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Chip sequencing after ER stress induced in HCC cells using tunicamycin

ABSTRACT: Chip sequencing after ER stress induced in HCC cells using tunicamycin

PROVIDER: PRJNA861140 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20403489.fastq.gz	Fastqsanger.gz
	SRR20403490.fastq.gz	Fastqsanger.gz
	SRR20403491.fastq.gz	Fastqsanger.gz
	SRR20403492.fastq.gz	Fastqsanger.gz
	SRR20403493.fastq.gz	Fastqsanger.gz

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Tunicamycin induced ER stress in liver of C57Bl/6N mice

Project description:ER stress could affect many tissues, especially liver, in which non-alcoholic fatty liver disease, liver steatosis, etc. have been reported relative. But there still lack systematic insight into ER stress in liver, which can be obtained by transcriptomics of the tissue. Here, tunicamycin was utilized to induce ER stress in C57BL/6N mice. And microarray was performed to get the transcriptome alteration. Microarray of liver from tunicamycin-injected C57Bl/6N mice

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Project description:Endoplasmic reticulum (ER) stress, a disruption of ER homeostasis, is involved in the pathophysiology of several human diseases, including metabolic dysfunction-associated steatotic liver disease (MASLD). MASLD, formerly known as nonalcoholic fatty liver disease (NAFLD), is characterized by an excessive accumulation of hepatic lipids. To characterize ER stress-induced changes in the expression of genes involved in lipid metabolism, HepG2 human hepatoma cells were exposed to tunicamycin, followed by transcriptome profiling. Among genes involved in lipid biosynthesis, GPAT3 was strongly activated by tunicamycin while many other genes involved in this process (e.g., DGAT2, AGPAT2, AGPAT3, GPAT1, DGAT1 and GPAT4) were downregulated. Since GPAT proteins catalyze rate-limiting step in the de novo synthesis of glycerophospholipids and triglycerides, the unique expression pattern of GPAT3 potentially links it to ER stress-associated accumulation of lipids in hepatic cells.

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RNA sequencing of HCC cells after endoplasmic reticulum stress induced by tunicamycin

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Chip sequencing after ER stress induced in HCC cells using tunicamycin

Project description:We report the application of the CHIP sequencing-based technology in the high-throughput analysis of histone modifications in HepG2 cells. Endoplasmic reticulum stress related super enhancers were identified and their regulatory target genes were predicted.

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Tunicamycin induced ER stress in liver of C57Bl/6N mice

Project description:Tunicamycin induced ER stress in liver of C57Bl/6N mice

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Development of mRNA and lincRNA expression signatures of MEFs deficient in ER stress mediators for tunicamycin treatment

Project description:To further development of our mRNA or lincRNA expression approach to ER stress, we have employed whole genome microarray expression profiling as a discovery platform to identify ER stress-responsible genes. Mouse embryonic fibroblasts (MEFs) deficient in each ER stress mediator (XBP1, ATF4, ATF6a or ATF6b) were treated with tunicamycin for 12 or 24 hrs. Genes responsible for tunicamycin in each mediator-dependent manner were extracted and categorized by Gene Ontology. Among them, expression of five ER-related genes (Derl1, Ssr3, Magt1, Bet1 and Mcfd2) was quantified in the RNA samples from COS7 cells by real-time PCR, confirming existence of similar mechanisms of trancriptional activation in ER stress by tunicamycin treatment.

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Development of miRNA expression signatures of MEFs deficient in a ER stress mediator XBP1 for tunicamycin treatment

Project description:To further development of our miRNA expression approach to ER stress, we have employed miRNA microarray expression profiling as a discovery platform to identify ER stress-responsible ones. Mouse embryonic fibroblasts (MEFs) deficient in a ER stress mediator XBP1 were treated with tunicamycin for 12 or 24 hrs. miRNAs responsible for tunicamycin-treatment for 12hrs in XBP1-dependent manner were extracted. Among them, expression of three miRNAs (miR-23a, miR-27a, miR-24-2) was quantified in the RNA samples from the same as the microarray, and COS7 cells by real-time PCR, confirming existence of similar mechanisms of trancriptional repression in ER stress by tunicamycin treatment.

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Development of miRNA expression signatures of MEFs deficient in a ER stress mediator ATF6a for tunicamycin treatment

Project description:To further development of our miRNA expression approach to ER stress, we have employed miRNA microarray expression profiling as a discovery platform to identify ER stress-responsible ones. Mouse embryonic fibroblasts (MEFs) deficient in a ER stress mediator ATF6a were treated with tunicamycin for 12 or 24 hrs. miRNAs responsible for tunicamycin-treatment for 12hrs in ATF6a-dependent manner were extracted. Among them, expression of three miRNAs (miR-26a, miR-27b, miR-143) was quantified in the RNA samples from the same as the microarray by real-time PCR.

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