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Mus musculus

ABSTRACT: Analysis of gene expression changes induced in wild-type or Atf6a-/- mice by treatment with tunicamycin for 8h

OTHER RELATED OMICS DATASETS IN: MTBLS472

PROVIDER: PRJNA212335 | ENA |

REPOSITORIES: ENA

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Mus musculus

Project description:Analysis of gene expression changes induced in wild-type or Atf6a-/- mice by treatment with tunicamycin for 34h

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Project description:Analysis of gene expression changes induced in wild-type or Atf6a-/- mice by treatment with tunicamycin

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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. Mouse embryonic fibroblasts (MEFs) deficient in a ER stress mediator ATF6a 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 ATF6a-dependent manner were extracted.

2015-01-18 | E-GEOD-35176 | biostudies-arrayexpress

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

2015-01-18 | GSE35176 | GEO

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. Mouse embryonic fibroblasts (MEFs) deficient in each ER stress mediator (XBP1, ATF4, ATF6a or ATF6b) were treated with 2ug/mL tunicamycin for 12 or 24 hrs. Two independent experiments were performed for each mediator-deficient MEF at each time (untreated, 12 or 24 hrs). Genes responsible for tunicamycin in each mediator-dependent manner were extracted and categorized by Gene Ontology in GeneRanker program of Genomatix platform.

2015-01-18 | E-GEOD-35173 | biostudies-arrayexpress

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

2015-01-18 | GSE35173 | GEO

Mus musculus

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

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RNAseq Analysis of TP53+/+ and TP53-/- HCT116 colon carcinoma cell lines after treatment with p53 or ATF4-activating compounds

Project description:We examined the gene expression changes resulting from treatment of either "wild-type" or "p53-deficient" human cell lines with compounds known to activate either p53 (nutlin-3A,etoposide) or the integrated stress response (ISR) transcription factor ATF4 (histidinol,tunicamycin)

2022-08-20 | GSE211244 | GEO

NHR-8 regulated P-glycoproteins uncouple xenobiotic stress resistance from longevity in chemosensory C. elegans mutants

Project description:Transcriptomics analysis of wild type and osm-3(dh441)IV under vehicle and tunicamycin treatment for 6 hours

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Analysis of gene expression changes induced in wild-type or Atf6a-/- mice by treatment with tunicamycin for 8h

Project description:Protein misfolding stress in the endoplasmic reticulum (ER) leads to dysregulation of lipid metabolism in the liver, and ER stress is associated with human diseases that are accompanied by hepatic lipid accumulation, including obesity, alcoholism, and viral hepatitis; yet the pathways leading from ER stress to the regulation of lipid metabolism are poorly understood. Working exclusively in vivo, we used a “bottom-up” approach to infer pathways in the genetic regulation of lipid metabolism by the UPR. We used a functional genomics to link gene expression patterns taken from microarray data to the severity and persistence of ER stress, using mice lacking the UPR signaling molecule ATF6α. This approach revealed that functionally related genes clustered into a small number of distinct expression profiles, and that lipid oxidation and efflux were targets for coordinated transcriptional suppression during ER stress.Our results establish a framework for hepatic gene regulation during ER stress. Atf6a-/- or +/+ mice of variable age and gender were injected intraperitoneally with 2 mg/kg tunicamycin or vehicle. 3 separate mice were used in each group. 8h after injection, mice were sacrificed and total RNA was prepared from resected livers.

2013-09-04 | E-GEOD-48932 | biostudies-arrayexpress

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