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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

2021-02-23 | GSE167299 | GEO

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

Project description:In order to explore the role of ER stress in the development and progression of HCC, RNA sequencing was performed to detect the differential RNA levels before and after ER stress, thus providing strong evidence for the search of ER stress-related genes.

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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.

2025-02-12 | GSE209520 | GEO

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

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Development of miRNA expression signatures of MEFs deficient in a ER stress mediator ATF6b for tunicamycin treatment

2015-01-18 | GSE35177 | GEO

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

2015-01-18 | GSE35176 | GEO

Development of miRNA expression signatures of MEFs deficient in a ER stress mediator ATF4 for 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. Mouse embryonic fibroblasts (MEFs) deficient in a ER stress mediator XBP1 were treated with 2ug/mL tunicamycin for 12 or 24 hrs. Two independent experiments were performed at each time (untreated, 12 or 24 hrs). miRNAs responsible for tunicamycin-treatment for 12hrs in XBP1-dependent manner were extracted.

2015-01-18 | E-GEOD-35174 | biostudies-arrayexpress

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