ライフサイエンスコーパス: DRE

1 DRE binding or to induce luciferase.

2 DRE females showed dysregulation of the classical comple

3 DRE males exhibited dysregulation of the classical, lect

4 DRE of the prostatic fossa and biopsy confirmation of lo

5 DRE of the prostatic fossa, prebiopsy PSA, and postrecur

6 DRE was defined as the use of 2 or more ASMs.

7 DRE-1 and SKR-1 form a complex, as do the human ortholog

8 DRE-1 functions in parallel to EGL-1, requires CED-9 for

9 DREs are the binding sites for the sequence-specific DNA

10 DREs with MS scores above the threshold were disproporti

11 ltichannel SEEG and video recordings from 14 DRE patients.

12 The 1.28 DRE contains in vitro binding sites for Deformed and DEA

13 four Deformed binding sites renders the 1.28 DRE inactive in vivo, demonstrating that these sites are

14 Comparisons of the 1.28 DRE with other known Deformed-responsive enhancers indic

15 ied a 664-bp Deformed Response Element (1.28 DRE) that directs maxillary-specific expression of a rep

16 A reconstructed eruption volume of >=5km(3) DRE is derived, suggesting a VEI 5 event or larger.

17 This Sp1(N)(4)DRE(core) motif has been identified in promoters of seve

18 with AhR-Arnt proteins bound to the Sp1(N)(4)DRE(core) motif were also dependent on the proximity of

19 In the mouse, 8 DREs are located in the 14-kb intergenic region between

20 regions that physically interact with the 92 DRE that were found at IBD susceptibility loci.

21 uently, genes that are regulated by these 92 DREs are to be considered as candidate genes.

22 -deficient cells that expressed AhRY9F and a DRE-driven luciferase construct with phorbol 12-myristat

23 ription from the TalphaREI-TK construct in a DRE-dependent manner.

24 uced a concentration-dependent response in a DRE-driven CAT reporter construct, with a greater than 1

25 d modulation is AhR specific and occurs in a DRE-independent manner.

26 ic mice expressing a wild-type (WT) Ahr or a DRE-binding mutant Ahr (A78D) on an ahr-null background

27 pression of CsRuby1 by directly binding to a DRE/CRT cis-element within the retrotransposon in the pr

28 y, of the mouse-rat orthologous genes with a DRE between -1500 and +1500, only 37% had an equivalent

29 Those with an abnormal DRE or a PSA above 4 ng/ml should be referred to a urolo

30 family history of prostate cancer, abnormal DRE result, African American race, and older age.

31 grade prostate cancer included PSA, abnormal DRE, and older age.

32 onse element (DRE) D, E, and A and abrogated DRE-driven gene induction mediated by the AhR with no ef

33 A4 transformed the Ah receptor to an active DRE-binding form in a concentration-dependent manner as

34 In addition, DRE was able to identify only 3 of 14 cases (21%) with a

35 polymorphism rs11959928 were shown to affect DRE function, illustrating that genes regulated by DREs

36 Results revealed that AhR DRE binding is not required for the suppression of genes

37 BLMP-1 and DRE-1 function together to regulate developmental timing

38 Combined with age and DRE findings, both 4Kscore and uCaP could accurately pre

39 Epilepsy and DRE were administratively identified based on criteria n

40 inding validates DiMNF as an AHR ligand, and DRE-dependent reporter assays with quantitative mRNA ana

41 The combination of PSA and DRE is an excellent cancer-screening tool with sensitivi

42 y of prostate cancer, PSA, PSA velocity, and DRE adjusting for history of prior prostate biopsy.

43 ction of more than one quarter of apparently DRE-detected prostate cancers and up to one quarter of a

44 d processes require a nuclear event, such as DRE binding, we used homologous recombination to generat

45 in order to analyze the relationship between DRE binding (determined in vitro using an electrophoreti

46 None of the EF-hand mutants bind DRE at saturating Ca(2+) levels, suggesting that binding

47 ng the four EF-hands (residues 65-256) binds DRE (K(d) = 200 nM) in a Ca(2+)-regulated and sequence-s

48 pressed, whereas FOX proteins enhanced, both DRE and FOXA-responsive element-driven gene expression.

49 ions of AhR/Arnt that are important for both DRE binding and induction of transcription.

50 iology was the strongest determinant of both DRE and GDD.

51 PsAP2 showed specific binding with both DRE and GCC box elements and it was able to transactivat

52 ranslational regulation of BLMP-1/BLIMP-1 by DRE-1/FBXO11 coordinates C. elegans developmental timing

53 the clinical DD score and were evaluated by DRE and BET [standard and variable volume (VV)].

