chipseq data  (Biotechnology Information)

Journal: bioRxiv

Article Title: Vascular smooth muscle cell atherosclerosis trajectories characterized at single cell resolution identify causal transcriptomic and epigenomic mechanisms of disease risk

doi: 10.1101/2025.06.04.655863

Figure Lengend Snippet: A. Hierarchically clustered heatmap of differential ChromVar scores ( Tcf21 -KO vs. control) labeled with selected representative TF motifs B. Jensen-Shannon divergence of observed Tcf21 -KO vs. control ChromVar scores showing motifs demonstrating significant probability divergence between conditions. Control JSD is calculated by randomly splitting control dataset into two equal distributions and calculating the JSD between these distributions. C. ChIPseq peak overlap between TCF21 and TEAD1. D. Representative pathways identified from shared ChIPseq peaks using Genomic Regions Enrichment of Annotations Tool (GREAT). E. GWASAnalytics analysis of GWAS SNP (EMBL-EBI GWAS Catalog) enrichment of overlapping ChIPseq peaks between TCF21 and TEAD1 showing highest enrichment for CAD traits. F. Proximity ligation assay showing nuclear fluorescent signal enrichment in the TCF21 + TEAD1 antibody group compared with TCF21+IgG control. G, H, I. Dual luciferase assay for overlapping regulatory regions ( SRF Intron, BMP1 Intron, LOXL1 Promoter) for TCF21 and TEAD1 demonstrating competitive repression and epigenetic fine-tuning of enhancer/promoter activity between regulatory elements.

Article Snippet: All ChIPseq data generated and analyzed (CEBPB, H3K27ac, TEAD1) are deposited to National Center for Biotechnology Information Gene Expression Omnibus (GEO) to be made available for public access.

Techniques: Control, Labeling, Proximity Ligation Assay, Luciferase, Activity Assay

Journal: bioRxiv

Article Title: Vascular smooth muscle cell atherosclerosis trajectories characterized at single cell resolution identify causal transcriptomic and epigenomic mechanisms of disease risk

doi: 10.1101/2025.06.04.655863

Figure Lengend Snippet: A. Top consensus TF motif sequences enriched amongst TCF21 HCASMC ChIPseq. B. Individual TF ChromVar scores for Tcf21 , Cebpb , and Tead1 across pseudotemporal bins comparing Tcf21 - KO (dotted) and control (solid) SMC lineage cells. C. Overlapping ChIPseq peak number between CEBPB and TCF21 and representative pathways identified by examining the intersected regions with the Genomic Regions Enrichment of Annotations Tool (GREAT). D-E. Heatmap of feature overlap for CEBPB+TCF21 and TEAD1+TCF21 ChIPseq F-K. GWASAnalytics results for GWAS SNP (EMBL-EBI GWAS Catalog) enrichment of overlapping ChIPseq peaks for TCF21, TEAD1, CEBPB, CEBPB+TCF21, HNF1A+TCF21 and HNF1A. HNF1A serves as negative control showing no significant CAD loci overlap with TCF21 despite both being CAD associated genes, suggesting of alternative mechanisms. L. ChIPseq annotation of TCF21+TEAD1 overlapping peaks and TCF21 -only peaks. Top panel shows peak overlap with H3K27ac regions and bottom panel showing peak annotations. M. TSS distance analysis of TCF21+TEAD1 peaks and TCF21-only peaks. N. O. Representative pathways of overlapping TCF21+TEAD1 and TCF21-only ChIPseq peaks identified by GREAT.

Article Snippet: All ChIPseq data generated and analyzed (CEBPB, H3K27ac, TEAD1) are deposited to National Center for Biotechnology Information Gene Expression Omnibus (GEO) to be made available for public access.

Techniques: Control, Negative Control

Journal: NPJ Precision Oncology

Article Title: Genome-wide analyses reveals an association between invasive urothelial carcinoma in the Shetland sheepdog and NIPAL1

doi: 10.1038/s41698-024-00591-0

Figure Lengend Snippet: LD between the top SNP and all others in the region is indicated by the color of the markers with red indicating highest value. Positions of predicted active regulatory regions are in the second panel. The third panel contains positions of the associated SNPs within the shared haplotype with the presumed functional SNP highlighted in green. The bottom panel contains regulatory regions from ChIPseq as well as gene annotations. Each gene is represented by the longest transcript from the Broad Improved Canine Annotation v.1 (UCSC). The components are plotted against the CanFam3.1 genome using custom tracks in the UCSC browser ( http://genome.ucsc.edu ). Genes highlighted in red were upregulated in iUC tumors .

Article Snippet: Specifically: Illumina SNP chip data and ChIPseq data from cell lines has been submitted to the NCBI GEO database under accession GSE241367 and GSE254079 respectively.

Techniques: Functional Assay

Journal: Genome Biology

Article Title: IDHwt glioblastomas can be stratified by their transcriptional response to standard treatment, with implications for targeted therapy

doi: 10.1186/s13059-024-03172-3

Figure Lengend Snippet: A The distribution of average promoter DNA methylation for all genes, JARID2 binding site (JBS)genes, LE50 and LE70 genes in primary (P) and recurrent (R) GBM tumors from all patients (top) and once separated into Down (middle) and Up (bottom) responders. B The proportion of differentially methylated promoters (DMP) between primary and matched recurrent GBM. C The average change in methylation between primary and matched recurrent tumors for the DMP from panel B . D The proportion of single GBM cell promoters that have different methylation status. E The proportion of promoters with the H3K27me3 mark in nine patient GBMs. F The proportion of JBSgene promoters that had EZH2 bound according to ChIPseq of paired patient samples from an Up and a Down responder. G The proportion of promoters with a specific change in EZH2 occupancy that belonged to each gene set

Article Snippet: EZH2, and matched input control DNA, ChIPseq data was created from samples in our Discovery cohort by Active Motif (Carlsbad, CA).

Techniques: DNA Methylation Assay, Binding Assay, Methylation