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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                                The SCAN box (SRE-ZBP; CT-fin51; AW-1; Number 18) is a highly-conserve
42 dence on the clinical and economic impact by SRE subtype.
43 gene, and inducible cis-elements (CRE, CaRE, SRE, AP1 or NF-kappaB) demonstrated that only CRFR1alpha
44        Here we develop CoSREM (Combinatorial SRE Miner), a graph mining algorithm to discover combina
45 h mining algorithm to discover combinatorial SREs in human exons.
46 r multiple tissues to identify combinatorial SREs which may be responsible for exon inclusion or excl
47                           The 7-bp consensus SRE is identical to the anaerobic response element, AR1c
48  SREs are likely different from constitutive SREs, since only 18% of our exonic splicing enhancers (E
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  sets of unbiased, experimentally determined SREs show a distinct strand-asymmetry pattern that is in
54 g its binding affinity to multiple different SRE sequences.
55 may arise from a long motif or two different SREs bound by different SFs.
56 proportion of extremely rare SNPs disrupting SREs is significantly higher in European than in African
57 formed by an upstream TRE and the downstream SRE and ATF sites and the cognate factors is necessary a
58 nsgenic studies show that mutation of either SRE, the TBE or the distal GATA element, strongly reduce
59 ce of a complex splicing regulatory element (SRE) sequence that interacts with the splicing factors h
60  identified three sterol regulatory element (SRE) sites in the Fbw8 promoter, where SRE-binding prote
61  regulated by the sterol regulatory element (SRE)-binding protein (SREBP) pathway, and RSV treatment
62  mapping through subtelomere repeat element (SRE) regions to unique chromosomal DNA while simultaneou
63 he activation of the serum response element (SRE) by preventing MAPK-mediated phosphorylation of the
64 ed a 7-bp consensus sterol-response element (SRE) common to genes involved in sterol biosynthesis and
65 l activation via the serum response element (SRE) in response to anti-CD3 antibody, phorbol ester, or
66            The c-fos serum response element (SRE) mediates transcriptional activation in response to
67  at both the ARE and serum response element (SRE) of the Egr-1 promoter, which facilitates binding of
68 factor (GEF)-induced serum response element (SRE) reporter activation in human embryonic kidney 293T
69 tains two canonical sterol response element (SRE) sites (-63 to -53 and -52 to -40 relative to the tr
70 to an LDLR promoter sterol response element (SRE), increasing LDLR gene expression and LDL-C uptake.
71 ranscription factor, serum response element (SRE), that was enhanced by p114RhoGEF.
72 9-583) of radixin on serum response element (SRE)-dependent gene transcription initiated by a constit
73 leton remodeling and serum response element (SRE)-dependent gene transcription.
74 d strongly activated serum response element (SRE)-dependent reporter genes through its direct binding
75  proteins, activates serum response element (SRE)-dependent transcription through changes in actin dy
76 nced the HGF-induced serum response element (SRE)-luciferase activity.
77 obes, we developed a serum response element (SRE)-luciferase-based screening approach to identify GPR
78  PI3K both stimulate serum response element (SRE)-mediated gene expression, and serum response factor
79 ry for activation of serum response element (SRE)-mediated transcription, a G12/13-stimulated pathway
80 ox) located within a serum response element (SRE).
81 d transcription of serum responsive element (SRE) but had a very small effect on the activity of estr
82 f an ERK-dependent serum-responsive element (SRE)-luciferase reporter gene, indicating that associati
83 otentiated) high insulin-induced SR element (SRE) activation and beta-MHC expression.
84 ollectively known as serum response element, SRE), and an ATF site, is also necessary for the FRA-1 i
85 tions within the set of regulatory elements (SRE) regulating ESR1 in 7% of ESR1-positive breast cance
86 ng site (CArG box), serum response elements (SRE) also typically contain a binding site for a member
87  promoter-imbedded sterol response elements (SRE) and co-induced by statins.
88 ntified switch (S) regulatory ATTT elements (SREs) in the Igamma and Iepsilon promoters and downstrea
89 ic variants in splicing regulatory elements (SREs) and evaluated the extent to which natural selectio
90  of cis-acting splicing regulatory elements (SREs) and their interactions.
91                Splicing regulatory elements (SREs) in pre-mature messenger RNA play a very important
92     There are two SREBP regulatory elements (SREs) in the PEPCK-C gene promoter (-322 to -313 and -59
93 t identifies synonymous regulatory elements (SREs) in vertebrate genomes.
94 ch site, other splicing-regulatory elements (SREs).
95 everal potential sterol regulatory elements (SREs).
96 tes are called splicing regulatory elements (SREs).
