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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.
32         Here we identify AUTEN-99 (autophagy enhancer-99), which activates autophagy in cell cultures
33  consuming for large scale identification of enhancers across a variety of tissues under different di
34             Here, we report that the rainbow enhancers activate RGB cone-specific transcription of th
35 etyltransferases CBP/p300 to recruit Brd4 to enhancers activated during differentiation.
36 TAT3 is not the limiting factor for collagen enhancer activation in human lung fibroblasts.
37 cate the pioneer factor FOXA1 as a driver of enhancer activation in this system, a mechanism that ren
38            Enhancer-bound loop formation and enhancer activation of preformed loops together form mul
39 1 and zygotic Foxa at these CRMs to maintain enhancer activation.
40 s associated with suppression of LPS-induced enhancer activation.
41 l count association near CEBPA overlapped an enhancer active in common myeloid progenitors and influe
42 cus to a 5 kb region that overlaps a stretch-enhancer active in islets.
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,
45  that alleles of rs7090445 have differential enhancer activity and influence RUNX3 binding.
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
48  of sequences examined display p53-dependent enhancer activity during the DNA damage response.
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
51 t on transcription factor (TF) occupancy and enhancer activity remains poorly understood.
52          Notably, we found that E93 controls enhancer activity through three different modalities, in
53              Loss of UTX leads to attenuated enhancer activity, characterized by reduced levels of H3
54 ided a quantitative metric of Tbx5-dependent enhancer activity, correlating with target gene expressi
55 nied by massive and recurrent alterations in enhancer activity.
56 enomic region surrounding the Eya1 locus for enhancer activity.
57 down reduces ARID5B expression and rs7090445 enhancer activity.
58 e effects, thereby buffering their impact on enhancer activity.
59 ssibility of an upstream genomic region with enhancer activity.
60 ets of features govern PPARgamma binding vs. enhancer activity.
61 to activation or inactivation of hundreds of enhancers along with drastic genome-wide reduction of HN
62                             Misregulation of enhancer and promoter associated noncoding RNAs (ncRNAs)
63 urther promotes spatial clustering of MIR335 enhancer and promoter elements along with overexpression
64 nuclear interior and to juxtapose the Bcl11b enhancer and promoter into a single-loop domain.
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
67                                        Super-enhancers and broad H3K4me3 domains showed higher associ
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
74 ption is more bidirectional at newly evolved enhancers and promoter regions.
75                          YY1 binds to active enhancers and promoter-proximal elements and forms dimer
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
79 estricting chromatin accessibility at B cell enhancers and promoters.
80                     A large number of distal enhancers and proximal promoters form enhancer-promoter
81 sense core promoter sequences, and that most enhancers and several families of repetitive elements ac
82     Our findings reveal a complex network of enhancers and TFs that dynamically cooperate to restore
83             Systematic mapping of functional enhancers and their biological contexts is required to u
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
87 ental stages and brain-specific promoter and enhancer annotations.
88 al lineage and that corneal epithelial super enhancers are already marked as potential regulatory dom
89         In mammalian cells, active or primed enhancers are commonly marked by monomethylation of hist
90                       Strikingly, Amphimedon enhancers are enriched in metazoan-specific microsynteni
91 y, our analyses revealed that most p53-bound enhancers are located within regions of inaccessible chr
92                    Results suggest that hkCP enhancers are more likely to form multi-TSS interaction
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
95                            Most pluripotency enhancers are selected later in the process and require
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,
104      The approach described here to identify enhancer-associated small insertion variants provides a
105 lation by Dve maintains expression from each enhancer at distinct homeostatic levels.
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
111                                        CCAAT/enhancer binding proteins (C/EBPs) are expressed in vari
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
115                            Ablation of CCAAT-enhancer-binding protein homologous protein (CHOP), the
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.
118                                              Enhancer-bound loop formation and enhancer activation of
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
124 md14-Enh by inducing enhancer components and enhancer chromatin accessibility.
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
127                                      Related enhancers colocalize to the same microenvironments indep
128      Anemia activated Samd14-Enh by inducing enhancer components and enhancer chromatin accessibility
129                      A large majority of new enhancers comprise transposable elements.
130 oma-specific BRD2/4-bound promoter and super-enhancer configuration.
