Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional Profiling of NASH mice with hepatocyte-specific knock down of Elf3 or Glis2

ABSTRACT: We performed RNA-seq of livers obtained from mice fed either a control or the NASH-inducing FPC diet (Wang et al., 2016) for 24wk. In some FPC-fed mice the NASH-activated transcription factors, Elf3 or Glis2, had been deleted specifically in hepatocytes, when mice reached a steatotic state.

ORGANISM(S): Mus musculus

PROVIDER: GSE162869 | GEO | 2021/07/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptional Profiling of NASH mice with hepatocyte-specific knock down of Elf3 or Glis2

Project description:Transcriptional Profiling of NASH mice with hepatocyte-specific knock down of Elf3 or Glis2

| PRJNA683618 | ENA

Fibrosis-activated transcriptional networks govern hepatocyte reprogramming and intra-hepatic communication in metabolic associated liver fibrosis

Project description:Liver fibrosis is a strong predictor of long-term mortality in patients with non-alcoholic fatty liver disease; yet the mechanisms underlying the progression from the comparatively benign fatty liver state to advanced non-alcoholic steatohepatitis (NASH) and liver fibrosis are incompletely under-stood. Using a cell type-resolved genomics approach, we show that comprehensive alterations in hepatocyte genomic and transcriptional settings during NASH progression, led to a partial loss of hepatocyte identity. The hepatocyte reprogramming was under tight cooperative control of a net-work of NASH-activated transcription factors (TFs), as exemplified by Elf3 and Glis2. Indeed, Elf3 and Glis2 controlled hepatocyte identity and fibrosis-dependent hepatokine genes targeting disease-associated hepatic stellate cell (HSC) gene programs. Thus, interconnected TF networks not only promoted hepatocyte dysfunction, but also directed the intra-hepatic crosstalk with HSCs necessary for NASH and fibrosis progression implying molecular “hub-centered” targeting strategies to be superior to existing mono-target approaches as currently used in NASH therapy.

2021-07-13 | PXD025691 | Pride

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

Expression profiling analysis of an inducible ELF3-expressing and control human bile duct cells [inducible ELF3]

Project description:An immortalized normal epithelial cell line of common bile duct origin (HBDEC2 cells) was established. An inducible ELF3-expressing was generated by infection with the retrovial vector pRetroX-TetOne-Puro-ELF3-flag, expressing ELF3 fused to a flag-tag.

2020-08-27 | GSE148107 | GEO

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

Impact of dietary cholesterol on Macrophages during non-alcoholic steatohepatitis progression

Project description:Inflammation, mediated by liver-resident Kupffer cells (KCs) and recruited infiltrating macrophages (IMs), plays a critical role in NAFLD pathogenesis. Cholesterol induces pro-inflammatory cytokine production by macrophages and has been identified as a key factor involved in progression from simple steatosis to NASH. In this study, using the fructose, palmitate, cholesterol & trans-fat (FPC) diet model which recapitulates human NAFLD, we aimed to determine the impact of cholesterol manipulation on NAFLD progression/regression and macrophage phenotype in vivo.The transcriptomic evaluation of hepatic macrophages from mice fed with FPC diet contained the highest concentration of cholesterol (1.25%) suggest these cells might contribute to liver inflammation, steatohepatitis, and hepatocarcinoma pathways during the progression phase.

2022-08-23 | GSE205776 | GEO

RNA-Seq and ChIP-Seq profiling of ELF3, an prion-like domain-containig in ELF3 that functions as a thermosensor in Arabidopsis.

Project description:Temperature is a major environmental variable governing plant growth and development. ELF3 contains a polyglutamine (polyQ) repeat 8–10, embedded within a predicted prion domain (PrD). We find the length of the polyQ repeat correlates with thermal responsiveness. Plants from hotter climates appear to have lost the PrD domain, and these versions of ELF3 are stable at high temperature and lack thermal responsiveness. ELF3 temperature sensitivity is also modulated by the levels of ELF4, indicating that ELF4 can stabilise ELF3 function. This RNA-Seq dataset provides evidence for the hypothetical ELF3 function of temperature sensing .

2020-06-21 | GSE137264 | GEO

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

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