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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
6 via the induced binding of SREBP to the -150 SRE and that USF binding to the -65 E-box is also requir
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
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
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
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
24 r other solid tumors, the proportion with an SRE was reduced in both zoledronic acid groups compared
38 d that DN-MKL1 and RNAi specifically blocked SRE-dependent reporter gene activation by serum and RhoA
43 gene, and inducible cis-elements (CRE, CaRE, SRE, AP1 or NF-kappaB) demonstrated that only CRFR1alpha
46 r multiple tissues to identify combinatorial SREs which may be responsible for exon inclusion or excl
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
51 al products was screened for GPR56-dependent SRE activation inhibitors that did not inhibit constitut
53 sets of unbiased, experimentally determined SREs show a distinct strand-asymmetry pattern that is in
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
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.
72 9-583) of radixin on serum response element (SRE)-dependent gene transcription initiated by a constit
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
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
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
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
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
92 There are two SREBP regulatory elements (SREs) in the PEPCK-C gene promoter (-322 to -313 and -59
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
101 ce MKP-1 null fibroblasts exhibited enhanced SRE activity in response to serum compared with wild-typ
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
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
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
116 gnificantly reduced skeletal-related events (SREs), and improved progression-free survival and overal
121 nanocopper (nCu) and synthetic root exudate (SRE) and its components (including sugars, organic acids
125 The primary end point was time to first SRE, defined as radiation to bone, clinical fracture, sp
128 m response factor (SRF) is indispensable for SRE-mediated transcription, we investigated whether SRF
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
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
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).
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
149 more, serum induction of two TCF-independent SRE target genes, SRF and vinculin, was nearly completel
152 terference method down-regulated HGF-induced SRE-luciferase activity and decreased Elk-1 activation.
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
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
163 ery 3 months, the incremental costs per mean SRE avoided for denosumab ranged from $162,918 to $347,6
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
168 t radixin via its C-terminal domain mediates SRE-dependent gene transcription through activation of R
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
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
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
184 lytic activation nor nuclear localization of SRE-BP was affected by disruption of the PDGF autocrine
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
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
195 In the analysis of position distribution of SREs, we found that a dozen of SREs were biased to a spe
197 SynoR performs de novo identification of SREs utilizing known patterns of TFBS in active regulato
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
204 c sequence conservation filters in search of SREs and the results are displayed such as to provide an
206 14; P = .81); ZA had a significant effect on SRE-free interval (HR, 0.78; 95% CI, 0.65-0.95; P = .01)
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
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 +/-
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
222 sterol regulatory element binding proteins (SRE-BP), consistent with a key role for these transcript
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
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
237 sulin alone, insulin+TNF-alpha increased SRF/SRE binding and beta-MHC expression, which was reversed
239 ostatin induced c-Fos expression, stimulated SRE reporter activity, and promoted cell proliferation.
241 Similarly, Gbetagamma subunits stimulated SRE activity induced by full-length and DH/PH domain of
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).
252 Our approach opens new directions to study SREs and the roles that AS may play in diseases and tiss
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
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 (
267 the transcription factors that binds to the SRE and has a consensus motif binding to EVH1 domain.
271 wever, in association with the -318 TRE, the SRE and ATF sites imparted a strong TPA-inducibility to
274 f acetylated histone H3 at lysine 9 with the SRE-containing region in the promoter of the lipin-1 gen
279 we firmly demonstrated the key role of this SRE motif in SREBP2-mediated activation of C-ACSL1 gene
281 n, SRF, Elk1, ATF1 and CREB proteins bind to SRE and ATF sites of the FRA-1 promoter, constitutively.
285 3 homolog Concertina was unable to signal to SRE in mammalian cells, and Galpha12:Concertina chimeras
288 with SRF and enhances the binding of SRF to SREs located in the c-fos, Nur77, and viral promoters.
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
294 e position of the previously described viral SRE (vSRE) within the HTLV-1 promoter can be extended fr
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
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