ライフサイエンスコーパス: super-enhancer

1 e proximal enhancer incapacitated the entire super-enhancer.

2 at bring the MYC gene under the control of a super-enhancer.

3 flanking the locus and two associated with a super-enhancer.

4 of constituent enhancers within the SLC25A37 super-enhancer.

5 stream somatic tissues, often expanding into super enhancers.

6 the distal regulatory sequences described as super-enhancers.

7 on such as tissue-specific transcription and super-enhancers.

8 ant regions of focal amplification harboring super-enhancers.

9 eviously, with particularly high turnover at super-enhancers.

10 ptional network controlled by TCF4-dependent super-enhancers.

11 many active enhancers, including almost all super-enhancers.

12 K7 inhibition and frequently associated with super-enhancers.

13 ciating domains (TADs) and the activation of super-enhancers.

14 rom other broad epigenetic features, such as super-enhancers.

15 nd GFI1 by repositioning these genes next to super-enhancers.

16 o active promoters and enhancers, especially super-enhancers.

17 ed with transcriptional regulators, known as super-enhancers.

18 control, suggesting unique RNA regulation at super-enhancers.

19 iation, while maintaining SWI/SNF binding at super-enhancers.

20 nhancer elements collectively referred to as super-enhancers.

21 nucleic acid structure, and two databases of super-enhancers.

22 bility often reside in enhancer clusters, or super-enhancers.

23 , we demonstrate EBNA2 activation of a RUNX1 super-enhancer (-139 to -250 kb) that results in low-lev

24 ow that two distinct focal amplifications of super-enhancers 3' to MYC in lung adenocarcinoma (MYC-LA

25 demonstrated that UTX-mediated regulation of super-enhancer accessibility was a key mechanism for com

26 constitute these domains and by identifying super-enhancers across the spectrum of human cell types.

27 sion of multiple weak constituents can alter super-enhancer activity in a manner greatly exceeding re

28 Furthermore, we find each super enhancer acts as a single regulatory unit within w

29 equencing are extensively transcribed within super enhancers and are dynamically regulated in respons

30 nded deposition of histone marks H3K27ac for super enhancers and H3K4me3 for broad domains, however l

31 H3K27ac) and define, for the first time, the super enhancers and typical enhancers active in primary

32 ssociation with the IgH 3' regulatory region super-enhancer and leads to decreased class switch recom

33 due to vulnerability conferred by the RUNX1 super-enhancer and the key role of RUNX1 in the core tra

34 By in vivo super-enhancer and transcriptional profiling, we uncover

35 2 and prevented H3K27me3 accumulation at ESC super-enhancers and associated promoters.

36 or SWI/SNF at typical enhancers than at most super-enhancers and at enhancers in untranscribed region

37 Several chromatin interactions involving super-enhancers and broad H3K4me3 domains are constituti

38 We connected super-enhancers and broad H3K4me3 domains in the K562 ch

39 Super-enhancers and broad H3K4me3 domains showed higher

40 Stretched histone regions, such as super-enhancers and broad H3K4me3 domains, are associate

41 ew layer of complexity in gene regulation by super-enhancers and broad H3K4me3 domains.

42 itor JQ1 led to preferential loss of BRD4 at super-enhancers and consequent transcription elongation

43 We identified iNKT cell super-enhancers and demonstrated that UTX-mediated regul

44 d for clusters of regulatory regions such as super-enhancers and for disease-associated single nucleo

45 imited in vivo evidence for CTCF demarcating super-enhancers and preventing cross talk between distin

46 genome but are predominantly grouped within super-enhancers and regulatory clusters.

47 We identified developmental-stage-specific super-enhancers and showed that most epigenetic changes

48 Super-enhancers and stretch enhancers (SEs) drive expres

49 factors contribute to this local activity of super-enhancers and that trans-acting factors modulate D

50 The identification of mammary-specific super-enhancers and the mechanistic exploration of the W

51 trolled by complex mechanisms involving both super-enhancers and the Polycomb repressive complex.

