ライフサイエンスコーパス: SRE

1 SRE encode all six known protein secretion systems prese

2 SRE SNPs in various SNP functional classes show differen

3 rate (beta coefficient = 0.0025, P = .001), SRE LA strain rate at early diastolic peak (beta coeffic

4 role in enhancing the HGF-induced Erk-Elk-1-SRE pathway.

5 In total, we identified 119 SRE pairs between different regions of cassette exons th

6 via the induced binding of SREBP to the -150 SRE and that USF binding to the -65 E-box is also requir

7 e prevented by mutation not only of the -150 SRE but, unexpectedly, of the -65 E-box as well.

8 n both fasted and refed mice, while the -150 SRE is bound by SREBP-1 only in refed mice.

9 also found that mutation of either the -150 SRE or the -65 E-box abolishes the feeding-induced activ

10 discontinued prematurely (645 patients; 299 SREs) after the corporate supporter withdrew study drug

11 We identified 37 SRE sets that include both enhancer and silencer element

12 Primary analysis was planned after 470 SREs.

13 xon or intron definition in splicing, and 77 SRE pairs from the same region that may arise from a lon

14 had a markedly increased ability to activate SRE reporter genes, suggesting that its activation of SR

15 In addition, SRE resulted in a complex transformation of nCu, where C

16 ficity of nuclear protein binding to the ADH-SRE site was confirmed using antibody and UV cross-link

17 The in vivo binding status of SREBP-1 to ADH-SRE sites, as measured by the chromatin immunoprecipitat

18 Functional analysis of the ADH-SREs demonstrated these sites to be essential for ADH tr

19 event analysis) counted hypercalcemia as an SRE.

20 +32 bp FRA-1 promoter fragment containing an SRE and an ATF site alone was also insufficient to confe

21 cement of KLF11 from an Sp1 site flanking an SRE, indicating that activation by SREBP/Sp1 requires an

22 nivariate predictor of the odds of having an SRE (P = 0.0445; odds ratio = 1.30; 95% confidence inter

23 redictive biomarker of OS and the risk of an SRE in patients treated with (223)Ra.

24 r other solid tumors, the proportion with an SRE was reduced in both zoledronic acid groups compared

25 nalgesic use, proportion of patients with an SRE, or mobility at week 9 or 27.

26 The interaction between Cu(2+) and SRE was stronger (Kd = 7.181 x 10(4) M(-1)) but varies f

27 , and phenolic acids), as well as Cu(2+) and SRE.

28 Upc2 and Candida glabrata CgUpc2 to AR1b and SRE/AR1c elements.

29 thrombin-induced stress fiber formation and SRE activation supports this hypothesis.

30 bin-induced actin stress fiber formation and SRE-dependent gene transcription.

31 trong interactions between nCu particles and SRE, as well as with individual organic acids.

32 one mass or prior osteoporotic fracture, and SREs by one-third in cancer patients.

33 Bone metastasis and SREs in prostate cancer patients are associated with con

34 regarding the burden of bone metastasis and SREs.

35 d SRE 6.9 restored late-phase LTD in Arc-/-, SRE 6.9 mutant BAC cells.

36 ogether with myocardin expression as well as SRE and NF-kappaB activities.

37 How subsequent events at SRE promoters stimulate initiation of transcription has

38 d that DN-MKL1 and RNAi specifically blocked SRE-dependent reporter gene activation by serum and RhoA

39 Whereas Galphaz also blocks SRE reporter induction by the activated mutant RhoAL63,

40 PCK-C gene promoter; this was lost when both SREs were mutated.

41 dence on the clinical and economic impact by SRE subtype.

42 gene, and inducible cis-elements (CRE, CaRE, SRE, AP1 or NF-kappaB) demonstrated that only CRFR1alpha

43 Here we develop CoSREM (Combinatorial SRE Miner), a graph mining algorithm to discover combina

44 h mining algorithm to discover combinatorial SREs in human exons.

45 r multiple tissues to identify combinatorial SREs which may be responsible for exon inclusion or excl

46 The 7-bp consensus SRE is identical to the anaerobic response element, AR1c

47 SREs are likely different from constitutive SREs, since only 18% of our exonic splicing enhancers (E

48 ast inhibitors such as bisphosphonates delay SREs but do not prevent skeletal complications or improv

49 vity analyses were performed where denosumab SRE probabilities were assumed to be 50%, 75%, and 90% l

50 bit constitutively active Galpha13-dependent SRE activation.

