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1 e were modest effects on genes regulated by 'super-enhancers'.
2  specificity is linked to enhancer clusters (super-enhancers).
3 ive immune responses, is also regulated by a super-enhancer.
4 es MYC, an important oncogene regulated by a super-enhancer.
5 flanking the locus and two associated with a super-enhancer.
6 of constituent enhancers within the SLC25A37 super-enhancer.
7 e proximal enhancer incapacitated the entire super-enhancer.
8 ctions between the MYC promoter and a distal super-enhancer.
9 rs to be either an alternative promoter or a super-enhancer.
10 ntact points were significantly enriched for super enhancers.
11 romatin interactions, particularly among the super enhancers.
12 s and antagonizes chromatin accessibility at super-enhancers.
13 disruption of several Warburg effect-related super-enhancers.
14 in accessible chromatin domains organized as super-enhancers.
15 regulation of lineage-specific enhancers and super-enhancers.
16 on factors, especially those associated with super-enhancers.
17 ed primary locations of transcription within super-enhancers.
18 ated in tissue-specific enhancer clusters or super-enhancers.
19 condensates with the Mediator coactivator at super-enhancers.
20  proximity of their genes to transcriptional super-enhancers.
21 r diseases, at ERG endothelial enhancers and super-enhancers.
22 o active promoters and enhancers, especially super-enhancers.
23 ed with transcriptional regulators, known as super-enhancers.
24 control, suggesting unique RNA regulation at super-enhancers.
25 iation, while maintaining SWI/SNF binding at super-enhancers.
26 nhancer elements collectively referred to as super-enhancers.
27 nucleic acid structure, and two databases of super-enhancers.
28 Aire-mediated induction of self-antigens via super-enhancers.
29 bility often reside in enhancer clusters, or super-enhancers.
30 the distal regulatory sequences described as super-enhancers.
31 on such as tissue-specific transcription and super-enhancers.
32 ant regions of focal amplification harboring super-enhancers.
33 eviously, with particularly high turnover at super-enhancers.
34 ptional network controlled by TCF4-dependent super-enhancers.
35  many active enhancers, including almost all super-enhancers.
36  at key downstream genes, often by targeting super-enhancers.
37 atin (DORCs) that significantly overlap with super-enhancers.
38  samples remains challenging, especially for super-enhancers.
39  role of ERG in controlling a core subset of super-enhancers.
40 MJD6 gene is associated with transcriptional super-enhancers.
41 r and concentrate in Mediator condensates at super-enhancers.
42 , we demonstrate EBNA2 activation of a RUNX1 super-enhancer (-139 to -250 kb) that results in low-lev
43 ow that two distinct focal amplifications of super-enhancers 3' to MYC in lung adenocarcinoma (MYC-LA
44  mediator are concentrated in condensates at super-enhancers(7,8), and large numbers of splicing fact
45 , as positive regulator of transcription and super-enhancer accessibility as well as establish this r
46 demonstrated that UTX-mediated regulation of super-enhancer accessibility was a key mechanism for com
47 gh-resolution map of eRNA loci through which super-enhancer activities can be quantified by RNA-seq a
48 sion of multiple weak constituents can alter super-enhancer activity in a manner greatly exceeding re
49                    Furthermore, we find each super enhancer acts as a single regulatory unit within w
50 ed blocking of Ash2l-binding motifs at these super-enhancers also prevents OSN recruitment and enhanc
51 d more closely aligned to cell identity than super-enhancer analysis does using multiple data sets.
52 d in chromatin regions denoted by typical or super enhancers and active markers, including histone H3
53 equencing are extensively transcribed within super enhancers and are dynamically regulated in respons
54 nded deposition of histone marks H3K27ac for super enhancers and H3K4me3 for broad domains, however l
55 H3K27ac) and define, for the first time, the super enhancers and typical enhancers active in primary
56 his cancer, focusing on the investigation of super-enhancer and its associated transcriptional regula
57                                   By in vivo super-enhancer and transcriptional profiling, we uncover
58 eals a novel positive regulatory function at super-enhancers and a unique lineage-specific role in re
59 o revealed >1,300 groups of islet enhancers, super-enhancers and active promoters that form 3D hubs,
60 2 and prevented H3K27me3 accumulation at ESC super-enhancers and associated promoters.
