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Transcriptome analysis of the D3 mouse embryonic stem cell line in comparison to the MIN6 pancreatic beta-cell insulinoma cell line

ABSTRACT: Analysis of the transcriptional differences between mouse ES cells from the D3 cell line and transformed beta-cells (MIN6 cell line) as determined by a direct comparative analysis of their transcriptome. The results show that 40% of transcripts were differentially expressed between D3 and MIN6 cells. There is thus a marked difference in the pattern of transcription between the ES cell and beta-cell genomes.

ORGANISM(S): Mus musculus

PROVIDER: GSE49077 | GEO | 2013/07/23

SECONDARY ACCESSION(S): PRJNA212924

REPOSITORIES: GEO

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Transcriptome analysis of the D3 mouse embryonic stem cell line in comparison to the MIN6 pancreatic beta-cell insulinoma cell line

Project description:Analysis of the transcriptional differences between mouse ES cells from the D3 cell line and transformed beta-cells (MIN6 cell line) as determined by a direct comparative analysis of their transcriptome. The results show that 40% of transcripts were differentially expressed between D3 and MIN6 cells. There is thus a marked difference in the pattern of transcription between the ES cell and beta-cell genomes. Total RNA was extracted from three independent replicates of passage 21 D3 cells and passage 23 MIN6 cells. A whole mouse genome comparison between D3 and MIN6 cells was performed using the Mouse WG-6 v2.0 Expression Beadchip from Illumina.

2013-07-23 | E-GEOD-49077 | biostudies-arrayexpress

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.

2024-03-13 | GSE183775 | GEO

Next Generation Sequencing Analysis of Gene expression of Min6 insulinoma cell line transfected with siNC, siSRSF1 or siSRSF2

Project description:Assessment of the impact of SRSF1 or SRSF2 silencing in Min6 cell lines

2024-04-28 | GSE178357 | GEO

MIN6 beta cell CtBP2 ChIP-seq

Project description:CtBP2 ChIP-seq analysis was performed in a murine pancreatic beta cell line MIN6.

2023-08-08 | GSE221257 | GEO

RNA-Seq of mouse beta cell line MIN6 after siRNA knockdown of lncRNA Pax6os1

Project description:Pax6os1 was knocked using by a pool of 3 siRNAs in the mouse insulinoma (beta cell) line MIN6. A parallel experiment using 3 control siRNAs was performed and RNA extracted 72 hours after transfection and subjected to RNA-Seq.

2021-06-01 | E-MTAB-9218 | biostudies-arrayexpress

Pla2g6-dependent cytokine signaling in MIN6 cells

Project description:Analysis of MIN6 murine beta cell line transfected with Pla2g6 RNAi and treated with pro-inflammatory cytokines TNF-alpha, IL-1beta and IFN-gamma.

2024-02-08 | PXD017863 | Pride

Transcription profiling by array of mouse pancreatic beta cells of MIN6 insulinoma cell line transfected with siRNA directed against murine Meis3 or non targeting control.

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.

2010-11-01 | E-MTAB-273 | biostudies-arrayexpress

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.

2013-04-22 | GSE43774 | GEO

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.

2023-09-25 | GSE221276 | GEO

Modulation of insulin secretion through RBFOX2-mediated alternative splicing [RNA-seq MIN6]

2023-09-25 | GSE221274 | GEO

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