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RNA-seq of Min6 cells were transfected with the GR cDNA expression vector or control vector

ABSTRACT: In order to investigated the underlying molecular mechanism of GR’s effects, we transfected the Min6 cell with the GR cDNA expression vector or control vector, and then extracted RNA of Min6 cells for RNA sequencing. We studied the gene-expression differences resulting in GR overexpress. A total of 21542 gene transcripts was captured,and 233 genes showed significant expression differences (p-value<0.05,|log2Foldchange|>1) between the two group. Further GO analysis and KEGG analysis found that GR overactivation instigates dysregulated autophagy in beta-cells

ORGANISM(S): Mus musculus

PROVIDER: GSE182267 | GEO | 2021/08/19

REPOSITORIES: GEO

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m6A-seq of Min6 cells were transfected with the GR cDNA expression vector or control vector

Project description:To further explore the underlying molecular mechanism of GR’s effects, we transfected the Min6 cell with the GR cDNA expression vector or control vector, and then extracted RNA of Min6 cells. M6A antibody was used to specifically recognize m6A on mRNA. methylation modified RNA fragments were obtained by immunoprecipitation and used for high-throughput sequencing. By comparing the captured RNA fragments, we found that there were 22381 difference peaks between GR overexpression group and control group, among which 3659 binding peaks were significantly different.Further analysis the MeRIP sequencing results of MIN6 cells overexpressing GR revealed that decreased m6A was detected in a large number of autophagy-related mRNAs.

2021-08-19 | GSE182268 | GEO

m6A-seq of Min6 cells were transfected with the GR cDNA expression vector or control vector

Project description:m6A-seq of Min6 cells were transfected with the GR cDNA expression vector or control vector

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RNA-seq of Min6 cells were transfected with the GR cDNA expression vector or control vector

Project description:RNA-seq of Min6 cells were transfected with the GR cDNA expression vector or control vector

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RNA-seq and m6A-seq of Min6 cells were transfected with the GR cDNA expression vector or control vector

Project description:RNA-seq and m6A-seq of Min6 cells were transfected with the GR cDNA expression vector or control vector

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Identification of a novel Glis3-348aa protein in MIN6 cells by LC-MS

Project description:To identify the novel protein encoded by circGlis3, total protein lysates were extracted from MIN6 cells transfected with circGlis3 plasmid or empty vector and separated by SDS-PAGE, followed by Coomassie brilliant blue staining. The differential gel bands near 35 kDa were excised and subjected to mass spectrometry.

2023-11-02 | PXD037447 | Pride

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

GRα-independent transcriptional activity of hGRβ in GR Liver Knockout Mouse

Project description:We used AAV as a vector to deliver hGRβ to the liver of GR Liver Knockout mice. We collected liver samples for microarray analysis to investigate any phenotype as well as the underlying specific signaling pathway. In particular, we would like to determine if and how hGRβ overexpression in liver affects mGRα’s gene transcription profile in GR Liver Knockout mice.

2015-12-11 | GSE75683 | GEO

Microarray Analysis of MIN6 cells treated with Exendin-4 over time

Project description:The aim of the study was to investigate the effect of Exendin-4 on MIN6 cells allowing for the elucidation of the various transcriptional programs initiated by this multifunctional peptide hormone. MIN6 cells were treated with Exendin-4 for 24, 48 and 72 hours. After these time points RNA was isolated and used for hybridization (on Cy3) against matched control MIN6 cells (on Cy5) using the Mouse PancChip 5.0 . Three assays were carried out for each time point.

2014-11-04 | E-MTAB-3071 | biostudies-arrayexpress

ChIP-MS of GR and GR-DZn in mouse embryonic fibroblasts

Project description:The Glucocorticoid Receptor (GR) is both one of the most widely used clinical drug targets and a very potent metabolic regulator. GR belongs to the nuclear hormone receptor family of ligand-gated transcription factors that govern mammalian physiology. Upon ligand binding, GR enters the nucleus to regulate gene expression both positively and negatively. It is known to bind to consensus DNA sequences termed glucocorticoid response elements (GREs), but the mechanisms determining transcriptional activation versus repression remain an unresolved molecular paradox. Prevailing models suggest that tethering of GR to AP-1 or NF-κB via protein-protein interactions, rather than direct DNA binding, specifies negative regulation. However, here we show that the repression of inflammatory genes as well as all other glucocorticoid responses, require direct DNA binding of GR. Generating GR point mutant mice that retain the ability to tether via protein-protein interactions while unable to recognize DNA sequences, we demonstrate that response element recognition via the Zinc finger is absolutely required for both transcriptional activation and repression. We have used ChIP-Seq and RNA-Seq in inflammatory and metabolic cells and tissues together with proteomics to reveal that DNA binding of GR is necessary for the assembly of a functional SWI/SNF coregulator complex. Generally, the desired anti-inflammatory actions of GR are attributed to the silencing of inflammatory genes, while its adverse effects are believed to result from the transcriptional upregulation of metabolic targets. Our findings not only challenge classical models and dogmas of GR mediated gene regulation, but will provide an important basis for the development of novel immunosuppressants with reduced side effect profiles.

2020-07-07 | PXD013772 | Pride

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.

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