ライフサイエンスコーパス: enhancer

1 tivation of an ATF4-bound, stress-responsive enhancer.

2 ging the chromatin accessibility of a DDIT4L enhancer.

3 I loading rate is primarily modulated by the enhancer.

4 sly activate and deactivate different target enhancers.

5 s that also act as gene expression-promoting enhancers.

6 stablishing low methylation levels at distal enhancers.

7 TEs are de-repressed, unleashing TE-encoded enhancers.

8 polymerase II (RNA Pol II) to promoters and enhancers.

9 l chromosomal fragments harboring CRC-driven enhancers.

10 icularly frequently incorporated by evolving enhancers.

11 valently vetted inventory of bona fide human enhancers.

12 tion of several Warburg effect-related super-enhancers.

13 h as the potential roles of transcription at enhancers.

14 sociated transcription factors and MLL3/4 on enhancers.

15 e AML in general was enriched for changes at enhancers.

16 y of DNNs to learn the regulatory grammar of enhancers.

17 effectors and transcription factors (TFs) on enhancers.

18 genes by altering the acetylation status at enhancers.

19 subtype of AML, the translocation of a GATA2 enhancer (3q21) to MECOM (3q26) results in overexpressio

20 We have identified an enhancer ~5 kb upstream of the IFNK gene driving its exp

21 aited enhancers amplify TF binding at target enhancers, a phenomenon we term cross-interaction stabil

22 still unknown, such pleiotropy suggests that enhancer accessibility could be one of the molecular mec

23 romoter regions and a large number of active enhancers across the genome.

24 Most other changes in gene expression and enhancer activation are imprecisely timed and poorly coo

25 regions and activate autophagy genes through enhancer activation.

26 olution map of eRNA loci through which super-enhancer activities can be quantified by RNA-seq and a u

27 systems display more robust perturbations of enhancer activity and gene transcription with minimal of

28 hancers, suggesting that these SNPs modulate enhancer activity and, consequently, gene expression.

29 factors, i.e. the regulatory grammar, drives enhancer activity have been proposed, ranging from the f

30 We propose a model for tissue-specific enhancer activity in which an HDAC-associated GLI repres

31 Notably, the precocious patterns of enhancer activity resemble the wild-type patterns that o

32 Variants observed to alter enhancer activity were further confirmed to cause polyda

33 nces, whose expression levels correlate with enhancer activity.

34 ivity and increases basal and DMRT2-mediated enhancer activity.

35 ly mutated in prostate cancer and can impact enhancer activity.

36 of these features functionally contribute to enhancer activity.

37 eletion from intron 1 abolishes hyperosmotic enhancer activity.

38 ulatory elements, such as gene promoters and enhancers, along the DNA.

39 The mouse SAN enhancer also directed reporter activity to the inflow t

40 Transcription factors (TFs) at baited enhancers amplify TF binding at target enhancers, a phen

41 amma-globin transcription, by binding to its enhancer and fostering enhancer-promoter contacts.

42 daunorubicin activated the stress-responsive enhancer and led to dose-dependent induction of ABCB1.

43 ablish a direct regulatory link between this enhancer and lncRNAs PCAT1, PRNCR1 and PVT1.

44 omoter activation rate is influenced by both enhancer and promoter sequences, whereas Pol II loading

45 ionally multifaceted transcription factor in enhancer and ribosomal RNA biology.

46 -range interaction between the +51 erythroid enhancer and TAL1 promoter-1 leading to inhibition of TA

47 CBS acts as critical regulator to define +19-enhancer and the leukemic prone promoter IV interaction

48 ocal epigenetic landscapes at sgRNA-targeted enhancers and associated genes.

49 Finally, the users can search enhancers and enhancer-target gene relationships through

50 ng a possible relationship between gene body enhancers and expression of key TME genes in both entiti

51 ith rapid DNA demethylation at reprogramming enhancers and increased chromatin accessibility later in

52 ries of this mammalian gene that function as enhancers and insulators.

53 structure of chromatin, including promoters, enhancers and insulators.

54 ics, metformin, acarbose, spermidine, NAD(+) enhancers and lithium.

55 anscriptional regulatory networks by linking enhancers and predicted bound transcription factors to t

56 rentially impact regulatory elements such as enhancers and promoters remains poorly understood.

