Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE125927 | GEO | 2020/05/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

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.

2020-05-01 | GSE125920 | GEO

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

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

| PRJNA517965 | ENA

Identification of ETO2-GLIS2 transcriptional targets

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 target genes, we performed two approaches: 1-Ectopic expression of ETO2-GLIS2, ETO2, GLIS2 and OTT-MAL in HEL cells, which does not endogenously express AMKL fusion oncogenes. Transduced cells marked by expression of the GFP were sorted by flow cytometry 24 hours after transduction and RNA was extracted with the Qiagen Rneasy kit including DNase treatment. 2-Expression of a small peptide (NC128), which interferes with the dimerization and cofactor recruitment by the ETO2-GLIS2 fusion, within MO7E cells derived from an AMKL patient and expressing endogenously the ETO2-GLIS2 fusion. Transduced cells marked by expression of the GFP were sorted by flow cytometry 7 days after transduction and RNA was extracted with the Qiagen Rneasy kit including DNase treatment. After quantification of biological replicates, and quality control (Bioanalyser, Agilent), RNA were hybridized on Agilent arrays as indicated below.

2017-05-05 | E-MTAB-4332 | biostudies-arrayexpress

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.

2017-05-22 | E-MTAB-4367 | biostudies-arrayexpress

Changes in gene expression in kidneys from Glis2-deficient mice

2009-01-01 | GSE8454 | GEO

Transcription profiling of mouse kidneys from Glis2-deficient animals

Project description:Glis2 is a member of the Gli-similar (Glis) subfamily of Kruppel-like zinc finger transcription factors. To obtain insights into the physiological functions of Glis2, mice deficient in Glis2 expression were generated. These mutant mice develop progressive renal disease associated with fibrosis and inflammation. Gene expression profiles were examined to identify changes in gene expression at early stages of progressive renal disease in Glis2 mutant mice. Experiment Overall Design: To analyze changes in gene expression, microarray analysis was performed using RNA from kidneys of PND25 and PND60 wild type and Glis2-mutant mice. Experiment Overall Design: Gene expression profiles were compared between kidneys of PND25 wt and Glis2 mutant mice and between PND60 wt and Glis2 mutants. RNA from three kidneys were pooled. RNA from two independent experiments was used and each microarray analysis was performed in duplicate.

2009-01-14 | E-GEOD-8454 | biostudies-arrayexpress

Transcriptome of HEL cells with inducible expression of ETO2-GLIS2

Project description:These data were generated to investigate the impact on the gene expression of the chimeric transcription factor CBFA2T3-GLIS2 (a.k.a ETO2-GLIS2 and abbreviated here as EG) which is associated with pediatric leukemia (LAM7), to assess the functional roles of several domains of this protein (the ETO2 and GLIS2 moiety) on the gene dysregulation induced by EG through the generation of several mutants (deleted for the NHR2 domain of ETO2: dNHR2 or with a C265G mutation in the GLIS2 moiety: C265G). The different EG forms were cloned into a doxycycline-inducible lentiviral vector and transcriptomes were performed 24 hours post doxycycline induction.

2022-12-31 | E-MTAB-12255 | biostudies-arrayexpress

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]

| PRJNA517954 | ENA

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

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

| PRJNA517964 | ENA

IPSC model of ETO2-GLIS2 expression

Project description:To characterize the molecular consequences of ETO2-GLIS2 expression in iPSC-derived cells, we performed a transcriptome analysis on control and two ETO2-GLIS2 clones at day18 of differentiation. From the control, the CD41+CD42- and CD41+CD42+ populations were sorted to obtain normal immature progenitors and maturing megakaryocytes. From ETO2-GLIS2-expressing cells, CD41+CD42+ and the aberrant CD41lowCD42low were analyzed.Whole transcriptome sequencing (WTS) was performed using Illumina Nextseq500 platform. cDNA libraries were synthesized from 250 ng total RNA using the TruSeq Stranded mRNA kit (Illumina) following manufacturers’ instructions. Briefly, poly-A containing mRNA molecules were reverse transcribed to double stranded cDNA fragments that were then adenylated at 3' ends and ligated to single-index adapters. PCR-enriched libraries were then quantified by Quant-It picogreen assay (Thermo-Fisher) and sized with the High Sensitivity kit on the 2100 Bioanalyzer (Agilent Technologies). Sequencing was performed at 2x80bp using Illumina Sequencing by synthesis (SBS) technology.

2020-04-27 | E-MTAB-7967 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data