Genome-wide mapping of the chromatin enrichment of CEBPB in NCM460 cell
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE165710 | GEO | 2025/12/31
REPOSITORIES: GEO
Similar Datasets
Project description:Genome-wide mapping of the chromatin enrichment of CEBPB in NCM460 cell
| PRJNA695514 | ENA
Project description:One of the strongest associated type 2 diabetes (T2D) loci reported to date resides within the TCF7L2 gene. Previous studies point to the T allele of rs7903146 in intron 3 as the causal variant at this locus. To aid in the identification of the actual gene(s) under the influence of this variant, we first generated a CRISPR/Cas9 mediated 1.4kb deletion of the genomic region harboring rs7903146 in the HCT116 cell line followed by global gene expression analysis (see experiment E-MTAB-4839). We then carried out high-throughput chromosome conformation capture assays in the HCT116 and NCM460 cell lines and in colon tissue in order to ascertain which of these perturbed genes promoters made consistent physical contact with the genomic region harboring the variant. To assess consistency and reproducibility we utilized two different techniques: Circularized Chromosome Conformation Capture (4C) and Capture C. In both types of assays, after preparing 3C libraries, our bait of interest was the region harboring rs7903146. Loci interacting with such bait are enriched for by inverse PCR in 4C and by oligonucleotide capture in capture C. 4C assays were carried out in the following samples: two on NCM460 cells (using different primer sets), one on HCT116 cells, one on HCT116 cells with a CRISPR/Cas9 mediated 1.4kb deletion of the genomic region harboring the SNP rs7903146, and one on colon tissue. Capture C assays were carried out in one sample each of the cell lines NCM 460 and HCT116. This experiment, coupled with the associated E-MTAB-4839, revealed just one gene, ACSL5, which resides in the same topologically associating domain as TCF7L2.
2016-08-15 | E-MTAB-4845 | biostudies-arrayexpress
Project description:One of the strongest associated type 2 diabetes (T2D) loci reported to date resides within the TCF7L2 gene. Previous studies point to the T allele of rs7903146 in intron 3 as the causal variant at this locus. To aid in the identification of the actual gene(s) under the influence of this variant, we first generated a CRISPR/Cas9 mediated 1.4kb deletion of the genomic region harboring rs7903146 in the HCT116 cell line followed by global gene expression analysis. HCT116 cells with or without a CRISPR/Cas9 mediated1.4kb deletion of the genomic region harboring the SNP rs7903146 were analyzed for expression, with 3 replicates per condition (DEL vs WT). We observed 99 genes with significant differential expression (FDR cut-off=10%) and an effect size of at least two-fold. We then carried out high-throughput chromosome conformation capture assays in the HCT116 and NCM460 cell lines and in colon tissue (see experiment E-MTAB-4845) in order to ascertain which of these perturbed genesâ promoters made consistent physical contact with the genomic region harboring the variant. This revealed just one gene, ACSL5, which resides in the same topologically associating domain as TCF7L2.
2016-08-16 | E-MTAB-4839 | biostudies-arrayexpress
Project description:WT HepG2 cells vs CEBPB knockout HepG2. CEBPB knockout HepG2 was generated from a single clone by CRISPR KO.
2026-06-14 | E-MTAB-16228 | biostudies-arrayexpress
Project description:CEBPB contributes to the migration of breast cancer cells. We used microarrays to detail the mechanism of CEBPB with downstream targets that drive breast cancer cell migration. CEBPB were overexpressed in MDA-MB231 cell for RNA extraction and hybridization on Agilent microarrays. We sought to obtain the mechanisms of CEBPB with downstream proteins that drive breast cancer cell migration.
2015-03-31 | E-GEOD-67425 | biostudies-arrayexpress
Project description:The bZIP homodimers CEBPB and CREB1 bind DNA containing methylated cytosines differently. CREB1 binds stronger to the C/EBP half-site GCAA when the cytosine is methylated. For CEBPB, methylation of the same cytosine does not affect DNA binding. The X-ray structure of CREB1 binding the half site GTCA identifies an alanine in the DNA binding region interacting with the methyl group of T, structurally analogous to the methyl group of methylated C. This alanine is replaced with a valine in CEBPB. To explore the contribution of this amino acid to binding with methylated cytosine of the GCAA half-site, we made the reciprocal mutants CEBPB(V285A) and CREB1(A297V) and used protein binding microarrays (PBM) to examine binding to four types of double-stranded DNA (dsDNA): 1) DNA with cytosine in both strands (DNA(C|C)), 2) DNA with 5-methylcytosine (M) in one strand and cytosine in the second strand (DNA(M|C)), 3) DNA with 5-hydroxymethylcytosine (H) in one strand and cytosine in the second strand (DNA(H|C)), and 4) DNA with both cytosines in all CG dinucleotides contain- ing 5mC (DNA(5mCG)). When binding to DNA(C|C), CEBPB (V285A) preferentially binds the CRE consensus motif (TGACGTCA), similar to CREB1. The reciprocal mutant, CREB1(A297V) binds DNA with some similarity to CEBPB with strongest binding to the methylated PAR site 8-mer TTACGTAA. These data demonstrate that V285 residue inhibits CEBPB binding to methylated cytosine of the GCAA half-site.
