202 bonding site) drug modification sites in the GC box region, demonstrating that these sites are in a b

203 al array with the N1 nucleosome spanning the GC box region.

204 hromatin segments containing the TRE and the GC box regions and the sliding of upstream nucleosomes t

205 Sp1 and to a lesser extent Sp3 bound to the GC box regions of eNOS and TNFalpha in intact cells.

206 activated the DOR promoter via the E box and GC box, respectively.

207 in the E box alone or in both the E box and GC box resulted in 90% loss of transcriptional activity.

208 REST and a higher stability of Sp1 on target GC boxes, resulting in an increase of SYN1 transcription

209 Mutation of both the S element and the GC box results in either no or little effect on transcri

210 cted in the protein complexes that bound the GC boxes revealed by electrophoretic mobility shift assa

211 Mutation of the two GC boxes revealed that these elements play two distinct

212 The inclusion of a consensus GC box sequence as a competitor in gel shift analysis re

213 The c.-172G>A mutation occurs within a GC box sequence element and was not found in 379 control

214 The addition of the Sp1/GC box sequence to this minimal promoter construct inhib

215 eam region of exon 1 revealed four consensus GC box sequences and a strong transcription initiation s

216 Three GC box sequences located between -25 and +10 were essent

217 Recombinant Zf9-GST also bound to GC box sequences within the promoters for the types I an

218 on indicated an absence of both TATA-box and GC-box sequences; this distinguishes it from the promote

219 er potential regulatory elements including a GC box (Sp1-binding site) and three NRF-2 sites, one of

220 r contained TATA and CCAT boxes as well as a GC-box (Sp1-binding site) situated upstream from the tra

221 ty to the G + C-rich Sp1 consensus sequence (GC box), Sp1 and Sp3 transcription factors could be show

222 scription factor consensus motifs, including GC-box, SP1, AP2, and GATA-box sites, in the absence of

223 a downstream promoter element, TATA box, and GC box/Sp1 site at -29 are all individually required for

224 Mutations that crippled both the EBS and GC box suppressed both basal and PMA-inducible SPRR1B tr

225 e Sp7's affinity for the Sp family consensus GC-box target; Dlx5 binding maps to this domain of Sp7.

226 he mouse DOR gene, containing an E box and a GC box that are crucial for DOR promoter activity in NS2

227 -bp minimal promoter containing an essential GC box that binds Sp1/Sp3 in vitro and in vivo.

228 ed affinity of DNA/protein interactions at a GC box that contains a binding site for Sp1, Sp2, and Sp

229 Es) that bind transcription factor NF-Y, two GC boxes that bind Sp1 and a TATA-like element that bind

230 1-dependent binding of two promoter-proximal GC boxes, the mutation of which attenuates alpha1dAR pro

231 TGF-beta1 promoter but minimally to a single GC box; these results correlated with transactivation by

232 the gene revealed the existence of three SP1/GC boxes, three AP1 and one AP2 binding sequences, a cyc

233 , analysis of methylation status of proximal GC boxes using sodium bisulfite sequencing reveals diffe

234 binding protein antiserum suggested that the GC box was bound by basic transcription element-binding

235 ecific and functional binding by Sp3 at this GC box was confirmed by in vitro gel-shift assays using

236 cetyltransferase reporter with a mutagenized GC box was not suppressed by dn-JUN and was not stimulat

237 The GC box was predominantly bound by the DNA binding transc

238 that this minimal region that contained both GC boxes was sufficient for promoter activity.

239 Mutation of one GC-box was particularly detrimental to GLTP transcriptio

240 For the various GC-boxes, we detect protein binding only to that GC-box

241 pecific factor binding to the NRF-1 site and GC boxes were demonstrated by gel mobility shifts and DN

242 Five GC boxes were identified in a 100-bp upstream region, al

243 Analogous to the human gammaENaC gene, two GC boxes were seen at -30 and -61 to the transcription s

244 Here, elements flanking GC boxes were tested for their role in determining wheth

245 Four GC-boxes were shown to be functional Sp1/Sp3 transcripti

246 The three GC boxes which bind Sp1 and Sp3 with high affinity, an A

247 Deletion of the GC box, which binds to zinc finger transcription factors

248 monstrated SP1 and Egr-1 binding to the CD19 GC box, while unknown nuclear proteins bound the PyG and

249 e revealed protection of a GC-rich sequence (GC box) with the same temporal pattern as that seen at t

250 ed to DNA elements comprising a Klf4 site or GC box, with adjacent Meis and Pbx sites.

251 A GC box within the 17-bp element is critical for both pro

252 ntrast, the binding of stable protein 1 to a GC box within the core promoter region was not affected

253 The HDC GC box within the proximal enhancer in the mouse and hum

254 r lacks a canonical TATA box and has several GC boxes within a highly GC-rich region.

255 factors regulate gene expression via binding GC boxes within promoter regions.

256 ophoretic mobility shift assay to two tandem GC boxes within the TGF-beta1 promoter but minimally to

257 mTERT promoters revealed that a nonconserved GC-box within the hTERT promoter was responsible for the