Similar Datasets
Project description:Macrophage CEBPD dependent gene expression
| PRJNA726152 | ENA
Project description:To investigate the effects of CEBPD on pancreatic ductal cell tumorigenicity, we established doxycycline-inducible MIA PaCa-2 cells for CEBPD over-expression, as well as non-control cells with an empty inducible construct. RNAseq was performed on these cells in the presence and absence of doxycycline and we showed that CEBPD activates gene signatures associated with cell motility.
2022-09-26 | GSE214028 | GEO
Project description:CCAAT/enhancer-binding protein delta (C/EBPδ) is a member of the C/EBP family of transcription factors. According to the current paradigm, C/EBPδ potentiates cytokine production and modulates macrophage function thereby enhancing the inflammatory response. Remarkably, however, C/EBPδ deficiency does not consistently lead to a reduction in Lipopolysaccharide (LPS)-induced cytokine production by macrophages. Here, we address this apparent discrepancy and show that the effect of C/EBPδ on cytokine production and macrophage function depends on both the macrophage subtype and the LPS concentration used. Using CRISPR-Cas generated macrophages in which the transactivation domain of C/EBPδ was deleted from the endogenous locus (ΔTAD macrophages), we next show that the context-dependent role of C/EBPδ in macrophage biology relies on compensatory transcriptional activity in the absence of C/EBPδ. We extend these findings by revealing a large discrepancy between transcriptional programs in C/EBPδ knock-out and C/EBPδ transactivation dead (ΔTAD) macrophages implying that compensatory mechanisms do not specifically modify C/EBPδ-dependent inflammatory responses but affect overall macrophage biology. Overall, these data imply that knock-out approaches are not suited for identifying the genuine transcriptional program regulated by C/EBPδ, and we suggest that this phenomenon applies for transcription factor families in general.
| S-EPMC8470509 | biostudies-literature
Project description:Cebpd is a transcription factor regulating cytokines. We determined the role of Cebpd in the regulation of transciptional output. We generated 4T1 breast cancer cells with CRISPR/Cas9 mediated Cebpd knockout. We treated control sgRosa26 and sgCebpd cells with vehicle or IFNgamma (20ng/ml) for 24 hours and isolated RNA for sequencing.
2021-04-27 | GSE173296 | GEO
Project description:In previous studies, we identified and demonstrated that a 1.2kb cebpd downstream element (CEN) is capable and neccessary for the induction of cebpd in the kidney after cardiac injury. The goal of this study is to unveal the Cebpd regulated responses of kidney to cardiac regeneration in zebrafish. we profiled responses by kidney in cebpd mutant and enhancer (CEN) mutant fish zebrafish to massive injuries of the heart.
2022-02-25 | GSE193630 | GEO
Project description:Purpose: To determine which genes are regulated by CEBPD in MCF-7 cells. Methods: MCF7 cells were transfected with siRNAs against CEBPD or control. After 48h transfection total RNAs from two independent experiments were extracted and subjected to deep sequencing following Illumina standard protocols. Results: Samples were aligned to the reference human genome hg19 with good alignment ranging from 84 – 85% for both reads and very low mismatch rates <0.35%. RNA mapping statistics calculated using Picard software reported mapping of samples to 86 % mRNA bases, 63-65% unique reads, and <2.6% ribosomal reads. The aligned BAM files were imported into Partek Genome Studio v6.4 following the RNA-Seq workflow. Briefly, metadata about the samples was added followed by normalizing counts and doing differential expression analysis with ANOVA for the siNS vs siCEBPD contrasts. Differential gene list were created based on a p-value cutoff of <0.05 and fold-change of >1.5 or < -1.5. Analysis revealed that C/EBPδ supports the expression of 319 genes (downregulated by siCEBPD) and attenuates the expression of 238 genes (induced by siCEBPD). For validation, 31 genes were assessed by QPCR with mRNA samples independent of those used for mRNA-Seq, and also by silencing CEBPD with either one of two siRNA sequences. About 90% of the tested genes from the mRNA-Seq approach were validated as C/EBPδ-regulated in MCF-7 cells by QPCR. Conclusions: Our study is the first characterization of the CEBPD transcriptome generated by RNA-seq in MCF7 cells with biological replicates.
