ライフサイエンスコーパス: hypersensitive site

1 ted enzymes were unable to erase the DNase I-hypersensitive site.

2 activity and corresponds to a major DNase I-hypersensitive site.

3 6-bp footprint separated from the first by a hypersensitive site.

4 esults in the appearance of multiple DNase I hypersensitive sites.

5 lso reiterated by their proximity to DNAse I-hypersensitive sites.

6 ct from, that observed for FAIRE and DNase I hypersensitive sites.

7 density, gene expression levels, and DNaseI hypersensitive sites.

8 t of nucleosome sequences containing KMnO(4) hypersensitive sites.

9 sites and greatly diminished at the DNase I hypersensitive sites.

10 the immediate 5' flanking region for DNase I hypersensitive sites.

11 her functional modalities encoded by DNase I hypersensitive sites.

12 in to either stably create or remove DNase I hypersensitive sites.

13 cers (hs3A, hs1,2, hs3B, and hs4) at DNase I-hypersensitive sites.

14 conditions caused rapid development of three hypersensitive sites.

15 T transcription start site and several minor hypersensitive sites.

16 binding within the LCR is restricted to the hypersensitive sites.

17 ome mobilization, which subsumed the DNase I hypersensitive sites.

18 ma cells by inducing and maintaining DNase I hypersensitive sites.

19 and termination sites, enhancers and DNase I hypersensitive sites.

20 r chromatin binding and induction of DNase I hypersensitive sites.

21 C with target-sequence enrichment of DNase I hypersensitive sites.

22 ct through binding events located in DNase I hypersensitive sites.

23 accessible regulatory DNA defined by DNase I hypersensitive sites.

24 associated histone modifications and DNase I hypersensitive sites.

25 n transcription-factor-binding-sites and DNA-hypersensitive-sites.

26 Deletion of this element, termed hypersensitive site 1 (HSS1), in a bacterial artificial

27 One region, DNase I-hypersensitive site 1 (HSS1), located 10 kb upstream of

28 rted between locus control region 5' DNase I-hypersensitive site 1 and the epsilon-globin gene was tr

29 folds from 1.36 to 3.1) as well as the DNase hypersensitive sites (1.58-2.42 fold), H3K4Me1 (1.23-1.4

30 ng in vivo in the beta-globin cluster to the hypersensitive site 2 (HS2) in the locus control region

31 element (MARE) in locus control region (LCR) hypersensitive site 2 (HS2) reveals a remarkably high de

32 s sequence in the enhancer region of the LCR hypersensitive site 2 (HS2).

33 ACCC site at -114 bp and enhancer sequences (hypersensitive site 2 [HS2]) from the beta-globin locus

34 The human beta-globin locus control region hypersensitive site 2 plays different roles on beta-glob

35 f transcription initiation within the LCR at hypersensitive sites 2 and 3.

36 on of the 234-bp core element of the DNase I hypersensitive site 3 (5'HS3) of the locus control regio

37 We conclude that the GT6 motif of hypersensitive site 3 of the LCR is required for normal

38 Our studies revealed a cluster of hypersensitive sites 30 kb upstream of the most 5' VH ge

39 -SAR) and the chicken beta-globin 5' DNase I hypersensitive site 4 (5'HS4) insulator both separately

40 Thus, the chicken hypersensitive site 4 DNA insulator is sufficient to pro

41 from the chicken beta-globin locus, chicken hypersensitive site 4, which contains CCCTC binding fact

42 gene led to the identification of a DNase I hypersensitive site 4.5 kb upstream of the Ly49A gene tr

43 Previous studies demonstrated that DNase I hypersensitive site -40 (HS-40) of the alpha-globin locu

44 odifications revealed that deletion of Rad50 hypersensitive site 6 impacted epigenetic modifications

45 These studies indicated that Rad50 hypersensitive site 6 was the singularly most important

46 Among these sites, Rad50 hypersensitive site 7 (RHS7) shows rapid T(H)2-specific

47 rad50 hypersensitive site 7 (RHS7), a hypersensitive site with

48 We used DNase-chip to identify DNase I hypersensitive sites accurately from a representative 1%

49 s and by mapping the previously known DNaseI hypersensitive sites across 240 kb of the human alpha-gl

50 ated the ADHM protocol by mapping the DNaseI hypersensitive sites across 250 kb of the human TAL1 loc

51 es a powerful approach to identifying DNaseI hypersensitive sites across large genomic regions.

