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Mus musculus

ABSTRACT: Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [H3.3 ChIP]

PROVIDER: PRJNA391903 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5755600.fastq.gz	Fastqsanger.gz
	SRR5755610.fastq.gz	Fastqsanger.gz
	SRR5755601.fastq.gz	Fastqsanger.gz
	SRR5755611.fastq.gz	Fastqsanger.gz
	SRR5755602.fastq.gz	Fastqsanger.gz

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Mus musculus

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

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Mus musculus

Project description:Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [ATAC-seq]

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Mus musculus

Project description:Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [RNA-seq]

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Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin

Project description:Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin

| PRJNA391898 | ENA

Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [RNA-seq]

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 | GSE100464 | GEO

Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [H3.3 ChIP]

2017-12-31 | GSE100463 | GEO

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

2017-12-31 | GSE100462 | GEO

Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [ATAC-seq]

2017-12-31 | GSE100461 | GEO

G-quadruplex stabilizer CX-5461 effectively combines with ionizing radiation to selectively target ATRX-deficient malignant glioma

Project description:Mutational inactivation of ?-thalassaemia/mental retardation X-linked (ATRX) represents a defining molecular feature in large subsets of adult and pediatric malignant glioma. ATRX deficiency gives rise to abnormal G-quadruplex (G4) DNA secondary structures at GC-rich regions of the genome, altering chromatin accessibility and enhancing DNA damage. Building on earlier work, we sought to assess the extent to which pharmacological G4 stabilization selectively enhances DNA damage and cell death in preclinical models of ATRX-deficient glioma. In this study, we assessed the extent to which G4 stabilization impacted genome-wide deposition of H3.3 in patient-derived glioma stem cells (GSCs). In order to evaluate the overlap of these H3.3 deposition sites with regions of the genome that bind ATRX, we performed cleavage under targets and tagmentation (CUT&Tag) for ATRX using GSC line TS 543. Our analyses show that G4 stabilizer CX-541 disrupts H3.3 deposition at regions of the genome that frequently bind ATRX.

2025-05-29 | GSE276481 | GEO

G-quadruplex stabilizer CX-5461 effectively combines with ionizing radiation to selectively target ATRX-deficient malignant glioma [CUT&Tag]

Project description:Mutational inactivation of ?-thalassaemia/mental retardation X-linked (ATRX) represents a defining molecular feature in large subsets of adult and pediatric malignant glioma. ATRX deficiency gives rise to abnormal G-quadruplex (G4) DNA secondary structures at GC-rich regions of the genome, altering chromatin accessibility and enhancing DNA damage. Building on earlier work, we sought to assess the extent to which pharmacological G4 stabilization selectively enhances DNA damage and cell death in preclinical models of ATRX-deficient glioma. To investigate the effect of G4 stabilization on histone variant H3.3 deposition on the genome, we treated patient-derived glioma stem cells (GSCs) with G4 stabilizer CX-5461 and performed cleavage under targets and tagmentation (CUT&Tag) for H3.3. Our analyses show that G4 stabilizer CX-541 disrupts H3.3 deposition in ATRX-deficient GSCs and likely enhances replication stress and DNA damage.

2024-03-18 | GSE261562 | GEO

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