ライフサイエンスコーパス: ChIP-seq

1 ecipitations and next-generation sequencing (ChIP-seq).

2 by chromatin immunoprecipitation sequencing (ChIP-seq).

3 gene expression, ATAC-seq, TF knockouts, and ChIP-seq).

4 hromatin immunoprecipitation-DNA sequencing (ChIP-Seq).

5 omated solution for individual or sequential ChIP-seq.

6 thylation, ATAC-seq and histone modification ChIP-seq.

7 t of a quantitative, physical model defining ChIP-Seq.

8 cts of an EZH2 inhibitor through the lens of ChIP-Seq.

9 ase II in the promoter region as detected by ChIP-seq.

10 from naive, EAE and CBD treated EAE mice by ChIP-seq.

11 diction methods, MocapG, MocapS, and Virtual ChIP-seq.

12 to address the major limitations of standard ChIP-seq.

13 induction by 1,25(OH)(2)D(3) Herein, we used ChIP-Seq analyses of mouse tissues to identify regulator

14 Previous ChIP-seq analyses of the murine uterus have revealed a p

15 Whole genome-wide scRNA-seq, ATAC-seq, and ChIP-seq analyses reveal that ARID1A is required to open

16 RNA-seq (sequencing) and ChIP-seq analyses revealed distinct IRF8 and PU.1 target

17 ChIP-seq analyses revealed that MYC2 and MYC3 bind direc

18 ChIP-seq analyses show high colocalization of HMGNs and

19 RNA-Seq and SALL4 ChIP-Seq analyses support the notion that Sall4 regulate

20 RNA-seq and H3.3-HA ChIP-seq analyses were performed on NAcc tissue collecte

21 In ChIP-seq analyses, antibodies selectively capture nucleo

22 ecipitation with high-throughput sequencing (ChIP-seq) analyses of TG from DeltaCTRL2-infected mice c

23 Chromatin immunoprecipitation sequencing (ChIP-seq) analyses revealed that cohesin binding to the

24 Subsequent ChIP-seq analysis confirmed increased H3.3 aggregation a

25 ChIP-seq analysis confirmed that LSH is a major regulato

26 Gene profiling and ChIP-Seq analysis identified Klk1b21 as an ICI-inducible

27 Comparative ChIP-seq analysis identifies genomic loci bound by both

28 lytene chromosomes of salivary glands and by ChIP-seq analysis in S2 cells.

29 ChIP-Seq analysis indicated that ER binding is reduced i

30 ChIP-Seq analysis of bone marrow cells derived from six

31 Combined RNA-seq and ChIP-seq analysis of lymphomas from Lck-Dlx5;Lck-MyrAkt

32 ChIP-seq analysis of the human CLB-GA neuroblastoma cell

33 Furthermore, ChIP-seq analysis of the polycomb repressive complex 1 c

34 Further, ChIP-seq analysis revealed a subset of genes for which A

35 ChIP-Seq analysis revealed three MafK binding regions (-

36 development and inflammatory response to LPS ChIP-seq analysis showed that despite its limited import

37 Our ChIP-seq analysis showed that mH2A1 and mH2A2 bind to di

38 Target engagement and ChIP-seq analysis showed that the compounds inhibited th

39 VirtUaL ChIP-seq Analysis through Networks (VULCAN) infers regul

40 At present, most ChIP-seq analysis tools adopt the command line, which la

41 By ChIP-seq analysis, CcpAV301A bound to DNA from 74% of ge

42 outperformed existing tools for differential ChIP-seq analysis, especially when the groups of samples

43 We embarked on a large-scale RBP ChIP-seq analysis, revealing widespread RBP presence in

44 graphical interfaces have been developed for ChIP-seq analysis, these sites cannot provide a comprehe

45 A, which can complete the whole procedure of ChIP-seq analysis.

46 in immunoprecipitation with deep sequencing (ChIP-seq) analysis showed the directionality of double-s

47 nd chromatin immunoprecipitation sequencing (ChIP-seq) analysis, we uncover a mechanism by which Tyr1

48 rates m(6)A/MeRIP-seq data with 1418 histone ChIP-seq and 118 DNase-seq data tracks from the ENCODE p

49 RNA-Seq/ChIP-Seq and a subsequent modifier screen reveal that pd

50 Gene expression profiling integrated with ChIP-seq and ATAC-seq data established that inactivation

51 SMAD3 ChIP-seq and ATAC-seq suggested that TGFbeta-mediated H3

52 vivo, we analysed human neuronal cells using ChIP-seq and ATAC-seq technologies.