54 nction, illustrating that genes regulated by DREs colocalizing with CKD-associated variation can be d

55 AM) binds to regulatory element sites called DRE in the DNA and represses transcription of target gen

56 type AHR could be dissociated from canonical DRE-dependent transactivation in a ligand-dependent mann

57 R by Way-169916 fails to stimulate canonical DRE-driven AHR-mediated CYP1A1 expression, thus eliminat

58 these genes possessed positionally conserved DREs as determined by multiple sequence alignment.

59 Conversely DRE activity was only inhibited by the COX2-selective in

60 esis analysis defined an essential 80bp core DRE sequence and its potential regulatory motifs.

61 ype pCD/L and constructs mutated in the core DRE (pCD/L(m1)) and Sp1 (pCD/L(m2)) sites, it was shown

62 some other genes whose promoters lack a CRT/DRE element.

63 ative effects on the function of the CBF-CRT/DRE regulatory module, and 11 transcription factors enco

64 lerance is dependent on a functional CBF-CRT/DRE regulatory module.

65 n is only partially dependent on the CBF-CRT/DRE regulatory module.

66 the C-repeat/drought-responsive element (CRT/DRE) DNA regulatory element.

67 motif or the drought-responsive element (CRT/DRE) in its promoter, failed to normally accumulate in t

68 C repeat/dehydration-responsive element (CRT/DRE) motif in their promoters.

69 C-REPEAT/DEHYDRATION RESPONSIVE ELEMENT (CRT/DRE) motifs, the cognate CBF binding site in its upstrea

70 tudies we conclude that CAS genes harbor CRT/DRE motifs, their proximity to one another is likely key

71 We hypothesize that these differences in CRT/DRE copy numbers in CAS30/CAS31 upstream regions combine

72 nsive in both species, harbored numerous CRT/DRE motifs, but only in the distal module.

73 (CAMTA3) in the rapid cold induction of CRT/DRE BINDING FACTOR (CBF) genes CBF1 and CBF2, and the re

74 The presence of CRT/DRE promoter cis-elements is consistent with the synchro

75 propose that cold-induced expression of CRT/DRE-containing COR genes involves a low temperature-stim

76 whether the failure of cold induction of CRT/DRE-containing genes in sfr 6 was due to altered low-tem

77 stream region whereas MtCAS31 lacked one CRT/DRE partner of the two proximal partner pairs.

78 ROST RESISTANCE-H2-H2 (FR-H2) possessing CRT/DRE sites in their upstream regions, the most notable of

79 he same C repeat/dehydration-responsive (CRT/DRE) element as cold induction.

80 ontaining a C-repeat/drought-responsive (CRT/DRE) promoter element and metabolic changes that enhance

81 We discuss the possibilities that CRT/DRE binding proteins (such as CBF1) require activation t

82 ncoded by this allele cannot bind to the CRT/DRE (C-repeat/ dehydration-responsive element) motif pre

83 ional activator, CBF1, that binds to the CRT/DRE and demonstrated that its overexpression in transgen

84 porter genes in yeast that contained the CRT/DRE as an upstream activator sequence.

85 nes carrying a minimal promoter with the CRT/DRE as an upstream regulatory element.

86 temperature, increased expression of the CRT/DRE binding factor (CBF) family of transcriptional activ

87 The role of the CRT/DRE has been empirically tested by use of a synthetic pr

88 synthetic promoter, confirming that the CRT/DRE is sufficient to confer the sfr6 effect upon express

89 pically harbor one or more copies of the CRT/DRE low temperature cis-acting DNA regulatory element.

90 CBF2, CBF3, and ATP5CS1, which lack the CRT/DRE motif, was not affected.

91 F transcriptional activators bind to the CRT/DRE regulatory element present in the promoters of many

92 nscriptional activator that binds to the CRT/DRE sequence, induced COR gene expression and increased

93 be general to cold-inducible genes with CRT/DRE promoter elements, but also that it extends to some

94 PPARdelta using an adenovirus not only drove DRE activity but also prevented RMIC death due to COX2 i

95 bretinal fluid [SRF], diffuse retinal edema [DRE], retinal pigment epithelial detachment [PED], and s

96 Destruction removal efficiency (DRE) was calculated by assuming a flare natural gas inpu

97 e, those with a significant change in either DRE or PSA results, or those at higher risk for prostate

98 Caenorhabditis elegans DRE-1/FBXO11 functions in an SCF E3-ubiquitin ligase com

99 rchitectures, for distal regulatory element (DRE) detection.