2016-06-04 | GSE69604 | GEO
Project description:We carried out CEBPD chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq) and revealed that the top motif enriched in CEBPD sites are identical to the CEBPD family motif and osteoblast differentiation/bone formation motifs like Fos1, Fra1, JUNB, RUNX and STAT3. The commitment of stem cells to an osteoblastic lineage is a complex and tightly regulated process, involving coordination between extrinsic signals and intrinsic transcriptional machinery. While many rodent osteoblast studies abound, human osteoblastic signaling networks are not as well-researched due to limitations in cell sources and existing models. Here, we generated human pluripotent stem cell (hPSC)-derived osteoblasts and used this modeling platform to identify functional osteoblastic surface receptors and their downstream transcriptional networks involved in human osteogenesis. We systematically dissected osteoblastic gene expression patterns and identified critical clusters associated with osteogenesis. The osteoblast surface receptor signature study revealed enriched CORIN expression in osteoblasts and enriched SDC1 expression in MSCs. In vitro calcified staining and 3D biomimetic GelMA/microCT (μCT) studies demonstrated that depletion of CORIN as well as ectopic expression of SDC1 significantly impaired osteogenesis. Transcriptome analyses revealed that dysregulation of CORIN or SDC1 alters biological processes and pathways mainly involved in bone formation associated signaling including TGFβ regulating extracellular matrix and Wnt signaling. Genome-wide ChIP enrichment analysis further indicated that CEBPD is a downstream transcription factor involved in CORIN and SDC1-modulated osteogenesis. CEBPD ChIP-seq and RNA-seq validated its role in controlling extracellular matrix organization, bone mineralization, and TGFβ, BMP, and Wnt signaling. Depletion of CEBPD led to impairment of osteoblastic differentiation. Differential expression analysis of single-cell transcriptomes revealed enriched expression of CEBPD and its transcriptional targets during the different stages of osteoblast differentiation. In summary, our findings elucidated the vital signaling in osteoblast lineage commitment.
2023-04-28 | GSE201836 | GEO
Project description:RNAseq data from hMPDMs (HoxB4 myeloid progenitor derived macrophages), BMDMs (bone-marrow derived macrophages), and Raw264.7 cell line in unstimulated condition and 3 hours post LPS stimulation (lipopolysaccharide). Gene expression demonstrates similarities between hMPDMs and BMDMs supporting use of hMPDMs in this study of NFkB stimulus response signaling dynamics, whereas Raw264.7 cells are more distinct from BMDMs in terms of expression LPS-inducible genes.
2024-06-03 | GSE246566 | GEO
Project description:NK cells engineered to express IL-21 (IL-21 NK) acquire strong antitumor activity, with the ability to respond to glioblastoma (GBM) rechallenge in vitro and in vivo. IL-21 NK cells have a unique signature of chromatin accessibility, with CCAAT/Enhancer-Binding Protein (C/EBP), especially CEBPD, serving as key transcription factors regulating their memory response.
2024-07-09 | GSE227098 | GEO
Project description:CCAAT/Enhancer Binding Protein D (CEBPD) is a transcription factor that regulates genes involved in immune and inflammatory responses. Based on our previous observation that CEBPD expression increases in airway smooth muscle (ASM) with glucocorticoid exposure, we sought to better understand its role in the ASM transcriptomic response to glucocorticoids via knockdown experiments. Primary human airway smooth muscle (ASM) cells from four non-asthma donors were transfected with 25pmol of siRNA non-targeting control or siCEBPD SMARTpool using RNAiMax. Three days after transfection, cells were treated with 100nM Budesonide, 10ng/ml TNF-alpha, or both for 18 hours. RNA-Seq libraries were prepared with the Kapa mRNA HyperPrep Illumina Library kit. An Illumina HiSeq 2500 instrument was used to generate 125 base pair paired-end reads. STAR was used to align sequencing reads to the hg38 reference genome, and HTSeq was used to quantify transcript levels. DESeq2 was used to perform differential expression analysis.
2020-12-31 | GSE146017 | GEO