53 nd plasticity of BAG neurons, we used tandem ChIP-seq and cell targeted RNA-seq to identify gene targ

54 xt-generation sequencing experiments such as ChIP-seq and ChIA-PET that generate coverage files for t

55 ChIP-seq and ChIP-qPCR provided evidence that the CDK in

56 Based on publicly available ChIP-seq and chromatin accessibility data as well as our

57 nput gene sets, Lisa first uses histone mark ChIP-seq and chromatin accessibility profiles to constru

58 atin states were characterized using histone ChIP-seq and cis-regulatory elements were identified in

59 In this study, we used combined ChIP-seq and RNA-seq analyses of prostate cancer cells t

60 Our ChIP-seq and RNA-seq analyses reveal that a key gene dir

61 Integration of ChIP-seq and RNA-seq data for master regulators of the H

62 Integration of ChIP-seq and RNA-seq data revealed direct and HOXB13-dep

63 Our ChIP-seq and RNA-seq data sets provide an excellent reso

64 used several global methodologies (ATAC-seq, ChIP-seq and RNA-seq) to assess the effect of GCN5 loss-

65 omic landscapes of primary OCs using H3K27ac ChIP-seq and RNA-seq, and then integrate these with whol

66 By combining ChIP-seq and single molecule live imaging we report that

67 We performed EGR1 ChIP-seq and validated thousands of EGR1 binding sites w

68 pled with massively parallel DNA sequencing (ChIP-seq) and coimmunoprecipitation experiments show tha

69 om Chromatin Immunoprecipitation sequencing (ChIP-seq) and DNA-RNA Immunoprecipitation sequencing (DR

70 e precipitation followed by deep sequencing (ChIP-seq) and POLR2A chromatin interaction analysis foll

71 II chromatin immunoprecipitation sequencing (ChIP-seq) and single-cell transcriptional measurements t

72 th chromatin immunoprecipitation sequencing (ChIP-seq) and transcriptomic analyses reveals that PITX1

73 g time-series chromatin immunoprecipitation (ChIP-seq) and/or DNA adenine methyltransferase identific

74 ), chromatin immunoprecipitation sequencing (ChIP-seq), and assay for transposase accessible chromati

75 Through integrated RNA-seq, genome-wide ChIP-seq, and CUT&RUN association profiling, we identify

76 ndrogen receptor) in Position Weight Matrix, Chip-Seq, and Hi-C experimental data, suggesting common

77 Using reporter assays, RNA-seq, ChIP-seq, and loss-of-function mutations, we can show th

78 Molecular profiling by RNA-seq, ChIP-seq, and metabolomics revealed that glycolytic and

79 We generated Hi-C, ChIP-seq, and RNA-seq data sets from CD4 T cells of B6,

80 data were compared with existing DNase-seq, ChIP-seq, and RNA-seq data to evaluate library quality,

81 nactivation combined with RNA-seq, ATAC-seq, ChIP-seq, and study of patient samples suggest that IRE1

82 RPE were analyzed using microarray, ChIP-seq, and whole-genome bisulfite sequencing approach

83 describe a tamoxifen-inducible, time-course ChIP-seq approach to measure transcription factor bindin

84 Using a combination RNAseq/ChIP-seq approach, we found that CcpA affects transcript

85 ia chromatin immunoprecipitation-sequencing (ChIP-seq) approach in wild-type and OsHOX24 over-express

86 immunoprecipitation followed by sequencing (ChIP-seq) approach to describe differences in gene expre

87 In this study, we combined RNA-seq and ChIP-seq approaches to identify direct transcriptional t

88 Using RNA-seq and ChIP-seq approaches we identified genes regulated direct

89 immunoprecipitation followed by sequencing (ChIP-seq), are widely used but have their drawbacks, inc