61 or SWI/SNF at typical enhancers than at most super-enhancers and at enhancers in untranscribed region
62     Several chromatin interactions involving super-enhancers and broad H3K4me3 domains are constituti
63                                 We connected super-enhancers and broad H3K4me3 domains in the K562 ch
64                                              Super-enhancers and broad H3K4me3 domains showed higher
65           Stretched histone regions, such as super-enhancers and broad H3K4me3 domains, are associate
66 ew layer of complexity in gene regulation by super-enhancers and broad H3K4me3 domains.
67                      We identified iNKT cell super-enhancers and demonstrated that UTX-mediated regul
68 ockdown abrogates the OSN recruitment to all super-enhancers and further hinders the enhancer activat
69 t ABBV-744 displaced BRD4 from AR-containing super-enhancers and inhibited AR-dependent transcription
70 ion, validating that Ash2l directly binds to super-enhancers and initiates the pluripotency network.
71 imited in vivo evidence for CTCF demarcating super-enhancers and preventing cross talk between distin
72 he spatiotemporal configuration of erythroid super-enhancers and promoter-centric interactions reveal
73 NKX2-2 co-bind to their own and each other's super-enhancers and promoters, forming an inter-connecte
74   We identified developmental-stage-specific super-enhancers and showed that most epigenetic changes
75 factors contribute to this local activity of super-enhancers and that trans-acting factors modulate D
76       The identification of mammary-specific super-enhancers and the mechanistic exploration of the W
77  a cardinal Aire partner that colocalized on super-enhancers and was required for the interaction of
78 nificantly, these duplications often contain super-enhancers and/or oncogenes (e.g. MYC) that are dys
79  associated with a 1.5-Mb region containing 'super-enhancers' and is the most highly expressed super-
80 ed in 8.6% of regular enhancers and 36.5% of super enhancers, and are associated with coding genes th
81  locus, and demonstrated mapping to a B-cell super-enhancer, and risk allele association with decreas
82 coming enriched on a subset of enhancers and super-enhancers, and leading to RNA polymerase II activa
83 anscription factors binding at enhancers and super-enhancers, and leads to transcriptional repression
84      Remarkably, Pax7 binds to a majority of super-enhancers, and together with a cadre of interactin
85 r histone H3K27ac signals, characteristic of super-enhancers, and were designated "EBV super-enhancer
86 ancer genome, with significant enrichment in super-enhancer architecture.
87 2D risk alleles residing in a muscle stretch/super enhancer are linked to increased expression and al
88 todermal lineage and that corneal epithelial super enhancers are already marked as potential regulato
89                   Broad domain promoters and super enhancers are regulatory elements that govern cell
90                                      Somatic super-enhancers are also enriched in genetic risk SNPs a
91                                              Super-enhancers are an emerging subclass of regulatory r
92                                 Somatic gain super-enhancers are associated with complex chromatin in
93                                 Furthermore, super-enhancers are characterized by pervasive interacti
94                  We show that these retained super-enhancers are essential for rhabdoid tumor surviva
95 y activated in CRC, most are constituents of super enhancers, are occupied by AP-1 and cohesin comple
96  assays has resulted in the establishment of super-enhancers as a widespread and useful tool for iden
97 teins, which has been shown to co-occupy the super enhancers associated with MYC.
98                         Both proteins prefer super-enhancers associated to genes that either define t
99 analysis of human NK subsets, which revealed super-enhancers associated with gene cohorts that may co
100                   Here, we show E2-dependent super enhancer-associated characteristics and suggest co
101                    Moreover, APCDD1, another super-enhancer-associated gene, acting as a downstream t
102 d were designated "EBV super-enhancers." EBV super-enhancer-associated genes included the MYC and BCL
103 orts, with the goal of identifying essential super-enhancer-associated genes on which tumour cells de
104 nd DNA-binding factors to selectively occupy super-enhancer-associated genes.
105 region mutation in the chondrocyte-specific, super-enhancer-associated MIR140 gene encoding microRNA-
106 -enhancers' and is the most highly expressed super-enhancer-associated transcription factor.