97 l boundaries of subtelomere repeat elements (SREs) in transformed lymphoblastoid cell lines (LCLs) an
98 ilizes three distal serum response elements (SREs) in the EGR1 promoter, which are transactivated by
99 of DNA sequences (steroid response elements, SREs).
100 EGF-induced ERK phosphorylation and enhanced SRE-dependent transcription.
101 ce MKP-1 null fibroblasts exhibited enhanced SRE activity in response to serum compared with wild-typ
102                 Soft-rot Enterobacteriaceae (SRE), which belong to the genera Pectobacterium and Dick
103  upregulates the expression of egr-1, an ERK/SRE target gene.
104 Error (MSE) and Signal Reconstruction Error (SRE) ratio of the proposed method was 39.6% less and 8%
105 ll survival (OS) and skeletal-related event (SRE) data have been reported for the overall trial popul
106 ts with at least one skeletal-related event (SRE), defined as pathologic fracture, spinal cord compre
107 on-free survival and skeletal-related event (SRE).
108 n of patients with a skeletal-related event (SRE; defined as pathologic fracture, radiation or surger
109 aying or preventing skeletal-related events (SRE) in patients with advanced cancer and bone metastase
110 ne or more on-study skeletal-related events (SRE), and safety were also evaluated.
111 reases the risk for skeletal-related events (SREs) in men with castration-resistant prostate cancer a
112 tment/prevention of skeletal-related events (SREs) in multiple myeloma and breast and prostate cancer
113 aying or preventing skeletal-related events (SREs) in patients with breast cancer with bone metastase
114 bone metastasis and skeletal-related events (SREs) in prostate cancer, and discuss current gaps in un
115             Purpose Skeletal-related events (SREs) such as pathologic fracture, spinal cord compressi
116 gnificantly reduced skeletal-related events (SREs), and improved progression-free survival and overal
117  reduce the risk of skeletal-related events (SREs), but only radium-223 improves survival.
118 ife or reduction in skeletal-related events (SREs).
119  reduce the risk of skeletal-related events (SREs).
120  (pain progression, skeletal-related events [SREs], or death) and cost-effectiveness.
121 nanocopper (nCu) and synthetic root exudate (SRE) and its components (including sugars, organic acids
122  secondary end points included time to first SRE and skeletal morbidity rate (SMR).
123                            The time to first SRE between treatment groups was not statistically signi
124                     The median time to first SRE was 31.9 months in the zoledronic acid group (95% CI
125      The primary end point was time to first SRE, defined as radiation to bone, clinical fracture, sp
126            Secondary analyses (time to first SRE, skeletal morbidity rate, and multiple event analysi
127  not associated with increased time to first SRE.
128 m response factor (SRF) is indispensable for SRE-mediated transcription, we investigated whether SRF
129  acid was not associated with lower risk for SREs.
130            Whereas RhoA stimulates the c-fos SRE by a recently elucidated mechanism that is dependent
131                                    The c-fos SRE is regulated by mitogen-activated protein kinase pho
132                      Activation of the c-fos SRE transcriptional activity by Gab2 required tyrosine 6
133 and the consequent expression from the c-fos SRE, while a parallel pathway connects ROCK to JNK, ther
134 cells led to transcriptional activation from SRE- and CRE-driven promoters, independent of exogenousl
135 1) binding site residing 28 bp upstream from SRE as a critical sequence motif for PCSK9 transcription
136          These results identify a functional SRE within the HTLV-1 LTR and suggest that both Elk-1 an
137 ntial SREs identified a conserved functional SRE in the mouse (TCGGTCCAT) and human (TCATTCCAT) promo
138 sponse factor (SRF)-dependent reporter gene (SRE-LUC) activity and mRNA expression of pro-proliferati
139 powerful discriminative approach to identify SREs.
140 ulation and is a useful tool for identifying SREs and their interactions.
141 tration down-regulated SRF binding to RIP II SRE, and this down-regulation was associated with decrea
142  1-sided 97.5% CI bound of the difference in SRE rate between arms, -9.8%; noninferiority P = .02).
143 ation of Galpha12 than Galpha13 signaling in SRE activation experiments.
144    The colocalized CTCF and cohesin sites in SRE regions are candidates for mediating long-range chro
145 of single nucleotide polymorphisms (SNPs) in SREs among human populations and applied long-range hapl
146 n has shaped extant patterns of variation in SREs.
147                  Secondary outcomes included SRE-free interval, pain progression-free interval, total
148 hese results, knockdown of Homer-3 increased SRE activation.
149 more, serum induction of two TCF-independent SRE target genes, SRF and vinculin, was nearly completel
150 x 10(4) M(-1)) but varies for the individual SRE components.
