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M6A-seq of Min6 cells were transfected with the GR cDNA expression vector or control vector

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE182268 | GEO | 2021/08/19

REPOSITORIES: GEO

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

Project description: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

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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 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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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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Direct GR binding sites potentiate clusters of TF binding across the human genome [4]

Project description:The glucocorticoid receptor (GR) binds the human genome at >10,000 sites, but only regulates the expression of hundreds of genes. To determine the functional effect of each site, we measured the glucocorticoid (GC) responsive activity of nearly all GR binding sites (GBSs) captured using chromatin immunoprecipitation (ChIP) in A549 cells. 13% of GBSs assayed had GC-induced activity. The responsive sites were defined by direct GR binding via a GC response element (GRE) and exclusively increased reporter- gene expression. Meanwhile, most GBSs lacked GC-induced reporter activity. The non-responsive sites had epigenetic features of steady state enhancers and clustered around direct GBSs. Together, our data support a model in which clusters of GBSs observed with ChIP-seq reflect interactions between direct and tethered GBSs over tens of kilobases. We further show that those interactions can synergistically modulate the activity of direct GBSs, and may therefore play a major role in driving gene activation in response to GCs. Glucoroticoid receptor binding site chip-seq libraries were cloned into STARR-seq for massively parallel functional analysis. The results were confirmed by ChIP-Exo performed on the GR in A549 cells treated with 100 nM dexamethasone for one hour. This dataset [4] contains the sequences of GR ChIP-seq fragments that have been cloned into the STARR-seq backbone. [4] *.fragments files contain DNA fragments that were cloned into a massively parallel reporter assay. These fragments were generated via ChIP-seq for the glucororticoid receptor. The ChIP-seq library that was used for this source material was sequenced and the data from that sequencing was deposited in [8]. The [4] *.fragments file contains the abundance of each reporter plasmid produced by cloning the GR ChIP-seq library into the reporter vector.

2016-08-25 | E-GEOD-79427 | biostudies-arrayexpress

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

GRÎ±-independent transcriptional activity of hGRÎ² in GR Liver Knockout Mouse

Project description:We used AAV as a vector to deliver hGRÎ² 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 hGRÎ² overexpression in liver affects mGRÎ±âs gene transcription profile in GR Liver Knockout mice. GR Liver Knockout mice were treated with PBS, AAV-GFP and AAV-hGRB, respectively. Each treatment group has four replicates.

2015-12-11 | E-GEOD-75683 | biostudies-arrayexpress

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

Identification of m6A-mediated changes in mouse liver after exposure to polychlorinated biphenyls (PCB126 and Aroclor1260) and high fat diet

Project description:Exposure to polychlorinated biphenyls (PCBs) has been associated with liver injury in human cohorts and with nonalcoholic steatohepatitis (NASH) in mice fed a high fat diet (HFD). N(6)-methyladenosine (m6A) modification of mRNA regulates transcript fate, but the contribution of m6A modification on regulation of transcription in PCB-induced steatosis and fibrosis is unknown. This study tested the hypothesis that PCB and HFD exposure alters the levels of m6A modification in transcripts that play a role in NASH in vivo. Male C57Bl6/J mice were fed a HFD (12 wks.) and administered a single oral dose of Aroclor1260, PCB126, or Aroclor1260 + PCB126. Genome-wide identification of m6A peaks was accomplished by m6A mRNA immunoprecipitation sequencing (m6A-RIP) and the mRNA transcriptome identified by RNA-seq. Exposure of HFD-fed mice to Aroclor1260 decreased the number of m6A peaks and m6A-containing genes relative to HFD control whereas PCB126 or the combination of Aroclor1260+PCB126 increased m6A modification frequency. ~ 41% of genes had one m6A peak and ~49% had 2-4 m6A peaks. 117 m6A peaks were common in the four experimental groups. The Aroclor1260 + PCB126 exposure group showed the highest number (52) of m6A-peaks. qRT-PCR confirmed enrichment of m6A-containing fragments of the Apob transcript with PCB exposure. Integrated analysis of m6A-RIP-seq and mRNA-seq identified 242 differentially expressed genes (DEGs) with increased or reduced number of m6A peaks. Comparative pathway analysis identified “Immune response: IL-6-induced acute-phase response in hepatocytes” in the Aroclor1260 + PCB126 samples, consistent with steatohepatitis in human PCB epidemiological studies. These data show that PCB exposure in HFD-fed mice alters the m6A landscape offering an additional layer of regulation of gene expression affecting a subset of gene responses in NASH.

2023-05-12 | GSE202386 | 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

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