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1 DRE binding or to induce luciferase.
2 DRE of the prostatic fossa and biopsy confirmation of lo
3 DRE of the prostatic fossa, prebiopsy PSA, and postrecur
4 DRE-1 and SKR-1 form a complex, as do the human ortholog
5 DRE-1 functions in parallel to EGL-1, requires CED-9 for
6 DREs are the binding sites for the sequence-specific DNA
7 DREs with MS scores above the threshold were disproporti
9 four Deformed binding sites renders the 1.28 DRE inactive in vivo, demonstrating that these sites are
11 ied a 664-bp Deformed Response Element (1.28 DRE) that directs maxillary-specific expression of a rep
13 with AhR-Arnt proteins bound to the Sp1(N)(4)DRE(core) motif were also dependent on the proximity of
17 -deficient cells that expressed AhRY9F and a DRE-driven luciferase construct with phorbol 12-myristat
19 uced a concentration-dependent response in a DRE-driven CAT reporter construct, with a greater than 1
21 ic mice expressing a wild-type (WT) Ahr or a DRE-binding mutant Ahr (A78D) on an ahr-null background
22 y, of the mouse-rat orthologous genes with a DRE between -1500 and +1500, only 37% had an equivalent
26 onse element (DRE) D, E, and A and abrogated DRE-driven gene induction mediated by the AhR with no ef
27 A4 transformed the Ah receptor to an active DRE-binding form in a concentration-dependent manner as
29 polymorphism rs11959928 were shown to affect DRE function, illustrating that genes regulated by DREs
31 inding validates DiMNF as an AHR ligand, and DRE-dependent reporter assays with quantitative mRNA ana
34 ction of more than one quarter of apparently DRE-detected prostate cancers and up to one quarter of a
35 d processes require a nuclear event, such as DRE binding, we used homologous recombination to generat
36 in order to analyze the relationship between DRE binding (determined in vitro using an electrophoreti
38 ng the four EF-hands (residues 65-256) binds DRE (K(d) = 200 nM) in a Ca(2+)-regulated and sequence-s
39 pressed, whereas FOX proteins enhanced, both DRE and FOXA-responsive element-driven gene expression.
42 ranslational regulation of BLMP-1/BLIMP-1 by DRE-1/FBXO11 coordinates C. elegans developmental timing
43 nction, illustrating that genes regulated by DREs colocalizing with CKD-associated variation can be d
44 AM) binds to regulatory element sites called DRE in the DNA and represses transcription of target gen
45 type AHR could be dissociated from canonical DRE-dependent transactivation in a ligand-dependent mann
46 R by Way-169916 fails to stimulate canonical DRE-driven AHR-mediated CYP1A1 expression, thus eliminat
50 ype pCD/L and constructs mutated in the core DRE (pCD/L(m1)) and Sp1 (pCD/L(m2)) sites, it was shown
52 ative effects on the function of the CBF-CRT/DRE regulatory module, and 11 transcription factors enco
56 motif or the drought-responsive element (CRT/DRE) in its promoter, failed to normally accumulate in t
58 C-REPEAT/DEHYDRATION RESPONSIVE ELEMENT (CRT/DRE) motifs, the cognate CBF binding site in its upstrea
59 tudies we conclude that CAS genes harbor CRT/DRE motifs, their proximity to one another is likely key
60 We hypothesize that these differences in CRT/DRE copy numbers in CAS30/CAS31 upstream regions combine
62 (CAMTA3) in the rapid cold induction of CRT/DRE BINDING FACTOR (CBF) genes CBF1 and CBF2, and the re
64 propose that cold-induced expression of CRT/DRE-containing COR genes involves a low temperature-stim
65 whether the failure of cold induction of CRT/DRE-containing genes in sfr 6 was due to altered low-tem
67 ROST RESISTANCE-H2-H2 (FR-H2) possessing CRT/DRE sites in their upstream regions, the most notable of
69 ontaining a C-repeat/drought-responsive (CRT/DRE) promoter element and metabolic changes that enhance
71 ncoded by this allele cannot bind to the CRT/DRE (C-repeat/ dehydration-responsive element) motif pre
72 ional activator, CBF1, that binds to the CRT/DRE and demonstrated that its overexpression in transgen
75 temperature, increased expression of the CRT/DRE binding factor (CBF) family of transcriptional activ
77 synthetic promoter, confirming that the CRT/DRE is sufficient to confer the sfr6 effect upon express
78 pically harbor one or more copies of the CRT/DRE low temperature cis-acting DNA regulatory element.
