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

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

PROVIDER: PRJNA913819 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25409721_1.fastq.gz	Fastqsanger.gz
	SRR25409721_2.fastq.gz	Fastqsanger.gz
	SRR25409722_1.fastq.gz	Fastqsanger.gz
	SRR25409722_2.fastq.gz	Fastqsanger.gz
	SRR25409723_1.fastq.gz	Fastqsanger.gz

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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.

2023-09-25 | GSE221276 | GEO

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

2023-09-25 | GSE221274 | GEO

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

2023-09-25 | GSE221275 | GEO

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

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

| PRJNA913812 | ENA

Modulation of insulin secretion through RBFOX2-mediated alternative splicing

Project description:Modulation of insulin secretion through RBFOX2-mediated alternative splicing

| PRJNA913814 | ENA

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

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

Project description:Modulation of insulin secretion through RBFOX2-mediated alternative splicing [RNA-seq Mouse Iselt]

| PRJNA913820 | ENA

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

| PRJNA761990 | ENA

Modulation of insulin secretion by RBFOX2-mediated alternative splicing.

Project description:Insulin secretion is a tightly regulated process that is vital for maintaining blood glucose homeostasis. Although the molecular components of insulin granule trafficking and secretion are well established, how they are regulated to rapidly fine-tune secretion in response to changing environmental conditions is not well characterized. Recent studies have determined that dysregulation of RNA-binding proteins (RBPs) and aberrant mRNA splicing occurs at the onset of diabetes. We demonstrate that the RBP, RBFOX2, is a critical regulator of insulin secretion through the alternative splicing of genes required for insulin granule docking and exocytosis. Conditional mutation of Rbfox2 in the mouse pancreas results in decreased insulin secretion and impaired blood glucose homeostasis. Consistent with defects in secretion, we observe reduced insulin granule docking and corresponding splicing defects in the SNARE complex components. These findings identify an additional mechanism for modulating insulin secretion in both healthy and dysfunctional pancreatic β cells.

| S-EPMC10676425 | biostudies-literature

Deciphering RBP - alternative splicing networks in ALS iPSC-MN: TDP-43, NOVA1, NOVA2 and RBFOX2 eCLIP-seq

Project description:We produced enhanced cross-linking immunoprecipitation (eCLIP) sequencing data of the RNA binding proteins (RBP) TDP-43, NOVA1, NOVA2 and RBFOX2 in iPSC motor neurons of two healthy control individuals, respectively.

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