52 a shared region of 39 kb that contains DNAse hypersensitive sites active at a restricted time window

53 equence homology analysis as well as DNase I-hypersensitive site analysis.

54 periments revealed that, although all of the hypersensitive sites analyzed are important for appropri

55 of the core promoter that contains a DNase I hypersensitive site and directs high level, erythroid-sp

56 r from EKLF-deficient cells lacked a DNase I hypersensitive site and exhibited histone hypoacetylatio

57 A DNase I hypersensitive site and extragenic transcripts at IFNgCN

58 Global analyses of DNase I-hypersensitive sites and 3D genome architecture, linking

59 ssible chromatin by global mapping of DNaseI hypersensitive sites and analyzed enriched TF-binding mo

60 Each enhancer contains DNase I-hypersensitive sites and appears to confer developmental

61 igh-throughput, automated mapping of DNase I-hypersensitive sites and associated cis-regulatory seque

62 lowed us to identify a number of novel DNase hypersensitive sites and characterize more distant regul

63 f functional elements, as we show for DNaseI hypersensitive sites and highly conserved regions with d

64 These elements contain DNase I hypersensitive sites and histone modification patterns c

65 l region (LCR), composed of multiple DNase I-hypersensitive sites and located far upstream of the gen

66 gh-throughput approach, we discovered DNaseI hypersensitive sites and potential regulatory elements a

67 ated gene 1 complex induces promoter DNase I hypersensitive sites and recruits other transcription fa

68 is region contained newly identified DNase I-hypersensitive sites and several CTCF target sites, some

69 trong topo II sites colocalized with DNase I hypersensitive sites and thus represent open chromatin r

70 mplexes are recruited to a subset of DNase I hypersensitive sites and to conserved noncoding sequence

71 overlap endogenous erythroid-specific DNase hypersensitive sites, and 1 of which includes the proxim

72 -5.3 kb, the promoter, the intronic DNase I hypersensitive sites, and 3' distal sites including the

73 ipts, double-strand-break hotspots and DNase hypersensitive sites, and can distinguish genes by expre

74 ranscription start sites, CpG islands, DNase-hypersensitive sites, and gene-dense regions; all are fe

75 for 17 TFs, 3 histone modifications, DNase I hypersensitive sites, and high-resolution promoter-enhan

76 ssible chromatin comprising clustered DNaseI hypersensitive sites, and that replication time is bette

77 Traditional methods used to identify DNaseI hypersensitive sites are cumbersome and can only be appl

78 Here we report identification of a DNaseI hypersensitive site at the 3' end of the Scl/Map17 domai

79 tein TFE3 was sufficient to induce a DNase I-hypersensitive site at the immunoglobulin heavy chain mi

80 nd cell division involves the formation of a hypersensitive site at the insulator during chromatin ma

81 did not participate in the formation of the hypersensitive site at the tRNA.

82 ription factor motifs in deoxyribonuclease I hypersensitive sites at cell-type-specific epigenetic lo

83 tion, we have identified two tissue-specific hypersensitive sites at the 5' CR of the PD-1 locus.

84 thermore, we were only able to detect DNaseI hypersensitive sites at the TBP and PSMB1 promoters pres

85 accompanied by the loss of multiple DNase I hypersensitive sites at the TERT promoters and their ups

86 tin architecture reflected by major nuclease hypersensitive sites, atypical distribution of epigeneti

87 e replacement closely correspond to nuclease-hypersensitive sites, binding sites for Polycomb and tri

88 The Lockd promoter contains a DNase-hypersensitive site, binds numerous transcription factor

89 te that both the distal and proximal DNase I-hypersensitive sites characteristic of the transcription

90 in wild-type cells, suggesting that the four hypersensitive sites contain most of the CSR-promoting f

91 gene comprises a 220 bp micrococcal nuclease hypersensitive site corresponding to the promoter regula

92 We demonstrate DNase hypersensitive sites corresponding to the lymphotoxin al

93 addition, transcription from within the LCR hypersensitive sites could compensate for the absence of

94 in various cells using Encode Roadmap DNase-hypersensitive site data.