57 co-bind to their own and each other's super-enhancers and promoters, forming an inter-connected auto

58 condary model that effectively distinguishes enhancers and promoters.

59 modellers and histone deacetylases-at active enhancers and promoters.

60 buted to altered regulatory elements such as enhancers and promoters.

61 gic for the concurrent activation of mitotic enhancers and suppression of meiotic enhancers in the so

62 abundance and facilitated NIPBL occupancy at enhancers and that active transcriptional elongation is

63 data demonstrating many similarities between enhancers and the gene promoters they control, and we hi

64 ecreases long-range contacts between ERalpha enhancers and their target promoters.

65 i database to predict and optimize candidate enhancers and to prioritize enhancer mutations.

66 more likely to occur near active promoters, enhancers and transcribed regions.

67 revealed that chromatin structure, dedicated enhancers and transcriptional networks are regulated in

68 Altered methylation in promoters, enhancers, and gene bodies, as well as in polycomb repre

69 high structural complexity, lacks key local enhancers, and instead contains distal chromosomal fragm

70 e found that during prometaphase, promoters, enhancers, and insulators retain H3K4me3 and H3K4me1, wh

71 h ectopic contacts between GDPD1 and retinal enhancers, and modeling of all RP17 SVs was consistent w

72 emarkably, Pax7 binds to a majority of super-enhancers, and together with a cadre of interacting tran

73 d carrying motifs potentially beneficial for enhancer architecture and immune functions were particul

74 vity analysis showed that both promoters and enhancers are activated by the same transcription factor

75 e novo long-range interactions, where primed enhancers are brought in contact with their respective p

76 last decade that not only promoters but also enhancers are characterized by bidirectional, divergent

77 ation of these data demonstrated novel heart enhancers are enriched near genes expressed more strongl

78 are active, suggesting the vast majority of enhancers are established de novo without prior priming

79 he Roadmap Epigenomics project revealed that enhancers are more distinct between cell-types compared

80 ysis also revealed that cardiac regeneration enhancers are not only activated by injury, but surprisi

81 s and other innate lymphoid cells, competent enhancers are primed during lineage acquisition, and for

82 Only 12% of enhancers are primed, and 78% are active, suggesting the

83 Although these enhancers are shared by both STAT3 and ER, IL6/STAT3 act

84 Using dual effectors capable of re-writing enhancer-associated chromatin modifications, we show tha

85 abase where we have comprehensively analyzed enhancer-associated insertion and deletion variants for

86 provide insights into the regulatory role of enhancer-associated non-coding variants in cancer epigen

87 cytosine base edits at the BCL11A erythroid enhancer at +58 with few indels.

88 5-9 transcription factors repress the Ealpha enhancer at early stages of T cell differentiation, whil

89 regeneration by silencing damage-responsive enhancers at multiple loci can be partially overcome by

90 in part, through p63-mediated activation of enhancers at pro-inflammatory cytokine loci, which inclu

91 We found that NRARP interacts with lymphoid enhancer-binding factor 1 (LEF1) and potentiates Wnt sig

92 catenin and increased expression of lymphoid enhancer-binding factor 1 (LEF1), a downstream effector

93 er against decapentaplegic (SMAD)7 and CCAAT/enhancer-binding protein (C/EBP)delta, the transcription

94 sted that the G allele interacted with CCAAT/enhancer-binding protein beta transcription factor (TF),

95 D34(+) cells revealing upregulation of CCAAT/enhancer-binding protein homologous protein and immunogl

96 We observed that C/EBP-alpha (CCAAT/enhancer-binding protein-alpha) can act as a transcripti

97 atin-conformation capture and dCas9 mediated enhancer blocking establish a direct regulatory link bet

98 In summary, definition of high-resolution enhancer boundaries enables deconvolution of complex reg

99 mark H3K4me1 and carry sequences that match enhancer boundary nucleotide composition.

100 istone marks are used to identify and define enhancers but do not consider the endogenous role of an

101 t studies have focused on activators such as enhancers, but regions that repress gene expression-sile

102 CRISPRi perturbation of these super-enhancers by tethering transcription repressors to enhan

103 vitro genome editing indicated that the SRF enhancer CArG box regulates transcription of the SRF gen

104 ineage acquisition, and formation of de novo enhancers characterizes the acquisition of innate memory

105 Using CRISPR/Cas9 genome editing, the enhancer cluster or parts thereof, Nppb and flanking reg

106 The enhancer cluster was essential for prenatal and postnata

107 In enhancer cluster-deficient animals, Nppa was induced but

108 These high-interaction-frequency enhancer-cluster 'superclusters' create nano-environment

109 e epigenetic modifications of the FOXP3 gene enhancer CNS2, necessary for indelible expression of thi

110 tion factors, rather than the canonical PDX1 enhancer complex, are predicted to drive INS transactiva

111 ption of the IL10 promoter or putative local enhancer constructs.