90 ification of enhancers by signal strength in ChIP-seq assays has resulted in the establishment of sup

91 rturbations, live imaging, and time-resolved ChIP-seq assays in Drosophila embryos were used to disse

92 Herein, using genome-wide ChIP-Seq assays of TRF2-bound chromatin from HT1080 fibr

93 romatin immunoprecipitation with sequencing (ChIP-seq) assays for histone modifications and 132 assay

94 e genome by the combination of experimental (ChIP-seq, ATAC-seq and GRO-seq) and computational approa

95 sequencing and its chromatin landscape using ChIP-seq, ATAC-seq and Hi-C.

96 ChIP-seq, ATAC-seq and RNA-seq experiments reveal that C

97 nuclear architecture by integrating RNA-seq, ChIP-seq, ATAC-seq, Hi-C, and Hi-ChIP data.

98 When tested on 12 ChIP-seq, ATAC-seq, RNA-seq and ChIA-PET datasets, pyBed

99 o stabilize this intermediate we developed a ChIP-Seq-based approach to locate, with single nucleotid

100 ChIP-seq-based genome-wide localization of the repressiv

101 hat characterize sequences of interest (e.g. ChIP-Seq binding regions).

102 l epigenome features around these OCRs using ChIP-seq, Bisulfite-seq, and RNA-seq datasets.

103 ed chromatin immunoprecipitation sequencing (ChIP-seq), bulk RNA sequencing, and an innovative dual l

104 Our genetic and ChIP-seq (chromatin immunoprecipitation [ChIP] combined

105 ChIP-seq (Chromatin Immunoprecipitation followed by sequ

106 ding of the latter, recent work has utilized ChIP-seq (chromatin immunoprecipitation followed by sequ

107 Chromatin-immunoprecipitation (ChIP-seq) confirmed its in vivo binding to sog_Distal bu

108 ducting a transcriptome analysis followed by ChIP-Seq coupled with a comprehensive metabolite analysi

109 ChIP and global ChIP-seq data also confirms that FOXM1 can also potentia

110 a hierarchical strategy for normalization of ChIP-seq data and assesses within-group variability of C

111 Multiple ChIP-seq data and DNA methylation data generated from br

112 Integrated analysis of ChIP-seq data and RNA sequencing revealed that H3K4 mono

113 binding motifs from differential acetylation ChIP-seq data compared to other methods.

114 generated transcription factor (TF) binding ChIP-seq data covering hundreds of TF proteins and cell

115 ChIP-seq data demonstrate that binding sites of FLI1, a

116 al HiChIP analysis with an option to utilize ChIP-seq data for further characterizing differential lo

117 Additional generation of ChIP-seq data for SWI/SNF and Polycomb group proteins an

118 this study, we aggregated publicly available ChIP-seq data from 469 human DAPs assayed in three cell

119 omatin accessibility data as well as our own ChIP-seq data from CLL patients, we identified six candi

120 We analyse ChIP-seq data from MEIS, TFs which are broadly expressed

121 The accession number for the NF-kappaB ChIP-seq data generated for this study is Gene Expressio

122 map Epigenomics and ENCODE, and from H3K27Ac ChIP-seq data generated in 26 ovarian cancer and precurs

123 n ATC cells decreased their growth rate, and ChIP-Seq data indicated that CCAT1 is likely a direct ta

124 method called "BioTarget" that incorporates ChIP-seq data into cellular pathway analysis.

125 The analysis of ChIP-seq data is important but poses a difficult computa

126 act of these factors on inferences made from ChIP-seq data is not entirely clear.

127 However, the huge volumes of ChIP-seq data make it almost impossible for human resear

128 tions and cofactors of a given HMR, based on ChIP-seq data mining.

