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Impaired gene expression in ATRX-depleted cells following interferon signaling

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

PROVIDER: PRJNA800422 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17737166_1.fastq.gz	Fastqsanger.gz
	SRR17737166_2.fastq.gz	Fastqsanger.gz
	SRR17737167_1.fastq.gz	Fastqsanger.gz
	SRR17737167_2.fastq.gz	Fastqsanger.gz
	SRR17737168_1.fastq.gz	Fastqsanger.gz

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

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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.

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

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Quantitative Analysis of Telomeric Nucleosomal Compaction following ATRX Depletion

Project description:Quantitative Analysis of Telomeric Nucleosomal Compaction following ATRX Depletion

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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.

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

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Impaired interferon-γ signaling promotes the development of silicosis

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Quantitative Analysis of Transcriptional Changes in Atrx Conditional Knockout Mice

Project description:ATP-dependent chromatin remodeling protein ATRX is an essential regulator involved in maintenance of DNA structure and chromatin state and regulation of gene expression during development. However, the impact of ATRX during early skeletal development has not been examined. To understand the underlying mechanisms that impaired osteoclast differentiation, we performed RNA-seq on the tibias harvested from control and Atrx cKO mice at 8 weeks of age.

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Atrx deletion impairs cGAS-STING signaling and increases response to radiation and oncolytic herpesvirus in soft tissue sarcoma

Project description:RNA sequencing of 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.

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Project description:Stimulating the innate immune system has been explored as a therapeutic option for the treatment of gliomas. Inactivating mutations in ATRX, a defining molecular alteration in IDH-mutant astrocytomas, have been implicated in dysfunctional immune signaling. However, little is known about the interplay between ATRX loss and IDH mutation on innate immunity. To explore this biology, we generated ATRX knockout glioma models in the presence and absence of the IDH1R132H mutation. ATRX-deficient glioma cells were sensitive to dsRNA-based innate immune agonism and exhibited impaired lethality and increased T-cell infiltration in vivo. However, the presence of IDH1R132H dampened baseline expression of key innate immune genes and cytokines in a manner restored by genetic and pharmacological IDH1R132H inhibition. IDH1R132H co-expression did not interfere with the ATRX KO-mediated sensitivity to dsRNA. Thus, ATRX loss primes cells for recognition of dsRNA, while IDH1R132H reversibly masks this priming. This work reveals innate immunity as a therapeutic vulnerability of astrocytoma.

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