ライフサイエンスコーパス: ChIP

1 ChIP analysis confirmed that PGR proteins were recruited

2 ChIP analysis of hTERT-HM cells stably expressing PRWT o

3 ChIP analysis showed that MYCN binds at the EZH2 promote

4 ChIP and reporter assays in HeLa cells with monoallelic

5 ChIP assay demonstrated estradiol (E2) induced ESR1 bind

6 ChIP assays confirmed occupancy of these sites by OCT4 a

7 ChIP experiments demonstrate that in vivo occupancy of F

8 ChIP experiments revealed a preferential binding of BRD4

9 ChIP indicated that Msn2 has increased occupancy on the

10 ChIP indicated that WT1(-KTS), but not WT1(+KTS), binds

11 ChIP sequencing of the major players NUT, ZNF532, BRD4,

12 ChIP-exo/nexus experiments rely on innovative modificati

13 ChIP-qPCR assay showed that pCREB enrichment on the C/EB

14 ChIP-seq (chromatin immunoprecipitation [ChIP] combined

15 ChIP-seq (chromatin immunoprecipitation [ChIP] combined

16 ChIP-seq (chromatin immunoprecipitation [ChIP] followed

17 ChIP-seq analysis revealed that rather than regulating t

18 ChIP-seq and DNase-seq have become the standard techniqu

19 ChIP-seq and genetic analyses demonstrate the importance

20 ChIP-seq and mechanistic studies in human RMS uncovered

21 ChIP-seq identified 1300 potential direct targets of Atr

22 ChIP-seq performed on lymphoblastoid cell lines (LCLs),

23 ChIP-Seq revealed robust interaction of Shox2 with cis-r

24 ChIP-seq studies revealed that KDM5i resulted in the bro

25 ChIP-seq was performed in adult cerebellum and Wiz peaks

26 ChIP-seq was used to identify the cytokinin-dependent ta

27 ChIP-sequencing experiments using an anti-O-GlcNAc antib

28 -based searches identified more than 120,000 ChIP-Seq motifs allowing for expansion and refinement of

29 on through transgenic reporter assays, ELT-2 ChIP and characterisation of in vitro DNA-protein intera

30 chromatin by micrococcal nuclease digest; 4) ChIP for open chromatin-associated histone methylation a

31 We present a ChIP-seq pipeline for epigenome mapping in the neuronal

32 Akt modulates PRB transcriptional activity, ChIP-Mass spectrometry was performed to identify potenti

33 We confirm our observations by analyzing ChIP-exo, chemical mapping, and ATAC-seq data from other

34 Using luciferase assay and ChIP, KLF6 was established as a direct transcriptional a

35 By integrating eQTL, Hi-C and ChIP-seq data, we show that the pleiotropic risk loci ar

36 e used qRT-PCR, Western blotting, ELISA, and ChIP (chromatin immunoprecipitation) to characterize Pb-

37 tone signatures, DNaseI hypersensitivity and ChIP-seq data to identify enhancers for the human NOTCH1

38 sequences as demonstrated by luciferase and ChIP analyses.

39 aracterized by RNA-seq, DNA methylation, and ChIP-seq analyses the epigenetic response of a set of co

40 Mechanistically, analyses of microarray and ChIP-seq datasets, coupled with the investigation of spi

41 discovery algorithms on independent PBM and ChIP-seq data.

42 By ChIP-seq and ChIP analyses, we unveil that BET proteins directly prom

43 Here, combined RNA-seq and ChIP-seq analysis reveals that REST is involved in epith

44 Finally, in RNA-seq and ChIP-seq experiments, EBF3 acted as a transcriptional re

45 on gene expression, we performed RNA-seq and ChIP-seq for H3K27ac on HepG2 cells, a human liver cell

46 ls from mouse fetal testes to DNaseI-seq and ChIP-seq for H3K27ac.

