Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Eacf0d42-4f44-476c-aef2-dd554a1e9d5f - samples

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

PROVIDER: EGAD00001005207 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

ad3d7e51-efd1-42bd-bdcf-dc95c81ad662 - samples

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

| EGAD00001005208 | 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

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

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

Expression microarray analysis of human pancreatic islets reveals CD59 function

Project description:Pancreatic islets are central in type 2-diabetes development, which coincides with increased activity of innate immunity. Intriguingly, human pancreatic islets express many complement genes. The most highly expressed gene was the complement inhibitor CD59 that is GPI anchored to the cell membrane, which unexpectedly was found in high amounts intracellularly in beta cells. Silencing of CD59 strongly suppressed insulin secretion. Importantly, this suppression was unrelated to established CD59 functions, but rather depletion of intracellular CD59. Imaging experiments identified a distal site of inhibition in the exocytotic pathway, but prior to emptying of the insulin granules. Proximity Ligation Assays pin-pointed the mechanism to impaired turnover of exocytosis-regulating SNARE-proteins and CD59 was detected in complex with VAMP2 and syntaxin. CD59 was downregulated by 24-h glucose incubations in human islets, rat cell lines and in islets from three rodent diabetes models. Islets from cadaver donors were provided by the Nordic Islet Transplantation Programme (www.nordicislets.org), Uppsala University. The microarrays were performed using GeneChipM-BM-. Human Gene 1.0 ST whole transcript according to Affymetrix standard protocol.

2014-03-02 | E-GEOD-54279 | biostudies-arrayexpress

Global transcriptomic analysis of human pancreatic islets reveals novel genes influencing glucose metabolism [expression array]

Project description:Here we harnessed the potential of expression arrays in 89 human pancreatic islet donors (different levels of blood glucose (HbA1c)) to identify genes regulated in this relevant tissue for type 2 diabetes (T2D). Islets from cadaver donors were provided by the Nordic Islet Transplantation Programme (www.nordicislets.org), Uppsala University. The microarrays were performed using GeneChipM-BM-. Human Gene 1.0 ST whole transcript according to Affymetrix standard protocol.

2014-07-17 | E-GEOD-50397 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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