52 We show that super-enhancers and their dense clusters ('epicentres')

53 a cardinal Aire partner that colocalized on super-enhancers and was required for the interaction of

54 by decommissioning old and establishing new super-enhancers and/or epicentres, an auto-regulatory pr

55 nificantly, these duplications often contain super-enhancers and/or oncogenes (e.g. MYC) that are dys

56 hromatin rheostat of hair follicle stem cell super-enhancers, and provide functional evidence that su

57 r histone H3K27ac signals, characteristic of super-enhancers, and were designated "EBV super-enhancer

58 2D risk alleles residing in a muscle stretch/super enhancer are linked to increased expression and al

59 todermal lineage and that corneal epithelial super enhancers are already marked as potential regulato

60 suggests that transcriptional activities at super enhancers are critical components to understand th

61 Broad domain promoters and super enhancers are regulatory elements that govern cell

62 s that there is not yet strong evidence that super-enhancers are a novel paradigm in gene regulation

63 r perspective regarding the proposition that super-enhancers are a regulatory entity conceptually dis

64 Somatic super-enhancers are also enriched in genetic risk SNPs a

65 Super-enhancers are an emerging subclass of regulatory r

66 Somatic gain super-enhancers are associated with complex chromatin in

67 Furthermore, super-enhancers are characterized by pervasive interacti

68 Super-enhancers are clusters of gene-regulatory sites bo

69 ancers, and provide functional evidence that super-enhancers are dynamic, dense transcription-factor-

70 We show that these retained super-enhancers are essential for rhabdoid tumor surviva

71 rs in embryonic stem cells and evidence that super-enhancers are highly transcribed.

72 Super-enhancers are large clusters of transcriptional en

73 y activated in CRC, most are constituents of super enhancers, are occupied by AP-1 and cohesin comple

74 road range of human cell types and find that super-enhancers associate with genes that control and de

75 teins, which has been shown to co-occupy the super enhancers associated with MYC.

76 Both proteins prefer super-enhancers associated to genes that either define t

77 -occupied a small set of exceptionally large super-enhancers associated with genes that feature promi

78 model system, we find that transcription of super enhancer-associated eRNAs is dynamically induced a

79 ins is further supported by the finding that super enhancer-associated transcription factor binding i

80 ermal-SCs induces hyperproliferation and SCC super-enhancer-associated genes Fos, Junb and Klf5.

81 d were designated "EBV super-enhancers." EBV super-enhancer-associated genes included the MYC and BCL

82 orts, with the goal of identifying essential super-enhancer-associated genes on which tumour cells de

83 tor cause preferential loss of expression of super-enhancer-associated genes relative to other genes,

84 EBV super-enhancer-associated genes were more highly express

85 rrelated with preferential downregulation of super-enhancer-associated genes, including MYCN and othe

86 We find that expression of super-enhancer-associated transcription factor genes, in

87 thermore, we find that cancer cells generate super-enhancers at oncogenes and other genes important i

88 l states recapitulate known patterns such as super-enhancers, bivalent promoters and Polycomb repress

89 cell-type-specific exploitation of RUNX gene super-enhancers by multiple EBV TFs via the Notch pathwa

90 Disrupting EBV super-enhancers by the bromodomain inhibitor JQ1 or cond

91 Cell-line-defined super-enhancers can be subclassified by their somatic al

92 structures, while also regulating long-range super-enhancer chromosomal interactions important for ce

93 ly up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases.

94 and Edkappa, interact simultaneously in this super-enhancer cluster, which add to our previous findin

95 Super-enhancers comprise dense transcription factor plat

96 ed TBX5 recruitment, particularly to cardiac super-enhancers, concomitant with dysregulation of genes

97 melanoma-specific BRD2/4-bound promoter and super-enhancer configuration.

98 These domains, which we call super-enhancers, consist of clusters of enhancers that a

99 CRISPR/Cas9 genomics revealed that super-enhancer constituents act cooperatively and facili

100 In other more differentiated cells, super-enhancers containing cell-type-specific master tra

101 utational analysis demonstrates that the Wap super-enhancer controls Ramp3, despite three separating

102 The super-enhancer corresponds to an expression quantitative

103 these proteins negatively regulate the RUNX1 super-enhancer, curbing EBNA2 activation.

