Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from S.cerevisiae treated with tunicamycin

ABSTRACT: S.cerevisiae cells carrying a wild-type TOR1 allele or hyperactive TOR1L2134M allele were treated with the ER stressor, tunicamycin, and differential gene expression was examined between WT TOR1 and hyperactive TOR1LM We used microarrays to examine differential gene expression in cells expressing hyperactive TOR1LM following ER stress . We identified changes in expression of cell wall genes.

ORGANISM(S): Saccharomyces cerevisiae Schizosaccharomyces pombe

PROVIDER: GSE129200 | GEO | 2019/05/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from S.cerevisiae treated with tunicamycin

Project description:Expression data from S.cerevisiae treated with tunicamycin

| PRJNA530518 | ENA

Effect of Tunicamycin on Bovine Capillary Endothelial Cells

Project description:GPT inhibitor Tunicamycin develops ER stress causing anti-angiogenic response in breast tumor microvasculature due to unfolded protein response-mediated apoptosis. cDNA microarray identified 123 and 454 differentially regulated genes with 10 genes overlapping between 3h and 32 h of Tunicamycin treatment. Alg-2 expression is inconsistent but not the Dpms. Evidences support that Tunicamycin completely destroys DPMS activity in capillary endothelial cells without affecting its protein or the mRNA levels but by knocking down the phosphorylation. DPMS’ contribution to developing upr during ER stress has therefore been evaluated because of its inherent regulatory property of GPT. FTIR spectroscopy confirmed protein denaturation. Restablishing the phosphorylation status helps the DPMS regaining its activity. As a result, ER stress is reduced reversing apoptosis and bringing more cells into cycling with normal cellular morphology. Furthermore, differential expression of DPMS in breast tumor microvasculature during Tunicamycin therapy raises its potential as a tumor prognostic marker in the clinic.

2017-11-15 | GSE33729 | GEO

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

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

2015-01-18 | GSE35173 | GEO

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 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

2015-01-18 | GSE35175 | 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 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data