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EBF1 ChIP-seq after NICD1 induction

ABSTRACT: EBF1 ChIP-seq after NICD1 induction

PROVIDER: PRJNA832129 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18920607_1.fastq.gz	Fastqsanger.gz
	SRR18920607_2.fastq.gz	Fastqsanger.gz
	SRR18920608_1.fastq.gz	Fastqsanger.gz
	SRR18920608_2.fastq.gz	Fastqsanger.gz

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Characterizing the profiles of Ebf1 in mouse fat cells (ChIP-seq)

Project description:ChIP-seq data from mouse adipocyte. Mature 3T3-L1 adipocytes were cross-linked with 1% formaldehyde 10 days after induction with MDI. Frozen cell pellets were submitted to the Broad Institute for subsequent analysis of Ebf1-bound regions using anti-Ebf1 antibody (Abnova H00001879-M01).

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EBF1 ChIP-seq after NICD1 induction

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Dynamic EBF1 occupancy directs sequential epigenetic and transcriptional events in B cell programming [EBF1-ChIP-Seq-Cre]

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Dynamic EBF1 occupancy directs sequential epigenetic and transcriptional events in B cell programming [Histone-ChIP-Seq-Cre]

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Dynamic EBF1 occupancy directs sequential epigenetic and transcriptional events in B cell programming [Pax5-ChIP-Seq-Tet-On]

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Dynamic EBF1 occupancy directs sequential epigenetic and transcriptional events in B cell programming [ATAC-Seq-Cre]

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Mapping ERβ genomic binding sites reveals unique genomic features and identifies EBF1 as an ERβ interactor [ChIP-Seq]

Project description:The C4-12/Flag.ERβ cell line which stably expressed Flag.ERβ is used to study ERβ genomic functions without ERα interference. Mapping ERβ binding sites in these cells reveals ERβ unique distribution and motif enrichment patterns. Accompanying our mapping results, nascent RNA profiling is performed on cells at the same treatment time. The combined results allow the identification of ERβ target genes. Gene ontology analysis reveals that ERβ targets are enriched in differentiation, development and apoptosis. Concurrently, E2 treatment suppresses proliferation in these cells. Within ERβ binding sites, while the most prevalent binding motif is the canonical ERE, motifs of known ER interactors are also enriched in ERβ binding sites. Moreover, among enriched binding motifs are those of GFI, REST and EBF1, which are unique to ERβ binding sites in these cells. Further characterization confirms the association between EBF1 and the estrogen receptors, which favors the N-terminal region of the receptor. Furthermore, EBF1 negatively regulates ERs at the protein level. In summary, by studying ERβ genomic functions in our cell model, we confirm the anti-proliferative role of ERβ and discover the novel cross talk of ERβ with EBF1 which has various implications in normal physiology. C4-12/Flag.ERβ cells were treated with 10nM E2 for 1 hour then crosslinked with 1% formaldehyde; EtOH treatment was used as control. Crosslinked samples were processed for ChIP-seq and sequenced with Illumina Genome Analyzer II and aligned to hg18. QuEST was used as the peak-calling software, using default parameters recommended to analyze transcription factor ChIP-seq data. The entire ChIP-seq process was performed once on each sample (Vehicle or E2-treated).

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