95 co-occurring DNA motifs in 349 human DNase I hypersensitive site datasets.

96 An additional hypersensitive site developed rapidly only under Th2 con

97 An airway-selective DNase-hypersensitive site (DHS) at kb -35 (DHS-35kb) 5' to the

98 Here we present PlantDHS, a plant DNase I hypersensitive site (DHS) database that integrates histo

99 ce, which leverages cell-type specific DNAse Hypersensitive Site (DHS) information from the NIH Epige

100 d that allows us to generate maps of DNase I-hypersensitive site (DHS) of mouse preimplantation embry

101 Here, we report that a strong DNase I hypersensitive site (DHS) resides approximately 25 kb up

102 vivo and encompasses a male-specific DNase I hypersensitive site (DHS).

103 y chromatin environments and mapped to DNase-hypersensitive sites (DHS) classified by sex bias in chr

104 We previously mapped DNase I hypersensitive sites (DHS) in 400 kb spanning the CFTR l

105 fication of hundreds of thousands of DNase I hypersensitive sites (DHS) per cell type has been possib

106 sequence corresponding to human CFTR DNase I hypersensitive sites (DHS) showed high homology in the c

107 scription of Ikaros, tissue-specific DNase I-hypersensitive sites (DHS) were mapped throughout the Ik

108 elements for CFTR is the mapping of DNase I hypersensitive sites (DHS) within the locus.

109 MRs mark an exclusive subset of active DNase hypersensitive sites (DHS), and that both developmentall

110 zes with the PWS-IC and contains two DNase I hypersensitive sites, DHS1 at the SNRPN promoter, and DH

111 DNase I hypersensitive sites (DHSs) are a hallmark of chromatin

112 DNase I hypersensitive sites (DHSs) are markers of regulatory DN

113 sistent patterns of gain and loss of DNase I-hypersensitive sites (DHSs) as cells progress from embry

114 tory elements; therefore, mapping of DNase I hypersensitive sites (DHSs) enables the detection of act

115 polymorphisms (SNPs) and deoxyribonuclease I hypersensitive sites (DHSs) from 112 different cell type

116 ale maps of regulatory DNA marked by DNase I hypersensitive sites (DHSs) from 138 cell and tissue typ

117 e standard approach to locating these DNaseI-hypersensitive sites (DHSs) has been to use Southern blo

118 , we mapped >1.3 million deoxyribonuclease I-hypersensitive sites (DHSs) in 45 mouse cell and tissue

119 drive gene-expression changes though DNase-I hypersensitive sites (DHSs) near transcription start sit

120 We mapped the DNase I-hypersensitive sites (DHSS) of the serglycin gene in res

121 DNase I hypersensitive sites (DHSs) provide important informatio

122 However, an extended analysis of DNase I-hypersensitive sites (DHSs) spanning the entire upstream

123 Over half of embryonic DNase I hypersensitive sites (DHSs) were annotated as noncoding,

124 cytes and glioma cells, six specific DNase I-hypersensitive sites (DHSs) were found located exclusive

125 We associated DNase I hypersensitive sites (DHSs) with genes, and trained clas

126 t defined more than 1800 clusters of DNase I hypersensitive sites (DHSs) with similar tissue specific

127 AP-1 which created thousands of new DNase I-hypersensitive sites (DHSs), enabling ETS-1 and RUNX1 re

128 ave created genome-scale catalogs of DNase I hypersensitive sites (DHSs), which demark potentially fu

129 associated with regulatory elements, DNase I hypersensitive sites (DHSs).

130 d by a 150 kb domain comprised of 16 DNase I hypersensitive sites (DHSs).

