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

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

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

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

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

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

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

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

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

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

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

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

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

99 The GC box binding transcription factor Sp3 both activates a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 -464 to -27) confirmed the importance of two GC-boxes (positions -317 to -309 and -213 to -206) and t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

222 1-dependent binding of two promoter-proximal GC boxes, the mutation of which attenuates alpha1dAR pro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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