51 al products was screened for GPR56-dependent SRE activation inhibitors that did not inhibit constitut

52 c G proteins stimulated p114RhoGEF-dependent SRE activity.

53 TAZ-dependent (TEAD) and MRTF-A/B-dependent (SRE.L) transcriptional activity.

54 sets of unbiased, experimentally determined SREs show a distinct strand-asymmetry pattern that is in

55 g its binding affinity to multiple different SRE sequences.

56 may arise from a long motif or two different SREs bound by different SFs.

57 proportion of extremely rare SNPs disrupting SREs is significantly higher in European than in African

58 formed by an upstream TRE and the downstream SRE and ATF sites and the cognate factors is necessary a

59 entified nine splicing regulatory effectors (SREs) from 87 P. infestans effectors.

60 nsgenic studies show that mutation of either SRE, the TBE or the distal GATA element, strongly reduce

61 ce of a complex splicing regulatory element (SRE) sequence that interacts with the splicing factors h

62 identified three sterol regulatory element (SRE) sites in the Fbw8 promoter, where SRE-binding prote

63 regulated by the sterol regulatory element (SRE)-binding protein (SREBP) pathway, and RSV treatment

64 mapping through subtelomere repeat element (SRE) regions to unique chromosomal DNA while simultaneou

65 he activation of the serum response element (SRE) by preventing MAPK-mediated phosphorylation of the

66 ed a 7-bp consensus sterol-response element (SRE) common to genes involved in sterol biosynthesis and

67 l activation via the serum response element (SRE) in response to anti-CD3 antibody, phorbol ester, or

68 The c-fos serum response element (SRE) mediates transcriptional activation in response to

69 at both the ARE and serum response element (SRE) of the Egr-1 promoter, which facilitates binding of

70 factor (GEF)-induced serum response element (SRE) reporter activation in human embryonic kidney 293T

71 tains two canonical sterol response element (SRE) sites (-63 to -53 and -52 to -40 relative to the tr

72 to an LDLR promoter sterol response element (SRE), increasing LDLR gene expression and LDL-C uptake.

73 ranscription factor, serum response element (SRE), that was enhanced by p114RhoGEF.

74 9-583) of radixin on serum response element (SRE)-dependent gene transcription initiated by a constit

75 leton remodeling and serum response element (SRE)-dependent gene transcription.

76 d strongly activated serum response element (SRE)-dependent reporter genes through its direct binding

77 proteins, activates serum response element (SRE)-dependent transcription through changes in actin dy

78 nced the HGF-induced serum response element (SRE)-luciferase activity.

79 obes, we developed a serum response element (SRE)-luciferase-based screening approach to identify GPR

80 PI3K both stimulate serum response element (SRE)-mediated gene expression, and serum response factor

81 ry for activation of serum response element (SRE)-mediated transcription, a G12/13-stimulated pathway

82 ox) located within a serum response element (SRE).

83 d transcription of serum responsive element (SRE) but had a very small effect on the activity of estr

84 f an ERK-dependent serum-responsive element (SRE)-luciferase reporter gene, indicating that associati

85 otentiated) high insulin-induced SR element (SRE) activation and beta-MHC expression.

86 ollectively known as serum response element, SRE), and an ATF site, is also necessary for the FRA-1 i

87 tions within the set of regulatory elements (SRE) regulating ESR1 in 7% of ESR1-positive breast cance

88 here it binds to sterol regulatory elements (SRE).

89 ng site (CArG box), serum response elements (SRE) also typically contain a binding site for a member

90 promoter-imbedded sterol response elements (SRE) and co-induced by statins.

91 ntified switch (S) regulatory ATTT elements (SREs) in the Igamma and Iepsilon promoters and downstrea

92 ic variants in splicing regulatory elements (SREs) and evaluated the extent to which natural selectio

93 of cis-acting splicing regulatory elements (SREs) and their interactions.

94 Splicing regulatory elements (SREs) in pre-mature messenger RNA play a very important

95 There are two SREBP regulatory elements (SREs) in the PEPCK-C gene promoter (-322 to -313 and -59

96 t identifies synonymous regulatory elements (SREs) in vertebrate genomes.

97 ch site, other splicing-regulatory elements (SREs).

98 everal potential sterol regulatory elements (SREs).

99 tes are called splicing regulatory elements (SREs).

