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1 lation of GR expression by a tissue-specific enhancer.
2 ely impairing the GR signaling axis via this enhancer.
3 em cell leukemia (SCL) gene driven by its 5' enhancer.
4 blood-brain barrier and acts as a cognitive enhancer.
5 s the N-terminal helix serves as an affinity enhancer.
6 lect the de novo acquisition of AML-specific enhancers.
7 , and considers the joint effect of multiple enhancers.
8 to be regulated by two nonredundant "shadow" enhancers.
9 with known cell type markers, promoters and enhancers.
10 en alpha- and beta-cells are concentrated in enhancers.
11 ERG enrichment at Dll4 promoter and multiple enhancers.
12 essential for LCL growth were linked to EBV enhancers.
13 ulatory sequences, including transcriptional enhancers.
14 cape of CRMs, to discriminate promoters from enhancers.
15 Thus, PcG targeting elements overlap with enhancers.
16 he other's binding at diverse sets of active enhancers.
17 stages and could thereby represent putative enhancers.
18 under the control of at least seven putative enhancers.
19 chromatin accessibility at temporal-specific enhancers.
20 marks of transcription, open chromatin, and enhancers.
21 and decreasing accessibility of early-acting enhancers.
22 F binding and the activity of the associated enhancers.
23 etal brain promoters and embryonic stem cell enhancers.
24 sk loci co-localize to recurrently activated enhancers.
25 ntegrator at immediate early genes and their enhancers.
26 encompassing 1,992 viral/cellular genes and enhancers.
27 echanism via conserved noncoding elements or enhancers.
28 These could serve as intronic splicing enhancers.
29 nd it accumulates in regions flanking active enhancers.
30 e genetically regulated CpGs are enriched in enhancers.
31 -CoR/SMRT-HDAC3 corepressor complex on these enhancers.
33 consuming for large scale identification of enhancers across a variety of tissues under different di
37 cate the pioneer factor FOXA1 as a driver of enhancer activation in this system, a mechanism that ren
41 l count association near CEBPA overlapped an enhancer active in common myeloid progenitors and influe
43 ion of DNA methylation targeted to candidate enhancers active in liver cells, enriched for the bindin
44 nstrated strong allele-specific promoter and enhancer activity and differential binding of HNF4alpha,
46 found that Sox9-Brn2 and Isl1-Lhx3 regulate enhancer activity and NFIA expression in glial and neuro
47 tinct underlying DNA sequences and divergent enhancer activity as marked by histone 3 containing the
49 r absence of tamoxifen, indicating divergent enhancer activity for tumors that develop in different e
50 leotide polymorphism, rs577676, which alters enhancer activity in a mouse atrial cell line and in emb
54 ided a quantitative metric of Tbx5-dependent enhancer activity, correlating with target gene expressi
61 to activation or inactivation of hundreds of enhancers along with drastic genome-wide reduction of HN
63 urther promotes spatial clustering of MIR335 enhancer and promoter elements along with overexpression
65 nic mouse under the regulation of the Nkx2.5 enhancer and showed that neonatal Nkx2.5+ cardiomyoblast
66 d with reduced chromatin looping between the enhancer and the CUPID1 and CUPID2 bidirectional promote
68 he EWS-FLI1 fusion protein to tumor-specific enhancers and contributes to target gene activation.