129 her performed an integrative analysis on the ChIP-seq data of 10 histone marks and hundreds of transc

130 Using ENCODE ChIP-seq data of surrogate cell lines and motif analysis

131 e increasingly large number of DAP motif and ChIP-seq data publicly available to explore how DAP asso

132 A549 and BEAS-2B ChIP-seq data reveal four common glucocorticoid-induced

133 een thousands of TF and histone modification ChIP-seq data sets with thousands of gene expression pro

134 Using a number of real ChIP-seq data sets, we observed that MAnorm2 clearly out

135 Further motif recognition analysis of the ChIP-seq data showed that cocaine-associated differentia

136 earch approach in conjunction with extensive ChIP-seq data to achieve a precise global distinction be

137 for combined analysis of gene expression and ChIP-seq data to enhance the inference of transcriptiona

138 q were integrated with our Hi-C and previous ChIP-seq data to identify cell- and developmental-stage-

139 for GenetIc Controllers (MAGIC), uses ENCODE ChIP-seq data to look for statistical enrichment of TFs

140 ata are processed against publicly available ChIP-Seq data using Model-based Analysis of Regulation o

141 ethod is inappropriate for the evaluation of ChIP-seq data when treatments or mutations have global e

142 anscription factor TF target genes (based on ChIP-seq data) with the status of upstream signaling com

143 challenge to define a quantitative scale for ChIP-Seq data, and as such, several approaches making us

144 llele-biased mutation detection from H3K27ac ChIP-seq data, to pinpoint potential enhancer-activating

145 Using ChIP-seq data, we demonstrate that evolutionary gene rel

146 By incorporating HiChIP data with H3K27ac ChIP-seq data, we identify interactions between enhancer

147 From WGS and ChIP-seq data, we show the potential relevance of recurr

148 We apply ncHMR detector in ChIP-seq data-rich cell types and predict non-classical

149 s a rigorous comparison of the corresponding ChIP-seq data.

150 ants for both human and murine samples using ChIP-Seq data.

151 tor in neural development, we generated Ars2 ChIP-seq data.

152 lation network from paired disease-to-normal ChIP-seq data.

153 which correlates strongly with REC8-cohesin ChIP-seq data.

154 hancers defined using ATAC-seq and published ChIP-seq data.

155 y literature-curated information followed by ChIP-seq data.

156 ultiple tissue types using readily available ChIP-seq data.

157 ublicly available tumor expression data onto ChIP-seq data.

158 Chromatin immunoprecipitation-sequencing (ChIP-seq) data indicated that FAD mice exhibited genome-

159 immunoprecipitation followed by sequencing (ChIP-seq) data.

160 A number of changes in community practice of ChIP-Seq, data reporting, and analysis are motivated by

161 d AIControl to 410 IP datasets in the ENCODE ChIP-seq database, using 440 control datasets from 107 c

162 Using in silico analysis of ATAC- and ChIP-Seq databases in conjunction with mouse gonad expla

163 The availability of numerous ChIP-seq datasets for transcription factors (TF) has pro

164 iously unseen genomic segments from multiple ChIP-seq datasets including benchmark datasets commonly

165 on of matched in situ Hi-C, RNA-seq and CTCF ChIP-seq datasets revealed widespread differences in int

166 ly state-of-the-art topic models to multiple ChIP-Seq datasets to decipher the combinatorial binding

167 For the different types of ChIP-seq datasets, CSA can provide the corresponding too

168 richment of TF binding motifs from ENCODE TF ChIP-seq datasets.

169 signals from many publicly available control ChIP-seq datasets.

170 hrough a re-analysis of existing RNA-seq and ChIP-seq datasets.

171 ChIP-Seq defined the RARgamma cistrome, which was signif

172 gly enriched for the AP-1 motif, and indeed, ChIP-seq demonstrated AP-1 binding at >70% of them.

173 Chromatin immunoprecipitation-sequencing (ChIP-seq) demonstrated that cyclin D1 inhibits the bindi

174 ecipitation with high-throughput sequencing (ChIP-seq) densities from macrophages and adipocytes to c

175 q, chromatin immunoprecipitation sequencing (ChIP-seq), DNase I hypersensitive sites sequencing (DNas

176 ouse cis-regulatory information derived from ChIP-seq, DNase-seq and ATAC-seq chromatin profiling ass

177 y element activities in bulk samples such as ChIP-seq, DNase-seq and FAIRE-seq cannot analyze samples

178 llow users to better utilize the large-scale ChIP-seq, DNase-seq, and ATAC-seq data.