100 l boundaries of subtelomere repeat elements (SREs) in transformed lymphoblastoid cell lines (LCLs) an

101 ilizes three distal serum response elements (SREs) in the EGR1 promoter, which are transactivated by

102 of DNA sequences (steroid response elements, SREs).

103 EGF-induced ERK phosphorylation and enhanced SRE-dependent transcription.

104 ce MKP-1 null fibroblasts exhibited enhanced SRE activity in response to serum compared with wild-typ

105 Soft-rot Enterobacteriaceae (SRE), which belong to the genera Pectobacterium and Dick

106 Error (MSE) and Signal Reconstruction Error (SRE) ratio of the proposed method was 39.6% less and 8%

107 ll survival (OS) and skeletal-related event (SRE) data have been reported for the overall trial popul

108 ts with at least one skeletal-related event (SRE), defined as pathologic fracture, spinal cord compre

109 on-free survival and skeletal-related event (SRE).

110 n of patients with a skeletal-related event (SRE; defined as pathologic fracture, radiation or surger

111 aying or preventing skeletal-related events (SRE) in patients with advanced cancer and bone metastase

112 ne or more on-study skeletal-related events (SRE), and safety were also evaluated.

113 reases the risk for skeletal-related events (SREs) in men with castration-resistant prostate cancer a

114 tment/prevention of skeletal-related events (SREs) in multiple myeloma and breast and prostate cancer

115 aying or preventing skeletal-related events (SREs) in patients with breast cancer with bone metastase

116 bone metastasis and skeletal-related events (SREs) in prostate cancer, and discuss current gaps in un

117 Purpose Skeletal-related events (SREs) such as pathologic fracture, spinal cord compressi

118 gnificantly reduced skeletal-related events (SREs), and improved progression-free survival and overal

119 reduce the risk of skeletal-related events (SREs), but only radium-223 improves survival.

120 ife or reduction in skeletal-related events (SREs).

121 reduce the risk of skeletal-related events (SREs).

122 ractures, and other skeletal-related events (SREs).

123 (pain progression, skeletal-related events [SREs], or death) and cost-effectiveness.

124 nanocopper (nCu) and synthetic root exudate (SRE) and its components (including sugars, organic acids

125 secondary end points included time to first SRE and skeletal morbidity rate (SMR).

126 The time to first SRE between treatment groups was not statistically signi

127 The median time to first SRE was 31.9 months in the zoledronic acid group (95% CI

128 The primary end point was time to first SRE, defined as radiation to bone, clinical fracture, sp

129 Secondary analyses (time to first SRE, skeletal morbidity rate, and multiple event analysi

130 not associated with increased time to first SRE.

131 m response factor (SRF) is indispensable for SRE-mediated transcription, we investigated whether SRF

132 acid was not associated with lower risk for SREs.

133 Whereas RhoA stimulates the c-fos SRE by a recently elucidated mechanism that is dependent

134 The c-fos SRE is regulated by mitogen-activated protein kinase pho

135 and the consequent expression from the c-fos SRE, while a parallel pathway connects ROCK to JNK, ther

136 cells led to transcriptional activation from SRE- and CRE-driven promoters, independent of exogenousl

137 1) binding site residing 28 bp upstream from SRE as a critical sequence motif for PCSK9 transcription

138 These results identify a functional SRE within the HTLV-1 LTR and suggest that both Elk-1 an

139 ntial SREs identified a conserved functional SRE in the mouse (TCGGTCCAT) and human (TCATTCCAT) promo

140 sponse factor (SRF)-dependent reporter gene (SRE-LUC) activity and mRNA expression of pro-proliferati

141 lishes a novel AS screening tool to identify SREs from a wide range of plant pathogens, providing opp

142 powerful discriminative approach to identify SREs.

143 ulation and is a useful tool for identifying SREs and their interactions.

144 tration down-regulated SRF binding to RIP II SRE, and this down-regulation was associated with decrea

145 1-sided 97.5% CI bound of the difference in SRE rate between arms, -9.8%; noninferiority P = .02).

146 ation of Galpha12 than Galpha13 signaling in SRE activation experiments.

147 The colocalized CTCF and cohesin sites in SRE regions are candidates for mediating long-range chro

148 of single nucleotide polymorphisms (SNPs) in SREs among human populations and applied long-range hapl

149 n has shaped extant patterns of variation in SREs.

150 Secondary outcomes included SRE-free interval, pain progression-free interval, total

151 hese results, knockdown of Homer-3 increased SRE activation.