104 idence interval 0.60-0.70), and resides in a super-enhancer defined by extensive acetylation of histo

105 In this respect, the super-enhancer definition is useful in identifying regul

106 d by upstream enhancers that reside within a super-enhancer delineated by histone H3 acetyl Lys27 (H3

107 Super-enhancers demarcate cohorts of cell-identity genes

108 is of SMARCA4 localization and SMARCA4-bound super-enhancers demonstrated extensive binding at interg

109 with topological complex, highly transcribed super-enhancers, demonstrating that these compartments a

110 review the identification and composition of super-enhancers, describe links between super-enhancers,

111 mmediately decommissioned, basal endothelial super enhancers, despite persistent histone hyperacetyla

112 ngly, we observe locally active fractions of super-enhancers detectable through hypomethylated region

113 Super-enhancers differ from typical enhancers in size, t

114 domain inhibitor JQ1 preferentially inhibits super-enhancer-directed cotranscriptional pri-miRNA proc

115 Human tumors undergo a shift in super-enhancer DNA methylation profiles that is associat

116 d by TLR4 signaling are also associated with super enhancer domains and accompanied by massive repres

117 Here, we report that super-enhancers drive the biogenesis of master miRNAs cr

118 hancer-promoter interactions and reveal that super-enhancer-driven genes generally occur within chrom

119 of super-enhancers, and were designated "EBV super-enhancers." EBV super-enhancer-associated genes in

120 g BRD4-mediated ALDH1A1 expression through a super-enhancer element and its associated enhancer RNA.

121 h inhibition of ALDH1A1 expression through a super-enhancer element and other stem-related genes in p

122 hat a recently evolved polymorphism within a super-enhancer element in the first intron of LMO1 influ

123 Additional EBV super-enhancer (ESE) targets included MCL1, IRF4, and EB

124 Epstein-Barr virus (EBV) super-enhancers (ESEs) are essential for lymphoblastoid

125 Inflammatory super enhancers formed by nuclear factor-kappa B accumul

126 Additionally, most endogenous super-enhancers found in T-ALL cells are occupied by MYB

127 ate broad domains from typical promoters and super enhancers from typical enhancers.

128 ions and regulating IgH 3' regulatory region super-enhancer function.

129 n of super-enhancers, describe links between super-enhancers, gene regulation and disease, and discus

130 We interrogated the Wap super-enhancer, generating mice carrying mutations in ST

131 7ac and MED1 identified 440 mammary-specific super-enhancers, half of which were associated with gene

132 s from subjects homozygous for the high-risk super-enhancer haplotype exhibited greater increase in p

133 The term 'super-enhancer' has been used to describe groups of puta

134 These super-enhancers have been proposed to manifest higher-or

135 Functional study of genes marked by super-enhancers identifies DLBCLs dependent on OCA-B and

136 hibition, including profiles associated with super-enhancers, immune and inflammatory responses and s

137 hnology, we uncovered many new enhancers and super enhancers in hematopoietic stem and progenitor cel

138 matin interactions between broad domains and super enhancers in three ENCODE cell lines (K562, MCF7,

139 further led to the formation of distinctive super enhancers in UV-irradiated cells.

140 3 through a specific element within a -97 kb super-enhancer in a manner dependent on the expression o

141 only 47 bp apart, located within a predicted super-enhancer in an intergenic region between HLA-DRB1

142 We produce a catalog of super-enhancers in a broad range of human cell types and

143 Integrator is recruited to enhancers and super-enhancers in a stimulus-dependent manner.

144 Identification of super-enhancers in DIPG provides insights toward the cel

145 ancer therapeutics directed at components of super-enhancers in diverse tumor types.

146 ators, and transcription apparatus occupying super-enhancers in embryonic stem cells and evidence tha

147 dissection of one of the strongest putative super-enhancers in erythroid cells.