47 Using RNA-seq and ChIP-seq we show that BMP/Smad1 regulates dorsal-ventral

48 how, using CRISPR gene editing, ATAC-seq and ChIP-seq, that specific Runx1-bound enhancer elements cr

49 n followed by deep sequencing (ChIP-seq) and ChIP-reChIP-seq analyses revealed that EIN2-C associates

50 DNA binding experiments using gel-shift and ChIP assays demonstrated a progressive reduction in Nrf2

51 sing CRISPR-Cas9-introduced affinity tag and ChIP-Seq analysis, the genome-wide occupancy of SLIRP, a

52 quiring only 1/10th the sequencing depth as ChIP, making CUT&RUN especially cost-effective for trans

53 large-scale sequencing experiments (such as ChIP-seq or DNase-seq) and models the change in enhancer

54 features from a variety of sources, such as ChIP-seq peaks for a given protein or transcription star

55 igh-throughput sequencing technology such as ChIP-seq, the genome-wide binding sites of many proteins

56 rand-specific paired-end ChIP-exo (termed as ChIP-ePENS) data of FOXA1 in LNCaP cells by our novel al

57 ough rapidly accumulating publicly available ChIP-seq, DNase-seq and ATAC-seq data are a valuable res

58 ications and RNAPII states derived from bulk ChIP-seq data with single-cell RNA-sequencing data.

59 By ChIP-seq and ChIP analyses, we unveil that BET proteins

60 Our genome-wide analysis by ChIP-seq shows that PfAP2-I interacts with a specific DN

61 etic marks present at a locus, as assayed by ChIP-Seq, and the genomic compartment in which those loc

62 This was confirmed by ChIP-seq and RNA-seq analyses, showing differential tran

63 f vasopressin-responsive genes (confirmed by ChIP-seq).

64 ue sites within the erythroid cell genome by ChIP-seq.

65 ntly, binding sites previously identified by ChIP-seq for islet-specific transcription factors, enhan

66 with the HSV-1 DNA during lytic infection by ChIP-seq, and its knockdown results in the reduction of

67 ne action in the Indian Hedgehog pathway, by ChIP analysis.

68 T-rich KLF-binding sites, which, as shown by ChIP-assays, bind KLF16 in vivo In electrophoretic mobil

69 tions we identified embryonic Grh targets by ChIP-seq and gene expression analysis.

70 ic sequences were independently validated by ChIP-qPCR (quantitative PCR), oligonucleotide-binding as

71 EMSA-FRET analysis and validated in vivo by ChIP-seq data from human cell lines.

72 Analyzing beta-catenin ChIP sequencing in human cells, we found the 11-bp NREs

73 egulated by CDX2 directly, we performed CDX2 ChIP-Seq on trophoblast stem (TS) cells.

74 modules in TFBSbank aimed at characterizing ChIP peaks, identifying putative targets, predicting TF

75 ical methods and machine learning to combine ChIP-Seq and RNA-Seq data, we found that specific histon

76 Competition ChIP is an experimental method that allows transcription

77 BP) across the yeast genome from competition ChIP data.

78 1.3 minutes, demonstrating that competition ChIP is a relatively high temporal-resolution approach.

79 ghput assays, including in situ Hi-C, DamID, ChIP-seq, and RNA-seq, we investigated roles of the Hete

80 Using our recently developed ChIP-nexus method, we find that Pol II pausing inhibits

81 ivity across species by testing differential ChIP-seq read depths directly measured for orthologous s

82 genome-wide methylation and TET1 and DNMT3B ChIP-seq analyses, we conclude that TET proteins safegua

83 Using EHF ChIP followed by deep sequencing (ChIP-seq) and RNA sequ

84 pproach to identify TF clusters using either ChIP-seq or motif search data.

85 eatures associated with regulatory elements (ChIP-seq, Bis-Seq, ChiA-PET).

86 We employed ChIP-seq and 4sU-RNA-seq to identify aberrant DNA-bindin

87 We employed ChIP-sequencing for H3K4me3 to examine effects of early

88 Employing ChIP assays, cFOS recruitment to the MMP13 promoter occu

89 Using 548 ENCODE ChIP-seq and six targeted FAIRE-seq samples, we show tha

90 ly many of which were not detected by ENCODE ChIP-Seq.