179 , the Toolkit can determine the most similar ChIP-seq, DNase-seq, and ATAC-seq samples in terms of ge

180 Despite AhR ChIP-seq enrichment at 2 h, OCM gene expression was not

181 s, (ii) a network topology assessment, (iii) ChIP-Seq evidence and (iv) the KnowEnG Knowledge Network

182 lidation and functional studies included WT1 ChIP-seq, EWS-WT1 knockdown using JN-DSRCT-1 cells and i

183 Further comparison of PRO-seq data with ChIP-seq/exo data for BCL6, SMRT, FOXO1 and H3K27ac iden

184 Our analysis on ChIP-seq experiment in human embryonic stem cells (hESC)

185 In addition, we performed a ChIP-Seq experiment that identified ANT binding sites in

186 ources of variation on several outcomes of a ChIP-seq experiment, viz., the recoverability of the TF

187 ce features found near a target protein in a ChIP-seq experiment.

188 ChIP-seq experiments for SUZ12 and BMI1 were performed t

189 The algorithms are employed to analyze 349 ChIP-Seq experiments from the ENCODE project, yielding a

190 ChIP-Seq experiments identify candidate targets unique t

191 provides the means to carry out ChIP-qPCR or ChIP-seq experiments involving dozens of samples.

192 ry network by integrating publicly available ChIP-seq experiments with gene-expression data from tiss

193 RNA-seq studies, TF-target associations from ChIP-seq experiments, and TF-gene co-occurrence computed

194 DeltarsfG strains combined with RNA-seq and ChIP-seq experiments, suggests the involvement of SigG1

195 R biases, are known to affect the outcome of ChIP-seq experiments.

196 tion followed by high-throughput sequencing (ChIP-seq) experiments using the human HepG2 cell line fo

197 Fixed-tissue ChIP-seq for H3K27 acetylation (H3K27ac) profiling (FiTA

198 vity in mouse granulosa cells using combined ChIP-seq for PGR and H3K27ac and gene expression microar

199 were isolated and subjected to mRNA-seq and ChIP-seq for the histone marks H3K4me3 and H3K27ac.

200 ChIP-seq for WT1 showed significant overlap with genes f

201 ed chromatin immunoprecipitation sequencing (ChIP-seq) for epigenetic marks and RNA-seq on trunk tiss

202 L-based fine mapping when applied to H3K27AC ChIP-seq from just 28 prostate tumor/normal samples.

203 s cannot provide a comprehensive analysis of ChIP-seq from raw data to downstream analysis.

204 sequence and epigenomic profiles derived by ChIP-seq from two species as input data, and outputs the

205 pendent genes were overlapped with PGC1alpha-ChIP-Seq genes and significantly associated in TCGA with

206 romatin immunoprecipitation with sequencing (ChIP-seq), genome-wide analysis of DNA methylation and i

207 overexpressing PAX2, when coupled with PAX2 ChIP-seq, identified common targets regulated by both PA

208 r by ATAC-seq that, in combination with Gli2 ChIP-seq, identified inner ear enhancers in the vicinity

209 erforming H3-lysine-27 acetylation (H3K27ac) ChIP-seq in Enz-resistant CRPC cells, we identified a gr

210 ransposon-dense heterochromatin, we repeated ChIP-seq in kyp suvh5 suvh6 H3K9me2 mutants.

211 We perform CTCF ChIP-seq in multiple mouse species to create genome-wide

212 er and super-enhancer landscape after AKI by ChIP-seq in uninjured and repairing kidneys on day two a

213 ng chromatin immunoprecipitation sequencing (ChIP-seq) in Arabidopsis (Arabidopsis thaliana).