69 uding promoting accessibility of late-acting enhancers and decreasing accessibility of early-acting e
70 TF)-dependence of ncRNA expression to define enhancers and enhancer-associated ncRNAs that are involv
71 discover three major co-regulation modes of enhancers and find defense-related genes often simultane
72 be trained on any tissue-specific dataset of enhancers and known functional variants and applied to p
73 educed chromatin accessibility at EBF2-bound enhancers and led to a decrease in basal and catecholami
76 mSWI/SNF assemblies, BAF and PBAF complexes, enhancers and promoters, respectively, suggesting that e
77 patterns of histone H3 Lys27 acetylation at enhancers and promoters, suggesting a cross-talk between
78 hromatin at lineage-specific transcriptional enhancers and promoters, which is mediated by pioneer tr
81 sense core promoter sequences, and that most enhancers and several families of repetitive elements ac
84 in conformation analysis revealed that these enhancers and transcription factors form distinct archit
85 binds to transcription-primed promoters and enhancers, and to CTCF occupied, untranscribed chromatin
86 an with mechanistic studies on a beta-globin enhancer- and promoter-binding factor, GATA-1, the found
88 al lineage and that corneal epithelial super enhancers are already marked as potential regulatory dom
91 y, our analyses revealed that most p53-bound enhancers are located within regions of inaccessible chr
93 associating domain (TAD) borders, while dCP enhancers are more often bound to one or two TSSs and ar
94 ed during patterning in the tissue where the enhancers are not induced, including at enhancers that a
96 ge interactions between the Emu and 3'Ealpha enhancers are significantly diminished in the absence of
97 oncoproteins or mutations/variants in CEBPA enhancers are suggested in principal to reveal novel mec
98 and differentiation through transcriptional enhancer associate domain (TEAD) and runt-related transc
99 hese findings unveil Jmjd2c and G9a as novel enhancer-associated factors, and implicate Jmjd2c as a m
100 s showed strong Hi-C interaction enrichment, enhancer-associated histone modifications were evident,
101 the annotated lncRNA, IFNG-AS1, or one IFNG enhancer-associated lncRNA abrogates IFNG expression by
102 of ncRNA expression to define enhancers and enhancer-associated ncRNAs that are involved in a TF-dep
103 occupancy of architectural proteins, typical enhancer-associated proteins, and histone modifications,
106 d to predict the genomic locations of active enhancers based on histone modifications, but the accura
107 ession (CAGE) demonstrate that promoters and enhancers, based on their expression profiles after stim
108 pecies petunia (Petunia hybrida), AP2B/BLIND ENHANCER (BEN) confines the C-function to the inner petu
109 the control of regulatory elements (Atoh1 3' enhancer/beta-globin basal promoter) to direct expressio
110 he DNA binding landscape of C/EBPbeta (CCAAT enhancer binding protein beta) without affecting its exp
112 ith some nuclear proteins, i.e. the lymphoid enhancer-binding factor 1 (Lef1), histone H3, and Brahma
113 on of adipogenic transcription factors CCAAT/enhancer-binding protein alpha (C/EBPalpha), C/EBPbeta,
114 eracts with Tbeta4 and is recruited by CCAAT/enhancer-binding protein beta (C/EBPbeta) to discrete re
116 (OC) precursors up-regulates c-Fos and CCAAT/enhancer-binding protein-alpha (C/EBPalpha), two critica
117 s often simultaneously regulated by multiple enhancers bound by different transcription factors.
119 ermined accessibility was enriched at distal enhancers, but random monoallelically accessible (RAMA)
120 likelihood of a genetic variant deactivating enhancers by disrupting the binding of transcription fac
121 stically, IFN-gamma disassembled a subset of enhancers by inducing coordinate suppression of binding
122 CRISPR interference and activation at linked enhancers, by the presence of expression quantitative tr
123 ange chromatin interactions, suggesting that enhancers can influence the pause-initiation limit to re
125 istone modifications, we determine that both enhancer classes are enriched for RNA Polymerase II, CBP
126 e studies utilizing STARR-seq identified two enhancer classes in Drosophila that interact with differ
128 Anemia activated Samd14-Enh by inducing enhancer components and enhancer chromatin accessibility
131 CRISPR/Cas9 genomics revealed that super-enhancer constituents act cooperatively and facilitate D
132 in transgenic mice and fine-mapped separate enhancers controlling expression in joints versus growin
133 This promotes the binding of C/EBPbeta at enhancers controlling the expression of adipogenic targe
135 nal analysis demonstrates that the Wap super-enhancer controls Ramp3, despite three separating CTCF s
137 al disaccharide trehalose, a known autophagy enhancer, delays SG assembly and facilitates their prema
138 ere we demonstrate that CFIm functions as an enhancer-dependent activator of mRNA 3' processing.