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
134              Thus, a GATA-2/anemia-regulated enhancer controls expression of an SAM domain protein th
135 nal analysis demonstrates that the Wap super-enhancer controls Ramp3, despite three separating CTCF s
136 sekeeping enhancers (hkCP) and developmental enhancers (dCP).
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
142                   Here, we report that super-enhancers drive the biogenesis of master miRNAs crucial
143                Analysis of 54 Grh-responsive enhancers during development and upon wounding suggests
144                                 By analyzing enhancers during dorsal-ventral (DV) axis formation in t
145                            A transcriptional enhancer element from the Mason-Pfizer monkey virus can
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
149 events occur predominantly within regulatory enhancer elements.
150 ing with stage-specific activity of multiple enhancer elements.
151 pressed genes by suppressing the function of enhancers enriched for binding by transcription factor M
152                         Additional EBV super-enhancer (ESE) targets included MCL1, IRF4, and EBF.
153 ns to genomic annotations (promoters, exons, enhancers, etc.).
154                 Finally, characterization of enhancers exhibiting differential expression of enhancer
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
157 represent a new family of viral transduction enhancers for potential use in gene therapy.
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
160 ription response subclasses of promoters and enhancers from two different stimulations.
161           We show that two MEF2 sites in the enhancer function cooperatively due to bridging of the M
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
165  the skull and long bones, showed that these enhancers function in an additive manner.
166                     Here we present the Limb-Enhancer Genie (LEG), a collection of highly accurate, g
167 l3 (Kmt2c) and Mll4 (Kmt2d, Mll2), the major enhancer H3K4 monomethyltransferases.
168                                 The study of enhancers has been hampered by the scarcity of methods t
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
171  with different core promoters: housekeeping enhancers (hkCP) and developmental enhancers (dCP).
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
174 e of beta cells and is a component of active enhancers in both murine and human islets.
175                      Identification of super-enhancers in DIPG provides insights toward the cell of o
176        Simultaneous deletion of these shadow enhancers in embryonic stem cells leads to impaired acti
177 ciated hypomethylation was enriched at super-enhancers in highly expressed genes critical for liver f
178 TPN6/PHB2, ANKRD11, and TNRC18 map to active enhancers in kidney cortex.
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
182 e KLF1 from key erythroid gene promoters and enhancers in vivo.
183 expressed by altering OSK targeting, somatic-enhancer inactivation, and pluripotency enhancer selecti
184 atus, making computational identification of enhancers indispensable.
185                                    Thus, two enhancers integrate combinatorial transcription factor i
186 ression, indicating that long-range promoter-enhancer interaction mediated by CTCF plays important ro
187 reas the mode of repression of the slp1 PESE enhancer is transcription factor specific.
188 hmC and preferential enrichment at oncogenic enhancers is a novel regulatory mechanism in human pancr
189                        By mapping changes in enhancer landscape and transcription factor occupancy (u
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
195 y separating the fetal globin genes from the enhancer (locus control region [LCR]).
196 ntitative trait loci, and by allele-specific enhancer loops in patient-derived primary cells.
197 MLV, suggesting MLV prefers smaller promoter-enhancer loops, whereas PB insertion encompasses larger
198 ion and indirect determination of the flavor enhancer maltol in foods and beverages.
199 toli and pregranulosa cells; however, active enhancers marked by H3K27ac were enriched proximal to on
200                                      Rainbow enhancers may represent a cis-regulatory mechanism to tu
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
209 phorylating nuclear factor kappa-light-chain-enhancer of activated B cells.
210         Our study introduces BA-DEG-BA as an enhancer of ADSC adipogenesis and suggests an integral i
211  bound to the H1-compacted promoter/proximal enhancer of the neuron-specific gene doublecortin (Dcx)
212                                Here, we show enhancer of zeste homolog 2 (EZH2), an enzyme that catal
213 BP to promote activation of C/EBPbeta-primed enhancers of adipogenic genes.
214 ulin, DHA & EPA, vitamins B6, K1, and D3) as enhancers of calcium bioavailability according to recomm
215                                           No enhancers of the APIP promoter were found.
216                    Sequence variation within enhancers plays a major role in both evolution and disea
217 Mll3/4 proteins leads to strong depletion of enhancer Pol II occupancy and eRNA synthesis, concomitan
218  and that the methylation levels at specific enhancers predict overall survival of AML patients.
