Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA128457 | ENA |
REPOSITORIES: ENA
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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
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. 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.
2010-07-29 | E-GEOD-22537 | biostudies-arrayexpress
Project description:Gene expression in response to short and long term cAMP stimulation in the INS-1 insulinoma cell line
| PRJNA145433 | ENA
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
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
Project description:Knee osteoarthritis (KOA), as a degenerative multifactorial disease, affects the quality of life and mental health of patients, and also brings a huge socioeconomic burden. Treating synovitis have shown promise as anti-inflammatory therapeutics in mitigating OA symptoms and disease progression. Here, by analysing synovial single-cell sequencing (scRNA-seq) data from KOA, we found that synovial fibroblasts (FLS) in OA synovium showed a distinct pro-inflammatory phenotype. We collected synovial tissue from patients with clinical OA as well as from healthy donors, and histological examination was consistent with findings in scRNA-seq. Inspired by recent cross-tissue fibroblast lineage studies, we identified by sequencing that healthy FLS in synovial tissues share transcriptome-level similarities with dermal fibroblasts (DFb). Subsequently, we revealed the local as well as systemic distribution of intra-articular injected DFbs by constructing/extracting two types of rat fibroblasts (luciferase DFbs as well as GFP DFbs). The results demonstrate that DFbs can be locally retained in the synovium for up to three weeks following targeted engrafting on it. And intra-articular injection does not result in DFbs migration to vital organs or the occurrence of histological changes in these organs. A rat model of KOA was constructed by anterior cruciate ligament transection (ACLT) in order to study the therapeutic effect of DFbs on KOA. After injection, the rats showed improvement in painful gait. In addition, histological as well as imaging results showed reduced synovitis and improvement in articular cartilage. Finally we verified the protective effect of DFbs on cytokine-stimulated chondrocytes in a co-culture system.
2026-06-24 | GSE304724 | GEO
Project description:Molecular basis for vulnerability to mitochondrial and oxidative stress in an insulinoma cell line
| PRJNA120183 | ENA
Project description:This SuperSeries is composed of the following subset Series:; GSE1589: Targets of HNF1b, HNF4a2 and HNF6 in INS-1 cells; GSE1590: Targets of HNF1b mutants in INS-1; GSE1591: INS-1 cell lines (FLP-In T-REx) Experiment Overall Design: Refer to individual Series
2007-11-29 | E-GEOD-6428 | biostudies-arrayexpress
Project description:This study aims at elucidating how Coxsackie B virus infection perturbs the host's miRNA regulatory pathways that may lead to different pathological events using the miRNA microarray approach. The rat pancreatic cell line - INS-1E, was infected with various preparations of Coxsackie B4 viruses was analysed for miRNA expression profiles subsequently. The miRNA expression profiles were measured at 48, and 72 hours post infection, respectively.
2015-01-01 | E-GEOD-58691 | biostudies-arrayexpress