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Characterization of genome-wide DNA binding rhythms of HNF4A

ABSTRACT: Characterization of genome-wide DNA binding rhythms of HNF4A

PROVIDER: PRJNA483995 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7634103.fastq.gz	Fastqsanger.gz
	SRR7634104.fastq.gz	Fastqsanger.gz
	SRR7634105.fastq.gz	Fastqsanger.gz
	SRR7634106.fastq.gz	Fastqsanger.gz
	SRR7634107.fastq.gz	Fastqsanger.gz

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Characterization of genome-wide DNA binding rhythms of HNF4A

Project description:HNF4A mRNA cycles over the coure of 24 h. To understand whether the chromatin binding of the transcription factor is also rhythmic, we performed ChIP-seq for HNF4A using mouse liver samples of ZT4 and ZT16. By analysing this dataset, we conclude that HNF4A binds chromatin much more robustly during the evening ( at ZT16).

2018-08-02 | GSE118007 | GEO

HNF4A defines tissue-specific circadian rhythms by beaconing BMAL1::CLOCK chromatin binding and shaping rhythmic chromatin landscape

Project description:ChIP-seqs of BMAL1, HNF4A, FOXA2, H3K4me1, and H3K27ac were profiled in mouse liver tissues upon Hnf4a or Bmal1 knockout. BMAL1, H3K4me1, and H3K27ac ChIP-seq were profiled in U2OS cells ectopically expressing HNF4A.

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HNF4A defines tissue-specific circadian rhythms by beaconing BMAL1::CLOCK chromatin binding and shaping rhythmic chromatin landscape

Project description:HNF4A defines tissue-specific circadian rhythms by beaconing BMAL1::CLOCK chromatin binding and shaping rhythmic chromatin landscape

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Genome-wide mapping of Hnf4a binding sites in the newborn mouse kidneys

Project description:Hnf4a is specifically expressed in developing proximal tubule cells in the newborn mouse kidney. In order to identify direct target genes of Hnf4a in the developing proximal tubules, we performed ChIP-Seq of Hnf4a in the mouse kidneys at P0.

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HNF4A-binding sites in HepG2 hepatoblastoma cells treated with TGF-beta

Project description:Specific regulation of target genes by transforming growth factor-β (TGF-β) in a given cellular context is determined in part by transcription factors and cofactors that interact with the Smad complex. In the present study, we determined Smad2 and Smad3 (Smad2/3) binding regions in the promoters of known genes in HepG2 hepatoblastoma cells, and compared them to those in HaCaT epidermal keratinocytes to elucidate the mechanisms of cell type- and context-dependent regulation of transcription induced by TGF-β. Our results show that 81% of the Smad2/3 binding regions in HepG2 cells were not shared with those found in HaCaT cells. Hepatocyte nuclear factor 4α (HNF4α) is expressed in HepG2 cells, but not in HaCaT cells, and the HNF4α binding motif was identified as an enriched motif in the HepG2-specific Smad2/3 binding regions. ChIP-sequencing analysis of HNF4A binding regions under TGF-β stimulation revealed that 32.5% of the Smad2/3 binding regions overlapped HNF4A bindings. MIXL1 was identified as a new combinatorial target of HNF4A and Smad2/3, and both the HNF4A protein and its binding motif were required for the induction of MIXL1 by TGF-β in HepG2 cells. These findings generalize the importance of binding of HNF4A on Smad2/3 binding genomic regions for HepG2-specific regulation of transcription by TGF-β, and suggest that certain transcription factors expressed in a cell-type-specific manner play important roles in the transcription regulated by the TGF-β-Smad signaling pathway. HepG2 cells were treated with TGF-beta for 1.5 h or left untreated. anti-HNF4A ChIP-seq was performed. One lane was used for each sample.

2011-06-08 | E-GEOD-28845 | biostudies-arrayexpress

HNF4A-binding sites in HepG2 hepatoblastoma cells treated with TGF-beta

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Project description:HNF4A

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Genome-wide DNA-binding profile of HNF4A and genome occupancy of the histone modifications H3K4me1, H3K27ac in kidneys from Bicc1 WT and KO mice by ChIPseq.

Project description:Mutations in Bicaudaul C 1 (BICC1), evolutionary conserved RNA-binding protein, cause renal cysts in mice and humans. These renal cysts are reminiscent of Polycystic Kidney Disease (PKD). How BICC1 is involved in the pathogenesis of polycystic kidney disease is still unknown. Recent studies highlighted that HNF4A plays a role in the regulation of metabolic pathways deregulated in this renal disease. Moreover, Menezes et al. [2012, https://doi.org/10.1371/journal.pgen.1003053] showed that combined kidney inactivation of Hnf4a and Pkd1 in mice significantly worsened the cystic phenotype. Here we investigated whether the DNA binding and transcriptional activity of HNF4A might be deregulated in kidneys from Bicc1 mouse model of polycystic kidney disease. HNF4A, H3K27ac, H3K4me1 ChIPseq experiments were performed in kidneys from male and female Bicc1 WT and KO mice. From the contralateral kidneys of the same animals used for the ChIPseq experiments, the total RNA was extracted for gene expression profiling by RNAseq. The RNAseq data was used to support the ChIP-seq analysis and to reveal deregulated pathways in BICC1 mutants.

2020-01-20 | E-MTAB-6424 | biostudies-arrayexpress

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Project description:Genome-wide mapping of Hnf4a binding sites in the newborn mouse kidneys

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Genome-wide map of binding sites for HNF4a during hepatic specification of iPS cells

Project description:HNF4a has been shown to be critical for hepatocyte differentiation from iPS cells.

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