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Mutant-CCAAT/enhancer-binding protein alpha target genes in myeloid progenitor cells by chromatin IP

ABSTRACT: CCAAT/enhancer-binding protein alpha (C/EBPα) is a lineage-specific transcription factor that directs development of granulocytes. To obtain insights into the genome-wide transcriptome of mutant C/EBPα, we have performed chromatin immunoprecipitation on DNA promoter microarrays (ChIP-chip) in the murine 32D myeloid progenitor cell line. These cells expressed an estradiol-inducible form of mutant C/EBPα.

ORGANISM(S): Mus musculus

PROVIDER: GSE36268 | GEO | 2013/12/01

SECONDARY ACCESSION(S): PRJNA153097

REPOSITORIES: GEO

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CCAAT/enhancer-binding protein alpha target genes in myeloid progenitor cells uncovered by chromatin IP

Project description:CCAAT/enhancer-binding protein alpha (C/EBPα) is a lineage-specific transcription factor that directs development of granulocytes. To obtain insights into the genome-wide transcriptome of wild type C/EBPα, we have performed chromatin immunoprecipitation on DNA promoter microarrays (ChIP-chip) in the murine 32D myeloid progenitor cell line. These cells expressed an estradiol-inducible form of wild-type C/EBPα.

2013-12-01 | GSE19321 | GEO

Mutant-CCAAT/enhancer-binding protein alpha target genes in myeloid progenitor cells by chromatin IP

Project description:CCAAT/enhancer-binding protein alpha (C/EBPM-NM-1) is a lineage-specific transcription factor that directs development of granulocytes. To obtain insights into the genome-wide transcriptome of mutant C/EBPM-NM-1, we have performed chromatin immunoprecipitation on DNA promoter microarrays (ChIP-chip) in the murine 32D myeloid progenitor cell line. These cells expressed an estradiol-inducible form of mutant C/EBPM-NM-1. In the murine 32D myeloid progenitor cell line, expressing an estradiol-inducible form of C-terminal mutant of C/EBPM-NM-1. (n=2, replicates). We have performed chromatin immunoprecipitation on DNA promoter microarrays (ChIP-chip) after 4 hours of estradiol incubation.

2013-12-01 | E-GEOD-36268 | biostudies-arrayexpress

CCAAT/enhancer-binding protein alpha target genes in myeloid progenitor cells uncovered by chromatin IP

Project description:CCAAT/enhancer-binding protein alpha (C/EBPM-NM-1) is a lineage-specific transcription factor that directs development of granulocytes. To obtain insights into the genome-wide transcriptome of wild type C/EBPM-NM-1, we have performed chromatin immunoprecipitation on DNA promoter microarrays (ChIP-chip) in the murine 32D myeloid progenitor cell line. These cells expressed an estradiol-inducible form of wild-type C/EBPM-NM-1. In the murine 32D myeloid progenitor cell line, expressing either an estradiol-inducible form of wild-type C/EBPM-NM-1. (C/EBPM-NM-1-ER, n=3, replicates), or as a control ER (n=2, replicates), we have performed chromatin immunoprecipitation on DNA promoter microarrays (ChIP-chip) after 4 hours of estradiol incubation.

2013-12-01 | E-GEOD-19321 | biostudies-arrayexpress

Homodimer-mediated phosphorylation of C/EBPα-p42 S16 modulates acute myeloid leukaemia differentiation through liquid-liquid phase separation [RNA-seq]

Project description:CCAAT/enhancer binding protein α (C/EBPα) regulates myeloid differentiation, and its dysregulation contributes to acute myeloid leukaemia (AML) progress. Clarifying its functional implementation mechanism is of great significance for its further clinical application. Here, we show that C/EBPα regulates AML cell differentiation through liquid-liquid phase separation (LLPS), which can be disrupted by C/EBPα-p30. Considering that C/EBPα-p30 inhibits the functions of C/EBPα through the LZ region, a small peptide TAT-LZ that could instantaneously interfere with the homodimerization of C/EBPα-p42 was constructed, and dynamic inhibition of C/EBPα phase separation was observed, demonstrating the importance of C/EBPα-p42 homodimers for its LLPS. Mechanistically, homodimerization of C/EBPα-p42 mediated its phosphorylation at the novel phosphorylation site S16, which promoted LLPS and subsequent AML cell differentiation. Finally, decreasing the endogenous C/EBPα-p30/C/EBPα-p42 ratio rescued the phase separation of C/EBPα in AML cells, which provided a new insight for the treatment of the AML.

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Homodimer-mediated phosphorylation of C/EBPα-p42 S16 modulates acute myeloid leukaemia differentiation through liquid-liquid phase separation [ChIP-seq]

2023-11-08 | GSE243423 | GEO

The CCAAT-Binding Complex Controls Mitochondrial Activity and Iron Homeostasis in Candida glabrata

Project description:We conducted a network-based analysis of the Hap5 transcription factor belonging to the CCAAT-Binding Complex in Candida glabrata.