151 sal level or epidermal growth factor-induced SRE-luciferase activity.
152 terference method down-regulated HGF-induced SRE-luciferase activity and decreased Elk-1 activation.
153 kinase inhibition of serum- and RhoA-induced SRE-dependent transcription.
154 jor role in the attenuation of serum-induced SRE activity, since MKP-1 null fibroblasts exhibited enh
155 z, but not Galphai, attenuates serum-induced SRE reporter activation, suggesting that Galphaz can dow
156           Moreover, Galphaz does not inhibit SRE reporter induction by an activated form of Rho kinas
157 dixin using small interference RNA inhibited SRE-dependent gene transcription and phosphorylation of
158 P) F/H and E/K are identified as interacting SRE pairs, and have been shown to be consistent with the
159      We also identified two very interesting SREs that can function as an enhancer in one tissue but
160 ng an increase in SREBP-2 binding to an LDLR SRE site.
161                        No binding to an LDLR SRE was observed in the presence of the HMG-CoA reductas
162 ay, CTDa produced better responses and lower SRE rates than melphalan and prednisolone.
163 ery 3 months, the incremental costs per mean SRE avoided for denosumab ranged from $162,918 to $347,6
164 up period, and the algorithm used to measure SRE.
165 S or OS but did significantly improve median SRE-free interval and reduced total SREs by around one-t
166 g pathway is involved in Galpha(13)-mediated SRE-dependent gene transcription, suggesting that radixi
167 ng serum stimulation, reduced serum-mediated SRE activity.
168 t radixin via its C-terminal domain mediates SRE-dependent gene transcription through activation of R
169 as the proportion of patients with 1 or more SRE on study (SRE rate).
170 roportion of patients experiencing 1 or more SRE.
171 ) or time to first-and-subsequent (multiple) SRE (rate ratio, 0.90; 95% CI, 0.77 to 1.04; P = .14).
172 -type Arc and SRF engineered to bind mutated SRE 6.9 restored late-phase LTD in Arc-/-, SRE 6.9 mutan
173 tion differentiation compared with their non-SRE counterparts.
174 r signaling events involved in activation of SRE-BP target genes.
175 inase (G-kinase) inhibits RhoA activation of SRE-dependent transcription.
176 TA sites altered the DNA binding affinity of SRE.
177 btelomere and haplotype-resolved analyses of SRE organization and variation, providing a window into
178 ure experiments indicate that the binding of SRE with nCu and dissolved Cu ions can significantly dec
179            In the United States, the cost of SRE ranged from $7553 per radiation episode to $88 838 p
180  of SRE, time to SRE occurrence, and cost of SRE varied across studies because of differences in stud
181 s revealed Galpha12-specific determinants of SRE activation within the switch regions and a C-termina
182 e findings identify Galpha12 determinants of SRE activation, implicate Galpha12:Hsp90 interaction in
183 ependence, including increased expression of SRE-BP target genes.
184 lytic activation nor nuclear localization of SRE-BP was affected by disruption of the PDGF autocrine
185           nCu dissolution in the presence of SRE was the predominant interaction.
186                                Prevalence of SRE, time to SRE occurrence, and cost of SRE varied acro
187 rs implies that Galphaz-induced reduction of SRE reporter activation occurs via a mechanism other tha
188 Homer-3 may be involved in the regulation of SRE activation in T cells via interaction between its EV
189 ean10 greater than 19 increasing the risk of SRE.
190  months was more CE in reducing the risks of SRE than monthly denosumab.
191  of VASP is required for VASP stimulation of SRE-dependent transcription, and that VASP is downstream
192 of ERK1/2, and the preferential targeting of SRE over the classic ERE pathway support a role for nong
193  asymmetry, expanding the current catalog of SREs.
194         Here, we studied the distribution of SREs in human genes in terms of DNA strand-asymmetry pat
195  In the analysis of position distribution of SREs, we found that a dozen of SREs were biased to a spe
196 stribution of SREs, we found that a dozen of SREs were biased to a specific region.
197     SynoR performs de novo identification of SREs utilizing known patterns of TFBS in active regulato
198  Calpha1/Calpha2 loci because of the lack of SREs in the Ialpha1/Ialpha2 promoters.
199  Our model does not assume a fixed length of SREs and incorporates experimental evidence as well to i
200 methodology, particularly the measurement of SREs, is necessary to allow comparison of estimates acro
201 limiting the algorithm to find only pairs of SREs.
202 o in palliation of bone pain or reduction of SREs.
203 erior to monthly ZA in reducing the risks of SREs.