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
221 tmentalization to direct with high precision enhancer-promoter communication.
222 acterize a previously unknown liver-specific enhancer-promoter element in the wild-type AAV2 genome t
223 r complex to facilitate the establishment of enhancer-promoter interaction.
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
226           Deletion of CTCF sites compromises enhancer-promoter interactions.
227 g sites or depletion of YY1 protein disrupts enhancer-promoter looping and gene expression.
228 ption factor Yin Yang 1 (YY1) contributes to enhancer-promoter structural interactions in a manner an
229                   We found that strong viral enhancers/promoters placed in foamy viral vectors caused
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
235              rs11708067 overlaps a predicted enhancer region in pancreatic islets.
236 f2 to an antioxidant response element in the enhancer region of the EDNRB gene.
237 e for the transcription factor ETS within an enhancer region.
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
240                                  It occupies enhancer regions near lung cancer-associated genes, and
241                  Chromatin rearrangements in enhancer regions occurred before the switch was complete
242 eq for islet-specific transcription factors, enhancer regions, and different histone marks were enric
243                                              Enhancers regulate gene expression through the binding o
244  that, in addition to regulating CCND1, this enhancer regulates two estrogen-regulated long noncoding
245 F binding sites, promoter-related marks, and enhancer-related histone modifications.
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
250           Collectively, our study implicates enhancer reprogramming, FOXA1 upregulation, and a retrog
251 comprising IGF2 and a lineage-specific super-enhancer, resulting in high-level gene activation.
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
254  histone-, promoter upstream transcript- and enhancer RNA-loci.
255            We discuss the potential roles of enhancer RNAs (eRNAs) in early elongation and highlight
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
258 s and is associated with an archetypal super-enhancer (SE).
259 atic-enhancer inactivation, and pluripotency enhancer selection.
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
262                                     However, enhancers/SEs mediating VSMC dysfunction remain uncharac
263 , CRISPR-Cas9-mediated deletion of candidate enhancers/SEs, targeting SEs with the bromodomain and ex
264                                Promoters and enhancers share similar architectures and functions, and
265               Explaining these observations, enhancers show TF-dependent binding of the H3K27 demethy
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
268                 Shorter introns that contain enhancers splice early.
269 rough the donation of alternative promoters, enhancers, splice sites, and termination signals.
270 o Paired MEF2 sites are prevalent in cardiac enhancers, suggesting that this might be a common mechan
271                           Finally, EBV super-enhancer-targeted IRF2 protected LCLs against Blimp1-med
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
274 blems, it could be useful to have salt taste enhancers that are not sodium based.
275 es accumulation of Pol II near promoters and enhancers that can best be explained by a rapid decrease
276 factors collaborate, they activate oncogenic enhancers that distinguish cancers from wounds.
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
282 F sites are porous borders, allowing a super-enhancer to activate a secondary target.
283 ilizing and antifouling agent, as well as an enhancer to the mechanical and rejection properties of t
284     Three transcription factors act on these enhancers to determine cell-type specificity.
285 is required to activate brown adipose tissue enhancers to ensure thermogenic aptitude.
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
288              We illustrate that TF-dependent enhancer transcription can illuminate components of TF-d
289 approach, we identified a novel Sertoli cell enhancer upstream of Wt1, and used it to drive expressio
290                              We predict limb enhancers using a combination of >50 published limb-spec
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
293                                  Within this enhancer, we identified a single-nucleotide polymorphism
294              Genes harbouring hypomethylated enhancers were enriched for genes that change expression
295 owed that this intron functions as a genomic enhancer where glucocorticoid receptor binding regulates
296 fficient repair depends on the recombination enhancer, which tethers HMLalpha near the DSB.
297                                           An enhancer with amalgamated E-box and GATA motifs (+9.5) c
298 ugation process that co-localizes permeation enhancer with the protein.
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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