139 sodium reduction and the addition of flavor enhancers did not constitute an obstacle to L. casei 01
140 inhibitor JQ1 preferentially inhibits super-enhancer-directed cotranscriptional pri-miRNA processing
141 mpletes complex bioinformatics tasks such as enhancer discovery and provides functions to integrate v
146 31746 mapped to a long-range neuron-specific enhancer element shown previously to regulate PCDH-alpha
147 -seq and ChIP-seq, that specific Runx1-bound enhancer elements critically modulate lineage-dependent
148 three-dimensional organization of the genes, enhancer elements, and transcription machinery plays an
151 pressed genes by suppressing the function of enhancers enriched for binding by transcription factor M
155 our characterization of a cell type-specific enhancer for the Wnt9b/beta-catenin target gene Fam19a5
156 atform that can identify stimulus-responsive enhancers for a target gene independent of stimulus expo
158 in, and we show that paired sites buffer the enhancer from integration site-dependent effects on tran
159 n-dependent looping to reposition the Bcl11b enhancer from the lamina to the nuclear interior and to
162 This highly sensitive phenotypic readout of enhancer function in a native genomic context reveals no
163 d by a similar cis mechanism to modulate LTR enhancer function in activating transcription of downstr
164 n "enhanceosome" and "smorgasbord" models of enhancer function, in which elements cooperate to bind c
169 a role in splicing modulation, exonic splice enhancers have a lower SSM density before and after cont
170 p sequencing techniques in the recent years, enhancers have been systematically identified in such pr
172 Taken together, our results validate our enhancer identification pipeline and reveal that enhance
173 arch for factors that relocalized the Bcl11b enhancer identified a non-coding RNA named ThymoD (thymo
177 ciated hypomethylation was enriched at super-enhancers in highly expressed genes critical for liver f
179 tigated the evolution of liver promoters and enhancers in six primate species using ChIP-seq (H3K27ac
180 highly accurate, genome-wide predictions of enhancers in the developing limb, available through a us
181 methods when predicting the target genes of enhancers in unseen samples, as evaluated by independent
183 expressed by altering OSK targeting, somatic-enhancer inactivation, and pluripotency enhancer selecti
186 ression, indicating that long-range promoter-enhancer interaction mediated by CTCF plays important ro
188 hmC and preferential enrichment at oncogenic enhancers is a novel regulatory mechanism in human pancr
190 idization, we examined the epigenome and the enhancer landscape in X. tropicalis x X. laevis hybrid e
191 es results in signal-specific alterations in enhancer landscapes and associate with coordinated bindi
192 ranscription is a defining feature of active enhancers, linking transcription factor (TF) binding to
193 emonstrate that a highly conserved ERG-bound enhancer located upstream of HLX (which encodes a transc
194 re enhanced by natural variation at the drl2 enhancer locus, including reduced expression of the drl2
197 MLV, suggesting MLV prefers smaller promoter-enhancer loops, whereas PB insertion encompasses larger
199 toli and pregranulosa cells; however, active enhancers marked by H3K27ac were enriched proximal to on
201 vance in colon cancer modeling and implicate enhancer-mediated gene regulation as a principal tumor-s
202 onstrate a physiological role for intragenic enhancer-mediated transcription attenuation in cell fate
203 SPR/Cas9 was used to delete defined rhomboid enhancers mediating expression at each site of Spitz pro
204 longation and highlight that transcriptional enhancers might modulate the release of paused RNAPII vi
205 s unified TAD, both proximal and distal limb enhancers nevertheless continued to work independently o
206 ough a TLR4/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB)/signal transdu
207 n levels of nuclear factor kappa-light-chain-enhancer of activated B cells and A20 were diminished in
208 kinase and nuclear factor kappa-light-chain-enhancer of activated B cells and negative regulators tu
211 bound to the H1-compacted promoter/proximal enhancer of the neuron-specific gene doublecortin (Dcx)
214 ulin, DHA & EPA, vitamins B6, K1, and D3) as enhancers of calcium bioavailability according to recomm
217 Mll3/4 proteins leads to strong depletion of enhancer Pol II occupancy and eRNA synthesis, concomitan
219 o the action of a putative intronic splicing enhancer present in intron 25, which appeared to functio
220 Chromatin per se can stimulate efficient enhancer-promoter communication (EPC); however, the role
