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
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Project description:Genome-wide mapping of the chromatin enrichment of CEBPB in NCM460 cell
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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
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 containing 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 | GSE112019 | GEO
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.
2015-03-31 | GSE67425 | GEO
Project description:The CCAAT/enhancer-binding proteins (CEBPs) are transcription factors involved in hematopoietic cell development and induction of several inflammatory mediators. Here, we generated CEBP-beta (CEBPB) and CEBP-epsilon (CEBPE) double-knockout (bbee) mice and compared their phenotypes to those of single-deficient (bbEE and BBee) and wild-type (BBEE) mice. The bbee mice were highly susceptible to fatal infections and died within 2-3 months. Morphologically, their neutrophils were blocked at the myelocytes/metamyelocytes stage, and clonogenic assays of bone marrow cells indicated a significant decrease in the number of myeloid colonies of the bbee mice. In addition, the proportion of hematopoietic progenitor cells [Lin(-)Sca1(+)c-Kit(+)] in the bone marrow of the bbee mice was significantly increased, reflecting the defective differentiation of the myeloid compartment. Furthermore, microarray expression analysis of lipopolysaccharide (LPS)- and interferon-gamma (IFN-gamma)-activated bone marrow-derived macrophages from bbee compared to single knockout mice revealed decreased expression of essential immune response-related genes and networks, including some direct CEBP targets such as Marco and Clec4e. Overall, the phenotype of the bbee mice is distinct from either the bbEE or BBee mice, demonstrating that both transcription factors are crucial for the maturation of neutrophils and macrophages, as well as the innate immune system, and can at least in part compensate for each other in the single knockout mice. To rule out the regulatory influence of both CEBPB and CEBPE on macrophage-related genes, expression analysis of bone marrow-derived macrophages was performed. Macrophages were derived from murine bone marrow with the use of murine M-CSF. The macrophages were stimulated with both LPS (100 ng) and IFN-gamma (100 ng) for 24h, and RNA was extracted for array analysis. Overall, RNA was extracted from stimulated macrophages of one WT mouse, one CEBPB-KO mouse, one CEBPE-KO mouse and one double-KO mouse.
2010-09-02 | E-GEOD-23821 | biostudies-arrayexpress