Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ad3d7e51-efd1-42bd-bdcf-dc95c81ad662 - samples

ABSTRACT: 7 RNA-Seq datasets in human pancreatic islets from 7 donors, where islets were using low (4mM) glucose conditions.

PROVIDER: EGAD00001005208 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

eacf0d42-4f44-476c-aef2-dd554a1e9d5f - samples

Project description:7 RNA-Seq datasets in human pancreatic islets from 7 donors, where islets were treated in high (11mM) glucose conditions

| EGAD00001005207 | EGA

18c3c6ae-3626-41c0-8f64-eeeebe56788b - samples

Project description:14 ChIP-Seq datasets of H3K27ac in human pancreatic islets from 14 donors, where islets were treated in high (11mM) glucose conditions. Samples IDs HI-129, HI-130, HI-131, HI-132, HI-135, HI-137 and HI-152 were also cultured in low glucose conditions.

| EGAD00001005204 | EGA

2a55ff79-e333-4e5c-b9cb-854fbf65deb3 - samples

Project description:7 H3K27ac ChIP-Seq datasets from 7 donors where islets were treated in low (4mM) glucose conditions.

| EGAD00001005205 | EGA

e2c51f53-edb0-4f6e-aa02-5b22bbb27c0b - samples

Project description:13 ATAC-Seq datasets of human pancreatic islets from 13 donors

| EGAD00001005201 | EGA

4142bbc0-4e34-41f4-ac1d-13706f7aceb3 - samples

Project description:3 ChIP-Seq datasets of Cohesin in human pancreatic islets from 3 donors

| EGAD00001005203 | EGA

bfec3c13-930c-4ff3-b710-ac86638f6ff4 - samples

Project description:6 ChIP-Seq datasets of Mediator in human pancreatic islets from 6 donors

| EGAD00001005202 | EGA

f43ad0e6-8478-4fa8-b474-8da7521749d1 - samples

Project description:4 Promoter-Capture Hi-C datasets of human pancreatic islets from 4 human islet donors

| EGAD00001005206 | EGA

Epigenomic plasticity enables human pancreatic alpha to beta cell reprogramming

Project description:Insulin-secreting β cells and glucagon-secreting α cells maintain physiological blood glucose levels, and their malfunction drives diabetes development. Using ChIP sequencing and RNA sequencing analysis, we determined the epigenetic and transcriptional landscape of human pancreatic α, β, and exocrine cells. We found that, compared with exocrine and β cells, differentiated α cells exhibited many more genes bivalently marked by the activating H3K4me3 and repressing H3K27me3 histone modifications. This was particularly true for β cell signature genes involved in transcriptional regulation. Remarkably, thousands of these genes were in a monovalent state in β cells, carrying only the activating or repressing mark. Our epigenomic findings suggested that α to β cell reprogramming could be promoted by manipulating the histone methylation signature of human pancreatic islets. Indeed, we show that treatment of cultured pancreatic islets with a histone methyltransferase inhibitor leads to colocalization of both glucagon and insulin and glucagon and insulin promoter factor 1 (PDX1) in human islets and colocalization of both glucagon and insulin in mouse islets. Thus, mammalian pancreatic islet cells display cell-type–specific epigenomic plasticity, suggesting that epigenomic manipulation could provide a path to cell reprogramming and novel cell replacement-based therapies for diabetes. Pancreatic islets were collected post-mortem from 6 human donors and subjected to FACS to separate populations of alpha, beta, and exocrine cells. Depending on the availability of resulting material, sorted islet cell populations were used for H3K4me3, H3K27me3 ChIP-seq, or RNA-seq analysis. All ChIP-seq samples have a corresponding input from the same sample.

2013-08-28 | E-GEOD-50386 | biostudies-arrayexpress

Single-cell transcriptomics of primary human pancreatic islet cells exposed to stress conditions associated with beta-cell failure.

Project description:Diabetes mellitus (DM) is a chronic disease associated with elevated blood glucose level and resulting from a loss of functional beta-cell mass. The goal of this study is to investigate the response of human pancreatic cells to pathophysiological conditions associated with beta-cell dysfunction, ultimately to identify molecular mechanisms contributing to the development of diabetes. Isolated primary human islets from three non-diabetic donors were exposed in vitro to pro-inflammatory, oxidative, metabolic and endoplasmic reticulum stress for up to 3 days. Subsequently the cells were processed for single-cell RNA sequencing (scRNA-seq). Analysis of the dataset revealed both common and specific molecular response of each pancreatic cell type to the various stress conditions.

2023-06-19 | GSE218316 | GEO

Mapping of INS promoter interactions reveals its role in long-range regulation of SYT8 transcription

Project description:Insulin (INS) synthesis and secretion from pancreatic M-NM-2 cells are tightly regulated; their deregulation causes diabetes. Here we map INS-associated loci in human pancreatic islets by 4C and 3C techniques and show that the INS gene physically interacts with the SYT8 gene, located over 300 kb away. This interaction is elevated by glucose and accompanied by increases in SYT8 expression. Inactivation of the INS promoter by promoter-targeting siRNA reduces SYT8 gene expression. SYT8-INS interaction and SYT8 transcription are attenuated by CTCF depletion. Furthermore, SYT8 knockdown decreases insulin secretion in islets. These results reveal a non-redundant role for SYT8 in insulin secretion and indicate that the INS promoter acts from a distance to stimulate SYT8 transcription. This suggests a function for the INS promoter in coordinating insulin transcription and secretion through long-range regulation of SYT8 expression in human islets. Circular Chromosome Conformation Capture (4C)-Seq experiments to profile interactions of INS promoter in human pancreatic islets isolated from two donors: donor 1 and donor 2.

2011-02-22 | E-GEOD-25862 | 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