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Genome-wide screen of transcription co-regulators identifies GLIS2 as a repressor for p53 target genes

ABSTRACT: Genome-wide screen of transcription co-regulators identifies GLIS2 as a repressor for p53 target genes

PROVIDER: PRJNA517965 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8509090_1.fastq.gz	Fastqsanger.gz
	SRR8509090_2.fastq.gz	Fastqsanger.gz
	SRR8509550_1.fastq.gz	Fastqsanger.gz
	SRR8509550_2.fastq.gz	Fastqsanger.gz
	SRR8509560_1.fastq.gz	Fastqsanger.gz

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Genome-wide screen of transcription co-regulators identifies GLIS2 as a repressor for p53 target genes [RNA-seq]

Project description:GLIS2, a member of the sub-family of Krüppel-like zinc finger proteins, has been linked to the development of nephronophthisis, while few studies have been conducted on the connection between tumorigenesis and GLIS2. In the current study, we identified GLIS2 as a repressor for p53 target genes, such as PUMA. GLIS2 ChIP-seq demonstrated that GLIS2 binds directly on PUMA promoter. In addition, GLIS2 inhibits the binding of p53 on PUMA promoter region and the modification of H3K27ac on PUMA enhancer. Taken together, GLIS2 is identified as an oncogene in colorectal cancer.

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Genome-wide screen of transcription co-regulators identifies GLIS2 as a repressor for p53 target genes [RNA-seq]

Project description:Genome-wide screen of transcription co-regulators identifies GLIS2 as a repressor for p53 target genes [RNA-seq]

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Genome-wide screen of transcription co-regulators identifies GLIS2 as a repressor for p53 target genes

Project description:This SuperSeries is composed of the SubSeries listed below.

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Identification of ETO2-GLIS2 targets by ChIP-sequencing

Project description:Acute megakaryoblastic leukemia (AMKL) is a subtype of leukemia primarily diagnosed in childhood and generally associated with poor prognosis. Genetic alterations found in de novo childhood AMKL include the OTT-MAL fusion, MLL and NUP98 fusions and the recently identified ETO2-GLIS2 fusion that involves two transcriptional regulators. In order to identify ETO2-GLIS2-bound regions as well as the chromatin landscape in human AMKL cells, we performed ChIP-seq analyses in AMKL MO7E cell line and in AMKL patient derived cells. Since existing GLIS2 antibodies could not successfully pull-down ETO2-GLIS2, we introduced the GFP at the endogenous GLIS2 loci in the MO7E cell line using a CRISPR/Cas9 approach to obtain physiological expression of a GFP-tagged ETO2-GLIS2 (MO7e-KI cell line). ChIP-seq were performed using antibody against GFP and ETO2 to identify ETO2-GLIS2-bound regions, against ERG to investigate colocalization and against chromatin marks to highlight repressed (H3K27me3) and active (H3K4me3: promoters; H3K27Ac, H3K4me1: enhancers) regions.

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