107                          We demonstrate that super-enhancer-associated transcripts are significantly
108 eased interactions between TNF-alpha-induced super enhancers at NF-kappaB-relevant loci, coinciding w
109 l states recapitulate known patterns such as super-enhancers, bivalent promoters and Polycomb repress
110                 Mir142 was associated with a super enhancer bound by the Treg lineage-determining tra
111 cell-type-specific exploitation of RUNX gene super-enhancers by multiple EBV TFs via the Notch pathwa
112                CRISPRi perturbation of these super-enhancers by tethering transcription repressors to
113                            Cell-line-defined super-enhancers can be subclassified by their somatic al
114 c data we uncovered an enhancer cluster with super enhancer characteristics upstream of Nppb.
115 and Edkappa, interact simultaneously in this super-enhancer cluster, which add to our previous findin
116                                     At these super-enhancers, co-occupancy of GATA2 (GATA-binding pro
117                                              Super-enhancers comprise dense transcription factor plat
118 on, such genetic dissection reveals that the super-enhancer concept can obscure important functions o
119 ed TBX5 recruitment, particularly to cardiac super-enhancers, concomitant with dysregulation of genes
120  melanoma-specific BRD2/4-bound promoter and super-enhancer configuration.
121           CRISPR/Cas9 genomics revealed that super-enhancer constituents act cooperatively and facili
122 utational analysis demonstrates that the Wap super-enhancer controls Ramp3, despite three separating
123                                          The super-enhancer corresponds to an expression quantitative
124 these proteins negatively regulate the RUNX1 super-enhancer, curbing EBNA2 activation.
125 d by upstream enhancers that reside within a super-enhancer delineated by histone H3 acetyl Lys27 (H3
126                                              Super-enhancers demarcate cohorts of cell-identity genes
127 is of SMARCA4 localization and SMARCA4-bound super-enhancers demonstrated extensive binding at interg
128 ngly, we observe locally active fractions of super-enhancers detectable through hypomethylated region
129 domain inhibitor JQ1 preferentially inhibits super-enhancer-directed cotranscriptional pri-miRNA proc
130              Human tumors undergo a shift in super-enhancer DNA methylation profiles that is associat
131            We previously found that a distal super-enhancer domain was important for Pmp22 expression
132                         Here, we report that super-enhancers drive the biogenesis of master miRNAs cr
133             More generally, the link between super enhancer-driven transcriptional networks and essen
134 integrative analysis, we identify MEIS1 as a super-enhancer-driven oncogene, which co-operates with E
135 eviously unrecognized mechanism feeding into super-enhancer-driven or other oncogenic transcriptional
136                                              Super-enhancers driving SC identity are decommissioned,
137 of super-enhancers, and were designated "EBV super-enhancers." EBV super-enhancer-associated genes in
138 g BRD4-mediated ALDH1A1 expression through a super-enhancer element and its associated enhancer RNA.
139 h inhibition of ALDH1A1 expression through a super-enhancer element and other stem-related genes in p
140 d loss widely impairs epigenomic signals for super-enhancers/enhancers, including the super-enhancer
141                               Additional EBV super-enhancer (ESE) targets included MCL1, IRF4, and EB
142                     Epstein-Barr virus (EBV) super-enhancers (ESEs) are co-occupied by all essential
143                     Epstein-Barr virus (EBV) super-enhancers (ESEs) are essential for lymphoblastoid
144 c modifications, chromatin accessibility and super-enhancer establishment.
145 for super-enhancers/enhancers, including the super-enhancer for the circadian rhythm repressor Per2.
146 ate broad domains from typical promoters and super enhancers from typical enhancers.
147 sulator that normally partitions a core GIST super-enhancer from the FGF4 oncogene.
148 specific promoters and enhancers, especially super-enhancers, from which a global promoter-enhancer c
149 apid histone deacetylase inhibition disrupts super enhancer function by creating many new aberrant co
150                      We interrogated the Wap super-enhancer, generating mice carrying mutations in ST
151  and IRF4 significantly reduces MYC and IRF4 super-enhancer H3K27ac signal.
152 7ac and MED1 identified 440 mammary-specific super-enhancers, half of which were associated with gene
153 s from subjects homozygous for the high-risk super-enhancer haplotype exhibited greater increase in p
154                                    The term 'super-enhancer' has been used to describe groups of puta
155                                        These super-enhancers have been proposed to manifest higher-or
156 s can be modulated through the regulation of super-enhancers; however, the underlying mechanisms are
157 hibition, including profiles associated with super-enhancers, immune and inflammatory responses and s
158         Our findings elucidate the role of a super enhancer in Igf1 regulation and uterine growth.
159 matin interactions between broad domains and super enhancers in three ENCODE cell lines (K562, MCF7,
160  further led to the formation of distinctive super enhancers in UV-irradiated cells.
