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Development of miRNA expression signatures of MEFs deficient in a ER stress mediator ATF4 for tunicamycin treatment

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE35175 | GEO | 2015/01/18

SECONDARY ACCESSION(S): PRJNA155985

REPOSITORIES: GEO

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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 XBP1 for tunicamycin treatment

2015-01-18 | GSE35174 | GEO

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 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 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

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 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

ChIP-seq and mRNA-seq experiment to find the direct target genes of ATF4 and CHOP

Project description:We report the direct target genes of ATF4 and CHOP in response to endoplasim reticulum stress through next generation sequencing. By obtaining genowide sequence from chromatin immunoprecipitated DNA with anti-CHOP and anit-ATF4, we identified direct binding sites of ATF4 and CHOP in promoter regions of their target genes in mouse embrynic fibroblasts (MEFs) in response to ER stress. In addition, we obtained list of genes which are differentially regulated in Atf4 or Chop-deficient MEFs compared to the wild-type MEFs in response to ER stress. We found that genes related with unfolded protein response and protein synthesis were directly regulated by ATF4 and CHOP. Through this observation, we conclude that main role of ATF4 and CHOP as transcription factors is to enhance mRNA translation in respone to ER stress. This sutdy provide new insight of genetic network of ATF4 and CHOP in response to ER stress. For ChIP-seq, Chop+/+ and Chop-/- MEFs were treated with Tunicamycin, N-glycosylation inhibitor, to induce ER stress for 8hr. Atf4+/+ and Atf4-/- MEFs were also treated same condition for ChIP-Seq. For mRNA-seq, wild-type, Atf4-/-, and Chop-/- MEFs were treated with tunicamycin for 8hr for experiments.

2013-04-11 | E-GEOD-35681 | biostudies-arrayexpress

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