ChIP-seq

Overview

Chromatin immunoprecipitation followed by next-generation sequencing (ChIP-seq); maps genome-wide protein–DNA interactions (transcription factor binding, histone modifications) at single-nucleotide resolution.

Used by

  • Used with a Flag antibody in EWS::FLI1-transduced heMSCs (GEO GSE272959) to map genome-wide EWS::FLI1 binding sites; identified 3,086 peaks predominantly in intronic (1,065) and intergenic (1,186) regions at tandem CA dinucleotide microsatellites — a binding pattern qualitatively distinct from GGAA promoter-enhancer occupancy in transformed A673 Ewing cells. PMID:25186949
  • Performed for H3K27ac, H3K4me1, H3K4me3, H3K36me3, H3K9me3, and H3K27me3 in three TERT-rearranged neuroblastoma tumours and cell lines, demonstrating enhancer-hijacking mechanism: rearrangements juxtapose TERT to super-enhancer clusters, spreading active chromatin marks and displacing H3K27me3 repression PMID:26466568
  • ChIP-seq for H3K4me3, H3K27ac, BRD4, MYB, and TP63 used to map chromatin landscapes and super-enhancer locations in 13 ACCs (5 primary + 8 primagrafts); identified translocated super-enhancers as drivers of MYB overexpression PMID:26829750
  • H3K27me3 ChIP-Seq on 35 MRTs vs normals identified 158 promoters with decreased H3K27me3 enriched for homeobox/HOX terms (FDR 4.17e-44 to 1.67e-37); H3K27ac ChIP-Seq on 10 MRTs identified 136 MRT-specific super-enhancers at HOX clusters, HISTH1, HISTH2, FLT3LG, and STAT3. PMID:26977886
  • DUX4 ChIP-seq in NALM-6 and Reh cells confirmed direct DUX4 binding at ERG exon 6 alt and other non-canonical transcription start sites deregulated in DUX4/ERG B-ALL. PMID:27776115
  • Employed ChIP-seq to assess chromatin occupancy and epigenomic state in tumor cells PMID:28196596
  • H3K27ac and CTCF ChIP-seq performed on a subset of 28 medulloblastoma cases; ChIP-seq data demonstrated Group 4-specific SNCAIP super-enhancer repositioning into the PRDM6 TAD (enhancer-hijacking mechanism) PMID:28726821
  • ChIP-seq for H3K27ac, H3K4me1, and H3K4me3 performed in prostate cancer cell lines and CPGEA tissues to map the rs4519489 enhancer; allele-specific USF1 ChIP-seq in heterozygous tissue confirmed preferential A-allele binding (A:T ratio shifted from 1:5 in input to 11:6 in USF1-IP) PMID:28927585

Notes

  • In the Ewing sarcoma heMSC study, ~85% of bound chromatin was in quiescent (low histone mark) regions.
  • Direct comparison with published A673 Ewing-cell ChIP-seq revealed virtually no peak overlap at the binding-site level, yet 37% of bound genes were shared — reflecting a transition from intronic/intergenic binding in the cell-of-origin context to promoter binding in established tumor cells.

Sources

This page was processed by crosslinker on 2026-05-14. - PMID:26466568

This page was processed by crosslinker on 2026-05-14. - PMID:26829750

This page was processed by entity-page-writer on 2026-05-15. - PMID:26977886

This page was processed by entity-page-writer on 2026-05-15. - PMID:27776115

This page was processed by entity-page-writer on 2026-05-15. - PMID:28196596

This page was processed by wiki-cli on 2026-05-14. - PMID:28726821

This page was processed by wiki-cli on 2026-05-15. - PMID:28927585

This page was processed by wiki-cli on 2026-05-15.