91 tential transcriptional regulators in ENCODE ChIP-seq database identified transcriptional repressor E

92 incorporating gene-based information, ENCODE ChIP-seq assays, eQTL, population haplotype, functional

93 s that are bound by SOX6 according to ENCODE ChIP-seq datasets and are possible direct SOX6 targets.

94 s' gene promoters were verified using ENCODE ChIP-Seq data.

95 nal analysis on a strand-specific paired-end ChIP-exo (termed as ChIP-ePENS) data of FOXA1 in LNCaP c

96 Genomic analyses using RNA-seq and ER ChIP-seq demonstrated that the Y537S mutation promotes c

97 rial cancers with publicly available ERalpha ChIP-seq data in breast tumors and found a striking rese

98 By evaluating ChIP-seq occupancy of architectural proteins, typical en

99 e chromatin immunoprecipitation-exonuclease (ChIP-exo) method allowed the identification of a previou

100 ducing technique-specific input controls for ChIP-based methods that utilize additional bead-bound pr

101 ial variability in the observed coverage for ChIP-seq experiments and that this variability leads to

102 eak annotation, and motif identification for ChIP-seq, differential gene expression analysis for RNA-

103 ing RNA-seq gene transcripton and up to four ChIP-seq histone modification measurements.

104 rements of transcription factor binding from ChIP-seq data are key to dissecting the allelic effects

105 f specific transcription factor binding from ChIP-seq supports mechanistic roles of CGIs on the regul

106 edicted protein-binding regions derived from ChIP-seq/ChIP-exo-seq experiments using human and mouse

107 pression and binding sites data, either from ChIP-seq experiments or motif predictions, and outputs a

108 nce genomes and for mapping short reads from ChIP-seq with antibodies to centromeric histone H3 (cenH

109 ional insight for motif finding results from ChIP-Seq data.

110 Furthermore, ChIP-PCR results showed that SR1 binds to promoters of s

111 Furthermore, ChIP-Seq analysis was used to determine genome-wide bind

112 ow overlap with experimentally derived (e.g. ChIP-chip and transcription factor (TF) knockouts) netwo

113 Techniques, e.g. ChIP-Seq can reveal genome-wide patterns of TF binding,

114 f next-generation sequencing datasets (e.g., ChIP-seq and RNA-seq).

115 Single-gene ChIP and genome-wide ChIP-sequencing (ChIP-seq) and RNA-

116 d by C/EBPepsilon, we performed whole-genome ChIP-Seq using mouse bone marrow cells.

117 analyzed by RNA-seq, exome-seq, and H3K27ac ChIP-seq at 4 h and 72 h following UVR.

118 s, we used DNase-seq and H3K4me1 and H3K27Ac ChIP-seq to map open and active chromatin respectively,

119 isk rs11708067-A allele showed fewer H3K27ac ChIP-seq reads in human islets, lower transcriptional ac

120 derived from 365 human and 267 mouse H3K27ac ChIP-seq data sets.

121 Our H3K27ac ChIP-seq identified 9,514 peaks that are PenStrep respon

122 The method has been validated in H3K4me3 ChIP-seq experiments, by the quantitative assessment of

123 However, the quality of histone ChIP-seq data is affected by many experimental parameter

124 ping from suboptimal to high-quality histone ChIP-seq data.

125 Thus, histone ChIP-seq experiments are essential to distinguish nucleo

126 However, ChIP-seq data have consistently shown GR to occupy AP-1

127 However, ChIP-seq is an ensemble measurement reporting the averag

128 where quality RNA can be acquired, However, ChIP-Seq and similar validation methods are challenging

129 ing sites, by chromatin immunoprecipitation (ChIP) analyses.