80 F transcriptional activators bind to the CRT/DRE regulatory element present in the promoters of many
81 nscriptional activator that binds to the CRT/DRE sequence, induced COR gene expression and increased
82 be general to cold-inducible genes with CRT/DRE promoter elements, but also that it extends to some
83 PPARdelta using an adenovirus not only drove DRE activity but also prevented RMIC death due to COX2 i
84 bretinal fluid [SRF], diffuse retinal edema [DRE], retinal pigment epithelial detachment [PED], and s
86 e, those with a significant change in either DRE or PSA results, or those at higher risk for prostate
88 usly identified a distal regulatory element (DRE) in the mouse serum amyloid A3 (SAA3) promoter that
90 ThPOK locus a key distal regulatory element (DRE) that mediated its differential expression in class
91 ting element, the distal regulatory element (DRE), is sufficient for this TCR-dependent induction.
92 ified a novel downstream regulatory element (DRE), which is bound by RUNX1 and is necessary for human
95 ance of the DNA replication-related element (DRE), the Initiator (Inr), and a new over-represented mo
97 dissociation of non-dioxin-response element (DRE) AHR activity from DRE-dependent xenobiotic gene exp
98 AHR binding to its dioxin response element (DRE) and driving expression of CYP1 family members, whic
99 d the presence of a dioxin response element (DRE) and five nuclear factor-kappaB (NF-kappaB) motifs o
100 delta binding to PPARdelta response element (DRE) and increased PPARdelta reporter activity, indicati
101 delta binding to PPARdelta response element (DRE) and increased PPARdelta reporter activity, which wa
102 bolished binding to dioxin response element (DRE) D, E, and A and abrogated DRE-driven gene induction
106 ore sequence of a dioxin responsive element (DRE) and binds the aryl hydrocarbon receptor (AhR)-AhR n
107 e C-repeat (CRT)/drought-responsive element (DRE) binding factor CBF1/DREB1b is a transcriptional reg
108 responding to the dioxin-responsive element (DRE) core binding sequence, which is the cognate respons
109 repeat (CRT)/dehydration-responsive element (DRE) DNA regulatory element present in the promoters of
110 the C-repeat/dehydration responsive element (DRE), that stimulates transcription in response to low t
112 evealed that dehydration-responsive element (DRE)B2A but not DREB1A, RD (response to dehydration)29A
115 inding of AhR to dioxin-responsive elements (DRE) in vitro; and 3) inhibit TCDD-induced transcription
116 slationally regulated by two 28 nt elements (DREs) located in the 3'UTR that bind a factor called DRF
117 ypothesized that distal regulatory elements (DREs) are involved in optimal expression of the NGB gene
121 l level by two 28 nt direct repeat elements (DREs) located in its 3' untranslated region (3'UTR).
122 man, mouse and rat dioxin response elements (DREs) in genomic sequences unambiguously assigned to a n
124 r (Arnt), binds to dioxin response elements (DREs) located in the promoter region of target genes, su
126 iption factor to dioxin-responsive elements (DREs) upstream of promoters that regulate the expression
127 on by binding to dioxin-responsive elements (DREs) within an enhancer upstream of the CYP1A1 gene.
129 g sequences, the damage-responsive elements (DREs), rendered these genes dependent upon TAF(II)s.
132 plex binds to "dioxin responsive enhancers" (DREs) and activates genes involved in the metabolism of
134 ening is performed with digital rectal exam (DRE) and measurement of serum prostate-specific antigen
135 at least one PSA and a digital rectal exam (DRE) during the year before biopsy, had at least two PSA
136 ly using PSA and digital rectal examination (DRE) alone and subsequently using the remaining variable
137 ue to suspicious digital rectal examination (DRE) findings and/or PSA levels (limit range, 2.0-20.0 n
138 rapy (CMT) using digital rectal examination (DRE) has been proposed as a means of assessing efficacy
139 me, and positive digital rectal examination (DRE) of the prostatic fossa were all statistically signi
140 ents with normal digital rectal examination (DRE) results but elevated prostate-specific antigen (PSA
142 d serendipity in digital rectal examination (DRE) screening as the discovery of a prostate cancer by
143 a expand the classes of AHR ligands exerting DRE-independent anti-inflammatory SAhRM activity, sugges
145 1% for macular fluid (kappa = 0.28), 79% for DRE (kappa = 0.10), 90% for PED (kappa = 0.78), and 79%
147 ls of luciferase induction (9 +/- 2-fold for DRE and 8 +/- 2-fold for NF-kappaBs of Fas promoter and
153 Epo gene and found that its promoter harbors DREs immediately upstream of its transcriptional start s
154 AhR nuclear translocator protein heterodimer DRE-binding activity as assessed by electrophoretic mobi
158 5-aza-CdR partially restores TCDD-inducible DRE occupancy, showing that DNA methylation indirectly s
160 f LT at 18 degrees C, suggesting that intact DRE is not required for transcription from the LT promot
161 erol biosynthesis pathway independent of its DRE-binding ability, and suggest that AhR may be a previ
167 ght-responsive/C-repeat) cis element but non-DRE/CRT type stress-responsive genes were less affected.