100 usly identified a distal regulatory element (DRE) in the mouse serum amyloid A3 (SAA3) promoter that

101 ived from the downstream regulatory element (DRE) of either the prodynorphin or c-fos genes.

102 ThPOK locus a key distal regulatory element (DRE) that mediated its differential expression in class

103 ting element, the distal regulatory element (DRE), is sufficient for this TCR-dependent induction.

104 ified a novel downstream regulatory element (DRE), which is bound by RUNX1 and is necessary for human

105 red to as the downstream regulatory element (DRE).

106 89 to -103) and a distal regulatory element (DRE, -121 to -128).

107 ance of the DNA replication-related element (DRE), the Initiator (Inr), and a new over-represented mo

108 well as the DNA replication-related element (DRE)-binding factor DREF.

109 dissociation of non-dioxin-response element (DRE) AHR activity from DRE-dependent xenobiotic gene exp

110 AHR binding to its dioxin response element (DRE) and driving expression of CYP1 family members, whic

111 d the presence of a dioxin response element (DRE) and five nuclear factor-kappaB (NF-kappaB) motifs o

112 delta binding to PPARdelta response element (DRE) and increased PPARdelta reporter activity, indicati

113 delta binding to PPARdelta response element (DRE) and increased PPARdelta reporter activity, which wa

114 bolished binding to dioxin response element (DRE) D, E, and A and abrogated DRE-driven gene induction

115 hich recognizes the dioxin response element (DRE) in the promoter of downstream genes.

116 P1A1) by binding to dioxin response element (DRE) sequences in their promoter region.

117 a specific reporter (delta response element (DRE)) by 90% above base line.

118 ore sequence of a dioxin responsive element (DRE) and binds the aryl hydrocarbon receptor (AhR)-AhR n

119 e C-repeat (CRT)/drought-responsive element (DRE) binding factor CBF1/DREB1b is a transcriptional reg

120 responding to the dioxin-responsive element (DRE) core binding sequence, which is the cognate respons

121 repeat (CRT)/dehydration-responsive element (DRE) DNA regulatory element present in the promoters of

122 the C-repeat/dehydration responsive element (DRE), that stimulates transcription in response to low t

123 tion driven by the DACH1-responsive element (DRE).

124 evealed that dehydration-responsive element (DRE)B2A but not DREB1A, RD (response to dehydration)29A

125 downstream and upstream regulatory elements (DRE and URE), and between the DRE and ygaY that lies imm

126 Drosophila DNA replication-related elements (DRE) and a single putative E2F binding site.

127 that works through dioxin response elements (DRE) to activate gene expression.

128 inding of AhR to dioxin-responsive elements (DRE) in vitro; and 3) inhibit TCDD-induced transcription

129 slationally regulated by two 28 nt elements (DREs) located in the 3'UTR that bind a factor called DRF

130 ypothesized that distal regulatory elements (DREs) are involved in optimal expression of the NGB gene

131 enetic variation on DNA regulatory elements (DREs).

132 ize with non-coding DNA regulatory elements (DREs).

133 h binding to downstream regulatory elements (DREs).

134 l level by two 28 nt direct repeat elements (DREs) located in its 3' untranslated region (3'UTR).

135 man, mouse and rat dioxin response elements (DREs) in genomic sequences unambiguously assigned to a n

136 c binding of DREAM to DNA response elements (DREs) in prodynorphin and c-fos genes.

137 r (Arnt), binds to dioxin response elements (DREs) located in the promoter region of target genes, su

138 s several putative dioxin response elements (DREs).

139 iption factor to dioxin-responsive elements (DREs) upstream of promoters that regulate the expression

140 on by binding to dioxin-responsive elements (DREs) within an enhancer upstream of the CYP1A1 gene.

141 g of the AHR to dioxin- responsive elements (DREs) within the genome.

142 g sequences, the damage-responsive elements (DREs), rendered these genes dependent upon TAF(II)s.

143 h specificity to dioxin-responsive elements (DREs).

144 ntrolled by four dioxin-responsive elements (DREs).

145 llision cell, the dynamic range enhancement (DRE) lens of a Waters Q-IM-TOF, or the exit lens of a tr

146 plex binds to "dioxin responsive enhancers" (DREs) and activates genes involved in the metabolism of

147 with epilepsy have drug-resistant epilepsy (DRE) and require surgical interventions.