130 Chromatin immunoprecipitation (ChIP) analysis showed that this stressor caused substant

131 show through chromatin immunoprecipitation (ChIP) and chemical inhibitor studies that RNA polymerase

132 Chromatin immunoprecipitation (ChIP) and chromatin isolation by RNA purification (ChIRP

133 Chromatin immunoprecipitation (ChIP) and micrococcal nuclease (MNase) digest assays wer

134 Chromatin immunoprecipitation (ChIP) assays established binding of c-Jun (an AP-1 facto

135 quantified by chromatin immunoprecipitation (ChIP) assays RNA polymerase II occupancy of SALL4 gene,

136 profiling and chromatin immunoprecipitation (ChIP) assays, we found that ALOX5 is especially down-reg

137 ation of 1870 chromatin immunoprecipitation (ChIP) datasets of 585 TFs in five species (human, mouse,

138 tion with the chromatin immunoprecipitation (ChIP) sequencing (ChIP-Seq) data shows that the domain b

139 it includes a chromatin immunoprecipitation (ChIP) step that enriches for interactions mediated by sp

140 Chromatin immunoprecipitation (ChIP) studies illustrated that M inhibited RNA polymeras

141 ctor, we used chromatin immunoprecipitation (ChIP) to assess PDC's ability to interact with STAT5 DNA

142 assay (EMSA), chromatin immunoprecipitation (ChIP), promoter cloning, and site-directed mutagenesis,

143 ay (EMSA) and chromatin immunoprecipitation (ChIP), we found evidence for the NREs binding to beta-ca

144 Unlike Chromatin Immunoprecipitation (ChIP), which fragments and solubilizes total chromatin,

145 nd Hmga2, and chromatin immunoprecipitation (ChIP)-quantitative PCR (qPCR) analysis of their promoter

146 enes, and ERG chromatin immunoprecipitation (ChIP)-seq revealed the presence of conserved ERG-bound p

147 Chromatin immunoprecipitation (ChIP-seq) is the omics technique that enables genome wid

148 ing in silico/chromatin-immunoprecipitation (ChIP) analysis we identify a conserved p53 DNA-binding s

149 Chromatin-immunoprecipitation (ChIP-seq) revealed BAZ1B target gene functions are enric

150 ChIP-seq (chromatin immunoprecipitation [ChIP] combined with high-throughput sequencing) analysis

151 p53 ChIP-seq (chromatin immunoprecipitation [ChIP] combined with high-throughput sequencing) and RNA-

152 ChIP-seq (chromatin immunoprecipitation [ChIP] combined with high-throughput sequencing) data sho

153 ChIP-seq (chromatin immunoprecipitation [ChIP] followed by deep sequencing) analyses in brown adi

154 Importantly, ChIP-seq analysis revealed that there is a higher level

155 However, accounting for GC content bias in ChIP-seq is challenging because the binding sites of int

156 of placenta development, were identified in ChIP-seq experiments.

157 new approach for finding TF-binding sites in ChIP-seq, with roots in digital signal processing that a

158 several commonly used NGS datasets including ChIP-seq, RNA-seq, MNase-seq, DNase-seq, GRO-seq, and AT

159 This resulted in increased ChIP signal of GFP-AR.

160 7, many methods have been developed to infer ChIP-target binding loci from the resultant reads after

161 ta from Mycobacterium tuberculosis involving ChIP-seq data on 113 TFs and matched gene expression dat

162 decreased Atf5 transcript, and primary islet ChIP-sequencing localized PDX1 to the Atf5 promoter, imp

163 pots', regions in 3-space for which the mean ChIP-seq peak height is significantly elevated.

164 nt of all MNase-sensitive complexes by MNase-ChIP-seq and sonication-ChIP-seq.

165 and provided further insights for modelling ChIP-exo data.

166 tion factor binding and histone modification ChIP-Seq data.

167 Moreover, ChIP analysis revealed that GnRH-activated MSK1 targets

168 alChIP allows the joint analysis of multiple ChIP-seq samples across a single variant and outperforms

169 When used in conjunction with native ChIP-seq and applied to human CTCF, CUT&RUN mapped direc

170 public ChIP-exo/nexus data and multiple, new ChIP-exo datasets from Escherichia coli.

171 a method for mapping new TFCT, for which no ChIP-seq data exists, onto our ensemble of classifiers a

172 background allele frequency on the observed ChIP-seq read counts.

173 tes the quality control and data analyses of ChIP-seq and DNase-seq data.

174 oQual, to enable exploration and analysis of ChIP-exo and related experiments.

