Differential gene expression in Glis2 knckdown tubular cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA554802 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Immortalized kidney tubular cells were obtained from immortomice. The gene Glis2 was knocked down by adenoviral-mediated infectipon of specific shRNAs
2019-09-04 | GSE134338 | GEO
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. Keywords: Glis2, kidney, fibrosis, nephropathy, inflammation
2009-01-01 | GSE8454 | GEO
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
Project description:Loss of function of the transcription factor GLIS2 in humans and mice causes nephronophthisis (NPHP). To obtain insights into the role of GLIS2 in the regulation of normal kidney functions and in the development of NPHP, we investigated GLIS2 direct target genes in kidney. Due to a lack of suitable GLIS2 antibody for chromatin immunoprecipitation (ChIP), we generated Glis2-HA mice in which HA tag was inserted before the TGA stop codon of GLIS2. Thereby, endogenous GLIS2 protein is expressed as a fusion protein with HA tag. GLIS2 ChIP-Seq was performed using HA antibody with kidneys from Glis2-HA mice. GLIS2 cistrome analysis identified many of genes associated with inflammation, ECM, and cell adhesion as direct targets by GLIS2.
2026-04-02 | GSE282341 | GEO
Project description:Eradication of chemotherapy-resistant leukemia stem cells is expected to improve treatment outcomes in patients with acute myelogenous leukemia (AML). In a mouse model of AML expressing the MOZ-TIF2 fusion, we found that Ring1A and Ring1B, components of Polycomb repressive complex 1, play crucial roles in maintaining AML stem cells. Deletion of Ring1A and Ring1B (Ring1A/B) from MOZ-TIF2 AML cells diminished self-renewal capacity and induced the expression of numerous genes including Gli-similar 2 (Glis2). Overexpression of Glis2 caused MOZ-TIF2 AML cells to differentiate into mature cells, whereas Glis2 knockdown in Ring1A/B-deficient MOZ-TIF2 cells inhibited differentiation. Thus, Ring1A/B regulates and maintains AML stem cells in part by repressing Glis2 expression, which promotes their differentiation. These findings provide new insights into the mechanism of AML stem cell homeostasis and reveal novel targets for cancer stem cell therapy.
2017-01-06 | GSE93214 | GEO
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
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
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
Project description:Profiling of H3K27ac in ETO2-GLIS2 positive AMKL cells and ETO2-GLIS2 binding
| PRJNA543772 | ENA
Project description:To characterize the consequences of cytokine stimulation, we compared ET02-GLIS2 expressing cells from different origins by single cell transcriptomes (scRNAseq). We analysed FL and CB ET02-GLIS2-expressing CD34+ progeny after 7 days in vitro, human cells from diseased NSG (FL- and FBM-derived) and NSGS (CB- and FL-derived) recipients.
2024-10-08 | E-MTAB-14140 | biostudies-arrayexpress