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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Seiichi Oyadomari

PROVIDER: E-GEOD-35209 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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 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

Development of miRNA expression signatures of MEFs deficient in a ER stress mediator ATF4 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 ATF4 were treated with tunicamycin for 12 or 24 hrs. miRNAs responsible for tunicamycin-treatment for 12hrs in ATF4-dependent manner were extracted. Among them, expression of three miRNAs (miR-193b, miR-423-5p, miR-199a-3p) 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 ATF4 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 ATF4-dependent manner were extracted.

2015-01-18 | E-GEOD-35175 | biostudies-arrayexpress

Development of miRNA expression signatures of MEFs deficient in a ER stress mediator ATF6b 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 ATF6b were treated with tunicamycin for 12 or 24 hrs. miRNAs responsible for tunicamycin-treatment for 12hrs in ATF6b-dependent manner were extracted. Among them, expression of three miRNAs (miR-15b, miR-20b, miR-92a) 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 ATF6b 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 ATF6b-dependent manner were extracted.

2015-01-18 | E-GEOD-35177 | biostudies-arrayexpress

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2015-09-01 | E-GEOD-49598 | biostudies-arrayexpress

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

Gene expression profile of ATF6a and ATF6b overexpression in LS174T cells

Project description:To further development of our mRNA expression approach to ER stress, we have employed whole genome microarray expression profiling as a discovery platform to identify ER stress-responsible genes. LS174T cells were overexpressed with ER stress mediators, ATF6a or ATF6b. Genes responsible for each mediator were extracted and categorized by Gene Ontology. ATF6a and ATF6b were overexpressed in LS174T. Subsequently, cells were treated with 2 mM sodium butyrate, which induces LS174T cells to differentiate to mature goblet cells. Genes responsible for each mediator were extracted and categorized by Gene Ontology in GeneRanker program of Genomatix platform.

2015-08-05 | E-GEOD-49567 | biostudies-arrayexpress

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2015-08-05 | E-GEOD-49645 | biostudies-arrayexpress

Saturated fatty acids induced genes and ISR target genes in pancreatic beta cells

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2015-08-01 | E-GEOD-49647 | biostudies-arrayexpress

Gene expression profile of ATF6a and ATF6b knockout mice with dextran sulfate sodium (DSS)-induced colitis

Project description:To understand the role of ATF6a and ATF6b in non-canonical endoplasmic reticulum stress response pathway, we have employed whole genome microarray expression profiling to identify the genes regulated by ATF6s. WIild type or, ER stress mediators,ATF6a or ATF6b-knockout mice were treated with 3% DSS for 3days. Genes responsible for DSS in each mediator-dependent manner were extracted and categorized by Gene Ontology. Among them, expression of three cell structure-related genes (Muc2, Muc3, Muc4) was quantified in the RNA samples from another mice treated with DSS by real-time PCR. Colitis was induced with 3% DSS, 36,000-50,000 M.W. (MP Biomedicals,) in the drinking water for 3 days. Genes responsible for DSS treatment in each mediator-dependent manner were extracted and categorized by Gene Ontology in GeneRanker program of Genomatix platform.

2015-02-08 | E-GEOD-35651 | biostudies-arrayexpress

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