175 Integrative analysis of ChIP-seq and microarray data sets also reveals a consist

176 In this study, genome-wide analysis of ChIP-seq data from human cancer and mouse embryonic cell

177 Re-analysis of ChIP-seq data identified several genomic regions where t

178 Analysis of ChIP-seq data in the ENCODE (Encyclopedia of DNA Element

179 The main application of ChIP-seq technology is the detection of genomic regions

180 built the Cistrome database, a collection of ChIP-seq and chromatin accessibility data (DNase-seq and

181 apply our method to numerous comparisons of ChIP-Seq datasets from the Human Epigenome Atlas and FAN

182 Finally, correlation across a time course of ChIP-seq and RNA-seq experiments was also predictive of

183 Since the inception of ChIP-seq in 2007, many methods have been developed to in

184 ylation; and 5) generation and sequencing of ChIP-seq libraries.

185 IP-exo data analysis are similar to those of ChIP-seq, these high throughput experiments pose a numbe

186 ough simultaneous evaluation of thousands of ChIP-seq peaks or differentially expressed genes possess

187 Using HTS data from a variety of ChIP-seq, DNase-seq, FAIRE-seq, and ATAC-seq experiments

188 On ChIP-seq datasets, our method obtains best AUC results o

189 nt of both known and de novo motifs based on ChIP data.

190 tional genomics' public catalogs is based on ChIP-seq data.

191 can be identified from a network trained on ChIP-seq data and that nucleosome positioning signals ar

192 w whole-genome analytic pipeline to optimize ChIP-Seq protocols on patient-derived xenografts from hu

193 ies (e.g. single-cell ATAC-seq, DNase-seq or ChIP-seq) have made it possible to assay regulome of ind

194 ypes of experimental data such as RNA-seq or ChIP-seq.

195 In addition, our ChIP-seq analysis reveals remarkable conservation in mec

196 On the basis of our ChIP data and these previous findings, we hypothesize th

197 ndreds of novel DV enhancers and outperforms ChIP-seq data of relevant transcription factors when ben

198 Here, we leveraged p53 ChIP-seq (chromatin immunoprecipitation [ChIP] combined

199 omatin immunoprecipitation quantitative PCR (ChIP-qPCR) indicate that in LCLs inhibition of CDKN2C (p

200 ly decreasing the sequencing cost to perform ChIP-seq.

201 f epiblast stem cells (EpiSCs), we performed ChIP-seq analysis of the genomic binding regions of five

202 using immunohistochemical staining of pSHF, ChIP-quantitative polymerase chain reaction and lucifera

203 torical data derived from over 23,677 public ChIP-seq and DNase-seq samples (11,265 datasets) from ei

204 We apply diHMM to analyse a public ChIP-seq data set.

205 peline with both large collections of public ChIP-exo/nexus data and multiple, new ChIP-exo datasets

206 ticoid-mediated ST2 was assessed by RT-qPCR, ChIP assay and luciferase reporter assay.

207 A quantitative ChIP-seq approach, which allows detection of global occu

208 Recent ChIP-seq and RNA expression analyses indicated that WhiA

209 Recently, ChIP-seq analysis revealed two classes of CTCF/BORIS-bou

210 Recently, ChIP-seq in mapping TF provides a large amount of experi

211 Comparisons with previously reported ChIP-seq datasets for primordial germ cell-like cells an

212 High resolution ChIP-exo was used to analyze in vivo the association of

213 affinity (VDR-BVs) using a high-resolution (ChIP-exo) genome-wide analysis of 27 HapMap lymphoblasto

214 tion)-seq datasets for 60 human RBPs and RIP-ChIP (RNP immunoprecipitation-microarray) data for 69 ye

215 Recent large-scale ChIP-seq studies and loss-of-function experiments have r

216 -accessible chromatin sequencing (ATAC-seq), ChIP-seq, and RNA-seq reveal that IL-10 represses the tr

217 ifying regulatory regions in DNA (DNase-seq, ChIP-seq, FAIRE-seq, ATAC-seq).

218 tions and analyses of datasets from RNA-Seq, ChIP-Seq and bisulfite sequencing experiments.

