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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression changes in response to doxycyline-induced expression of proinsulin (C96Y)-GFP in an INS-1 insulinoma cell line

ABSTRACT: A doxycyline-inducible INS-1 insulinoma cell line expressing proinsulin (C96Y)-GFP was engineered. Addition of doxycyline causes the production of the proinsulin (C96Y)-GFP, which is retained in the endoplasmic reticulum. This study analyzes the gene expression changes that occur after doxycyline-induced expression of proinsulin (C96Y)-GFP for 24h, 48h and 5 days. Expression changes were compared between control un-induced cells and cells treated with doxycyline. Three replicates (experiments) were performed for each time point. Stable mutant insulin-expressing insulinoma cells were treated or not with doxycyline for 24h, 48h or 5 days and RNA was extracted for expression analysis.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Allen Volchuk

PROVIDER: E-GEOD-22537 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression changes in response to doxycyline-induced expression of proinsulin (C96Y)-GFP in an INS-1 insulinoma cell line

Project description:A doxycyline-inducible INS-1 insulinoma cell line expressing proinsulin (C96Y)-GFP was engineered. Addition of doxycyline causes the production of the proinsulin (C96Y)-GFP, which is retained in the endoplasmic reticulum. This study analyzes the gene expression changes that occur after doxycyline-induced expression of proinsulin (C96Y)-GFP for 24h, 48h and 5 days. Expression changes were compared between control un-induced cells and cells treated with doxycyline. Three replicates (experiments) were performed for each time point.

2010-06-24 | GSE22537 | GEO

Expression data of rat insulinoma cells induced with ER stress +/- IRE1 inhibitor treatment

Project description:The Akita mutation (C96Y) in the insulin gene results in early onset diabetes in both humans and mice. Expression of the mutant proinsulin (C96Y) causes endoplasmic reticulum (ER) stress in pancreatic ?-cells and consequently the cell activates the unfolded protein response (UPR). Since the proinsulin is terminally misfolded however, the ER stress is irremediable and chronic activation of the UPR eventually activates apoptosis in the cell population. We used microarray gene expression arrays to analyze the IRE1-dependent activation of genes in response to misfolded proinsulin expression in an inducible mutant proinsulin (C96Y) insulinoma cell line by inhibiting the IRE1 endoribonucleas activity with a specific inhibitor, 4u8c. Insulinoma cells with doxycycline inducible C96Y-proinsulin expression were either untreated, treated with doxycycline alone or treated with dox and 4u8c. This was done with two biological replicates.

2014-07-16 | E-GEOD-58866 | biostudies-arrayexpress

Expression data of rat insulinoma cells induced with ER stress +/- IRE1 inhibitor treatment

Project description:The Akita mutation (C96Y) in the insulin gene results in early onset diabetes in both humans and mice. Expression of the mutant proinsulin (C96Y) causes endoplasmic reticulum (ER) stress in pancreatic -cells and consequently the cell activates the unfolded protein response (UPR). Since the proinsulin is terminally misfolded however, the ER stress is irremediable and chronic activation of the UPR eventually activates apoptosis in the cell population. We used microarray gene expression arrays to analyze the IRE1-dependent activation of genes in response to misfolded proinsulin expression in an inducible mutant proinsulin (C96Y) insulinoma cell line by inhibiting the IRE1 endoribonucleas activity with a specific inhibitor, 4u8c.

2014-07-16 | GSE58866 | GEO

Rattus norvegicus

Project description:Gene expression changes in response to doxycyline-induced expression of proinsulin (C96Y)-GFP in an INS-1 insulinoma cell line

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Time course treatment with Palmitate and thapsigargin of insulinoma INS-1E cells

Project description:Time course treatment with 0.4 mM Palmitate and 200 nM thapsigargin of insulinoma INS-1E cells. Timepoints; 0, 4, 16 and 24h in biological duplicates within an iTRAQ 8 set for palmitate and thapsigargin, respectively.

2020-08-18 | PXD020851 | JPOST Repository

Glycosaminoglycan domain mapping of proteoglycans

Project description:We have developed a strategy for the detailed structural characterization of complex proteoglycan-derived glycosaminoglycans. Chondroitin/dermatan sulfate isolated from rat INS-1 832/13 insulinoma cells known to produce primarily one proteoglycan was used to evaluate and demonstrate the efficacy of the strategy.

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Genome-wide analysis of tumor regression upon K-RAS inactivation

Project description:We performed expression profiling on micro-dissected lung tumors derived from a doxycycline-inducible K-RAS mouse model in order to gain mechanistic insight into K-RAS-mediated tumor maintenance. In this model, the tumors were induced with doxycycline for 11 weeks (in order to obtain lung tumors). At this point the doxycyline was withrawn from the food of the mice and consequently K-RAS inactivated. Thus, the genome-wide analysis was performed on tumors at timepoints 0, 24h and 48h after K-RAS inactivation. Total RNA obtained from mouse lung tumors at time 0 and 24h or 48h after K-RAS inactivation.

2012-09-06 | E-GEOD-40606 | biostudies-arrayexpress

Genome-wide analysis of tumor regression upon K-RAS inactivation

2012-09-06 | GSE40606 | GEO

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Project description:Genomics and Transcriptomics of Human Insulinoma

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Effect of Fzd9 knock-out on MycER-BclXl insulinoma progression

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2021-02-20 | GSE167073 | GEO

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