ライフサイエンスコーパス: ChIP-seq

1 12.5 followed by next-generation sequencing (ChIP-seq).

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

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

4 ng chromatin immunoprecipitation sequencing (ChIP-seq).

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

6 as Chromatin Immunoprecipitation sequencing (ChIP-Seq).

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

8 an chromatin immunoprecipitation sequencing (ChIP-seq).

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

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

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

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

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

14 rium bovis BCG genome, were identified using ChIP-seq.

15 e JAK2 promoter in vitro and was enriched by ChIP-seq.

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

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

18 e address this through the development of G4 ChIP-seq, an antibody-based G4 chromatin immunoprecipita

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

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

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

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

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

24 ChIP-seq analysis for the master regulator STAT5A, the g

25 ever, the biological insights generated from ChIP-seq analysis have been limited to predictions of bi

26 ChIP-seq analysis identified target genes that are coreg

27 ChIP-seq analysis identified thousands of regions that a

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

29 ChIP-seq analysis of SMARCA4 localization and SMARCA4-bo

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

31 CBP indicated overlapping gene control, and ChIP-seq analysis of these commonly controlled genes sho

32 ChIP-seq analysis revealed that rather than regulating t

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

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

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

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

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

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

39 get gene of the NFkB transcription factor by ChIP-seq analysis, is also upregulated in the peripheral

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

41 tion followed by next-generation sequencing (ChIP-seq) analysis from archived tissue samples.

42 noprecipitation followed by deep sequencing (ChIP-Seq) analysis of Sir proteins in T. delbrueckii rev

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

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

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

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

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

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

49 neages and intersected these data with TBX20 ChIP-seq and chromatin loop maps to determine that TBX20

50 and QC tools have been reported, few combine ChIP-seq and DNase-seq data analysis and quality control

51 e model of transcription factor binding from ChIP-seq and DNase-seq data, and scores variants by comp

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

53 d for large collaborative projects involving ChIP-seq and DNase-seq from different designs.

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

55 this atlas represents the most comprehensive ChIP-seq and DNase-seq related quality metric resource c

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

57 of sequencing-based genomics assays such as ChIP-seq and DNase-seq, the epigenomic characterization

58 ypes of data including sequence, expression, ChIP-seq and epigenetic data.

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

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

61 ChIP-seq and genetic analyses demonstrate the importance

62 sent the first study that integrates protein ChIP-seq and Hi-C data to systematically identify both t

63 Using integrated SRF ChIP-seq and Hi-C data, we identified over 700 TCF-depen

64 ChIP-seq and mechanistic studies in human RMS uncovered

65 s whose expression level changes in previous ChIP-seq and microarray analyses in Isl1-deficient cell

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

67 Combining ChIP-seq and molecular approaches we identified a single

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

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

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

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

72 By ChIP-seq and RNA-seq analysis, we demonstrate that histo

73 Integrative analysis of ChIP-Seq and RNA-Seq data and transgenic enhancer assays

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

75 nt signaling pathway were highly enriched in ChIP-seq and RNA-seq datasets and members of those pathw

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

77 can be assessed for an individual by mapping ChIP-seq and RNA-seq reads to a personal genome, and the

78 ChIP-seq and RNA-seq reveal enrichment of Lin28A binding

79 We propose a user-friendly ChIP-seq and RNA-seq software suite for the interactive

80 Using both ChIP-Seq and RNA-Seq we identify those regions of the F.

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

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

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

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

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

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

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

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

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

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

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

92 By examining nascent transcript RNA-seq, ChIP-seq, and binding motif datasets from lipid A-stimul

93 RO-seq provides much higher sensitivity than ChIP-seq, and it generates a much larger fraction of usa

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

95 knockout mutations in clock genes, RNA-seq, ChIP-seq, and reporter gene assays coupled with measurem

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

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

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

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

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

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

102 eover, 43% of Dux-responsive genes contained ChIP-seq binding sites for both Dux and DUX4, and both p

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

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

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

106 ChIP-seq (chromatin immunoprecipitation [ChIP] combined

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

108 ChIP-seq (chromatin immunoprecipitation [ChIP] combined

109 ChIP-seq (chromatin immunoprecipitation [ChIP] followed

110 advances have been implemented into the core ChIP-seq (chromatin immunoprecipitation coupled with nex

111 cations, which were essentially confirmed by ChIP-seq (chromatin immunoprecipitation followed by mass

112 P53 bind to cis-overlapping motifs within a ChIP-seq co-occupied region in Chr12.

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

114 ped a thermodynamic model that parameterizes ChIP-seq coverage in terms of genome accessibility and b

115 IT to find target genes from NOTCH3 and PBX1 ChIP-seq data acquired from MCF-7 breast cancer cells.

116 ownloaded and installed locally using ENCODE-ChIP-Seq data and showed that rGADEM was the best-perfor

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

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

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

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

121 We generated 101 bps paired-end ChIP-seq data for many transcription factors from human

122 nscription factor flexible models trained on ChIP-seq data for vertebrates, which capture dinucleotid

123 enza A virus (IAV) infection, as well as the CHIP-seq data from ENCODE on transcription factor (TF) a

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

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

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

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

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

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

130 Comprehensive analysis of 23 TFs, each with ChIP-seq data in four to 12 different cell types, shows

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

132 Multifactorial ChIP-seq data integration from the endometrial cancer ce

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

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

135 We found that ChIP-seq data of RNA polymerase II and histone modificat

136 Furthermore, ChIP-seq data often poorly correlate with in vitro measu

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

138 data as position-specific scoring matrices, ChIP-seq data or conservation scores is currently availa

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

140 We applied ChromNet to all available 1451 ChIP-seq data sets from the ENCODE Project, and showed t

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

142 ndence relationships among a large number of ChIP-seq data sets.