204 c sequence conservation filters in search of SREs and the results are displayed such as to provide an
205           CoSREM is able to identify sets of SREs and is not limited to SRE pairs as are current appr
206 14; P = .81); ZA had a significant effect on SRE-free interval (HR, 0.78; 95% CI, 0.65-0.95; P = .01)
207 re suggested by their synergistic effects on SRE.L- and TEAD-luciferase expression.
208 etaxel improved CPFS but did not improve OS, SRE-free interval, or total SREs; ZA did not improve CPF
209 s role in serum induction of c-fos and other SRE-regulated genes with a dominant negative MKL1 mutant
210 patients with baseline bone disease or other SREs.
211      A relatively small portion (20%) of our SREs is included in tissue-specific SREs in human identi
212 atrium strain rate at early diastolic peak ( SRE LA strain rate at early diastolic peak ) (-0.77 +/-
213      Methods Using a Markov model, costs per SRE avoided were calculated for the three treatments.
214       Site-directed mutagenesis of potential SREs identified a conserved functional SRE in the mouse
215            The N-terminal domain potentiated SRE activation induced by Galpha(13)Q226L; RhoGDI inhibi
216 ing of tissue-specificities of the predicted SREs.
217 developed a method that effectively predicts SREs based on strand asymmetry, expanding the current ca
218 to zoledronic acid in delaying or preventing SREs in patients with breast cancer metastatic to bone a
219 o-event end points of metastasis prevention, SRE, time to progression, and overall survival in the co
220 omplex from the Igamma and Iepsilon promoter SREs, thereby relieving the IH-CH transcriptional repres
221 of one SRF-binding site in the Arc promoter (SRE 6.9) blocked this rescue.
222  sterol regulatory element binding proteins (SRE-BP), consistent with a key role for these transcript
223 human ACSL1 gene and identified one putative SRE site.
224 splicing and give a set of valuable putative SREs for further experimental investigations.
225             Introduction of the LDL receptor SRE into the PEPCK-C gene promoter increased SREBP-1c bi
226 Ps in suppressing bone turnover and reducing SRE risk.
227 or less, ZOL was superior to CLO in reducing SREs (P = .048), whereas for patients in CR, both agents
228 ent system, plays a major role in regulating SRE-dependent transcription, and that G-kinase regulates
229 hromatin interactions in the transcript-rich SRE region.
230 ponding mutants of Galpha13 exhibited robust SRE activation, suggesting a Galpha12-specific mechanism
231  a reliable negative data set where the same SREs are most likely under-represented for a specific ti
232 nding site (TBE), and two SRF binding sites (SREs).
233  assays were conducted using an ADH-specific SRE site.
234                  Most of our tissue-specific SREs are likely different from constitutive SREs, since
235 ) of our SREs is included in tissue-specific SREs in human identified in two recent studies.
236 ates TNF-alpha in inducing NF-kappaB and SRF/SRE activities.
237 sulin alone, insulin+TNF-alpha increased SRF/SRE binding and beta-MHC expression, which was reversed
238 he phosphorylation of CaMKII, and stimulated SRE-dependent gene transcription.
239 ostatin induced c-Fos expression, stimulated SRE reporter activity, and promoted cell proliferation.
240 ous expression prevented Galpha13-stimulated SRE activity.
241    Similarly, Gbetagamma subunits stimulated SRE activity induced by full-length and DH/PH domain of
242 t fashion serum-, RhoA-, and VASP-stimulated SRE-dependent transcription.
243 at VASP is downstream of RhoA in stimulating SRE-dependent transcription.
244 primary end point was time to first on-study SRE (defined as pathologic fracture, radiation or surger
245 onic acid in delaying time to first on-study SRE (hazard ratio, 0.82; 95% CI, 0.71 to 0.95; P = .01 s
246 ior to ZA in delaying time to first on-study SRE (hazard ratio, 0.84; 95% CI, 0.71 to 0.98; P = .0007
247 ior to ZA in delaying time to first on-study SRE (P = .03 unadjusted; P = .06 adjusted for multiplici
248 primary end point was time to first on-study SRE (pathologic fracture, radiation or surgery to bone,
249  ZA in preventing or delaying first on-study SRE in patients with advanced cancer metastatic to bone
250  to first and subsequent (multiple) on-study SREs (rate ratio, 0.77; 95% CI, 0.66 to 0.89; P = .001).
251                                     On-study SREs were experienced by 9% of denosumab-treated patient
252   Our approach opens new directions to study SREs and the roles that AS may play in diseases and tiss
253 ion of patients with 1 or more SRE on study (SRE rate).
254  ratio quantitative trait loci (trQTLs) than SRE SNPs in general and includ outlier trQTLs for cross-
255 retic mobility shift assays demonstrate that SRE binds with high affinity to a DNA probe containing t
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.

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