214 on analysis and ChIP followed by sequencing (ChIP-seq) in MCF-7 breast cancer cells treated with the

215 de chromatin immunoprecipitation sequencing (ChIP-seq) in wild-type and mutant cells showed that abla

216 Here, combination of in vivo (genetics and ChIP-seq), in vitro (surface plasmon resonance) and phyl

217 ChIP-Seq is a widespread experimental method for determi

218 e-specific transcription factor binding from ChIP-seq is enriched among ASM loci, but most ASM differ

219 ChIP-seq is one of the core experimental resources avail

220 ChIP followed by next-generation sequencing (ChIP-Seq) is a key technique for mapping the distributio

221 Chromatin immunoprecipitation sequencing (ChIP-seq) is a technology that combines chromatin immuno

222 hod, EpiMethylTag, that combines ATAC-seq or ChIP-seq (M-ATAC or M-ChIP) with bisulfite conversion, t

223 of chromatin immunoprecipitation-sequencing (ChIP-seq), microarray transcriptional profiling and bioi

224 nts on hypertrophic cardiomyopathy patients (ChIP-seq N=14 and RNA-seq N=11) and nondiseased hearts (

225 14 and RNA-seq N=11) and nondiseased hearts (ChIP-seq N=4 and RNA-seq N=11).

226 ChIPseqSpikeInFree is a novel ChIP-seq normalization method to effectively determine s

227 ChIP-seq of DNA associated with DONSON or FANCM confirms

228 in silico and chromatin studies in SCC25 by ChIP-seq of KLF4 and identify DeltaNp63 as a co-oncogeni

229 o examine gene-specific H2Bub1, we performed ChIP-seq of mouse ciliated and nonciliated tissues and s

230 thod that integrates data from DNase-seq and ChIP-seq of TFs and histone marks.

231 nd chromatin immunoprecipitation-sequencing (ChIP-seq) of IL-6 responses in naive and effector memory

232 Here, we perform ChIP-seq on distinct subtypes of Drosophila FACS-purifie

233 Here, we used ChIP-seq on synchronized cells at different stages after

234 l utilizes approaches initially designed for ChIP-seq or DNase-seq, without considering the transposa

235 bed TIRs that were not identified by H3K27ac ChIP-seq or DNase-seq.

236 rome-GO has two working modes: solo mode for ChIP-seq peak analysis; and ensemble mode, which integra

237 genome can alter histone H3K4me1 and H3K27ac ChIP-seq peak calls either by creating new personal peak

238 e new formats for chromosome interactions, a ChIP-Seq peak display for track hubs and improved suppor

239 r example, FOX family motifs are enriched in ChIP-seq peaks of 37 other CAPs.

240 Using TR ChIP-seq peaks or imputed TR binding sites, Lisa probes

241 supervised learning approach for identifying ChIP-seq peaks using CNNs, and integrate it into a softw

242 nalysis; and ensemble mode, which integrates ChIP-seq peaks with DGE data.

243 a widely used method, BETA, to integrate TF ChIP-seq peaks with differential gene expression (DGE) d

244 By comparing results with RNA-seq data, ChIP-seq peaks, and DNase-seq footprints, we show that M

245 for a motif originally identified under tMAC ChIP-seq peaks.

246 ing, we systematically analyze over 700 CTCF ChIP-seq profiles across human tissues and cancers and i

247 torial binding patterns of TFs from multiple ChIP-Seq profiles, interpret and visualize the combinato

248 gh single-cell transcriptomics, ATAC-Seq and ChIP-Seq profiling, we expose a key role for NFIB and NF

249 genetic and cis-regulatory datasets, such as ChIP-Seq, Promoter-Capture Hi-C or eQTL, and presents th

250 We previously developed a modified ChIP-seq protocol (FiT-seq) for chromatin profiling in F

251 C2 in vitro, verified its enrichment in BNC2 ChIP-seq regions, and validated a set of its downstream

252 immunoprecipitation followed by sequencing (ChIP-seq) remains a tedious (>2 d), manually intensive,

253 y, our simulations reveal that the number of ChIP-seq replicates needed to accurately measure in vivo

254 By combining this data set with the modERN ChIP-seq resource, we are able to support and predict ge

255 xpression analysis (RNA sequencing) with the ChIP-seq results at the same stage in developing chondro

256 The quantitative scale on which ChIP-Seq results should be compared emerges from the mod

257 ChIP-Seq revealed that CBFA2T3 targets the RARalpha/RXRa

258 Further ChIP-seq reveals that global effects on Pol II-binding a

259 immunoprecipitation followed by sequencing (ChIP-seq) reveals direct binding of URI to promoters of

