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Mouse Insulinoma 6 (MIN6) transcriptome data at 2.8mM and 25mM extracellular glucose concentrations.

ABSTRACT: Mouse Insulinoma 6 (MIN6) transcriptome data at 2.8mM and 25mM extracellular glucose concentrations.

PROVIDER: PRJNA941054 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23701892_1.fastq.gz	Fastqsanger.gz
	SRR23701892_2.fastq.gz	Fastqsanger.gz
	SRR23701893_1.fastq.gz	Fastqsanger.gz
	SRR23701893_2.fastq.gz	Fastqsanger.gz

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Beta cells (MIN6) treated with amylin at different times and doses and growth at different concentrations of glucose

Project description:Murine pancreatic beta cell line MIN6 was growth at two different concentrations of glucose (22,2 and 5,5 mM of glucose), 37ºC, 5% CO2 and was treated at four different concentrations of human amylin (0, 1, 10 and 20 uM) during three different times (2, 12 and 24 hours) Keywords = pancreatic beta cell Keywords = amylin Keywords = glucose Keywords: time-course

2005-04-12 | GSE2253 | GEO

Mouse Insulinoma 6 (MIN6) transcriptome data at 2.8mM and 25mM extracellular glucose concentrations.

Project description:To investigate whether the upregulated proteins identified through transcriptome studies have any possible direct interaction with intracellular and unphosphorylated glucose. To investigate whether enhanced insulin secretion is at the cost of other secretory proteins.

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Transcription profiling of mouse pancreatic beta cell line (MIN6) treated with amylin at different times and doses and growth at different concentrations of glucose

Project description:Murine pancreatic beta cell line MIN6 was growth at two different concentrations of glucose (22,2 and 5,5 mM of glucose), 37ÂºC, 5% CO2 and was treated at four different concentrations of human amylin (0, 1, 10 and 20 uM) during three different times (2, 12 and 24 hours)

2009-04-10 | E-GEOD-2253 | biostudies-arrayexpress

Transcription profiling of mouse MIN6 insulinoma beta cells following knock-down of murine Pdx1

Project description:In order to identify genes that are regulated by Pdx1, MIN6 insulinoma cells were transduced with adenovirus expressing a short hairpin RNA directed against murine Pdx1 (AdshPdx1) or luciferase (AdshLuc) or not transduced at all (untreated). RNA was harvested and reverse transcribed. Reduced expression of Pdx1 and established Pdx1 targets was confirmed. The RNA was then submitted for labeling and hybridization to the PancChip cDNA microarray.

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Selenomethionine Modulates Insulin Secretion in the MIN6-K8 Mouse Insulinoma Cell Line

Project description:Selenium is an essential trace element that has gained interest for its potential role in glucose homeostasis. The purpose of the present study was to investigate the impact of selenium supplementation as selenomethionine (SeMet) on insulin secretion in MIN6-K8 cells, a model of pancreatic -cells. We found that 40 μM and 80 μM SeMet significantly enhanced percent insulin secretion at low (2.8 mM), intermediate (11.7 mM), and high (16.7 mM) glucose stimulation. SeMet also increased tolbutamide- or KCl-induced percent insulin secretion at 40 μM and 80 μM. Ca2+ influx was only reduced with 80 μM SeMet. RNA-sequencing showed that 40 μM SeMet supplementation upregulated expression of selenoprotein H (SelH) and thioredoxin reductase 1 (Txnrd 1) and downregulated expression of glutathione peroxidase 3 (Gpx3), selenoprotein O (SelO), and selenoprotein P (SelP). Gpx3 knockdown increased both percent and total insulin release with high glucose stimulation. SelP knockdown increased insulin release at high glucose. In conclusion, high SeMet supplementation augments insulin secretion, while reductions in Gpx3 and SelP expression, from SeMet supplementation or via silencing, augment -cell function in the MIN6-K8 cell line. These studies support a putative role for selenium and selenoproteins in the regulation of glucose homeostasis and diabetes risk.

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Project description:In order to identify genes that are regulated by Meis3, MIN6 insulinoma cells were transfected with siRNA directed against murine Meis3 (siMeis3) or non targeting control (siControl). RNA was harvested and reverse transcribed. Reduced expression of Meis3 was confirmed. The RNA was then submitted for labeling and hybridization to the Agilent cDNA microarray.

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Selenomethionine Modulates Insulin Secretion in the MIN6-K8 Mouse Insulinoma Cell Line

Project description:Selenomethionine Modulates Insulin Secretion in the MIN6-K8 Mouse Insulinoma Cell Line

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Modulation of insulin secretion through RBFOX2-mediated alternative splicing [eCLIP-Seq MIN6]

Project description:Recent studies have identified dysregulation of RNA-binding proteins (RBPs) and aberrant mRNA splicing in the onset of diseases including diabetes. Here we investigated the role of RBFOX2 in the pancreatic β cell through the conditional mutation of Rbfox2 in the mouse pancreas (Pdx1:Cre; Rbfox2fl/lf) and RNAi experiments in the mouse insulinoma cell line, MIN6. We then identified the direct targets of RBFOX2 in the mouse β cell transcriptome my eCLIP-Seq in MIN6 cells.

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Expression data from mouse insulinoma cells

Project description:We previously isolated a subclone, MIN6 clone 4, from the parental MIN6 cells, that shows well-regulated insulin secretion in response to glucose, glybenclamide, and KCl, even after prolonged culture. To investigate the molecular mechanisms responsible for preserving GSIS in this subclone, we compared four groups of MIN6 cells: Pr-LP (parental MIN6, low passage number), Pr-HP (parental MIN6, high passage number), C4-LP (MIN6 clone 4, low passage number), and C4-HP (MIN6 clone 4, high passage number). Based on their capacity for GSIS, we designated the Pr-LP, C4-LP, and C4-HP cells as “responder cells.” In a DNA microarray analysis, we identified a group of genes with high expression in responder cells (“responder genes”), but extremely low expression in the Pr-HP cells.

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