Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

27 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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. 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.

ORGANISM(S): Mus musculus

SUBMITTER: Chris O'Neill

PROVIDER: E-GEOD-49077 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

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.

2013-07-23 | GSE49077 | GEO

Expression data from mouse insulinoma cells

2013-04-22 | GSE43774 | GEO

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 M-bM-^@M-^\responder cells.M-bM-^@M-^] In a DNA microarray analysis, we identified a group of genes with high expression in responder cells (M-bM-^@M-^\responder genesM-bM-^@M-^]), but extremely low expression in the Pr-HP cells. MIN6 clone 4 cells are a subclone isolated from low-passage-number parental MIN6 cells by the limiting dilution method (JM, unpublished). This subclone was maintained in the same culture conditions as the parental cells, and retained good GSIS even after 6 months of continuous culture. For the low-passage-number parental MIN6 cells (Pr-LP), we used cells passaged 17-20 times; for the high-passage-number MIN6 cells (Pr-HP), we used cells passaged 35-40 times. Seventeen to 20 passages were also used for the low-passage-number MIN6 clone 4 cells (C4-LP), and the high-passage ones (C4-HP) were used after 40 to 50 passages.

2013-04-22 | E-GEOD-43774 | 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

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

RNA-seq of MIN6 cells overexpressing Hnf1a through CRISPR activation

Project description:To determine the impact of Hnf1a overexpression on gene expression in mouse beta cells, we performed RNA-seq experiments on MIN6 where Hnf1a was overexpressed using CRISPR activation (SAM system).

2022-05-01 | E-MTAB-11474 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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