2017-04-30 | GSE91371 | GEO

A C/EBPα–Wnt connection in gut homeostasis and carcinogenesis

Project description:We explored the connection between C/EBPα (CCAAT/enhancer binding protein α) and Wnt signaling in gut homeostasis and carcinogenesis. C/EBPα was expressed in human and murine intestinal epithelia in the transit amplifying region of the crypts and was absent in intestinal stem cells and Paneth cells with activated Wnt signaling. In human colorectal cancer and murine APCMin/+ polyps, C/EBPα was absent from nuclear β-catenin–positive tumor cells. In chemically induced intestinal carcinogenesis, C/EBPα KO in murine gut epithelia increased tumor volume. C/EBPα deletion extended the S-phase cell zone in intestinal organoids and activated typical proliferation gene expression signatures, including that of Wnt target genes. Genetic activation of β-catenin in organoids attenuated C/EBPα expression. Comparing gene expression of wild type and C/EBPα KO organoids by RNA sequencing aimed to identify C/EBPα dependent alterations in gene expression.

2018-12-24 | GSE123925 | GEO

Transcriptional repression of c-Myb and GATA-2 is involved in the effects of C/EBPα in p210 BCR/ABL-expressing cells

Project description:Levels of C/EBPα are low in myeloid blast crisis (BC) of chronic myelogenous leukemia (CML) and its expression in p210BCR/ABL-expressing hematopoietic cells induces granulocytic differentiation, inhibits proliferation and suppresses leukemogenesis. To assess the mechanisms involved in these effects, C/EBPα targets were identified by microarray analyses. Upon C/EBPα activation, expression of c-Myb and GATA-2 was repressed in 32D-BCR/ABL, K562 and CML-BC primary cells but only c-Myb levels decreased slightly in CD34+ normal progenitors. The role of these two genes for the biological effects of C/EBPα was assessed by perturbing their expression in K562 cells. Expression of c-Myb blocked the proliferation inhibition and differentiation-inducing effects of C/EBPα while c-Myb siRNA treatment enhanced C/EBPα-mediated proliferation inhibition and induced changes in gene expression indicative of monocytic differentiation. GATA-2 expression suppressed the proliferation inhibitory effect of C/EBPα but blocked in part the effect on differentiation; GATA-2 siRNA treatment had no effects on C/EBPα induction of differentiation but inhibited proliferation of K562 cells, alone or upon C/EBPα activation. In summary, the effects of C/EBPα in p210BCR/ABL -expressing cells depend, in part, on transcriptional repression of c-Myb and GATA-2. Since perturbation of c-Myb and GATA-2 expression has non identical consequences for proliferation and differentiation of K562 cells, the effects of C/EBPα appear to involve different transcription-regulated targets.

2008-06-13 | GSE11766 | GEO

The genome-scale binding profile of the CCAAT-binding complex in Aspergillus fumigatus

Project description:The CCAAT-binding complex (CBC) is a heterotrimetric transcription factor conserved in all eukaryotes. The CBC specifically interacts with the pentanucleotide motif known as the CCAAT box, which is one of the most ubiquitous cis-acting elements on the eukaryotic promoters. In Aspergillus fumigatus, the CBC consists of three subunits HapB, HapC, and HapE, which are all required for specific binding to the target sequences. This regulatory complex has been shown to be involved in the regulation of a wide range of cellular processes, including primary and secondary metabolism, iron homeostasis, as well as azole drug resistance and virulence in mammalian hosts. In this study, we investigated the genome-wide binding profile of the CBC using the chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). We identified over 1,000 peak regions, which showed more than 5-fold enrichment compared to the input control in steady-state iron-replete (+Fe) and iron-starvation (-Fe) conditions. Bioinformatic analysis of the peak regions revealed the 5’-CSAATVR-3’ sequence as the most enriched nucleotide motif, suggesting that this motif acts as the consensus binding sequence for the CBC in vivo.

2019-12-31 | GSE129966 | GEO

Transcription factor C/EBP⍺ is required for the development of Ly6Chi monocytes but not Ly6Clo monocytes

Project description:Monocytes comprise two major subsets, Ly6Chi classical monocytes and Ly6Clo non-classical monocytes. Notch2 signaling in Ly6Chi monocytes triggers transition to Ly6Clo monocytes, which require Nr4a1, Bcl6, Irf2 and Cebpb. By comparison, less is known about transcriptional requirements for Ly6Chi monocytes. We find transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα) is highly expressed in Ly6Chi monocytes, but down-regulated in Ly6Clo monocytes. A few previous studies described the requirement of C/EBPα in the development of neutrophils and eosinophils. However, role of C/EBPα for in vivo monocyte development has not been understood. We deleted the Cebpa +37 kb enhancer in mice, eliminating hematopoietic expression of C/EBPα, reproducing the expected neutrophil defect. Surprisingly, we also discovered a severe and selective loss of Ly6Chi monocytes, while preserving Ly6Clo monocytes. We find that BM progenitors from Cebpa +37–/– mice rapidly progress through the cMoP stage to develop directly into Ly6Clo monocytes even in the absence of Notch2 signaling. These results identify a previously unrecognized role for C/EBPα in maintaining Ly6Chi monocyte identity.

2024-03-18 | GSE254202 | GEO

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