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Homo sapiens

ABSTRACT: Repression of stress-induced LINE-1 expression protects cancer cell populations from lethal drug-exposures [ATAC-Seq]

PROVIDER: PRJNA392915 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5800660_1.fastq.gz	Fastqsanger.gz
	SRR5800660_2.fastq.gz	Fastqsanger.gz
	SRR5800670_1.fastq.gz	Fastqsanger.gz
	SRR5800670_2.fastq.gz	Fastqsanger.gz
	SRR5800661_1.fastq.gz	Fastqsanger.gz

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Homo sapiens

Project description:Repression of stress-induced LINE-1 expression protects cancer cell populations from lethal drug-exposures [ATAC-Seq]

| PRJNA301678 | ENA

Repression of stress-induced LINE-1 expression protects cancer cell populations from lethal drug-exposures

Project description:Repression of stress-induced LINE-1 expression protects cancer cell populations from lethal drug-exposures

| PRJNA301676 | ENA

Homo sapiens

Project description:Repression of stress-induced LINE-1 expression protects cancer cell populations from lethal drug-exposures [ChIP-Seq]

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Homo sapiens

Project description:Repression of stress-induced LINE-1 expression protects cancer cell populations from lethal drug-exposures [RNA-Seq]

| PRJNA392914 | ENA

Repression of stress-induced LINE-1 expression protects cancer cell populations from lethal drug-exposures [ATAC-Seq]

Project description:Establishing and maintaining phenotypic heterogeneity within cell and organismal populations is an evolutionarily conserved strategy that ensures survival of the population following stressful exposures. We previously identified a transient, reversible, drug-tolerant cancer cell subpopulation that survives otherwise lethal drug exposures. Here we show that these drug-tolerant persisters (DTPs) assume a highly heterochromatic state, which requires factors that modify or bind trimethylated H3 lysine 9 (H3K9me3). The increased H3K9me3 in DTPs is largely restricted to evolutionarily young Long Interspersed Repeat elements (LINEs). This transcriptionally repressive state, which decreases the expression of these retrotransposable elements, is critical for DTP survival, and disruption of this heterochromatic state results in re-expression of LINE elements and ablation of this subpopulation. Together, these findings establish a role for epigenetic silencing of transposable elements as a population survival strategy to maintain genomic integrity in subpopulations of cancer cells during lethal drug exposures.

2017-07-03 | GSE73874 | GEO

Drug-tolerant cancer cell persisters survive lethal exposures by silencing transposable elements [ChIP-Seq]

2017-07-03 | GSE74179 | GEO

Adrenal stress response is an essential host response against lethal T cell activation

Project description:Cytokine release syndrome (CRS) is a major cause of death in lethal T cell activation and presents a significant barrier for CAR-T immunotherapy or allogenic hematopoietic cell transplantation. We reported here that adrenal stress response, defined by a 5-10-fold increase in induced glucocorticoid (iGC) production, is an essential host response against lethal T cell activation. We identified scavenger receptor BI (SR-BI), a HDL receptor, as a key regulator for iGC production. Using SR-BI null mice as an adrenal stress response deficiency model, we demonstrated that adrenal stress response protects anti-CD3 induced death through keeping CRS under control and relative adrenal insufficiency (RAI) – lacking adrenal stress response, is a risk factor.

2023-04-19 | GSE179837 | GEO

Transcription profiling of mouse embryonic fibroblasts (MEF) from wild type vs CHOP-/- genotypes treated with tunicamycin reveals CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum

Project description:Primary mouse embryonic fibroblasts (pass 3 to 4) were treated with tunicamycin (2 micrograms/ml) for specified times - genotypes were WILDTYPE and CHOP-/-. Each time point n=4. C/EBP homologous protein CHOP is activated by ER stress, and CHOP deletion protects against its lethal consequences.

2007-12-11 | E-GEOD-2082 | biostudies-arrayexpress

Homo sapiens

Project description:Drug-tolerant cancer cell persisters survive lethal exposures by silencing transposable elements [ChIP-Seq]

| PRJNA301677 | ENA

Protective monocytes in cerebral ischemia

Project description:Stroke is a highly prevalent and devastating disease with limited therapeutic options. Most efforts to develop treatments for stroke have thus far met with limited success in large clinical trials. The brain has an enormous capacity for self-preservation, and elucidating how the brain protects itself may provide novel insights into stroke treatment. Ischemic tolerance (IT), a phenomenon in which application of sub-lethal stress [preconditioning (PC) stimulus; PC] induces a state of tolerance to a subsequent ischemic insult, represents an example of endogenous neuroprotection. IT can be induced in brain by systemic administration of the Toll-like receptor-4 ligand lipopolysaccharide (LPS). Different populations of immune cell could potentially play a role in PC induced by LPS. In particular, monocytes, which are the main target of LPS, can exert a powerful protective effect either directly or by modulating the immune system.

2016-07-13 | GSE84327 | GEO

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