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Alterations in chromatin accessibility in ATRX-depleted cells following interferon signaling

ABSTRACT: Alterations in chromatin accessibility in ATRX-depleted cells following interferon signaling

PROVIDER: PRJNA800424 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17737122_1.fastq.gz	Fastqsanger.gz
	SRR17737122_2.fastq.gz	Fastqsanger.gz
	SRR17737123_1.fastq.gz	Fastqsanger.gz
	SRR17737123_2.fastq.gz	Fastqsanger.gz
	SRR17737124_1.fastq.gz	Fastqsanger.gz

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Alterations in chromatin accessibility in ATRX-depleted cells following interferon signaling

Project description:We investigated the role of the chromatin remodeling protein ATRX on chromatin accessibility specifically upon IFN-β stimulation utilizing stable ATRX knockdown cells.

2022-08-03 | GSE194395 | GEO

Impaired gene expression in ATRX-depleted cells following interferon signaling

Project description:Impaired gene expression in ATRX-depleted cells following interferon signaling

| PRJNA800422 | ENA

Impaired gene expression in ATRX-depleted cells following interferon signaling

Project description:We investigated the role of the chromatin remodeling protein ATRX on ISG expression upon stimulation with IFN-β utilizing doxycycline-inducible ATRX knockdown cells.

2022-08-03 | GSE194396 | GEO

Quantitative Analysis of Telomeric Nucleosomal Compaction following ATRX Depletion

Project description:The goal of this experiment is to determine the effect of ATRX depletion on telomeric chromatin compaction. We adapted the ATAC-seq to quantify telomere chromatin accessibility. By scoring the ratio of sequence reads that contained 3 - 12 tandem telomeric repeats over the total number of reads in wild-type and ATRX deplted cells, our analysis revealed that CRISPR/Cas9-mediated ATRX depletion induces a progressive telomere de-compaction.

2019-08-26 | GSE130640 | GEO

ATRX reduces the accessibility of HCMV genomes during lytic infections

Project description:We investigated the role of the chromatin remodeling protein ATRX on chromatin accessibility of HCMV genomes during the IE phase of lytic infections

2024-08-28 | GSE262839 | GEO

Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [Atrx ChIP]

Project description:The chromatin regulator ATRX is inactivated in large subsets of adult and pediatric glioma. Whether and how ATRX deficiency promotes oncogenesis by epigenomic dysregulation remains unclear. We found that Atrx loss, especially when coupled with Tp53 inactivation, promoted cell motility and modulated differentiation state in primary murine neuroepithelial progenitors, recapitulating characteristic disease phenotypes and molecular features. Moreover, Atrx deficiency induced widespread shifts in chromatin accessibility, histone composition, and gene transcription at vacant Atrx binding sites distributed across the genome. Finally, target genes mediating Atrx-deficient phenotypes in vitro exhibited similarly selective misexpression in ATRX-mutant human glioma tissues and cell lines. These findings demonstrate that, in appropriate physiological contexts, ATRX deficiency and its epigenomic sequelae are sufficient to induce disease-defining oncogenic phenotypes.

2017-12-31 | GSE100462 | GEO

ATRX reduces the accessibility of HCMV genomes during lytic infections

Project description:ATRX reduces the accessibility of HCMV genomes during lytic infections

| PRJNA1093462 | ENA

ATRX promotes heterochromatin formation to protect cells from G-quadruplex DNA-mediated stress [ATAC-Seq]

Project description:We analyze the contribution of ATRX, DAXX and HIRA to the chromatin accessibility at G-quadruplex in mESC We analyze the contribution of ATRX and ESET to the chromatin accessibility at G-quadruplex in mESC

2021-05-17 | GSE151053 | GEO

RNA-sequencing of primary soft tissue sarcomas and cell lines with ATRX deletion

Project description:RNA sequencing of a primary tumors from a sarcoma genetically engineerted mouse model with activation of oncogenic Kras, deletion of p53 and deletion of Atrx, as compared to control sarcomas with identical genetic alterations but with wild-type Atrx. Tumors were either untreated or recieved 20 Gy of ionizing radiation and were harvested at 4 hrs, 3 day, or 6 day timepoints post treatment. For cell lines, isogenic ATRX wild-type (WT) and ATRX knockout (KO) paired isogenic cell lines treated with either 1.)interferon stimulatory DNA (ISD) and harvested 24 hours after treatment, 2)4 Gy ionizing radiation and harvested 36 hours after treatment, or 3) untreated control. These experiments help determine the differential impact of ATRX mutational status on cGAS-STING and type-I interferon signaling in soft tissue sarcoma.

2021-03-06 | GSE167537 | GEO

ATRX guards against aberrant differentiation in mesenchymal progenitor cells [CUT&RUN]

Project description:Alterations in the tumor suppressor ATRX are recurrently observed in several cancer types including sarcomas, which are mesenchymal neoplasms. ATRX has multiple epigenetic functions including heterochromatin formation and maintenance and regulation of transcription through modulation of chromatin accessibility. Here, we show in murine mesenchymal progenitor cells (MPCs) that Atrx deficiency aberrantly activated mesenchymal differentiation programs. This includes adipogenic pathways where ATRX loss induced expression of adipogenic transcription factors (Pparγ and Cebpα) and enhanced adipogenic differentiation in response to differentiation stimuli. These changes are linked to loss of heterochromatin near mesenchymal lineage genes together with increased chromatin accessibility and gains of active chromatin marks at putative enhancer elements and promoters. Finally, we observed depletion of H3K9me3 at transposable elements, which are derepressed including near mesenchymal genes where they could serve as regulatory elements. Our results demonstrate ATRX functions to buffer against differentiation in mesenchymal progenitor cells, which has implications for understanding ATRX loss of function in sarcomas.

2024-03-13 | GSE252531 | GEO

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