168 vone (alphaNF) mediates the suppressive, non-DRE dependent effects on SAA1 expression and partial DRE
170 otic stress, ERF1 bound to GCC boxes but not DRE elements; conversely, under abiotic stress, we obser
172 conformation capture we identified two novel DREs located -70 kb upstream and +100 kb downstream from
173 anti-inflammatory activity in the absence of DRE-mediated expression fulfills the major criteria of a
174 Parental genes also show an abundance of DRE and Inr motifs, but these do not seem to have been c
176 192837, were found to be potent inducers of DRE-driven transcriptional activity; AGN 190730 was the
181 and 3) inhibit TCDD-induced transcription of DRE-dependent luciferase in stably transfected hepatoma
185 ntially to only one among several GCC box or DRE/CRT elements in the promoter region of its target ge
189 eviously reported product complexes of other DRE-TIM metallolyases and induced fit substrate docking
190 ls after the first several years, but in our DRE cohort, mortality remains elevated despite a median
192 impact of serendipity, the currently popular DRE- and PSA-based screening strategy may not be optimal
196 y for men receiving finasteride include PSA, DRE, age, race, family history, and history of a prior n
199 ding the important transcriptional regulator DRE-binding protein 2A (DREB2A), two heat shock transcri
201 on of reporter genes containing the C-repeat/DRE as an upstream activator sequence but not mutant ver
203 dopsis thaliana cDNA that encodes a C-repeat/DRE binding factor, CBF1 (C-repeat/DRE Binding Factor 1)
204 ptional activator that binds to the C-repeat/DRE DNA regulatory element and, thus, is likely to have
205 s site shows some similarity to the C-repeat/DRE elements bound by proteins that contain a single AP2
208 the AHR-ARNT heterodimer binds to a specific DRE that overlaps binding sequences for peroxisome proli
211 nsient transfection assays, we observed that DRE driven transcription was markedly inhibited by hypox
219 ven of these DREs, collectively known as the DRE cluster (DREC), are located 1.4 kb upstream of the C
222 n-DRE binding AHR mutant has established the DRE-independent suppression of inflammatory markers by t
224 trast, although PGE2 treatment increased the DRE reporter activity in intact cells, it failed to indu
227 lineage choice, whereby inactivation of the DRE silencer by a strong TCR signal leads to CD4 commitm
228 ion and base substitution mutagenesis of the DRE sites demonstrated that they are required for effici
231 ion and antibody studies determined that the DRE contains a binding site for the transcription factor
232 that leads to trans-activation and that the DRE is the minimal DNA element required for PMA to enhan
233 formation capture assays in LT-HSCs that the DRE physically interacts with the human CD34 promoter.
235 ding of the transcription factor USF1 to the DRE-associated E-box domain in the gene encoding A20 act
237 Plasmids in an hns strain from which the DRE has been deleted still produce elevated levels of LT
238 ian AHR-ARNT heterodimer in complex with the DRE, in which ARNT curls around AHR into a highly intert
239 pression of stress-responsive genes with the DRE/CRT (drought-responsive/C-repeat) cis element but no
246 ls, it failed to induce PPARdelta binding to DRE in cell-free system, suggesting that cPLA2alpha-medi
247 ivity, DiMNF fails to promote AHR binding to DRE probes as determined through electromobility shift a
249 ent (residues 1-70) binds nonspecifically to DRE in a Ca(2+)-independent manner, whereas a C-terminal
250 xtracts enhanced the binding of PPARdelta to DRE in vitro, suggesting a direct role of arachidonic ac
251 his, AA enhanced the binding of PPARdelta to DRE, in vitro, suggesting a direct role of AA for PPARde
256 rinting experiments reveal that unmethylated DRE sites do not bind protein in response to TCDD in LNC
260 ore, we observed supershift in mobility when DRE and NF-kappaB probes were incubated in the presence
261 ctal cancer (T3/4 or N1) were evaluated with DRE and sigmoidoscopy in order to determine the followin
262 , we identified a total of 433 patients with DRE defined as at least one seizure per month and failur
263 Under identical conditions, zfAHR1/zfARNT2b/DRE complexes are formed; however, the interactions are
264 TG with the attached dorsal root entry zone (DRE) into the central nervous system (CNS) were stained
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