131 ormation of 17 expression-associated DNase I-hypersensitive sites (DHSs).

132 bility and DNA methylation patterns at DNase hypersensitive sites (DHSs).

133 ory DNA elements are associated with DNase I hypersensitive sites (DHSs).

134 DNA marked by deoxyribonuclease I (DNase I) hypersensitive sites (DHSs).

135 Two strong DNase I-hypersensitive sites (DHSSs) were identified in the IL-1

136 a functional role for an intergenic DNase I hypersensitive site distal to LTA in Jurkat cells based

137 Sequencing of DNase I hypersensitive sites (DNase-seq) is a powerful technique

138 nclude that favored integration near DNase I-hypersensitive sites does not imply that integration tak

139 developmentally specific erythroid enhancer, hypersensitive site-embryonic 1 (HS-E1), located within

140 DNase I hypersensitive sites exhibit marked aggregation around t

141 In particular, hypersensitive sites flanking the Cse4 containing nucleo

142 n approach that can rapidly identify DNase I hypersensitive sites for any region of interest, or pote

143 specific small hairpin RNA inhibits DNase I hypersensitive site formation and down-regulates target

144 However, GATA-1 binding, DNase I hypersensitive site formation and several histone modifi

145 AP-1 elements that colocalized with DNase I-hypersensitive sites found in astrocytes and glioma cell

146 art sites, most often contained within DNase hypersensitive sites, frequently conserved, and near gen

147 -50), and a novel Sarkosyl-sensitive DNase I-hypersensitive site generated by Ets-1 binding to chroma

148 n start sites, reduces the number of DNase I-hypersensitive sites genome wide, and decreases the numb

149 with, and maintain the intensity of DNase I hypersensitive sites genome wide, in resting but not in

150 ion (LCR), was revealed by analyzing DNase I hypersensitive sites, H3K4 trimethylation marks and GATA

151 An MSL-binding site (DHS, DNaseI hypersensitive site) has been identified in each roX gen

152 The 3' Igh enhancers, DNase I hypersensitive site (hs) 3B and/or hs4, are required for

153 Here we focus on DNase hypersensitive site (HS) 6 of the TCRalpha LCR.

154 We previously identified two upstream hypersensitive site (HS) clusters in mast cells and mela

155 function of the locus control region DNase I hypersensitive site (HS) core elements.

156 inants of this activity coincide with DNaseI hypersensitive site (HS) I of the LCR.

157 DNase I hypersensitive site (HS) mapping revealed five liver-spe

158 (ANK1E) core promoter contains a 5' DNase I hypersensitive site (HS) with barrier insulator function

159 t it is phosphorylated and lost over DNase I hypersensitive site (HS)2, HS3, HS4, and the human beta-

160 However, at DNase I-hypersensitive site (HS)3 of the beta-globin locus contr

161 We previously defined novel DNase I hypersensitive sites (hs) 5, 6, 7 immediately downstream

162 l promoter displays three constitutive DNase hypersensitive sites (HS) and a moderate level of histon

163 The LCR is marked by five DNase I-hypersensitive sites (HS) approximately 15 kb upstream o

164 Several deoxyribonuclease (DNase) I-hypersensitive sites (HS) have been located in the dista

165 This LCR is composed of DNase I-hypersensitive sites (HS) located -14.5 kb to -32 kb rel

166 ent physically characterized by five DNase I-hypersensitive sites (HS), designated HS1-HS5.

167 normal cells and is spanned by three DNase I-hypersensitive sites (HS).

