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SRX903246: GSM1625973: ChIP-Seq of H3K4me1 in baseline Macrophages; Homo sapiens; ChIP-Seq
3 ILLUMINA (Illumina HiSeq 1500) runs: 31.3M spots, 1.6G bases, 914.9Mb downloads

Submitted by: Gene Expression Omnibus (GEO)
Study: Epigenomic landscapes of human inflammation associated macrophages [ChIP-seq]
show Abstracthide Abstract
We previously demonstrated by genomic and bioinformatical approaches that human macrophage (MF) activation is best described by a spectrum model (Xue et al, Immunity, 2014). MF integrate exogenous input signals on transcriptional level in a unique fashion to generate specific functional programs, enabling the plasticity in disease-related pathophysiologies. Such versatile responsiveness requires fast changes of transcription mediated by transcriptional regulators (TRs) or epigenomic changes. To better understand the principles of this regulation during human MF activation, we assessed histone modifications including H3K4me1, H3K4me3, H3K27me3, and H3K27Ac by ChIP-sequencing allowing us to characterize the functional state of promoters (active, poised, repressed) and enhancers (active, inactive, intermediate). Using transcriptome data from our MF spectrum model, we generated a co-regulation network of all TRs. Next, we overlaid epigenomic information and transcriptional changes of major TRs over time onto the TR network. We observed that input signals like IFN? or TNFa induce a specific network of TRs that are transcriptionally regulated themselves, the combination of regulated TRs changes over time with a boost of transcriptional regulation of dozens of TRs 4 to 12 hrs post input signal exposure, almost all TRs within the network show active promoters, even if the TR itself is not expressed, and similar results are obtained for enhancers with open or at least intermediated states. These findings strongly suggest that in MF, the TR-defined cellular ‘switch panel’ is always accessible thereby allowing MF to quickly respond to the diverse input signal repertoire from the environment. Overall design: Epigenetic analysis of promoter and enhancer sites in primary human macrophage subtypes and correlation to RNA-seq expression data
Sample: ChIP-Seq of H3K4me1 in baseline Macrophages
SAMN03389883 • SRS865664 • All experiments • All runs
Organism: Homo sapiens
Library:
Instrument: Illumina HiSeq 1500
Strategy: ChIP-Seq
Source: GENOMIC
Selection: ChIP
Layout: SINGLE
Construction protocol: Chromatin from 0.5x10E6 macrophages was cross-linked for ChIP reactions with 1 % formaldehyde. Nuclei were lysed and chromatin was sheared with the Covaris S220 ultrasound system. For ChIP antibody reactions polyclonal rabbit antibodies were used (H3K4me1 (Abcam), H3K27Ac (Abcam), H3K27me3 (Millipore)). Washing and DNA purifications as well as size selections were performed with AMPure XP SPRI beads (Beckman Coulter). Published library construction protocol was adapted (Blecher-Gonen et al., Nature Protocols, 2013) and performed with 0.5 ng ChIP DNA. Barcodes from the NEXTflex adapter oligonucleotides kit (Bioo Scientific) were ligated to the ChIP-seq DNA fragments. Final DNA purification with additional size selection was performed with SPRI beads. ChIP-seq libraries were sequenced on the HiScanSQ/Hiseq 1000 sequencer (Illumina)
Experiment attributes:
GEO Accession: GSM1625973
Links:
External link:
Runs: 3 runs, 31.3M spots, 1.6G bases, 914.9Mb
Run# of Spots# of BasesSizePublished
SRR184272316,815,485857.6M496.1Mb2016-02-28
SRR18427243,954,267201.7M112.2Mb2016-02-28
SRR184272510,529,142537M306.6Mb2016-02-28

ID:
1297444

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