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Glucose deprivation induced gene expression

ABSTRACT: Glucose deprivation induced gene expression

PROVIDER: PRJNA668528 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15210159.fastq.gz	Fastqsanger.gz
	SRR15210160.fastq.gz	Fastqsanger.gz

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Function of YAP in glucose deprivation-induced gene expression

Project description:Function of YAP in glucose deprivation-induced gene expression

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Function of YAP in glucose deprivation-induced gene expression

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Single six hours sleep deprivation causes glucose intolerance and hepatic steatosis.

Project description:To assess the effect of sleep deprivation on glucose metabolism and elucidate the mechanism, we established the mouse model wth C57BL/6J that is useful for the intervention on sleep deprivation associated diabetes and evaluate the liver metabolism and gene expression. Single six hours sleep deprivation induced increased hepatic glucose production assessed by pyruvate tolerance test and the hepatic triglyceride content was significantly higher in the sleep deprivation group than freely sleeping control group. Liver metabolites such as ketone bodies were increased in sleep deprivation group. Some gene expressions which associated with lipogenesis were increased.

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KMT2D regulates gene expression through regulating promoters/enhances upon glucose deprivation.

Project description:KMT2D regulates gene expression through regulating promoters/enhances upon glucose deprivation.

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Glucose deprivation induced gene expression

Project description:Glucose is the main substrates of cancer cell metabolism. Relying on glucose for rapid proliferation and maintaining intracellular redox homeostasis is one of the hallmarkers of cancer cells. During physiology or cancer treatment, cancer cells will face a limited supply of glucose. In these case, cancer cells will undergo cell death . The plasticity of cancer cells is the main factor that allows cancer cells to survive this difficult situation. So in order to better understand the cplasticity of cancer cells, we use glucose-free medium to treat the colorectal cancer cell line HCT116, and perform RNA-Seq analysis on the treated samples.

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Role of 4EBP1/2 in the response to glucose deprivation

Project description:We investigated the function of the mTORC1 substrates and mRNA translation regulators 4EBP1/2 in the response to glucose deprivation. We uncovered that targeting 4EBP1/2 expression had a direct impact on the survival rates of cells challenged with glucose deprivation. To further define the mechanisms underlying 4EBP1/2 function under glucose deprivation, we conducted a proteomics analysis of HEK293 shRNA control and HEK293 shRNA 4EBP1/2 grown in basal media or under glucose deprivation (1 mM glucose containing media) for 30 hours.

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Gene expression profile of microglial cells under oxygen-glucose deprivation

Project description:Migroglia cells were exposed to oxygen-glucose deprivation (OGD) for 3 h. The mRNA was isolated and the expression profiles of OGD-activated cells were compared with the profiles of resting cells.

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Expression data from human astrocytes (HA) under oxygen-glucose deprivation / reoxygenation

Project description:Ischemia lead to neuronal injury. Dexmedetomidine and astrocytes are likely to protect neuronal cells against ischemia-induced injury. We used microarrays to examine the gene expression variation in astrocytes activated by oxygen-glucose deprivation and reoxygenation stress and identified distinct classes of genes up- and down-regulated by dexmedetomidine pretreatment.

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The vulnerability of actin cytoskeleton to disulfide stress dictates high SLC7A11-driven cell death upon glucose deprivation

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