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

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

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

146 d in Tbr1 knockouts, which together with the ChIP-seq data, suggests direct transcriptional regulatio

147 on to documenting the prevalence of mtDNA in ChIP-seq data, the results of our mitochondrial heteropl

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

149 Through analysis of deep RAG1 ChIP-seq data, we provide a quantitative description of

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

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

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

153 o existing methods in RNA-seq, DNase-seq and ChIP-seq data.

154 ranscription factors without matched H3K27ac ChIP-seq data.

155 sults with hepatic FOXO1 and THRB1 (TRbeta1) ChIP-Seq data.

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

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

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

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

160 ChIP-sequencing (ChIP-Seq) data on other transcription factors has shown

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

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

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

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

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

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

167 ng algorithms, making it ideal for analyzing ChIP-seq datasets, especially those that contain a mixtu

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

169 sing H3K27me3, H3K36me3, GABP, ESR1 and FOXA ChIP-seq datasets.

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

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

172 Additionally, Y14 ChIP-seq demonstrates that association with transcribed

173 first systematic evaluation of the impact of ChIP-seq designs on allele-specific binding detection an

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

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

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

177 hromatin immunoprecipitation and sequencing (ChIP-seq) does not capture quantitative information on h

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

179 ChIP-seq enables genome-scale identification of regulato

180 ed in adult cerebellum and showed strong Wiz ChIP-seq enrichment.

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

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

183 ate that the sequencing coverage of mtDNA in ChIP-seq experiments is sufficient for heteroplasmy dete

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

185 Lastly, ChIP-seq experiments show that OGA maps to the transcrip

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

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

188 igators in deciding sequencing parameters in ChIP-seq experiments.

189 vations with our meta-analyses of the ENCODE ChIP-Seq experiments.

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

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

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

193 Chromatin immunoprecipitation sequencing (ChIP-seq) experiments demonstrated KDM6A binding to puta

194 immunoprecipitation followed by sequencing (ChIP-seq) experiments revolutionized genome-wide profili

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

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

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

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

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

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

201 We performed ChIP-seq for TBR1 during mouse cortical neurogenesis and

202 ndamentally on sequencing based methods like ChIP-seq for the detection of DNA-protein interactions.

203 opterus natalensis and performed RNA-seq and ChIP-seq (H3K27ac and H3K27me3) analyses on its developi

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

205 immunoprecipitation followed by sequencing (ChIP-seq) has been instrumental to our current view of c

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

207 tion with massively parallel DNA sequencing (ChIP-seq) has greatly improved the reliability with whic

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

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

210 ChIP-seq identified 1300 potential direct targets of Atr

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

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

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

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

215 ChIP-seq in mouse THY1(+) spermatogonia identified 4176

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

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

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

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

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

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

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

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

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

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

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

227 pression (RNA-seq) and genome-wide profiles (ChIP-seq) of histone post-translational modifications an

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

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

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

231 arger fraction of usable sequence reads than ChIP-seq or NET-seq (native elongating transcript sequen

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

233 Moreover, our framework enables de novo ChIP-seq peak prediction and is useful for inferring TF-

234 g. chromatin immunoprecipitation-sequencing (ChIP-seq) peak height) are lacking.

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

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

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

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

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

240 ere we perform bioinformatics of RNA-Seq and ChIP-seq pluripotency data sets for two replicate Asian

241 lity led to a model that explains 63% of the ChIP-seq profile variance, while a model based in motif

242 Even when the matching H3K27ac ChIP-seq profiles are available, MARGE leverages public

243 ework on newly generated RNA-seq and H3K27ac ChIP-seq profiles upon siRNA silencing of multiple trans

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

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

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

247 ChIP-Seq quantification of binding sites for RNA polymer

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

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

250 ariants by computing the change of predicted ChIP-seq reads between the reference and alternate allel

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

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

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

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

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

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

257 profiling experiments (microarrays, RNA-seq, ChIP-seq, ribosome profiling, LC-ms proteomics), gene es

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

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

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

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

262 unoprecipitation followed by DNA sequencing (ChIP-seq) showed a striking overlap in Jun- and Sox9-bou

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

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

265 ial (RP) for each gene as the sum of H3K27ac ChIP-seq signals weighted by a function of genomic dista

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

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

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

269 al progenitor cells, and together with BAZ1B ChIP-seq target genes, explained 42% of the transcriptio

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

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

272 r set of transcription factors, validated by ChIP-seq, that is responsible for subgroup divergence, a

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

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

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

276 e applied genome-wide chromatin dynamics and ChIP-seq to determine these transcription factors' (TFs)

277 Here, using a combination of Chip-seq to enrich enhancer DNA and a computational appr

278 Using ChIP-seq to interrogate all 70 exemplar genes in single,

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

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

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

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

283 Here, we report comprehensive ChIP-Seq, transgenic and reporter gene experimental data

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

285 ChIP-seq using mouse embryonic stem cells and enrichment

286 rkflows and reporting templates for RNA-Seq, ChIP-Seq, VAR-Seq and Ribo-Seq.

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

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

289 Using immunofluorescence and ChIP-seq we determine the distribution of H4K20me3 in pr

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

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

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

293 omatin immunoprecipitation-based sequencing (ChIP-seq), we demonstrated that KLLN binds to DNA region

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

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

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

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

298 Using ChIP-seq, we identified Src kinase signaling inhibitor 1

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

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