112 as incorporated in liposomes and penetration enhancer-containing vesicles (PEVs) modified with glucid

113 eathers, claws, etc.) established by typical enhancers control five subclusters located within the ep

114 lly characterized MM-specific active distant enhancers controlling the expression of thioredoxin (TXN

115 While promoters and enhancers convey cell-type specific activating signals,

116 , to advance the application of genome-scale enhancer data, we offer a primer on current models of en

117 Sequence polymorphisms in enhancer DNAs are a major source of population diversity

118 enic mice carrying the intronic multimerized enhancer drove high expression of a betaGeo reporter in

119 Among these, the TCRA gene enhancer (Ealpha) is in an open and unmethylated chromat

120 To identify candidate tissue regeneration enhancer elements (TREEs) important for zebrafish fin re

121 ene juxtaposes the coding sequence to strong enhancer elements, leading to TERT overexpression and po

122 hown many variants are found within putative enhancer elements.

123 e modifications that typify active genes and enhancer elements.

124 umerous multi-enhancer genes and multi-genic enhancers engaged in the control of divergent molecular

125 del where the combined action of RhoA and an enhancer ensures the spatio-temporal regulation of actin

126 A distal candidate Runx1 enhancer exhibits high chromatin accessibility specifica

127 pertrophic transcription factor (TF) myocyte enhancer factor-2 (MEF2).

128 Myocyte enhancer factor-2B (MEF2B) has the unique capability of

129 of latency genes, while oriP functions as an enhancer for these promoters.

130 Using epigenetic signatures, we identified enhancers for each developmental stage.

131 ing that may distinguish productivity of new enhancer formation.

132 Deletion of this enhancer from the genome of mice resulted in SAN hypopla

133 ary vessels, visualized by a specific neural enhancer from the Nestin gene that is strongly induced i

134 erlap may thereby play a determinant role in enhancer function and evolution.

135 cordance has not been achieved for models of enhancer function in eukaryotes.

136 ic data presents a challenge to interpreting enhancer function in normal and pathogenic neurobiologic

137 PRa and enCRISPRi, for efficient analysis of enhancer function in situ and in vivo.

138 data, we offer a primer on current models of enhancer function in the CNS, we review how enhancers re

139 bipartite architecture of enhancers, inform enhancer function, and can be used as an indicator of th

140 hese boundaries are sufficient for capturing enhancer function, and confirm that core promoter sequen

141 actions play a key role in the regulation of enhancer function, and that HICE are important for both

142 neo-TADs leading to ectopic retinal-specific enhancer-GDPD1 accessibility.

143 ty with transcriptomics to identify putative enhancer-gene linkages and transcription factors that re

144 r configurations encompassing numerous multi-enhancer genes and multi-genic enhancers engaged in the

145 d, Genome engineering-based Interrogation of Enhancers (GenIE), which assesses the effects of defined

146 e comprehensively examine DNA methylation at enhancers, genome-wide, in neurons of patients with PD a

147 matin region and resides in the double-elite enhancer, GH22J020947, that is predicted to regulate CRK

148 inactivating mutations within the Drosophila enhancer H3K4 mono-methyltransferase Trr and its mammali

149 While transcriptional enhancers have been studied extensively, few transcripti

150 Thus, ectopic enhancer hijacking can compensate for the loss of local

151 a mutually exclusive manner documenting that enhancer hubs impinging on MYC detected in large cell po

152 sk variants are enriched in myeloid-specific enhancers, implicating myeloid cells in AD etiology.

153 on tropical forest: in the Andes, a putative enhancer in HAND2-AS1 (heart and neural crest derivative

154 ut do not consider the endogenous role of an enhancer in the context of native chromatin.

155 We dissected a cardiac regeneration enhancer in zebrafish to elucidate the mechanisms govern

156 regulated by AD risk variants within myeloid enhancers in a cell type-specific manner.