2019-03-01 | GSE112018 | GEO
Project description:Endothelial cell (EC) dysfunction is crucial in chronic vascular inflammation and diseases like atherosclerosis. An unknown endothelial pathological phenotype potentially driving atherosclerosis was hinted in our previous study. However, the detailed characterizations and underlying molecular mechanisms remain unclear. Here, we have defined a new endothelial pathological phenotype, characterized by high expression of fibroblast and pro-inflammatory genes with a rapid reduction in EC fate genes by performing single-cell RNA sequencing. Further analysis revealed that increased CEBPB contributes to the fibroblast and inflammatory feature of these atherogenic ECs, which was further confirmed in cultured human aortic ECs. Mechanistically, IL-1β-induced high expression of CEBPB triggers TGF-β signaling and subsequent regulation of downstream genes. This occurs through direct interaction of CEBPB with the promotor region of TGF-β receptor type I (TGFBR1), resulting in its upregulation. Furthermore, exacerbating atherosclerotic plaque area, enhanced vascular inflammation and increased endothelial TGFBR1 expression were confirmed by endothelial overexpression of CEBPB in vivo. These findings suggest endothelial CEBPB functions as a novel regulator of TGFBR1, driving endothelial pathological phenotype, promoting vascular inflammation and atherosclerosis. Targeting endothelial CEBPB may offer new therapeutic avenues for atherosclerotic diseases.
2025-12-10 | GSE278346 | GEO
Project description:Endothelial cell (EC) dysfunction is crucial in chronic vascular inflammation and diseases like atherosclerosis. An unknown endothelial pathological phenotype potentially driving atherosclerosis was hinted in our previous study. However, the detailed characterizations and underlying molecular mechanisms remain unclear. In the present study, using single-cell RNA sequencing, the new endothelial pathological phenotype was defined by high expression of fibroblast markers, extracellular matrix, and inflammatory genes, concurrently with a rapid decline in endothelial markers. By performing RNA-seq, we found that increased CEBPB contributes to the fibroblast and inflammatory feature of these atherogenic ECs. Further analysis revealed that IL-1β-induced high expression of CEBPB triggers TGF-β signaling and subsequent regulation of downstream genes. This occurs through direct interaction of CEBPB with the promotor region of TGF-β receptor type I (TGFBR1), resulting in its upregulation. Furthermore, exacerbating atherosclerotic plaque area, enhanced vascular inflammation and increased endothelial TGFBR1 expression were confirmed by endothelial overexpression of CEBPB in vivo. These findings suggest endothelial CEBPB functions as a novel regulator of TGFBR1, driving endothelial pathological phenotype, promoting vascular inflammation and atherosclerosis.
2025-12-10 | GSE278347 | GEO
Project description:Endothelial cell (EC) dysfunction is crucial in chronic vascular inflammation and diseases like atherosclerosis. An unknown endothelial pathological phenotype potentially driving atherosclerosis was hinted in our previous study. However, the detailed characterizations and underlying molecular mechanisms remain unclear. In the present study, using single-cell RNA sequencing, the new endothelial pathological phenotype was defined by high expression of fibroblast markers, extracellular matrix, and inflammatory genes, concurrently with a rapid decline in endothelial markers. Further analysis revealed that increased CEBPB contributes to the fibroblast and inflammatory feature of these atherogenic ECs, which was further confirmed in cultured human aortic ECs. Mechanistically, IL-1β-induced high expression of CEBPB triggers TGF-β signaling and subsequent regulation of downstream genes. By performing CUT&Tag analysis, we further investigated that CEBPB directly regulates TGFBR1 expression in endothelial cells through direct interaction of CEBPB with the promotor region of TGF-β receptor type I (TGFBR1). These findings suggest endothelial CEBPB functions as a novel regulator of TGFBR1, driving endothelial pathological phenotype, promoting vascular inflammation and atherosclerosis.
2025-12-10 | GSE278348 | GEO
Project description:Data from the immunoprecipitation of CEBPB from bone marrow derived macrophages.
2020-03-17 | MSV000085112 | MassIVE