148 Drug-resistant epilepsy (DRE) is thought to be associated with increased mortalit

149 Drug-resistant epilepsy (DRE) presents significant challenges in treatment and ma

150 that patients with drug-resistant epilepsy (DRE) undergo comprehensive neurodiagnostic evaluation, i

151 es considered to be drug-resistant epilepsy (DRE).

152 peutic approach for drug-resistant epilepsy (DRE).

153 me in children with drug resistant epilepsy (DRE).

154 ptic drug trials in drug resistant epilepsy (DRE).

155 ening is performed with digital rectal exam (DRE) and measurement of serum prostate-specific antigen

156 at least one PSA and a digital rectal exam (DRE) during the year before biopsy, had at least two PSA

157 ly using PSA and digital rectal examination (DRE) alone and subsequently using the remaining variable

158 with findings on digital rectal examination (DRE) and magnetic resonance imaging, specific endoscopic

159 ue to suspicious digital rectal examination (DRE) findings and/or PSA levels (limit range, 2.0-20.0 n

160 rapy (CMT) using digital rectal examination (DRE) has been proposed as a means of assessing efficacy

161 me, and positive digital rectal examination (DRE) of the prostatic fossa were all statistically signi

162 ents with normal digital rectal examination (DRE) results but elevated prostate-specific antigen (PSA

163 ad heme-positive digital rectal examination (DRE) results or hematochezia at routine follow-up.

164 test (BET) and a digital rectal examination (DRE) score were evaluated as separate or combined tests

165 d serendipity in digital rectal examination (DRE) screening as the discovery of a prostate cancer by

166 a expand the classes of AHR ligands exerting DRE-independent anti-inflammatory SAhRM activity, sugges

167 A total of 13 bona fide DREs, all including the substitution intolerant core seq

168 1% for macular fluid (kappa = 0.28), 79% for DRE (kappa = 0.10), 90% for PED (kappa = 0.78), and 79%

169 asic regions of AhR and Arnt are crucial for DRE binding.

170 ls of luciferase induction (9 +/- 2-fold for DRE and 8 +/- 2-fold for NF-kappaBs of Fas promoter and

171 TT is an effective and safe intervention for DRE with different disease aetiologies.

172 ly safe and effective treatment modality for DRE, although it is not yet ready for use in humans outs

173 Probes for DRE or NF-kappaB motifs of Fas and/or FasL promoters dem

174 is not a phosphorylated residue required for DRE binding.

175 xin-response element (DRE) AHR activity from DRE-dependent xenobiotic gene expression.

176 Previously identified functional DREs in well-characterized AhR-regulated genes including

177 echanism involving an invariant Asp-Arg-Glu (DRE) triplet.

178 7%) had epilepsy, of whom 55 571 (33.8%) had DRE.

179 Epo gene and found that its promoter harbors DREs immediately upstream of its transcriptional start s

180 AhR nuclear translocator protein heterodimer DRE-binding activity as assessed by electrophoretic mobi

181 rity (MS) score threshold to rank identified DREs.

182 ally, the benefit of effective management in DRE lacks evidence.

183 Mutations in DRE of Fas promoter or NF-kappaBs of FasL promoter led t

184 Mutations in DREs can contribute to IBD pathogenesis through dysregul

185 5-aza-CdR partially restores TCDD-inducible DRE occupancy, showing that DNA methylation indirectly s

186 se to TCDD in LNCaP cells, whereas inducible DRE occupancy occurs in RWPE-1 cells.

187 f LT at 18 degrees C, suggesting that intact DRE is not required for transcription from the LT promot

188 erol biosynthesis pathway independent of its DRE-binding ability, and suggest that AhR may be a previ

189 h a mutation in the AHR nuclear localization/DRE binding domain.

190 We propose the name "DRE-TIM metallolyases" for this newly identified enzyme

191 B (NF-kappaB) motifs on Fas promoter, and no DRE but two NF-kappaB motifs on FasL promoter.

192 Recent evidence using a non-DRE binding AHR mutant has established the DRE-independe

193 Microarray studies with a non-DRE binding but otherwise functional AHR mutant identifi

194 ght-responsive/C-repeat) cis element but non-DRE/CRT type stress-responsive genes were less affected.

195 vone (alphaNF) mediates the suppressive, non-DRE dependent effects on SAA1 expression and partial DRE

196 sitive cores in biopsy-naive men with normal DRE results and elevated PSA levels.

197 otic stress, ERF1 bound to GCC boxes but not DRE elements; conversely, under abiotic stress, we obser

198 op formed between its promoter and the novel DRE.

