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CHD4 remodels cellular chromatin accessibility and activates c-Myc pathway via phase separation in multiple myeloma

ABSTRACT: CHD4 remodels cellular chromatin accessibility and activates c-Myc pathway via phase separation in multiple myeloma

PROVIDER: PRJNA1201201 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31795918_1.fastq.gz	Fastqsanger.gz
	SRR31795918_2.fastq.gz	Fastqsanger.gz
	SRR31795919_1.fastq.gz	Fastqsanger.gz
	SRR31795919_2.fastq.gz	Fastqsanger.gz

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CHD4 remodels cellular chromatin accessibility and activates c-Myc pathway via phase separation in multiple myeloma

Project description:Multiple myeloma (MM) is an incurable hematologic malignancy, which is inherently related to chromatin abnormalities. Chromatin remodeling factors play an important role in the regulation of chromatin abnormalities, among which chromodomain-helicase-DNA-binding protein 4 (CHD4) was positive-associated with poor outcomes in MM patients and an elevated level of CHD4 promoted MM cell proliferation. Mechanistically, CHD4 untwisted c-Myc G4 and regulated chromatin accessibility through ATPase domain. Additionally, CHD4 recruited c-Myc though chromatin domain and stabilized c-Myc to chromatin by liquid–liquid phase separation, which up-regulated the expression of c-Myc. Furthermore, Luteolin 7-O-glucuronide and Idarubicin were identified as potential drugs targeting ATPase domain and chromatin domain for MM by a de novo design. Our study highlights the role of CHD4 as a high-risk gene in MM and suggests that remodels cellular chromatin accessibility and activates c-Myc pathway via phase separation in MM.

2024-12-25 | GSE285112 | GEO

CHD4 remodels cellular chromatin accessibility and activates c-Myc pathway

Project description:To investigate whether there is a physiological interaction between CHD4 and c-Myc, we conducted MS and found that CHD4 interacted with c-Myc.

2024-12-12 | PXD058803 |

ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression [ChIP-Seq]

Project description:Metazoan transcription factors typically regulate large numbers of genes. Here we identify via a CRISPR-Cas9 genetic screen ZNF410, a pentadactyl DNA binding protein that in human erythroid cells directly and measurably activates only one gene, the NuRD component CHD4. Specificity is conveyed by two highly evolutionarily conserved clusters of ZNF410 binding sites near the CHD4 gene with no counterparts elsewhere in the genome. Loss of ZNF410 in adult type human erythroid cell culture systems and xenotransplant settings diminishes CHD4 levels and derepresses the fetal hemoglobin genes. While previously known to be silenced by CHD4, the fetal globin genes are exposed here as among the most sensitive to reduced CHD4 levels. In vitro DNA binding assays and crystallographic studies reveal the ZNF410-DNA binding mode. ZNF410 is a remarkably selective transcriptional activator in erythroid cells whose perturbation might offer new therapeutic opportunities in the treatment of hemoglobinopathies.

2020-12-09 | GSE154960 | GEO

ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression [RNA-Seq]

2020-12-09 | GSE154961 | GEO

CD138-positive cell separation affects cancer gene expression in human myeloma cell lines

Project description:Gene expression (GE) profiling of multiple myeloma (MM) cells is a promising means of identifying high-risk MM patients. The analyses depend on plasma cell purification by CD138+ cell separation. Considering the sensitivity of gene transcription, we wanted to test if cell separation distorts true in vivo GE patterns. We performed a controlled study of running 4 human myeloma cell lines (HMCLs: U266, INA-6, RPMI 8226, and NCI H929) through a CD138+ separation procedure identical to the handling of clinical samples. We then compared the resulting effects on gene expression. Using U266 as a screening model, we performed global GE analysis using the Affymetrix Human Gene 1.0 ST array. Sample cells showed significant changes (adj. p<0,05) in 670 genes compared to the non-separated controls. We searched for upregulated genes of myeloma and/or cancer relevance and chose (in decending fold change order) FOS, DUSP1, MIRN21, NFKBIA, and ATF4 for PCR validation. Note: Only U266 cells were used for microarray analysis. The other cell lines were used later to validate the array results.

2012-03-01 | E-MEXP-2961 | biostudies-arrayexpress

ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression

Project description:ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression

| PRJNA648059 | ENA

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

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

ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression [ChIP-Seq]

Project description:ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression [ChIP-Seq]

| PRJNA648058 | ENA

ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression [RNA-Seq]

Project description:ZNF410 uniquely activates the NuRD component CHD4 to silence fetal hemoglobin expression [RNA-Seq]

| PRJNA648061 | ENA