161 3 through a specific element within a -97 kb super-enhancer in a manner dependent on the expression o
162 only 47 bp apart, located within a predicted super-enhancer in an intergenic region between HLA-DRB1
163                     We find that loss of the super-enhancer in mice reduces Pmp22 expression througho
164 nvestigate the consequences of deleting this super-enhancer in vivo.
165                            Identification of super-enhancers in DIPG provides insights toward the cel
166  dissection of one of the strongest putative super-enhancers in erythroid cells.
167  understanding the functional roles of these super-enhancers in gene regulation.
168 e-associated hypomethylation was enriched at super-enhancers in highly expressed genes critical for l
169 hair follicle stem cells dynamically remodel super-enhancers in response to changes in their microenv
170 and an unrecognized higher-order property of super-enhancers in RNA processing beyond transcription.
171 (GBM) cultures and patients' tumors harbored super-enhancers in several genes related to the Warburg
172 ional data led us to investigate the role of super-enhancers in the mammary gland, an organ character
173                   At a subset of endothelial super-enhancers (including DLL4 and CLDN5), loss of ERG
174  muscle is highly enriched in muscle stretch/super enhancers, including some that overlap T2D GWAS va
175 re predominantly located within enhancers or super-enhancers, including bi-directionally transcribed
176 ially affect the transcription of genes with super-enhancers, including oncogenes.
177 five regulatory elements of the alpha-globin super-enhancer individually and in informative combinati
178            Combination therapy with the CDK7/super-enhancer inhibitor THZ1 and the histone deacetylas
179         In these networks, broad domains and super enhancers interact more frequently with each other
180 itive cells and is associated with oncogenic super-enhancers involving long-range regulatory regions.
181                EBNA2 activation of the RUNX1 super-enhancer is also dependent on RBP-J.
182 although the recruitment of GATA4 to cardiac super-enhancers is retained, it no longer functions in p
183         Herein we establish the enhancer and super-enhancer landscape after AKI by ChIP-seq in uninju
184 me-wide reprogramming of the GC enhancer and super-enhancer landscape during tumorigenesis, contribut
185  deep sequencing, we mapped the enhancer and super-enhancer landscapes in antigen-specific naive, dif
186  consistent with activation of NCP genes and super-enhancers leading to melanoma.
187 cy with BRD4 at H3K27ac-marked enhancers and super-enhancers, leading to drastic suppression of drive
188 tors NANOG, OCT4 and SOX2 to an ESC-specific super enhancer located in the 5' region of Rex1.
189 on of the chromatin around broad domains and super enhancers: loci critical for pathologies and cell-
190 se a key role for NFIB and NFIX in governing super-enhancer maintenance of the key hair follicle SC-s
191 ct CRCs in poorly studied cell types through super-enhancer mapping.
192                                 Here, we use super-enhancer maps to generate CRC models for 75 human
193                                     Finally, super-enhancers mark multiple miRNAs associated with can
194                         These data delineate super-enhancer-mediated transcriptional deregulation in
195                      Moreover, they identify super-enhancers mediating these effects, highlighting ho
196        We next demonstrate that the dominant super-enhancer modulates Nanog globally and operates by
197 fic targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer prog
198  number gains of noncoding regions harboring super-enhancers near KLF5, USP12, PARD6B and MYC are ass
199 ntogeny, including NC-specific enhancers and super-enhancers, novel trans-factors, and cis-signatures
200 ion of genes associated with cancer-acquired super-enhancers, NSD2 inhibition affects the expression
201  elements, such as the pluripotency-specific super enhancers of Sox2 and miR290.
202 driver for this cancer, directly establishes super-enhancers of each of these three TFs to activate t
203 Nanog (OSN) to form Ash2l/OSN complex at the super-enhancers of Jarid2, Nanog, Sox2 and Oct4, and fur
204 l mechanism in which Ash2l directly binds to super-enhancers of several stemness genes to regulate pl
205 f RUNX1 enhancer (eR1) within its intragenic super-enhancer, or BET protein BRD4 depletion by short h
206 lates transcriptional activity in T cells at super-enhancers, or regions of high transcriptional acti
207 saic-seq to 71 constituent enhancers from 15 super-enhancers, our analysis of 51,448 sgRNA-induced tr
208 erentially acetylated enhancers ( P=0.8) and super-enhancers ( P=0.025).