260 NET-seq, 3' mRNA-seq, chromatin RNA-seq, and ChIP-seq, reveals that PCF11 enhances transcription term

261 immunoprecipitation followed by sequencing (ChIP-seq), RNA sequencing (RNA-seq), and assay for trans

262 ), chromatin immunoprecipitation sequencing (ChIP-seq), RNA sequencing (RNA-seq), and Hi-C assays, we

263 Through ChIP seq, RNA seq, hormone and sugar measurements on 1 m

264 Integrated analyses of ChIP-seq, RNA-seq, and patient prognosis identified sphi

265 e a comprehensive atlas comprising ATAC-seq, ChIP-seq, RNA-seq, and proteomics datasets.

266 tool for quantitatively comparing groups of ChIP-seq samples.

267 -low-input micrococcal nuclease-based native ChIP-seq) shows that EZH1 could partially safeguard the

268 ata and assesses within-group variability of ChIP-seq signals based on an empirical Bayes framework.

269 rk, MAnorm2 allows for abundant differential ChIP-seq signals between groups of samples as well as ve

270 noprecipitation followed by deep sequencing (ChIP-seq) signals for H3K27ac or other transcription fac

271 Here, via a detailed ChIP-seq simulation pipeline, ChIPulate, we assess the i

272 ChIP-seq studies demonstrate that the H3K36 methylation

273 However, most ChIP-seq studies overlook the normalization that must be

274 (TF)-binding region hits extracted from 1945 ChIP-seq studies; and (iii) the latest GWAS catalog with

275 Chromatin immunoprecipitation sequencing (ChIP-seq) studies determined that some U(S)3-regulated g

276 ogy to also act as a microfluidic sequential ChIP-seq system.

277 NA-seq to identify Loz1-regulated genes, and ChIP-seq to analyze the recruitment of Loz1 to target ge

278 We performed RNA-seq and histone mark ChIP-seq to define the transcriptomes and epigenomes of

279 skeletogenesis by Alx1, we used genome-wide ChIP-seq to identify Alx1-binding sites and direct gene

280 In addition, we utilized ChIP-seq to identify H3K18ac, H3K27ac and H3K27me3 histo

281 In this study, we use large-scale ChIP-seq to reconstruct it in the maize leaf, and train

282 is combined with next generation sequencing (ChIP-seq) to obtain a genome wide profile of protein bin

283 oci at the Hoxa/b gene clusters and Meis1 in ChIP-seq, together with NMR analysis of the H3K4me3-bind

284 ENCODE archives 2314 ChIP-seq tracks of 684 TFs and cofactors assayed across

285 A number of algorithms draw on ChIP-seq tracks to define TFs and cofactors behind gene

286 for pregenerated candidate binding sites or ChIP-seq training data.

287 ed chromatin immunoprecipitation sequencing (ChIP-seq) using developing limb buds and male gonads fro

288 tion followed by next-generation sequencing (ChIP-seq) was used to assess a range of N-terminal postt

289 n immunoprecipitation and direct sequencing (ChIP-seq), we show that CA12 is regulated by AP-2gamma t

290 Using RNA-seq and ChIP-seq, we determined that H-NS and LuxR co-regulate a

291 Using ATAC-seq and ChIP-seq, we found that activation of JUN rendered promo

292 Using iCLIP and ChIP-seq, we found that human cyclin-dependent kinase 11

293 ibrary, combined with RNA-seq, ATAC-seq, and ChIP-seq, we have dissected the regulatory circuitry gov

294 By performing ChIP-seq, we show that ACF leads to a general increase i

295 Using ChIP-seq, we show that PTEN co-localizes with RNAPII and

296 Using calibrated ChIP-seq, we show that remodelling of histones during sp

297 Using ChIP-seq, we show, surprisingly, that the FGF signaling

298 in the PLASMA credible sets for RNA-seq and ChIP-seq were enriched for open chromatin and chromatin

299 Whole genome BRD4 and gammaH2AX ChIP-Seq with R-loop IP qPCR reveals that BRD4 inhibitio

300 pared using PIXUL can be used in an existing ChIP-seq workflow.