219 equencing, whole-genome sequencing, RNA-seq, ChIP-seq, targeted sequencing and single-cell whole-geno

220 rotein-binding regions derived from ChIP-seq/ChIP-exo-seq experiments using human and mouse cells.

221 immunoprecipitation followed by sequencing (ChIP-Seq) has been utilized to study genome-wide chromat

222 immunoprecipitation followed by sequencing (ChIP-seq) method.

223 immunoprecipitation followed by sequencing (ChIP-Seq) of 104 DNA binding proteins in embryonic stem

224 immunoprecipitation followed by sequencing (ChIP-seq), and in theory it should overcome antibody iss

225 immunoprecipitation followed by sequencing (ChIP-seq), and then links the binding sites to putative

226 immunoprecipitation, followed by sequencing (ChIP-seq), in parallel with transcriptome analysis (RNA-

227 Here we use ChIP sequencing (ChIP-seq) to identify domains enriched for the histone m

228 Using ChIP sequencing (ChIP-seq), we compared the ERalpha profiles of 10 endome

229 matin immunoprecipitation (ChIP) sequencing (ChIP-Seq) data shows that the domain boundaries identifi

230 e-gene ChIP and genome-wide ChIP-sequencing (ChIP-seq) and RNA-seq studies extended these findings to

231 noprecipitation followed by deep sequencing (ChIP-seq) and ChIP-reChIP-seq analyses revealed that EIN

232 Using EHF ChIP followed by deep sequencing (ChIP-seq) and RNA sequencing after EHF depletion, we sho

233 noprecipitation followed by deep sequencing (ChIP-seq) datasets from postmortem brains are needed.

234 noprecipitation followed by deep sequencing (ChIP-seq), we found that DnaA was associated with eight

235 noprecipitation followed by deep sequencing (ChIP-seq).

236 unoprecipitation followed by DNA sequencing (ChIP-seq).

237 12.5 followed by next-generation sequencing (ChIP-seq).

238 nd chromatin immunoprecipitation sequencing (ChIP-seq) analyses revealed that, similar to those of th

239 Chromatin immunoprecipitation sequencing (ChIP-seq) and chromatin immunoprecipitation quantitative

240 ng chromatin immunoprecipitation sequencing (ChIP-seq) combined with assay for transposase-accessible

241 Chromatin immunoprecipitation sequencing (ChIP-seq) experiments show that H3K4 methylation pattern

242 Chromatin immunoprecipitation sequencing (ChIP-seq) reveals extensive interaction of RBFox2 with c

243 ng chromatin immunoprecipitation sequencing (ChIP-Seq) we refined AR-binding and AREs at a genome-sca

244 of chromatin immunoprecipitation sequencing (ChIP-seq), protein-binding microarrays, and transcriptom

245 an chromatin immunoprecipitation sequencing (ChIP-seq).

246 as Chromatin Immunoprecipitation sequencing (ChIP-Seq).

247 st chromatin immunoprecipitation-sequencing (ChIP-seq) analyses have focused on a few immortalized ce

248 th chromatin immunoprecipitation-sequencing (ChIP-seq) experiments to provide information on both the

249 Chromatin-immunoprecipitation-sequencing (ChIP-seq)-reported H3K27ac and H3K4me3 levels are positi

250 om chromatin immunoprecipitation-sequencing (ChIP-Seq).

251 Chromatin immune-precipitation sequencing (ChIP-seq) experiments are commonly used to obtain genome

252 unoprecipitation high-throughput sequencing (ChIP-seq) revealed that the TET2 gene contains EBNA2-dep

253 EMSA) or genome-wide assays (RNA-sequencing, ChIP-sequencing), we have assembled a comprehensive regu

254 ddition, bioinformatics analyses, sequential ChIP and coimmunoprecipitation experiments reveal that A

255 AT3 in HBV replicating cells, and sequential ChIP assays demonstrated co-occupancy with chromatin rem

256 ioinformatic analysis of human SIX1 and SIX2 ChIP-seq showed each factor targeted a similar set of ci

257 ysis, chromatin fragmentation by sonication, ChIP, proximity ligation with a bridge linker, Tn5 tagme

258 e complexes by MNase-ChIP-seq and sonication-ChIP-seq.