209  genome editing validation, that variants in super enhancers play an important role in controlling ar
210 stinctive lineage-specific transcriptome and super-enhancer profiles.
211 gions that are highly transcribed or contain super-enhancers, providing a level of insight into genom
212 dothelial cells showed that ERG binds 93% of super-enhancers ranked according to H3K27ac, a mark of a
213             We hypothesized that this distal super-enhancer region controls E2-responsive induction o
214 a 538 kb deletion of the entire MYC upstream super-enhancer region in mice results in 50% to 80% decr
215 ncogenic driver mutations depend on the 8q24 super-enhancer region, and indicate that targeting the a
216 eractions play important roles in condensing super-enhancer regions into a cohesive transcriptional a
217    We identify >300,000 eRNA loci in ~377 Mb super-enhancer regions that are regulated by evolutionar
218 ted histones, which occurs preferentially at super-enhancer regions that control oncogene expression.
219                        Here, we characterize super-enhancer regions using aggregated RNA sequencing (
220    These data suggest distinct mechanisms of super-enhancer regulation in endothelial cells and highl
221 ple proximal stimuli to chromatin, acting at super-enhancer regulatory regions to direct gene express
222 odds ratio (OR) = 4.28) and breast-specific 'super-enhancer' regulatory elements (OR = 3.54).
223 is of differentially regulated enhancers and super-enhancers reinforced inter-subgroup heterogeneity
224 , persister status is generated via adaptive super-enhancer remodeling that reprograms transcription
225 esults suggest that genomic amplification of super-enhancers represents a common mechanism to activat
226 ,973 predicted enhancers and 3,759 predicted super-enhancers respectively.
227 ing an MYCN core transcriptional network and super-enhancers resulting from long-range MYCN DNA inter
228 omain comprising IGF2 and a lineage-specific super-enhancer, resulting in high-level gene activation.
229  genes adjacent to traditional enhancers and super-enhancers revealed signaling networks, metabolic p
230 d cis-elements and developmentally regulated super-enhancers reveals spatial features that causally c
231 istone H3K27 acetylation and methylation and super-enhancer RNA transcription.
232 ia (AML) leads to the aberrant activation of super enhancer (SE) landscapes that drive the expression
233 nerates high-quality enhancer landscapes and super-enhancer (SE) annotation in numerous archived FFPE
234 ed the macrophage genome and participated in super-enhancer (SE) formation.
235 ural stem cells (NSCs) to identify essential super-enhancer (SE)-associated genes and the core transc
236 hocytes and is associated with an archetypal super-enhancer (SE).
237 ic transcriptional amplification mediated by super-enhancers (SE) as a key mechanism underlying the v
238  identified unique sets of distal enhancers, super-enhancers (SE), and their gene targets that coordi
239 ave been proposed to function by dismantling super-enhancers (SE), the LIN9 gene lacks an SE but was
240                   Active chromatin-enriched "super-enhancer" (SE) regions, mainly observed in in vitr
241 s in the Wap locus with its mammary-specific super-enhancer separated by CTCF sites from widely expre
242                                              Super enhancers (SEs) play critical roles in cell type-s
243 sistant CRPC cells, we identified a group of super enhancers (SEs) that are abnormally activated in E
244 (CR) TFs, are governed by cell-type specific super enhancers (SEs).
245                                              Super-enhancers (SEs) are clusters of enhancers marked b
246 ature suggests that epigenetically regulated super-enhancers (SEs) are drivers of aberrant gene expre
247                     We identify two distinct super-enhancers (SEs) associated with CD47 in certain ca
248 ions (DMRs) overlapping enhancers, including super-enhancers (SEs) associated with key cell identity
249 trate that the genome-wide reorganization of super-enhancers (SEs) drives bursts in germline gene exp
250 nisms underlying TE development, here we map super-enhancers (SEs) in trophoblast stem cells (TSCs) a
251               Further, MLL4 and CBP identify super-enhancers (SEs) of adipogenesis and that MLL3/MLL4
252                                          The super-enhancers (SEs) of lineage-specific genes in B cel
253                                Enhancers and super-enhancers (SEs) play critical roles in driving dis
254 27ac) at transcription start sites (TSS) and super-enhancers (SEs) prominently in stem-like BrCa cell
255 actors (CR TFs) orchestrate the placement of super-enhancers (SEs) to activate transcription of cell-
256                                              Super-enhancers (SEs), also known as stretch-enhancers,
257         Large regulatory elements, so-called super-enhancers (SEs), are central to the maintenance of
258        Clusters of enhancers, referred as to super-enhancers (SEs), control the expression of cell id
259 ntify cell- and developmental-stage-specific super-enhancers (SEs).