168 t a 650-bp sequence corresponding to DNase I hypersensitive sites HS1-2 within the mouse Igkappa gene

169 Thus, our studies demonstrate that DNase I hypersensitive sites HS1-2 within the Vkappa-Jkappa inte

170 This silencer activity requires DNase I hypersensitive sites HS2 and HS3 but not HS4.

171 An evolutionarily conserved DNase hypersensitive site (HS3) within intron 2 was found to a

172 These elements, hypersensitive site (HSS)-9 and HSS+3 (9 kb upstream and

173 Strikingly, a novel DNase I-hypersensitive site (HSS-4.5) was identified in stimulat

174 ctive globin genes, as well as the remote 5' hypersensitive sites (HSs) (HS-60/-62 in mouse, HS-110 i

175 hey can be detected experimentally as DNaseI hypersensitive sites (HSs) in vivo, though the process i

176 noncoding regulatory elements within DNase I-hypersensitive sites (HSS) located 9 kb upstream (HSS-9)

177 Clusters of epidermal-specific DNaseI-hypersensitive sites (HSs) mapped to specific CNSs.

178 The DNaseI hypersensitive sites (HSs) of the human beta-globin locu

179 The LCR encompasses 6 DNaseI hypersensitive sites (HSs) that bind transcription facto

180 The overall structure of the DNase I hypersensitive sites (HSs) that comprise the beta-globin

181 by two partially overlapping sets of DNase I hypersensitive sites (HSs) that constitute the pituitary

182 ne the contribution of individual LCR DNaseI hypersensitive sites (HSs) to transcription and nuclear

183 ch for genome-scale identification of DNaseI hypersensitive sites (HSs) via isolation and cloning of

184 the transcriptionally active state, DNase I hypersensitive sites (HSs) were detected at the -3.9- an

185 ning a defined set of liver-specific DNase I hypersensitive sites (HSs), is robustly expressed in mou

186 The LCR is composed of a number of DNase I-hypersensitive sites (HSs), which are believed to encomp

187 n (LCR) composed of five deoxyribonuclease I hypersensitive sites (HSs).

188 ll characterized LCR containing four DNase I hypersensitive sites (HSs).

189 tary-specific locus control elements DNase I-hypersensitive site I (HSI) and HSII, located 14.5 kb 5'

190 DNase I-hypersensitive site I (HSI) of the LCR is essential to f

191 Pituitary-specific DNase I hypersensitive site I (HSI), the dominant hGH LCR elemen

192 isruptive mutations within fetal CNS DNase I hypersensitive sites (i.e., putative regulatory regions)

193 ally, a lipopolysaccharide-inducible DNase I hypersensitive site identified 10 kb upstream of the sta

194 s information from H3K27ac signal at DNase I hypersensitive sites identified from published human and

195 uadruplexes strongly associate with nuclease hypersensitive sites identified throughout the genome vi

196 We describe three paternal-specific nuclease hypersensitive sites immediately upstream from the start

197 In transgenic mice, these hypersensitive sites impart strong, Th2-specific enhance

198 nhancer, we show that TFE3 induces a DNase I-hypersensitive site in an ATP-dependent reaction that re

199 xhibits a plasmacytoma cell-specific DNase I-hypersensitive site in chromatin, henceforth termed HS10

200 site mapping demonstrated the presence of a hypersensitive site in the 5' flanking region of the hEP

201 his technique enables genome-wide mapping of hypersensitive sites in a wide range of cell populations

202 The identification of nuclease-hypersensitive sites in an active globin gene and in the

203 erization of the most highly mutated DNase I hypersensitive sites in breast cancer (using in silico a

204 didate noncoding driver mutations in DNase I hypersensitive sites in breast cancer and experimentally

205 enoc7arcinoma cell line (LNCaP) or by DNaseI hypersensitive sites in cancer cell lines.

206 DNase I-hypersensitive sites in cellular chromatin are usually b

207 tion were positively correlated with DNase I-hypersensitive sites in chromatin.

208 We map the location of 17 DNase I-hypersensitive sites in different murine T cell populati

209 e observed significant enrichment in DNase I hypersensitive sites in fetal heart and lung.

210 we profile parental allele-specific DNase I hypersensitive sites in mouse zygotes and morula embryos

211 the TNF gene, respectively), contain DNase I hypersensitive sites in naive, T helper 1, and T helper

212 protein-coding genes, enhancers, and DNase-I hypersensitive sites in over 100 tissues and cell lines.

