Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from rat INS-1E cells

ABSTRACT: Cytokine-induced beta-cell apoptosis is a key event for the death of pancreatic beta cells in the development of type-1 diabetes. We identified BRD0476 as a novel suppressor of cytokine-induced beta-cell apoptosis. We used microarrays to look for gene set(s) that are regulated by BRD0476.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE42897 | GEO | 2012/12/14

SECONDARY ACCESSION(S): PRJNA183731

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression data from rat INS-1E cells

Project description:Cytokine-induced beta-cell apoptosis is a key event for the death of pancreatic beta cells in the development of type-1 diabetes. We identified BRD0476 as a novel suppressor of cytokine-induced beta-cell apoptosis. We used microarrays to look for gene set(s) that are regulated by BRD0476. Rat INS-1E cells were treated with cytokine cocktails (IL-1b, IFN-g and TNF-a) and/or BRD0476 for 6 or 12 hours. Total RNAs were isolated using the RNEasy kit from Qiagen.

2012-12-14 | E-GEOD-42897 | biostudies-arrayexpress

Rat insulin-producing INS-1E exposed to cytokines IL-1β and IFN-γ

2013-12-19 | GSE53453 | GEO

Rat insulin-producing INS-1E exposed to cytokines IL-1β and IFN-γ

Project description:In the context of T1 Diabetes, pro-inflammatory cytokines IL-1β and IFN-γ are known to contribute to β-cell apoptosis; The measurement of mRNA expression following β-cell exposure to these cytokines gives a picture of the changes in gene expression characterizing the path to β-cell dysfunction and death. INS1 cell lines were cultured in medium with or without IL-1β and IFN-γ. The samples were collected at various time points for profiling with Affymetrix Rat ST arrays. These experiments were performed on two separate occasions.

2013-12-19 | E-GEOD-53453 | biostudies-arrayexpress

Transcription profiling of rat insulinoma-beta (INS-1E) cells exposed to the cytokines IL-1-beta and IFN-gamma for six different lengths of time and with or without the inducible NO synthase blocker NMA

Project description:Locally released cytokines contribute to beta cell dysfunction and apoptosis in Type 1 diabetes. In vitro exposure of insulin producing INS-1E cells to the cytokines interleukin (IL)-1beta + interferon (IFN) gamma leads to a significant increase in apoptosis. To characterize the genetic networks implicated in beta cell dysfunction and apoptosis and its dependence on nitric oxide (NO) production, we performed a time course analysis using the Affymetrix RG U34A microarry. INS-1E cells were exposed in duplicate to IL-1beta + IFN-gamma for six different time points (1, 2, 4, 8, 12, and 24 h) with or without the inducible NO synthase blocker.

2006-06-14 | E-CBIL-10 | biostudies-arrayexpress

Transcription profiling of rat pancreatic beta-cells in response to cytokine exposure and NF-kappa B activation blocking

Project description:Type 1 diabetes mellitus results from an autoimmune destruction of pancreatic beta-cells. Based on findings suggesting NF-kappa B plays a role in beta cell apoptosis, we blocked NF-kappa B activation in cytokine-exposed FACS sorted beta cells by a recombinant adenovirus (AdI kappa B((SA)2)) containing an inhibitor of NF kappa B alpha (I kappa Bac) super-repressor (S32A/S36A). The expression profile was then analyzed with the Affymetrix RG U34a microarray.

2006-06-16 | E-CBIL-9 | biostudies-arrayexpress

Interactome of Ca2+-bound secretagogin in INS-1E cells

Project description:By using His6-tagged recombinant human secretagogin in the presence of Ca2+ (100 µM), we precipitated putative interacting partners from INS-1E cells and identified their amino acid sequences by mass spectrometry. We detected canonical interacting proteins participating in vesicle-mediated transport, exocytosis and cytoskeletal organization. Besides, we captured proteins controlling protein folding and (de-)ubiquitination. Our data support that secretagogin modulates protein folding and degradation through protein-protein interactions and interacts with USP9X in β cells to control cell survival.

2017-06-21 | PXD006544 | Pride

Sfrp5 increases glucose-stimulated insulin secretion in the rat pancreatic beta cell line INS-1E.

Project description: Not available

| S-EPMC6438539 | biostudies-literature

Gene expression profile at single cell level of GFP labeled islet β cells from streptozotocin (STZ) treated Ins/β-lineage-labeled mice

Project description:Islet β cells suffer from de- and trans-differentiation after injury. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of β cells in from STZ-induced diabetes.

2023-05-01 | GSE203042 | GEO

Transcriptome profile of INS-1E Ctrl and DKO cells

Project description:To analyse gene expression differences between the TFEB/TFE3 KO cells vs. Controls, under growing conditions (GC) vs. Fasting conditions (Fast)

2023-07-31 | GSE153709 | GEO

Paternal high-fat diet elicits early-onset se-specific islet inflammation in rat progeny

Project description:Progressive β–cell failure and apoptosis, resultant of innate immune system activation1,2 is gaining traction as a converging point for type 1 (T1D) and type 2 (T2D). Islet inflammation (insulitis), a hallmark of T1D, occurs typically during the initiation phase of the disease, subsequently orchestrating an autoimmune assault against β–cells. Whether this is a primary event or a consequence of glucotoxicity or lipotoxicity is undetermined3 but metabolic stress is demonstrated to prompt islet inflammation1,2. Here we show that paternal consumption of high fat diet (HFD) invoked distinct immuno-inflammatory transcriptional response in the pancreatic islets of their weanling daughters, in contrast to compensatory changes in the sons. Importantly, these changes occurred in conjunction with transition in islet repertoire resembling the spectrum of T2D, along with progressive development of β–cell dysfunction4. Note, these females were lean, normolipidaemic and insulin sensitive4. These findings provide experimental support for the notion that islet inflammation could be an antecedent event in T2D, leading to β–cell secretory defect, repair/regeneration and apoptosis. Importantly, these effects were transmitted via paternal nutrient stress to offspring.

2021-12-29 | GSE89138 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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