260                                              Super-enhancers showed enrichment for STAT5 binding and
261 upperhand (Uph), is required to maintain the super-enhancer signature and elongation of RNA polymeras
262 monstrate that SMARCB1 is essential for hESC super-enhancer silencing in neural differentiation condi
263  which show specific binding at enhancer and super-enhancer sites, revealing enhancer dynamics and tr
264 iptional addiction in this disease, we chart super-enhancer structures in both LPS tissues and cell l
265 s, such as SPRY1, and other lineage-specific super-enhancers, such as SOX2 in brain-derived rhabdoid
266 iated single nucleotide polymorphisms at ERG super-enhancers suggests that ERG-dependent transcriptio
267                                 Finally, EBV super-enhancer-targeted IRF2 protected LCLs against Blim
268 iched for EBV-induced genes, including viral super-enhancer targets.
269        KLF6 expression is driven by a robust super enhancer that integrates signals from multiple pat
270  The close proximity of EBV episomes and the super enhancers that are enriched for transcription cofa
271 ization of Bloodlinc, an eRNA derived from a super-enhancer that also functions as a lncRNA, suggests
272 mpartments and then form a multi-chromosomal super-enhancer that associates with the single active ol
273  with additional variants that are part of a super-enhancer that physically interacts with promoters
274 a highly lineage-specific and tumor-acquired super-enhancer that shows long-range interaction with AZ
275                             Here, we defined super-enhancers that bind to ERalpha in vivo within horm
276 n chromatin looping lead to the formation of super-enhancers that drive the ectopic expression of a s
277     Interestingly, we identified a subset of super-enhancers that overlap with broad H3K4me3 domains
278 tein 1) is significantly lower compared with super-enhancers that remained constant following ERG inh
279 l identity and highlight parallels with the 'super-enhancers' that regulate mammalian cell fate.
280 lian Csf1r locus contains a highly conserved super-enhancer, the fms-intronic regulatory element (FIR
281      These features include the formation of super-enhancers, the sensitivity of super-enhancers to p
282 ation, including the convergence of multiple super enhancers to individual stemness genes within indi
283 at CTCF sites are porous borders, allowing a super-enhancer to activate a secondary target.
284   We propose a model that entails looping of super-enhancers to efficiently deliver Aire-containing c
285                     HiChIP further links PEL super-enhancers to PEL dependency factors MYC, IRF4, MCL
286 ation of super-enhancers, the sensitivity of super-enhancers to perturbation, the transcriptional bur
287 ct chromosomal rearrangements that juxtapose super-enhancers to the MYB locus.
288 ase 2 to enhancers and promoters, especially super-enhancers, to inhibit gene transcription.
289                                              Super-enhancers, together with broad H3K4me3 domains, sh
290                   Thus, our study identifies super-enhancer translocations that drive MYB expression
291                             Here we identify super-enhancer translocations that drive overexpression
292             We found that Treg cell-specific super-enhancers (Treg-SEs), which were associated with F
293                                              Super-enhancers usually contain discrete loci featuring
294  active transcriptional loci with at least 2 super-enhancers, we detail the many-body functional land
295 y, NuRD complex containing CHD4 localizes to super-enhancers where CHD4 generates a chromatin archite
296 istically explained by its enrichment at ESC super-enhancers, where Spt6 controls histone H3K27 acety
297 resting patterns of spatial distributions of super-enhancers which can provide useful insights into u
298 ntrolled in a competitive manner by a shared super enhancer, which is also required to augment stress
299 omic regions distributed among enhancers and super-enhancers, which are conserved and occupied by p63
300 points to locally active regulatory sites at super-enhancers, which are targeted by specific aberrant
301 over, SAFA is required for the activation of super-enhancers, which direct vigorous immune gene trans
302 ng known core TFs forming CRCs are driven by super-enhancers, which provides an opportunity to system

 
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