Ch IP ‐Atlas: a data‐mining suite powered by full integration of public Ch IP ‐seq data

Abstract

We have fully integrated public chromatin chromatin immunoprecipitation sequencing (ChIP‐seq) and DNase‐seq data (n > 70,000) derived from six representative model organisms (human, mouse, rat, fruit fly, nematode, and budding yeast), and have devised a data‐mining platform—designated ChIP‐Atlas (http://chip-atlas.org). ChIP‐Atlas is able to show alignment and peak‐call results for all public ChIP‐seq and DNase‐seq data archived in the NCBI Sequence Read Archive (SRA), which encompasses data derived from GEO, ArrayExpress, DDBJ, ENCODE, Roadmap Epigenomics, and the scientific literature. All peak‐call data are integrated to visualize multiple histone modifications and binding sites of transcriptional regulators (TRs) at given genomic loci. The integrated data can be further analyzed to show TR–gene and TR–TR interactions, as well as to examine enrichment of protein binding for given multiple genomic coordinates or gene names. ChIP‐Atlas is superior to other platforms in terms of data number and functionality for data mining across thousands of ChIP‐seq experiments, and it provides insight into gene regulatory networks and epigenetic mechanisms.

Synergistic activation of p53 by actinomycin D and nutlin-3a is associated with the upregulation of crucial regulators and effectors of innate immunity

“…The presence of the peak, located on chromosome 11, positions: 119,037,091-119,037,351 (genome version hg19) was reported in meta-analysis performed by Nguyen et al [32]. The p53 ChIP-Seq peaks identified by others in this region and publically available through ChIP-Atlas tool [33] are visualized in supplementary Fig. S2.…”

“…B. Genome browser (IGV) views of p53 binding peak at the exon1/intron1 border of IL7 gene. Using ChIP-Atlas tool [33] we imported publically available coverage tracks from four ChIP-Seq experiments aimed at finding p53 binding sites in MCF-7 cell line exposed to ionizing radiation and Nutlin (sample ID SRX2924018), SAOS-2 cell line ectopically expressing wild-type p53 (sample ID SRX016980), SAOS-2 ectopically expressing pair of engineered p53 molecules with strong cooperative binding of p53 monomers [31] (sample ID ERX181467) or in MCF7 cells treated with Nutlin (sample ID SRX2060922). C. Measurement of relative IL7 mRNA levels in A549 cells exposed to indicated substances or combination treatments for 30 h. D. Relative IL7 mRNA levels in p53 knockdown A549 cells (p53-SH), and control cells (Con-SH), exposed to A + N or CPT for 30 h (p values from three repeats calculated by Student's t-test).…”

“…To find out if A + N treatment can induce genes coding for immunerelated extracellular molecules we searched for p53 ChIP-Seq peaks in genes encoding various cytokines and chemokines. Interestingly, using ChIP-Atlas [33], we found p53 ChIP-Seq peak at the exon 1/intron 1 border of interleukin-7 gene (Fig. 12B).…”

Combined mRNA and protein single cell analysis in a dynamic cellular system using SPARC

“…A set of genes where POU5F1 binds in the vicinity of the TSS in primed hESCs were identified using ChIPseq data 35 . An initial set of 11 hESC samples (SRX017276, SRX021069, SRX021071, SRX1053369, SRX1053370, SRX1053378, SRX1053379, SRX266859, SRX702065, SRX702066, SRX702069) were collected from CHiP-Atlas 35 by filtering with POU5F1 as antigen and a distance from TSS as 1 kb. For the remaining samples hierarchical clustering of the euclidean distance all samples binding scores across all genes compared to each other was done.…”

Cis‐control of Six1 expression in neural crest cells during craniofacial development

“…To further confirm the functions of the TFBS, we searched the interaction of transcriptional factors with the enhancer on ChIP-Atlas (http://chip-atlas.org). 18 We found a strong peak overlapping the enhancer in a ChIP-seq of LHX6 performed on E11.5 maxillary arch cells ( Figure 4M). 19 The peak is flanked by a H3K27ac peak detected in the E11.5 mouse maxillary arch, 20 suggesting the binding site is located in an active enhancer.…”