157 MYC thus interacts with its flanking enhancers in a mutually exclusive manner documenting tha

158 bserve enrichment of heritability in FANTOM5 enhancers in asthma, eczema, thyroid and autoimmune diso

159 firmed that our model can accurately predict enhancers in different species without re-parameterizati

160 y highlights the role of chromatin state and enhancers in disease-relevant cell types of PAH.

161 We believe the new annotation of enhancers in EnhancerAtlas 2.0 will facilitate users to

162 Notably, Ars2 preferentially occupies DNA enhancers in NSCs, where it colocalizes broadly with NSC

163 comprise the most frequently mutated set of enhancers in OC (P = 0.003).

164 ilencers that we identified were also active enhancers in other cellular contexts.

165 l, we observe extensive remodeling at active enhancers in PAH PAECs and identify hundreds of differen

166 spread increase in cytosine modifications at enhancers in PD neurons, which is partly explained by el

167 t looping are maintained at a subset of Pax7 enhancers in the absence of Pax7.

168 mitotic enhancers and suppression of meiotic enhancers in the somatic and/or mitotic proliferation ph

169 ers to perform useful functional analysis of enhancers in various genomes.

170 mall DNA regions containing each of the four enhancers, including two whose activity was stimulated b

171 with low dox, AR binding to sARE-containing enhancers increased, whereas AR was lost from cAREs.

172 CRISPR/Cas9 knockout of this enhancer induces downregulation of both genes.

173 ion cores-define a bipartite architecture of enhancers, inform enhancer function, and can be used as

174 Multi-enhancer interactions formed at genomic regions harborin

175 Collectively, these results indicate that enhancer interactions play a key role in the regulation

176 ops and to de novo formation of new promoter/enhancer interactions.

177 he analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable.

178 modularity, considered a defining feature of enhancers [J.

179 FiTAc-seq generates high-quality enhancer landscapes and super-enhancer (SE) annotation i

180 bacterial translation is often modulated by enhancer-like elements upstream of the SD, sRNA-mediated

181 pecifically interacts with the +19 stem cell enhancer located 19 Kb downstream of TAL1 and this inter

182 ions of selected gene loci suggest that some enhancers located within HCDs work at least in part via

183 Characterization of enhancer loci has identified the molecular features of a

184 d on human data and found that the predicted enhancer loops outputs were highly conserved.

185 rnover is important for maintaining promoter-enhancer loops.

186 used to determine the quantitative impact of enhancer loss on gene expression in different genetic ba

187 , that LSD1 associates with FOXA1 and active enhancer markers, and that LSD1 inhibition globally disr

188 selectively enriched for poised and bivalent enhancer marks.

189 gs of an evolutionary fail-safe, a duplicate enhancer mechanism that is hard-wired in the machinery o

190 rgeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer progressio

191 timize candidate enhancers and to prioritize enhancer mutations.

192 (JNK), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) as key signali

193 on controls nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) signaling, cel

194 spase-1 and nuclear factor kappa-light-chain-enhancer of activated B cells inhibitor that blocks IL-1

195 NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells)-dependent inflammation, c

196 10-step total synthesis of garsubellin A, an enhancer of choline acetyltransferase and member of the

197 gineic acid (DMA), a related Fe chelator and enhancer of Fe bioavailability, and increased NA/DMA bio

198 lex containing WEREWOLF (WER), GLABRA3 (GL3)/ENHANCER OF GLABRA3, and TRANSPARENT TESTA GLABRA1.

199 Thus, EDC4 not only serves as an enhancer of mRNA turnover that binds DCP2, but also as a

200 ing Yxx motif converted human IFITM3 into an enhancer of SARS-CoV-2 infection, and cell-to-cell fusio

201 AP/TAZ interact with Groucho/Transducin-Like Enhancer of Split (TLE) to block Wnt/T-cell factor (TCF)

202 A higher hairy and enhancer of split 1:mouse atonal homolog 1 ratio in ilea

203 ostane 3,17-dione, detected as the strongest enhancer of the pkd2 phenotype but whose effect was foun

204 form amyloid fibrils, known as semen-derived enhancer of viral infection (SEVI), that enhance the vir

205 s to the conserved histone methyltransferase enhancer of zest homolog 2 (EZH2) and specifically cause

