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Expression data from glioblastoma cells after ZFHX4 or CHD4 suppression.

ABSTRACT: ZFHX4 and CHD4 suppression independently shift tumor initiating cells out of a stem like state and toward a differentiated morphology. After gene suppression via transduction of a lentivirally mediated shRNA construct, RNA was extracted 3 and 5 days later and was hybridized on Affymetrix microarrays.

ORGANISM(S): Homo sapiens

PROVIDER: GSE52363 | GEO | 2014/01/16

SECONDARY ACCESSION(S): PRJNA227498

REPOSITORIES: GEO

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Expression data from glioblastoma cells after ZFHX4 or CHD4 suppression.

Project description:ZFHX4 and CHD4 suppression independently shift tumor initiating cells out of a stem like state and toward a differentiated morphology. After gene suppression via transduction of a lentivirally mediated shRNA construct, RNA was extracted 3 and 5 days later and was hybridized on Affymetrix microarrays. Total RNA was extracted 3 and 5 days after shRNA transduction of 0308 TICs, for 3 (for CHD4) or 5 (ZFHX4) independent experiments. Complementary RNA synthesis and hybridization/scanning of U133 plus 2.0 microarrays using GeneChip products (Affymetrix) was done as described in the GeneChip manual.

2014-01-16 | E-GEOD-52363 | biostudies-arrayexpress

ZFHX4 and CHD4 ChIP sequencing in glioblastoma tumor initiating cells

Project description:Glioblastomas (GBM) harbor subpopulations of therapy-resistant tumor initiating cells (TICs) that are self-renewing and multipotent. To understand the regulation of the TIC state, we performed an image-based screen for genes regulating GBM TIC maintenance and identified ZFHX4, a 397-kDa transcription factor. ZFHX4 is required to maintain TIC-associated phenotypes in vitro, suggesting that ZFHX4 regulates TIC differentiation, and its suppression increases glioma-free survival in intracranial xenografts. ZFHX4 interacts with CHD4, a core member of the NuRD (nucleosome remodeling and deacetylase) complex. ZFHX4 and CHD4 bind to overlapping sets of genomic loci and control similar gene expression programs. Using expression data derived from GBM patients, we demonstrate ZFHX4 is a master regulator of CHD4-mediated gene expression. These observations define ZFHX4 as a regulatory factor that links the chromatin remodeling NuRD complex and the GBM TIC state. Examination of binding of ZFHX4 and CHD4 across the human genome, using the 0308 tumor initiating cell line. Two replicates for each protein, compared to whole cell extract inputs.

2014-01-16 | E-GEOD-52419 | biostudies-arrayexpress

ZFHX4 and CHD4 ChIP sequencing in glioblastoma tumor initiating cells

2014-01-16 | GSE52419 | GEO

Homo sapiens

Project description:ZFHX4 and CHD4 ChIP sequencing in glioblastoma tumor initiating cells

| PRJNA228347 | ENA

Homo sapiens

Project description:Expression data from glioblastoma cells after ZFHX4 or CHD4 suppression.

| PRJNA227498 | ENA

RNA-seq analysis of THP-1 cell line upon knockdown of CHD4

Project description:Epigenetic alterations contribute to leukemogenesis in childhood acute myeloid leukemia (AML). We used RNAi screens of AML cells together with non-transformed bone marrow cells and identified CHD4 as being required for AML maintenance. RNAi and CRISPR-Cas9 approaches, showed that CHD4 is essential for cell growth of leukemic cells in vitro, and disease progression in vivo, including primary childhood AML cells. Loss of function of CHD4 arrests AML cells in the G0 phase of the cell cycle, which is associated with downregulation of MYC and its target genes. Conversely, CHD4 suppression is not essential for normal blood cells. Taken together, our results identify CHD4 as a potential therapeutic target in childhood AML.

2018-11-01 | GSE106392 | GEO

Expression data from glioblastoma cells after ZFHX4 or CHD4 suppression

| S-ECPF-GEOD-52363 | biostudies-other

Chd4 deficiency effect on mouse embryonic stem cells

Project description:Our study reveal that Chd4 is essential for stemness maintenance of ESCs. As Chd4 deficient ESCs show attentuated self-renewal ability and induced differentiation marker gene expression. To confirm the effect of Chd4 on the transcriptome profile of ESCs, we performed microarray analyses for Chd4 deficient ESCs.

2017-05-01 | GSE89675 | GEO

Chd4 controls Ripk3 dependent necroptosis during muscle regeneration

Project description:We performed a label-free LC-MS/MS study to analyse the role of Chd4 regulation in MuSC in suppressing genes enabling programmed cell death as part of the muscle regeneration program. Lox-cre recombination was used to create a deletion mutant of the CHD4 chromatin modifier (exons 12-21). A pseudo "infection" with GFP was used as control. Proteomics analysis here serves as a method to compare the differentially deregulated proteins upon knockdown of Chd4 in MuSCs using Adenoviral CRE recombination.

2020-04-02 | PXD010370 | Pride

Transcriptome of E18.5 CHD4-M195I mouse hearts

Project description:Purpose: The goal of this study is to compare the cardiac transcriptome profiling (RNA-seq) of WT and CHD4-M195I hearts at E18.5 to conclude genes affected by this CHD4 mutation. Methods: mRNA profiles of E18.5 WT and CHD4-M195I mouse hearts were generated by deep sequencing, n=4 for each genotype, using Illumina HiSeq2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: RNA-sequencing (RNA-seq) analyses on E18.5 WT and CHD4-M195I hearts and identified 323 genes that were differentially expressed [adjusted P value <0.05, |log2(Fold Change)| > 0.5], 113 upregulated and 210 downregulated in CHD4-M195I hearts.

2023-05-08 | GSE229050 | GEO

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