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Homo sapiens

ABSTRACT: ChIP-seq analysis of LSD2/DNA interaction in HepG2 cells in normal condition

PROVIDER: PRJNA255972 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1523282.fastq.gz	Fastqsanger.gz
	SRR1523283.fastq.gz	Fastqsanger.gz
	SRR1523284.fastq.gz	Fastqsanger.gz
	SRR1523285.fastq.gz	Fastqsanger.gz
	SRR1523286.fastq.gz	Fastqsanger.gz

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ChIP-seq analysis of LSD2/DNA interaction in HepG2 cells in normal condition

Project description:ChIP-seq analysis of HepG2 cells revealed that many of the target genes of LSD2 were related to lipid metabolism. We found that LSD2 is an important epigenetic regulator of hepatic lipid metabolism. Examination of LSD2/DNA interaction in HepG2 cells in normal condition.

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ChIP-seq analysis of LSD2/H3K4me1 interaction in control and LSD2-knockdowned HepG2 cells

Project description:ChIP-seq analysis of LSD2-depleted HepG2 cells revealed that many of the target genes were related to lipid metabolism. We found that LSD2 is an important epigenetic regulator of hepatic lipid metabolism. Examination of LSD2/H3K4me1 interaction in control and LSD2-knockdowned HepG2 cells.

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Project description:ChIP-seq analysis of LSD2/H3K4me1 interaction in control and LSD2-knockdowned HepG2 cells

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ChIP-seq analysis of LSD2/H3K4me1 interaction in control and LSD2-knockdowned HepG2 cells

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ChIP-seq analysis of LSD2/DNA interaction in HepG2 cells in normal condition

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Transcriptome analysis of LSD2-depleted HepG2 cells

Project description:Transcriptome analysis of LSD2-depleted HepG2 cells revealed that many of the target genes were related to lipid metabolism. We found that LSD2 is an important epigenetic regulator of hepatic lipid metabolism. We depleted LSD2 in HepG2 human hepatic cells using three different siRNAs, and then carried out an expression microarray experiment.

2015-02-02 | E-GEOD-56645 | biostudies-arrayexpress

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Project description:Transcriptome analysis of LSD2-depleted HepG2 cells

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The transcriptional coactivator RUVBL2 regulates Pol II clustering with diverse transcription factors

Project description:RUVBL2 is most important AAA+ ATPase for RNA polymerase II assembly and transcription regulation, through DNA remodeling or by directly interaction with PIC，this study will comprehensively to study the promiscuous functions of this proteins through the ChIP-MS, ChIP-seq, RNA-seq and nascent RNA seq and biochemistry analysis. Our study would provide more systematic and novel responsibility of this molecule, especially for the development and carcinomas.

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IFI16-mediated suppression of HSV-1 protein expression

Project description:Human cells identify invading pathogens and activate immune signaling pathways through a wide array of pattern recognition receptors, such as DNA sensors. The interferon-inducible protein 16 (IFI16) is a nuclear DNA sensor that recognizes double-stranded DNA from a number of viral sources, including genomes of nuclear-replicating viruses such as the prevalent human pathogen, herpes simplex virus 1 (HSV-1). Upon binding to the DNA genome of HSV-1, IFI16 both induces antiviral cytokine expression and suppresses virus gene expression. Here, we use a multi-omics approach of DNA sequencing techniques paired with targeted mass spectrometry to obtain an extensive view of the interaction between IFI16 and the HSV-1 genome, and how this binding affects the viral DNA structure and protein expression. Through ChIP-seq, we find that IFI16 binds to the HSV-1 genome in a sequence-independent manner while simultaneously exhibiting broad enrichment at two loci: UL30, the viral DNA polymerase gene, and US1-US7. ATAC-seq analysis reveals that these two regions are among the most accessible stretches of DNA on the genome, thereby facilitating IFI16 binding. Accessibility of the entire HSV-1 genome is elevated upon IFI16-KO, indicating that expression of IFI16 globally induces chromatinization of viral DNA, regardless of IFI16 enrichment. Deletion of IFI16 also results in a global increase in the expression of HSV-1 proteins, as measured by parallel reaction monitoring-mass spectrometry. Altogether, we demonstrate that IFI16 interacts with the HSV-1 genome in a sequence-independent manner, and this interaction coordinates epigenetic silencing of the viral genome, resulting in decreased protein expression and virus replication.

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