Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bfec3c13-930c-4ff3-b710-ac86638f6ff4 - samples

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

PROVIDER: EGAD00001005202 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

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

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

| EGAD00001005203 | EGA

acfa5398-83e8-4ae8-b3c5-f35677cd6f1a - samples

Project description:Input dataset of human islets. To be used in conjuction with Cohesin and Mediator ChIP-Seq datasets.

| EGAD00001005209 | EGA

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

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

| EGAD00001005201 | EGA

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

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

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

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

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

ATAC-seq on human pancreatic islets

Project description:We have studied the impact of T2D on open chromatin in human pancreatic islets. We used assay for transposase-accessible chromatin using sequencing (ATAC-seq) to profile open chromatin in islets from T2D and non-diabetic donors. We identified ATAC-seq peaks representing open chromatin regions in islets of non-diabetic and diabetic donors. The majority of ATAC-seq peaks mapped near transcription start sites. Additionally, peaks were enriched in enhancer regions and in regions where islet-specific TFs bind. Islet ATAC-seq peaks overlap with SNPs associated with T2D and with additional SNPs in LD with known T2D SNPs. There was enrichment of open chromatin regions near highly expressed genes in human islets.

2019-04-06 | GSE129383 | 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