206 2 (PRC2) is composed of three core subunits, enhancer of zeste 2 (EZH2), embryonic ectoderm developme

207 FZD10 and beta-catenin co-localization with enhancer of zeste 2 polycomb repressive complex 2 subuni

208 Enhancer of zeste homolog 2 (EZH2) is the catalytic subu

209 ropic functions in tumor and immune cells of enhancer of zeste homolog 2 (EZH2), the catalytic subuni

210 via the polycomb histone methyltransferase, enhancer of zeste homologue 2 [Ezh2]) showed that this p

211 Myt1 binds putative enhancers of Atf4 and Hsps, whose overexpression largely

212 for this cancer, directly establishes super-enhancers of each of these three TFs to activate their t

213 lo-Repeat Kinesin1) via a genetic screen for enhancers of the rhd3 mutant phenotype.

214 tion, and co-localized with eQTLS and (genic enhancers of) of transcription sites in brain and blood.

215 Transgenic mice with a knock-in mole CYP17A1 enhancer or overexpressing FGF9 showed phenotypes recapi

216 moter-interacting DNAm sites are enriched in enhancers or near expression QTLs.

217 s produced by transcription at promoters and enhancers, our method identifies transcription-coupled a

218 A single therapeutic base edit of the BCL11A enhancer prevented sickling and ameliorated globin chain

219 Hi-C) analysis revealed multiplex, activated enhancer-promoter configurations encompassing numerous m

220 on, by binding to its enhancer and fostering enhancer-promoter contacts.

221 he formation of fused-TADs promoting ectopic enhancer-promoter interactions that were likely to be in

222 as transcripts, revealing roles for eRNAs in enhancer-promoter looping, recruiting transcriptional ma

223 Hnf4alpha, relied on activation of preformed enhancer/promoter loops.

224 Thus, enhancer properties of locally produced WntD directly im

225 this study, we identified that Insulin Gene Enhancer Protein (ISL2) and its angiogenic capacity were

226 kely drives its communications with flanking enhancers, rather than vice versa.

227 dentified an AR binding site in the promoter/enhancer region of BMI1, and confirmed BMI1 as the direc

228 We also found that fetal-enhancer regions methylated by Dnmt3a and Dnmt3b were en

229 TCF/LEF factors to the promoter and putative enhancer regions of CSF3R.

230 MTG16 also bound to previously reported enhancer regions of genes regulated by ATOH1, including

231 enhancer function in the CNS, we review how enhancers regulate gene expression across the neuronal l

232 th increased numbers or greater proximity of enhancer regulatory elements near the gene.

233 oximal stimuli to chromatin, acting at super-enhancer regulatory regions to direct gene expression.

234 ed the traditional notion that promoters and enhancers represent distinct classes of regulatory eleme

235 te that PGA-FLUO within an HA-CP penetration enhancer represents an effective topical treatment for p

236 conserved motif in the orthologous mouse SRF enhancer revealed decreased SRF expression in aorta and

237 ulatory factors for both mitotic and meiotic enhancers, revealing a molecular logic for the concurren

238 l expression of regional genes and a retinal enhancer RNA at this locus was assessed by qPCR.

239 induction kinetics, chromosome looping, and enhancer RNA production to understand the distinct regul

240 coordinate induction of TNF, LTA, and hHS-8 enhancer RNA transcription occurs.

241 Enhancer RNAs (eRNA) are unstable non-coding RNAs, trans

242 ons with enhancer RNAs emphasize the role of enhancer RNAs and the overall structural aspects of tran

243 A complex of protein interactions with enhancer RNAs emphasize the role of enhancer RNAs and th

244 Our studies demonstrated that enhancer RNAs were produced from a subset of the regulat

245 for the biogenesis of small nuclear RNAs and enhancer RNAs.