148 e-associated hypomethylation was enriched at super-enhancers in highly expressed genes critical for l

149 responsible for the generation of oncogenic super-enhancers in malignant cells.

150 hair follicle stem cells dynamically remodel super-enhancers in response to changes in their microenv

151 and an unrecognized higher-order property of super-enhancers in RNA processing beyond transcription.

152 ional data led us to investigate the role of super-enhancers in the mammary gland, an organ character

153 ers and in particular at enhancer arrays or "super-enhancers" in mouse thymocytes.

154 muscle is highly enriched in muscle stretch/super enhancers, including some that overlap T2D GWAS va

155 ects that preferentially impacted genes with super-enhancers, including MYC.

156 ially affect the transcription of genes with super-enhancers, including oncogenes.

157 five regulatory elements of the alpha-globin super-enhancer individually and in informative combinati

158 BP, which suggests a general role for MYB in super-enhancer initiation.

159 ximal to active enhancer elements, including super-enhancers, instigating oncogenic activity.

160 In these networks, broad domains and super enhancers interact more frequently with each other

161 EBNA2 activation of the RUNX1 super-enhancer is also dependent on RBP-J.

162 although the recruitment of GATA4 to cardiac super-enhancers is retained, it no longer functions in p

163 ETS2-deficiency disrupts the SCC-SC super-enhancer landscape and downstream cancer genes whi

164 me-wide reprogramming of the GC enhancer and super-enhancer landscape during tumorigenesis, contribut

165 deep sequencing, we mapped the enhancer and super-enhancer landscapes in antigen-specific naive, dif

166 matic shifts in large open-chromatin domain (super-enhancer) landscapes underlie these differences an

167 consistent with activation of NCP genes and super-enhancers leading to melanoma.

168 on of the chromatin around broad domains and super enhancers: loci critical for pathologies and cell-

169 ct CRCs in poorly studied cell types through super-enhancer mapping.

170 Here, we use super-enhancer maps to generate CRC models for 75 human

171 Finally, super-enhancers mark multiple miRNAs associated with can

172 BET bromodomain inhibition abrogates super enhancer-mediated inflammatory transcription, athe

173 Moreover, they identify super-enhancers mediating these effects, highlighting ho

174 number gains of noncoding regions harboring super-enhancers near KLF5, USP12, PARD6B and MYC are ass

175 ion of genes associated with cancer-acquired super-enhancers, NSD2 inhibition affects the expression

176 elements, such as the pluripotency-specific super enhancers of Sox2 and miR290.

177 ated variation is especially enriched in the super-enhancers of disease-relevant cell types.

178 lates transcriptional activity in T cells at super-enhancers, or regions of high transcriptional acti

179 saic-seq to 71 constituent enhancers from 15 super-enhancers, our analysis of 51,448 sgRNA-induced tr

180 genome editing validation, that variants in super enhancers play an important role in controlling ar

181 Improved understanding of the roles that super-enhancers play in biology would be afforded by kno

182 Thus, super-enhancers play key roles in human cell identity in

183 These super-enhancers prove particularly sensitive to bromodom

184 gions that are highly transcribed or contain super-enhancers, providing a level of insight into genom

185 OTCH MYC enhancer, is located within a broad super-enhancer region +1.47 Mb from the MYC transcriptio

186 a 538 kb deletion of the entire MYC upstream super-enhancer region in mice results in 50% to 80% decr

187 ncogenic driver mutations depend on the 8q24 super-enhancer region, and indicate that targeting the a

188 ted histones, which occurs preferentially at super-enhancer regions that control oncogene expression.

189 ss the AML genome, and each is released from super-enhancer regions upon chemical inhibition of BET b

190 odds ratio (OR) = 4.28) and breast-specific 'super-enhancer' regulatory elements (OR = 3.54).

191 is of differentially regulated enhancers and super-enhancers reinforced inter-subgroup heterogeneity

192 esults suggest that genomic amplification of super-enhancers represents a common mechanism to activat

193 ,973 predicted enhancers and 3,759 predicted super-enhancers respectively.

194 omain comprising IGF2 and a lineage-specific super-enhancer, resulting in high-level gene activation.