199 conformation capture we identified two novel DREs located -70 kb upstream and +100 kb downstream from

200 anti-inflammatory activity in the absence of DRE-mediated expression fulfills the major criteria of a

201 Parental genes also show an abundance of DRE and Inr motifs, but these do not seem to have been c

202 Given the inaccuracy of DRE following preoperative CMT, it should not be used as

203 192837, were found to be potent inducers of DRE-driven transcriptional activity; AGN 190730 was the

204 .55 ng/mL for further work-up, regardless of DRE findings.

205 The specific regulation of DRE/CRT class of genes by FRY2 appears to be caused by r

206 When we investigated the role of DRE and NF-kappaB, we observed varying levels of lucifer

207 The role of DRE-1 in regulating BLMP-1 stability is evolutionary con

208 and 3) inhibit TCDD-induced transcription of DRE-dependent luciferase in stably transfected hepatoma

209 restimation of the true information value of DRE and PSA screening.

210 ristics examined had a significant impact on DRE estimation of response.

211 One DRE molecule binds tightly to the protein with a dissoci

212 ntially to only one among several GCC box or DRE/CRT elements in the promoter region of its target ge

213 and COLD-REGULATED 15A (COR15A) with GCC or DRE elements, thereby promoting their expression.

214 tresses by stress-specific binding to GCC or DRE/CRT.

215 opsy of all patients with an abnormal PSA or DRE.

216 biopsy confirmation of local recurrence, or DRE of the prostatic fossa.

217 eviously reported product complexes of other DRE-TIM metallolyases and induced fit substrate docking

218 ls after the first several years, but in our DRE cohort, mortality remains elevated despite a median

219 ndent effects on SAA1 expression and partial DRE-mediated CYP1A1 induction.

220 impact of serendipity, the currently popular DRE- and PSA-based screening strategy may not be optimal

221 Hematochezia or positive DRE findings are frequent sequelae of definitive radiati

222 Runx1 in mice harbouring human CD34 promoter-DRE constructs abrogates human CD34 expression.

223 tivation in vivo involving the F-box protein DRE-1.

224 y for men receiving finasteride include PSA, DRE, age, race, family history, and history of a prior n

225 nsiveness of 192 genes possessing a putative DRE.

226 Putative DREs were identified in 48 out of 2437 human-mouse-rat o

227 ding the important transcriptional regulator DRE-binding protein 2A (DREB2A), two heat shock transcri

228 regulatory element termed the CRT (C-repeat)/DRE (dehydration-responsive element).

229 on of reporter genes containing the C-repeat/DRE as an upstream activator sequence but not mutant ver

230 C-repeat/DRE binding factor, CBF1 (C-repeat/DRE Binding Factor 1).

231 dopsis thaliana cDNA that encodes a C-repeat/DRE binding factor, CBF1 (C-repeat/DRE Binding Factor 1)

232 ptional activator that binds to the C-repeat/DRE DNA regulatory element and, thus, is likely to have

233 s site shows some similarity to the C-repeat/DRE elements bound by proteins that contain a single AP2

234 Binding of CBF1 to the C-repeat/DRE was demonstrated in gel shift assays using recombina

235 tion factor BLMP-1 as a substrate of the SCF(DRE-1/FBXO11) complex.

236 the AHR-ARNT heterodimer binds to a specific DRE that overlaps binding sequences for peroxisome proli

237 We wished to determine whether such DRE-independent repression with wild-type AHR could be d

238 g that DNA methylation indirectly suppresses DRE occupancy.

239 nsient transfection assays, we observed that DRE driven transcription was markedly inhibited by hypox

240 phoretic mobility shift analyses showed that DRE binding factor (DREF) binds to these sites.

241 Our results suggest that DRE-1/FBXO10 is a conserved regulator of apoptosis.

242 ctivity, and binds to CED-9, suggesting that DRE-1 promotes apoptosis by inactivating CED-9.

243 The DRE score displayed an AUC of 0.56 (SE = 0.063, p = 0.30

244 The DRE was both necessary for suppression of ThPOK expressi

245 hese lines had reached the periphery and the DRE where the adjacent CNS was also stained.

246 of the interactions between AhR/Arnt and the DRE.

247 Another, the DRE/TGE element of the tra-2 3' UTR, was not detected by

248 ven of these DREs, collectively known as the DRE cluster (DREC), are located 1.4 kb upstream of the C

249 tory elements (DRE and URE), and between the DRE and ygaY that lies immediately downstream of proVWX.