213 itro mapping of the nucleosome positions and hypersensitive sites in specific genes such as the yeast

214 One of the three nuclease hypersensitive sites in the Fab-7 boundary, HS1, contain

215 rate localization of the majority of DNase I-hypersensitive sites in the human genome without requiri

216 fraction of the proviruses) of both DNase I hypersensitive sites in the long terminal repeats and in

217 tin structure were the occurrence of DNase I-hypersensitive sites in the promoter region of nearly ev

218 We identify several DNase I-hypersensitive sites in the SLP-76 locus, with a promine

219 ld tend to contain more micrococcal nuclease hypersensitive sites in their promoters, a proxy for ope

220 ects Mi2beta to erase an established DNase I-hypersensitive site, in an ATP-dependent reaction subseq

221 Bound regions covered 80% of DNase I hypersensitive sites including 99.7% of TSS and 98% of e

222 Analysis of DNase I hypersensitive sites indicated that only two of these ma

223 at the occupancy of nucleosomes at a DNase I hypersensitive site is a developmental stage-related eve

224 This DNase I-hypersensitive site is the only known regulatory element

225 Mapping DNase I hypersensitive sites is an accurate method of identifyin

226 from everywhere in the Il4-Il13 locus except hypersensitive site IV, suggesting a critical role for t

227 DNA fragment including only its four DNase I hypersensitive sites (lacking the large spacer regions)

228 by a 3.4-kb DNA fragment including a DNase I hypersensitive site located 14 kb upstream of the transc

229 uence element mapping to a chromatin DNase I hypersensitive site located within intron 1.

230 ammalian cohesins occupy a subset of DNase I hypersensitive sites, many of which contain sequence mot

231 novel genomic array-based approach to DNaseI hypersensitive site mapping (ADHM) that permits precise,

232 xperimental approaches - for example, DNaseI hypersensitive site mapping and analysis of chromatin in

233 By hypersensitive site mapping and chromosome conformation

234 We first performed DNase I hypersensitive site mapping and demonstrated that the pr

235 In this study, DNaseI hypersensitive site mapping demonstrated the presence of

236 Here we utilized DNase I hypersensitive site mapping, chromatin immunoprecipitati

237 nucleosome positioning for MNase-seq, DNase hypersensitive site mapping, site annotation and motif i

238 Here, we identify a double DNaseI hypersensitive site, mHS-25/6, as having erythroid but n

239 h tri-methyl K4 of histone H3, correspond to hypersensitive sites, notably in exon 4 of LTB.

240 In the vicinity of active genes and DNase I hypersensitive sites nucleosomes are organized into peri

241 Nuclease-hypersensitive sites occur in species from yeast to huma

242 n with the restriction enzyme Fnu4HI reveals hypersensitive sites occurring approximately 125 bp apar

243 promoter was found to be localized in DNaseI hypersensitive site of chromatin in cancer cells but not

244 demonstrate that nucleosomes at the DNase I hypersensitive sites of the LCR could be either depleted

245 l level; and formation of all the 5' DNase I hypersensitive sites of the LCR was disrupted.

246 ofile across the whole locus; the 5' DNase I hypersensitive sites of the LCR were formed, but to a le

247 The DNase I hypersensitive sites of the LCR were well formed and the

248 s strong enhancer regions containing DNase I hypersensitive sites overlapping the rs874040 linkage di

249 iated with the appearance of a major DNase I-hypersensitive site positioned around the hTERT transcri

250 served functional enhancer marked by DNase 1 hypersensitive sites present upstream of the gene.

251 ction with the RNA polymerase, and a DNase I-hypersensitive site, pronounced in the promoter DNA of t

252 were capable of pinpointing the most likely hypersensitive sites related to cell-type-specific expre

253 e and replication initiation lie outside the hypersensitive sites removed by the deletion.

254 Establishing and erasing the DNase I-hypersensitive site required transcriptional activation

255 Genome-wide mapping of DNase I hypersensitive sites revealed an open chromatin region b

256 gene RAD50, containing several RAD50 DNase1-hypersensitive sites (RHS), have been robustly associate

257 which is characterized by four Rad50 DNase I hypersensitive sites (RHS4-7).