152 more, serum induction of two TCF-independent SRE target genes, SRF and vinculin, was nearly completel

153 x 10(4) M(-1)) but varies for the individual SRE components.

154 sal level or epidermal growth factor-induced SRE-luciferase activity.

155 terference method down-regulated HGF-induced SRE-luciferase activity and decreased Elk-1 activation.

156 kinase inhibition of serum- and RhoA-induced SRE-dependent transcription.

157 jor role in the attenuation of serum-induced SRE activity, since MKP-1 null fibroblasts exhibited enh

158 z, but not Galphai, attenuates serum-induced SRE reporter activation, suggesting that Galphaz can dow

159 Moreover, Galphaz does not inhibit SRE reporter induction by an activated form of Rho kinas

160 dixin using small interference RNA inhibited SRE-dependent gene transcription and phosphorylation of

161 P) F/H and E/K are identified as interacting SRE pairs, and have been shown to be consistent with the

162 We also identified two very interesting SREs that can function as an enhancer in one tissue but

163 ng an increase in SREBP-2 binding to an LDLR SRE site.

164 No binding to an LDLR SRE was observed in the presence of the HMG-CoA reductas

165 ay, CTDa produced better responses and lower SRE rates than melphalan and prednisolone.

166 ery 3 months, the incremental costs per mean SRE avoided for denosumab ranged from $162,918 to $347,6

167 up period, and the algorithm used to measure SRE.

168 S or OS but did significantly improve median SRE-free interval and reduced total SREs by around one-t

169 g pathway is involved in Galpha(13)-mediated SRE-dependent gene transcription, suggesting that radixi

170 ng serum stimulation, reduced serum-mediated SRE activity.

171 t radixin via its C-terminal domain mediates SRE-dependent gene transcription through activation of R

172 as the proportion of patients with 1 or more SRE on study (SRE rate).

173 roportion of patients experiencing 1 or more SRE.

174 ) or time to first-and-subsequent (multiple) SRE (rate ratio, 0.90; 95% CI, 0.77 to 1.04; P = .14).

175 -type Arc and SRF engineered to bind mutated SRE 6.9 restored late-phase LTD in Arc-/-, SRE 6.9 mutan

176 tion differentiation compared with their non-SRE counterparts.

177 r signaling events involved in activation of SRE-BP target genes.

178 inase (G-kinase) inhibits RhoA activation of SRE-dependent transcription.

179 btelomere and haplotype-resolved analyses of SRE organization and variation, providing a window into

180 ure experiments indicate that the binding of SRE with nCu and dissolved Cu ions can significantly dec

181 In the United States, the cost of SRE ranged from $7553 per radiation episode to $88 838 p

182 of SRE, time to SRE occurrence, and cost of SRE varied across studies because of differences in stud

183 s revealed Galpha12-specific determinants of SRE activation within the switch regions and a C-termina

184 e findings identify Galpha12 determinants of SRE activation, implicate Galpha12:Hsp90 interaction in

185 ependence, including increased expression of SRE-BP target genes.

186 lytic activation nor nuclear localization of SRE-BP was affected by disruption of the PDGF autocrine

187 nCu dissolution in the presence of SRE was the predominant interaction.

188 Prevalence of SRE, time to SRE occurrence, and cost of SRE varied acro

189 rs implies that Galphaz-induced reduction of SRE reporter activation occurs via a mechanism other tha

190 Homer-3 may be involved in the regulation of SRE activation in T cells via interaction between its EV

191 ean10 greater than 19 increasing the risk of SRE.

192 months was more CE in reducing the risks of SRE than monthly denosumab.

193 of VASP is required for VASP stimulation of SRE-dependent transcription, and that VASP is downstream

194 of ERK1/2, and the preferential targeting of SRE over the classic ERE pathway support a role for nong

195 asymmetry, expanding the current catalog of SREs.

196 Here, we studied the distribution of SREs in human genes in terms of DNA strand-asymmetry pat

197 In the analysis of position distribution of SREs, we found that a dozen of SREs were biased to a spe

198 stribution of SREs, we found that a dozen of SREs were biased to a specific region.

199 SynoR performs de novo identification of SREs utilizing known patterns of TFBS in active regulato

200 Calpha1/Calpha2 loci because of the lack of SREs in the Ialpha1/Ialpha2 promoters.

201 Our model does not assume a fixed length of SREs and incorporates experimental evidence as well to i

202 methodology, particularly the measurement of SREs, is necessary to allow comparison of estimates acro

203 limiting the algorithm to find only pairs of SREs.