259 e amount of input DNA, antibody specificity, ChIP enrichment and sequencing depth.

260 ASD genes with adjacent cortical TBR1 ChIP-seq peaks also showed unusually low levels of LoF m

261 Moreover, both TopoIIalpha and TCF4 ChIP with the N-cadherin promoter, which is a new discov

262 ith matched ENCODE transcription factor (TF) ChIP-seq data, we connected miRNAs into the transcriptio

263 From the ChIP assay, we found that SIRT6 controls Mstn expression

264 Although many aspects of the ChIP-exo data analysis are similar to those of ChIP-seq,

265 o far unknown DNA regions identified through ChIP-sequencing.

266 s by CUT&RUN is an attractive alternative to ChIP-seq.

267 the patient rule induction method (PRIM) to ChIP-seq data superposed on a Saccharomyces cerevisiae 3

268 ut sequencing produce peaked data similar to ChIP-Seq experiments.

269 nsity, and possible results make traditional ChIP-Seq analysis methods inappropriate for use with rep

270 Here we use ChIP sequencing (ChIP-seq) to identify domains enriched

271 nnovative modifications of the commonly used ChIP-seq protocol for high resolution mapping of transcr

272 We used ChIP and differential gene-expression analyses in Arabid

273 We used ChIP-Seq to profile the binding locations for these fact

274 Using ChIP and one-hybrid assays, we find evidence for direct

275 Using ChIP sequencing (ChIP-seq), we compared the ERalpha prof

276 Using ChIP-nexus, we find that Hippo signaling keeps Ras targe

277 Using ChIP-Seq and promoter analysis, we demonstrate that GLIS

278 Using ChIP-seq and RNA-seq analyses, we define the global targ

279 Using ChIP-seq, RNA-seq, and GRO-seq, here we demonstrate a gl

280 Using ChIP-seq, we demonstrate that the cistrome for the AP-1

281 Using ChIP-seq, we found that UzcR binds extensively throughou

282 ent the first genomic analysis of Atro using ChIP-seq against endogenous Atro.

283 the genome-wide binding profile of Bcd using ChIP-seq in embryos expressing single, uniform levels of

284 validate these structural ensembles by using ChIP-Seq tracks alone to predict Hi-C maps, as well as d

285 me-wide binding of Tbrain orthologs by using ChIP-sequencing and associates these orthologs with puta

286 e, central and effector memory T cells using ChIP-Seq and found that unlike the naive cells, the regu

287 g GRO-seq and RNA-seq) and epigenomes (using ChIP-seq) of 11 different human breast cancer cell lines

288 ersal model, BPAC, which was generated using ChIP-Seq data from multiple TFs in various cell types.

289 nding site in the murine Dnajc22 locus using ChIP-qPCR and luciferase assays and verified this regula

290 pe and transcription factor occupancy (using ChIP-seq), we show that synergistic gene induction is ac

291 d the genome-wide distribution of ORCA using ChIP-seq during specific time points of G1.

292 nalyze more than 440,000 binding sites using ChIP-seq data for 20 DAPs in two human liver tissue samp

293 s and enhancers in six primate species using ChIP-seq (H3K27ac and H3K4me1) to profile cis-regulatory

294 Following genome-wide analyses utilizing ChIP-Seq and RNA-Seq, GOF p53-induced origin firing, mic

295 nd cancer cell line models, here we show via ChIP-seq and biochemical assays that SWI/SNF complexes a

296 polyubiquitination both in vivo and in vitro ChIP-Seq analysis and biochemical experiments demonstrat

297 Genome-wide ChIP-seq shows that NFATc1 binds many genes that control

298 Single-gene ChIP and genome-wide ChIP-sequencing (ChIP-seq) and RNA-seq studies extended

299 ngside, chromatin architecture combined with ChIP-seq analysis suggest that Oct4 competes with variou

300 Using this assay in conjunction with ChIP-Seq, in vitro transcription, and a chromatin retent