258 Further, one of the hypersensitive sites (RHS7) is rapidly demethylated in T

259 ing (snDrop-seq) and single-cell transposome hypersensitive site sequencing (scTHS-seq).

260 n sequencing and microarray data and DNase I hypersensitive site sequencing data.

261 In this study, we applied DNase-seq (DNase I hypersensitive site sequencing) to study changes of chro

262 We present a transposome hypersensitive sites sequencing assay for highly sensiti

263 sequence alone, with the highest accuracy at hypersensitive sites shared across cell types.

264 beta-globin locus, well-established DNase I hypersensitive sites stand out against a background in w

265 blockade did not redistribute Pol II at the hypersensitive sites, suggesting that Pol II is recruite

266 single guide RNA libraries to target DNase I hypersensitive sites surrounding a gene of interest, we

267 e also discovered a cell-type specific DNase hypersensitive site that maps to the Sp1/Sp3 and adjacen

268 genes with paternal allele-specific DNase I hypersensitive sites that are devoid of DNA methylation

269 ecific footprints were detected within DNase hypersensitive sites that are present in multiple cell t

270 We identify ten DNase I hypersensitive sites that are significantly mutated in b

271 ns are, however, highly enriched for DNase I-hypersensitive sites that comprehensively mark cell-type

272 DNase I hypersensitive sites that comprise the T(H)2 LCR develop

273 occurs primarily within narrow, highly DNase hypersensitive sites that frequently coincide with trans

274 he traditional method of identifying DNase I hypersensitive sites, the conventional manual method is

275 remodeling and formation of multiple DNase I-hypersensitive sites throughout the locus.

276 (DRR) containing previously described DNaseI hypersensitive sites, to allow direct comparison between

277 site methylation, CGIs, co-localized DNase I hypersensitive sites, transcription factor binding sites

278 s DNA coincident with the location of DNaseI hypersensitive sites, transcriptional start sites, and a

279 ation analysis indicated that NF-E2 occupies hypersensitive site two (HS2) of the beta-globin locus c

280 By analyzing the DNase I hypersensitive sites under 349 experimental conditions,

281 We provide evidence that DNaseI hypersensitive site V in the Il4 3' enhancer is the like

282 Enrichment of SNPs associated with DNase I-hypersensitive sites was also found in many tissue types

283 However, correlations with DNase I hypersensitive sites were different for all vectors, ind

284 veral traits, and cell-type-specific DNase-I hypersensitive sites were enriched with SNPs associated

285 We found that although most DNase I hypersensitive sites were present in both cell types stu

286 We found that 40% DHSs (DNaseI hypersensitive sites) were diminished under darkness.

287 anscription in the presence and absence of a hypersensitive site, whereas endonuclease accessibility

288 arge (100-500 kb) 'superclusters' of DNase I hypersensitive sites, which encompass both gene-rich and

289 he insulator itself contains several DNase I hypersensitive sites whose occurrence is dependent on th

290 functional elements coinciding with DNase I hypersensitive sites will substantially expand our knowl

291 sitions of 4 histone modifications and DNase hypersensitive sites, Wilson et al reveal many more of t

292 of the KRAS gene contains a GC-rich nuclease hypersensitive site with three potential DNA secondary s

293 ergenic transcription start sites and DNaseI hypersensitive sites with allelic differences.

294 wherein we localized 2,690 classical DNase I hypersensitive sites with high sensitivity and specifici

295 We identified 71,264 hypersensitive sites, with 1,284 showing robust sex-rela

296 rad50 hypersensitive site 7 (RHS7), a hypersensitive site within this LCR, becomes demethylate

297 the presence of a single cluster of DNase I hypersensitive sites within the 5' flanking region, and

298 ting regions correspond to prominent DNase I hypersensitive sites within the locus.

299 fic demethylation were restricted to DNase I hypersensitive sites within this locus.

300 However, PU.1 binding erased the DNase I-hypersensitive site without abolishing TFE3 binding.