204 o in palliation of bone pain or reduction of SREs.

205 erior to monthly ZA in reducing the risks of SREs.

206 c sequence conservation filters in search of SREs and the results are displayed such as to provide an

207 CoSREM is able to identify sets of SREs and is not limited to SRE pairs as are current appr

208 14; P = .81); ZA had a significant effect on SRE-free interval (HR, 0.78; 95% CI, 0.65-0.95; P = .01)

209 re suggested by their synergistic effects on SRE.L- and TEAD-luciferase expression.

210 etaxel improved CPFS but did not improve OS, SRE-free interval, or total SREs; ZA did not improve CPF

211 s role in serum induction of c-fos and other SRE-regulated genes with a dominant negative MKL1 mutant

212 patients with baseline bone disease or other SREs.

213 A relatively small portion (20%) of our SREs is included in tissue-specific SREs in human identi

214 atrium strain rate at early diastolic peak ( SRE LA strain rate at early diastolic peak ) (-0.77 +/-

215 Methods Using a Markov model, costs per SRE avoided were calculated for the three treatments.

216 Site-directed mutagenesis of potential SREs identified a conserved functional SRE in the mouse

217 The N-terminal domain potentiated SRE activation induced by Galpha(13)Q226L; RhoGDI inhibi

218 ing of tissue-specificities of the predicted SREs.

219 developed a method that effectively predicts SREs based on strand asymmetry, expanding the current ca

220 to zoledronic acid in delaying or preventing SREs in patients with breast cancer metastatic to bone a

221 o-event end points of metastasis prevention, SRE, time to progression, and overall survival in the co

222 omplex from the Igamma and Iepsilon promoter SREs, thereby relieving the IH-CH transcriptional repres

223 of one SRF-binding site in the Arc promoter (SRE 6.9) blocked this rescue.

224 sterol regulatory element binding proteins (SRE-BP), consistent with a key role for these transcript

225 human ACSL1 gene and identified one putative SRE site.

226 splicing and give a set of valuable putative SREs for further experimental investigations.

227 Introduction of the LDL receptor SRE into the PEPCK-C gene promoter increased SREBP-1c bi

228 Ps in suppressing bone turnover and reducing SRE risk.

229 or less, ZOL was superior to CLO in reducing SREs (P = .048), whereas for patients in CR, both agents

230 ent system, plays a major role in regulating SRE-dependent transcription, and that G-kinase regulates

231 hromatin interactions in the transcript-rich SRE region.

232 ponding mutants of Galpha13 exhibited robust SRE activation, suggesting a Galpha12-specific mechanism

233 a reliable negative data set where the same SREs are most likely under-represented for a specific ti

234 assays were conducted using an ADH-specific SRE site.

235 Most of our tissue-specific SREs are likely different from constitutive SREs, since

236 ) of our SREs is included in tissue-specific SREs in human identified in two recent studies.

237 ates TNF-alpha in inducing NF-kappaB and SRF/SRE activities.

238 sulin alone, insulin+TNF-alpha increased SRF/SRE binding and beta-MHC expression, which was reversed

239 he phosphorylation of CaMKII, and stimulated SRE-dependent gene transcription.

240 ostatin induced c-Fos expression, stimulated SRE reporter activity, and promoted cell proliferation.

241 ous expression prevented Galpha13-stimulated SRE activity.

242 Similarly, Gbetagamma subunits stimulated SRE activity induced by full-length and DH/PH domain of

243 t fashion serum-, RhoA-, and VASP-stimulated SRE-dependent transcription.

244 at VASP is downstream of RhoA in stimulating SRE-dependent transcription.

245 primary end point was time to first on-study SRE (defined as pathologic fracture, radiation or surger

246 onic acid in delaying time to first on-study SRE (hazard ratio, 0.82; 95% CI, 0.71 to 0.95; P = .01 s

247 ior to ZA in delaying time to first on-study SRE (hazard ratio, 0.84; 95% CI, 0.71 to 0.98; P = .0007

248 ior to ZA in delaying time to first on-study SRE (P = .03 unadjusted; P = .06 adjusted for multiplici

249 primary end point was time to first on-study SRE (pathologic fracture, radiation or surgery to bone,

250 ZA in preventing or delaying first on-study SRE in patients with advanced cancer metastatic to bone

251 to first and subsequent (multiple) on-study SREs (rate ratio, 0.77; 95% CI, 0.66 to 0.89; P = .001).