250 he Drosophila mtSSB gene is regulated by the DRE/DREF system.

251 This element, the DRE (downstream repressive element), was mapped to the 1

252 n-DRE binding AHR mutant has established the DRE-independent suppression of inflammatory markers by t

253 3-base pair mismatches was identified in the DRE.

254 trast, although PGE2 treatment increased the DRE reporter activity in intact cells, it failed to indu

255 The crucial role of the DRE in NGB expression activation was further confirmed b

256 Specific recognition of the DRE is determined locally by the DNA-binding residues, w

257 lineage choice, whereby inactivation of the DRE silencer by a strong TCR signal leads to CD4 commitm

258 ion and base substitution mutagenesis of the DRE sites demonstrated that they are required for effici

259 level after CRISPR-mediated deletion of the DRE.

260 Placing the DRE in different promoter contexts indicated that its ac

261 ion and antibody studies determined that the DRE contains a binding site for the transcription factor

262 that leads to trans-activation and that the DRE is the minimal DNA element required for PMA to enhan

263 formation capture assays in LT-HSCs that the DRE physically interacts with the human CD34 promoter.

264 ed that this flavone elicited binding to the DRE by guinea pig but not mouse AhR complex.

265 n showed that ZmDREB2A directly binds to the DRE motif of the promoters of both ZmGH3.2 and ZmRAFS.

266 ding of the transcription factor USF1 to the DRE-associated E-box domain in the gene encoding A20 act

267 partway toward the periphery and toward the DRE.

268 Plasmids in an hns strain from which the DRE has been deleted still produce elevated levels of LT

269 ian AHR-ARNT heterodimer in complex with the DRE, in which ARNT curls around AHR into a highly intert

270 pression of stress-responsive genes with the DRE/CRT (drought-responsive/C-repeat) cis element but no

271 DRF is a factor that binds the DREs and may be a trans-acting translational regulator o

272 Here, we rename the DREs to TGEs (tra-2 and GLI elements).

273 Seven of these DREs, collectively known as the DRE cluster (DREC), are

274 To identify target genes of these DREs, we used circular chromosome conformation capture (

275 Within this DRE, three functional elements interact with CCAAT/enhan

276 CDD regulates Fas and FasL promoters through DRE and/or NF-kappaB motifs via AhR.

277 ls, it failed to induce PPARdelta binding to DRE in cell-free system, suggesting that cPLA2alpha-medi

278 ivity, DiMNF fails to promote AHR binding to DRE probes as determined through electromobility shift a

279 ess, we observed specific binding of ERF1 to DRE elements.

280 ent (residues 1-70) binds nonspecifically to DRE in a Ca(2+)-independent manner, whereas a C-terminal

281 nctions upstream of CED-9 and in parallel to DRE-1, another CED-9 and tail-spike cell death regulator

282 xtracts enhanced the binding of PPARdelta to DRE in vitro, suggesting a direct role of arachidonic ac

283 his, AA enhanced the binding of PPARdelta to DRE, in vitro, suggesting a direct role of AA for PPARde

284 FBXO10, a human protein related to DRE-1, binds BCL2 and promotes its degradation, thereby

285 The EF-hand mutants bind specifically to DRE, suggesting they are functionally intact.

286 elements that are functionally equivalent to DREs.

287 rthermore, the former is not blocked by two "DRE-decoy" treatments.

288 rinting experiments reveal that unmethylated DRE sites do not bind protein in response to TCDD in LNC

289 Clinical assessment using DRE underestimated pathologic response in 73 cases (78%)

290 g surgeon's ability to assess response using DRE.

291 in these tumor characteristics, assessed via DRE.

292 ore, we observed supershift in mobility when DRE and NF-kappaB probes were incubated in the presence

293 ctal cancer (T3/4 or N1) were evaluated with DRE and sigmoidoscopy in order to determine the followin

294 , we identified a total of 433 patients with DRE defined as at least one seizure per month and failur

295 A total of 33 542 patients with DRE were included in the Medicaid cohort, 22 496 in the

296 for treatment, offering hope to people with DRE for freedom from seizure.

297 etiology was determined in 82% of those with DRE, and 75% of those with GDD.

298 Among US veterans with DRE, the mean (SD) age was 58.3 (15.4) years, and 49 430

299 Under identical conditions, zfAHR1/zfARNT2b/DRE complexes are formed; however, the interactions are

300 TG with the attached dorsal root entry zone (DRE) into the central nervous system (CNS) were stained