195 genes adjacent to traditional enhancers and super-enhancers revealed signaling networks, metabolic p

196 d cis-elements and developmentally regulated super-enhancers reveals spatial features that causally c

197 istone H3K27 acetylation and methylation and super-enhancer RNA transcription.

198 hocytes and is associated with an archetypal super-enhancer (SE).

199 ic transcriptional amplification mediated by super-enhancers (SE) as a key mechanism underlying the v

200 ave been proposed to function by dismantling super-enhancers (SE), the LIN9 gene lacks an SE but was

201 s in the Wap locus with its mammary-specific super-enhancer separated by CTCF sites from widely expre

202 Super-enhancers (SEs) are large clusters of transcriptio

203 Super-enhancers (SEs) are regions of the genome consisti

204 We identify two distinct super-enhancers (SEs) associated with CD47 in certain ca

205 Further, MLL4 and CBP identify super-enhancers (SEs) of adipogenesis and that MLL3/MLL4

206 Enhancers and super-enhancers (SEs) play critical roles in driving dis

207 cers, they bind multiple sites on almost all super-enhancers (SEs) present in RCS cells.

208 Super-enhancers (SEs), also known as stretch-enhancers,

209 Large regulatory elements, so-called super-enhancers (SEs), are central to the maintenance of

210 Super-enhancers (SEs), which are composed of large clust

211 Intriguingly, some key super-enhancers shift epicentres, enabling their genes t

212 Super-enhancers showed enrichment for STAT5 binding and

213 upperhand (Uph), is required to maintain the super-enhancer signature and elongation of RNA polymeras

214 ide in enhancer-dense genomic regions (i.e., super enhancers, stretch enhancers).

215 s, such as SPRY1, and other lineage-specific super-enhancers, such as SOX2 in brain-derived rhabdoid

216 and Elk3, are themselves regulated by SCC-SC super-enhancers suggesting a cooperative feed-forward lo

217 Finally, EBV super-enhancer-targeted IRF2 protected LCLs against Blim

218 iched for EBV-induced genes, including viral super-enhancer targets.

219 ization of Bloodlinc, an eRNA derived from a super-enhancer that also functions as a lncRNA, suggests

220 Interestingly, we identified a subset of super-enhancers that overlap with broad H3K4me3 domains

221 riven from large regulatory elements, called super-enhancers, that recruit much of the cell's transcr

222 These features include the formation of super-enhancers, the sensitivity of super-enhancers to p

223 Super-enhancers thus play key roles in the control of ma

224 Super-enhancers thus provide a platform for signaling pa

225 at CTCF sites are porous borders, allowing a super-enhancer to activate a secondary target.

226 We propose a model that entails looping of super-enhancers to efficiently deliver Aire-containing c

227 ation of super-enhancers, the sensitivity of super-enhancers to perturbation, the transcriptional bur

228 ct chromosomal rearrangements that juxtapose super-enhancers to the MYB locus.

229 Super-enhancers, together with broad H3K4me3 domains, sh

230 Thus, our study identifies super-enhancer translocations that drive MYB expression

231 Here we identify super-enhancer translocations that drive overexpression

232 We found that Treg cell-specific super-enhancers (Treg-SEs), which were associated with F

233 Here we show that super-enhancers underlie the identity, lineage commitmen

234 in a precise noncoding site, which creates a super-enhancer upstream of the TAL1 oncogene.

235 EBV super-enhancers were enriched for B cell transcription f

236 Super-enhancers were found at key oncogenic drivers in m

237 istically explained by its enrichment at ESC super-enhancers, where Spt6 controls histone H3K27 acety

238 omic regions distributed among enhancers and super-enhancers, which are conserved and occupied by p63

239 points to locally active regulatory sites at super-enhancers, which are targeted by specific aberrant

240 ng known core TFs forming CRCs are driven by super-enhancers, which provides an opportunity to system

241 of tissue-specific transcription factors and super-enhancers, while additive enhancer activity isolat

242 m antisense transcription that emanates from super-enhancers within sense transcribed gene bodies.