252 On-study SREs were experienced by 9% of denosumab-treated patient

253 Our approach opens new directions to study SREs and the roles that AS may play in diseases and tiss

254 ion of patients with 1 or more SRE on study (SRE rate).

255 ratio quantitative trait loci (trQTLs) than SRE SNPs in general and includ outlier trQTLs for cross-

256 Trial data indicate that SREs occur in half of prostate cancer patients with bone

257 The SRE at -590 differs by a single base pair from the SRE i

258 The SRE at -590 overlaps an Sp1 site on the opposite strand

259 The SRE includes a recurrently mutated enhancer whose activi

260 n of the CYP51A1 gene revealed that both the SRE and nLXRE are required for normal oxysterol-dependen

261 -590 differs by a single base pair from the SRE in the low density lipoprotein (LDL) receptor gene (

262 promoter at -582, compared with an A in the SRE of the gene for the LDL receptor promoter).

263 in of radixin synergistically stimulated the SRE activation; RhoGDI inhibited this effect.

264 y, the C-terminal domain also stimulated the SRE-dependent gene transcription.

265 We also show that the SRE set GGGAGG and GAGGAC identified by CoSREM may play

266 However, hnRNP H binding to the SRE acts as an enhancer of exon 6D inclusion in the pres

267 the transcription factors that binds to the SRE and has a consensus motif binding to EVH1 domain.

268 Sp1 does not bind to the SRE at -322.

269 ted kinase (ERK)-phosphorylated Elk-1 to the SRE, activating the Egr-1 promoter.

270 inclusion independent of its binding to the SRE.

271 wever, in association with the -318 TRE, the SRE and ATF sites imparted a strong TPA-inducibility to

272 ther than an inhibition as observed with the SRE in the PEPCK-C gene promoter.

273 ealed that ATF6(N) formed a complex with the SRE-bound SREBP2(N).

274 f acetylated histone H3 at lysine 9 with the SRE-containing region in the promoter of the lipin-1 gen

275 The SREs include exonic splicing enhancers (ESEs), exonic sp

276 tive regulatory regions corresponding to the SREs in the PEPCK-C gene promoter.

277 These SREs bound SREBP-1a and SREBP-1c with low affinity but t

278 Mutating these SREs increased both unstimulated (5-fold) and protein ki

279 we firmly demonstrated the key role of this SRE motif in SREBP2-mediated activation of C-ACSL1 gene

280 2 and Ecm22 function through binding to this SRE site.

281 n, SRF, Elk1, ATF1 and CREB proteins bind to SRE and ATF sites of the FRA-1 promoter, constitutively.

282 Thus, SRF binding to SRE 6.9 in the Arc promoter is required for the late pha

283 identify sets of SREs and is not limited to SRE pairs as are current approaches.

284 ress-activated kinase (MSK) are recruited to SRE promoter complexes in vitro and in vivo.

285 3 homolog Concertina was unable to signal to SRE in mammalian cells, and Galpha12:Concertina chimeras

286 Prevalence of SRE, time to SRE occurrence, and cost of SRE varied across studies be

287 y outcomes of interest were SREs and time to SRE.

288 with SRF and enhances the binding of SRF to SREs located in the c-fos, Nur77, and viral promoters.

289 erval, pain progression-free interval, total SREs, and overall survival (OS).

290 not improve OS, SRE-free interval, or total SREs; ZA did not improve CPFS or OS but did significantl

291 e median SRE-free interval and reduced total SREs by around one-third, suggesting a role as postchemo

292 as the start of each terminal repeat tract, SRE identity and organization, and subtelomeric gene mod

293 After 1 year of follow-up, SREs occurred in 44 patients (22.0%) in the zoledronic a

294 e position of the previously described viral SRE (vSRE) within the HTLV-1 promoter can be extended fr

295 The primary outcomes of interest were SREs and time to SRE.

296 ment (SRE) sites in the Fbw8 promoter, where SRE-binding protein 1c binds and induces the expression

297 data to determine a positive data set where SREs are over-represented and a reliable negative data s

298 ting that HNF1 site works cooperatively with SRE as HNF1 mutation significantly attenuated the activi

299 and abolishing unfavorable interactions with SRE; also required were numerous permissive substitution

300 ed to be 50%, 75%, and 90% lower than the ZA SRE probabilities.