222 acterize a previously unknown liver-specific enhancer-promoter element in the wild-type AAV2 genome t
224 e that our method is effective in predicting enhancer-promoter interactions as compared to the state-
225 distal enhancers and proximal promoters form enhancer-promoter interactions to regulate target genes
228 ption factor Yin Yang 1 (YY1) contributes to enhancer-promoter structural interactions in a manner an
230 rovirus/lentivirus vectors carrying the same enhancers/promoters, an effect not explained solely by f
231 ing mutations in PSENEN, encoding presenilin enhancer protein 2, in 6 unrelated patients and families
232 cular scaffold for the assembly of essential enhancer-protein complexes with an impact on timely gene
233 ding Panicum mosaic virus-like translational enhancer (PTE) and ribosome-binding 3' T-shaped structur
234 n factor EB or treatments with the autophagy enhancers rapamycin and Tat-Beclin-1 increased ureagenes
238 DNA methylation is significantly altered at enhancer regions and that the methylation levels at spec
239 illustrate how sequences outside of minimal enhancer regions can evolve functionally through mechani
242 eq for islet-specific transcription factors, enhancer regions, and different histone marks were enric
244 that, in addition to regulating CCND1, this enhancer regulates two estrogen-regulated long noncoding
246 the Satb1-NuRD complex for binding to Pdcd1 enhancers, releasing Pdcd1 expression from Satb1-mediate
247 dinate with cell-type-specific TFs to select enhancer repertoires that enable differentiation during
248 show that in developing T cells, the Bcl11b enhancer repositioned from the lamina to the nuclear int
249 on of pancreatic cancer involves large-scale enhancer reprogramming by Foxa1, which activates transcr
252 g putative targets, predicting TF responsive enhancers, revealing potential cofactors/collaborators a
253 nal global connectivity map of promoters and enhancers, revealing transcription-activity-linked genom
256 ancers exhibiting differential expression of enhancer RNAs pointed a central role for Kruppel-like fa
257 of lncRNA biology, such as the functions of enhancer RNAs, circular RNAs and chemical modifications
260 s/transcription factors in trans to hot spot enhancers serves as an effective biological strategy for
261 Large regulatory elements, so-called super-enhancers (SEs), are central to the maintenance of cance
263 , CRISPR-Cas9-mediated deletion of candidate enhancers/SEs, targeting SEs with the bromodomain and ex
266 e Drosophila embryo, we find that the poised enhancer signature is specifically generated during patt
267 that the mode of slp1 repression by Runt is enhancer specific, whereas the mode of repression of the
270 o Paired MEF2 sites are prevalent in cardiac enhancers, suggesting that this might be a common mechan
272 by DNA methylation, including at an upstream enhancer that is protected by TET2, to allow Tet1 expres
273 the enhancers are not induced, including at enhancers that are known to be repressed by a transcript
275 es accumulation of Pol II near promoters and enhancers that can best be explained by a rapid decrease
277 overed extensive allelic interactions within enhancers that have opposite effects, thereby buffering
278 we identified hundreds of tissue-restricted enhancers that require the transcription factor (TF) CDX
279 e identified an emerging program of putative enhancers that revise H3.3 occupancy during regeneration
280 romatin remodeling complex to brown fat gene enhancers, thereby regulating chromatin accessibility.
281 otein complex associated with Wnt-responsive enhancers through T cell factors (TCF) and kept silent b
283 ilizing and antifouling agent, as well as an enhancer to the mechanical and rejection properties of t
286 llel, we found that PAX6 binds promoters and enhancers to repress alternative islet cell genes includ
287 ncer identification pipeline and reveal that enhancers transcribed in breast cancer cells direct crit
289 approach, we identified a novel Sertoli cell enhancer upstream of Wt1, and used it to drive expressio
291 resolving causal mutations in developmental enhancers, validated transcription-factor-binding sites
292 the physical proximity of a promoter and an enhancer, we constructed a three-dimensional global conn
295 owed that this intron functions as a genomic enhancer where glucocorticoid receptor binding regulates
299 5i induced a dramatic increase in H3K27ac at enhancers with an associated significant increase in tar
300 that CTCF binding sites are interwoven with enhancers within topologically associated domains (TADs)
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