246 nse revealed several regeneration-responsive enhancers (RREs), including an element upstream to inhib

247 Deletion of a Samd14 enhancer (Samd14-Enh), occupied by GATA2 and SCL/TAL1 tr

248 s high-quality enhancer landscapes and super-enhancer (SE) annotation in numerous archived FFPE sampl

249 L) leads to the aberrant activation of super enhancer (SE) landscapes that drive the expression of ke

250 of mRNAs that are enriched for translational enhancer sequences in the 5' untranslated region (UTR) a

251 tually resumed, showing that the presence of enhancer sequences, rather than either their exact topol

252 HoxD, both containing a range of appropriate enhancer sequences.

253 that the genome-wide reorganization of super-enhancers (SEs) drives bursts in germline gene expressio

254 Super enhancers (SEs) play critical roles in cell type-specifi

255 t CRPC cells, we identified a group of super enhancers (SEs) that are abnormally activated in Enz-res

256 We show that transcribed enhancers share a number of CGI-dependent characteristic

257 depletion of archaic alleles, but only brain enhancers show evidence of unusually stringent purifying

258 oetal brain and muscle are the tissues whose enhancers show the strongest depletion of archaic allele

259 Independent analyses of enhancers showed an excess of DNVs in associated genes (

260 ers by tethering transcription repressors to enhancers significantly reduces target gene expression a

261 Our findings identify LSD1-mediated enhancer silencing as a cell-intrinsic epigenetic feedba

262 e elements upstream of the SD, sRNA-mediated enhancer silencing could be a common mode of gene regula

263 d Prdm1 and Vsx2 or their cell type-specific enhancers simultaneously using a CRISPR/Cas9 in vivo ret

264 more common than previously suspected, with enhancers sometimes located megabases away.

265 rently independent of Tcfs, whereas on other enhancers, Sox17 represses beta-catenin/Tcf-mediated tra

266 of these SINEs harbor a high density of the enhancer-specific histone mark H3K4me1 and carry sequenc

267 meability in transdermal patches, permeation enhancers such as alkanols, fatty acids, prodrugs, and v

268 s overlap with putative endocrine pancreatic enhancers, suggesting that these SNPs modulate enhancer

269 on or epigenetic silencing of an ERV-derived enhancer suppresses cell growth by inducing apoptosis in

270 Finally, the users can search enhancers and enhancer-target gene relationships through five user-fri

271 Here we describe CRISPR/dCas9-based enhancer-targeting epigenetic editing systems, enCRISPRa

272 tiglobin gene locus, which contains a remote enhancer that drives globin expression in erythroid cell

273 Furthermore, set-based tests identified an enhancer that is predicted to target CRKL and is signifi

274 identified the molecular features of active enhancers that accompany the binding of transcription fa

275 n of hundreds of cell-type-specific neuronal enhancers that appear to be modulated by neuronal activi

276 lose proximity of EBV episomes and the super enhancers that are enriched for transcription cofactors

277 and overlap with subsets of putative somatic enhancers that are methylated in ESCs and can be activat

278 that these five loci contained cell-specific enhancers that differed between normal luminal and basal

279 enesis may involve the epigenetic control of enhancers that modify neuronal functions.

280 Among several novel SAN enhancers that were experimentally validated using trans

281 rs using its CXXC domain, TET1 also binds to enhancers, though the mechanism involved is unknown.

282 STAT3 hijacks a subset of ER enhancers to drive a distinct transcriptional program.

283 HiChIP further links PEL super-enhancers to PEL dependency factors MYC, IRF4, MCL1, CCN

284 t expression of E93 alters the competence of enhancers to respond to spatial cues.

285 , requiring the intersection of two promoter/enhancers to target gene expression to precise cell type

286 d the specificity of action of promoters and enhancers towards their targets in a tissue specific man

287 Using an enhancer trapping assay, we discovered a novel osmosensi

288 B in regulating the activity of ESC-specific enhancer units and propose that the developmentally regu

289 We show that active enhancer units are precisely delineated by active transc

290 ere, we report the existence of two types of enhancer units within SEs typified by distinctive CpG me

291 In support, we discover a causal enhancer variant (rs6060369) present in billions of peop

292 strated positive selection in Europe for the enhancer variant responsible for light eye color.

293 The enhancer was active independently of orientation and whe

294 NASH-induced changes in Kupffer cell enhancers were driven by AP-1 and EGR that reprogrammed

295 ritical role for morphogen sensing by a gene enhancer, which ultimately determines the final global d

296 Enhancers, which comprise DNA elements bound by regulato

297 Overall, the database contains 13 494 603 enhancers, which were obtained from 16 055 datasets usin

298 ologically associating domain (TAD), rich in enhancers with binding sites for retinal transcription f

299 Genome engineering revealed that two enhancers with half EREs could not compensate for the la

300 port a 'bind and discard' mechanism in which enhancers with specific binding sites promote rapid Cdk8