Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression in pancreatic beta-cells post EMC-D virus infection

ABSTRACT: Gene expression in pancreatic beta-cells post EMC-D virus infection

PROVIDER: PRJNA547795 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Gene expression in pancreatic beta-cells post EMC-D virus infection

Project description:In order to reveal context specific gene expression in pancreatic beta-cells, beta-cells were purified by flow cytometry from two days after EMC-D virus infected mice, and performed microarray analysis.

2019-12-31 | GSE132388 | GEO

Rhesus macaque model of hCoV-EMC respiratory infection

Project description:Microarray analysis of peripheral blood mononuclear cells (PBMCs), lungs, and lung lesions collected over the course of hCoV-EMC infection of 6 rhesus macaques.

2013-08-29 | GSE44542 | GEO

Rhesus macaque model of hCoV-EMC respiratory infection

Project description:Microarray analysis of peripheral blood mononuclear cells (PBMCs), lungs, and lung lesions collected over the course of hCoV-EMC infection of 6 rhesus macaques. 6 rhesus macaques were infected intratracheally with hCoV-EMC. PBMCs were collected at days 0, 1, 3, and 6, and lungs were collected from serial sacrifices of 3 animals each at day 3 and day 6. Infection produced a mild-moderate, self-limiting respiratory infection, and was not lethal. We performed microarray analysis (using Agilent Rhesus arrays) on all lungs, lung lesions, and PBMCs collected for the study.

2013-08-29 | E-GEOD-44542 | biostudies-arrayexpress

Cell host-response to infection with novel human coronavirus EMC predict potential antivirals and important differences with SARS-coronavirus.

Project description:Differential expression was determined in Calu-3 cells between mock infected and infection with either Human coronavirus EMC and SARS coronavirus at different times post infection. Calu-3 2B4 cells were infected with Human Coronavirus EMC 2012 (HCoV-EMC) or mock infected. Samples were collected 0, 3, 7, 12, 18 and 24 hpi. There are 3 mock and 3 infected replicates for each time point, except for 12 hpi for which there are only 2 infected replicates (one replicate did not pass RNA quality check). There were no mock sampes at 18 hpi, and therefore infected samples at 18 hpi were compared with mocks at 24 hpi. For direct comparison with SARS-CoV infected cells, raw data from HCoV-EMC experiments were quantile normalized together with the SARS-CoV dataset (GEO Series accession number GSE33267).

2013-05-03 | E-GEOD-45042 | biostudies-arrayexpress

Cell host-response to infection with novel human coronavirus EMC predict potential antivirals and important differences with SARS-coronavirus.

2013-05-03 | GSE45042 | GEO

Phosphoproteome of mouse pancreatic beta cell

Project description:TMT-labeled phosphoproteome data of mouse pancreatic beta cell

2021-05-11 | PXD022745 | JPOST Repository

Functional analysis of CNOT3 in pancreatic beta cells

Project description:Pancreatic β-cells are responsible for production and secretion of insulin in response to increasing blood glucose levels. Therefore, defects in pancreatic β-cell function lead to hyperglycemia and diabetes mellitus. Understanding the molecular mechanisms governing β cell function is crucial for development of novel treatment strategies for this disease. The aim of this project was to investigate the role of Cnot3, part of CCR4-NOT complex, major deadenylase complex in mammals, in pancreatic β cell function. Cnot3βKO islets display decreased expression of key regulators of β cell maturation and function. Moreover, they show an increase of progenitor cell markers, β cell-disallowed genes and genes relevant to altered β cell function. Cnot3βKO islets exhibit altered deadenylation and increased mRNA stability, partly accounting for the increase of those genes. Together, these data reveal that CNOT3-mediated mRNA deadenylation and decay constitute previously unsuspected post-transcriptional mechanisms essential for β cell identity.

2020-08-31 | PXD018403 | Pride

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 RNA sequencing of zebrafish pancreatic cells during beta-cell regeneration

Project description:To better understand the underlying mechanism of beta-cell regeneration in adult zebrafish, we performed single-cell transcriptomic profiling of the pancreatic tissue (using 10X Genomics) at various stages post beta-cell ablation.

2022-06-21 | GSE166052 | GEO

Transcriptional profiling of pancreatic beta cells during maturation and with function-inactivating mutations

Project description:Islet β-cells from newborn mammals need a maturation process to become mature functional beta cells. The detailed molecular mechanisms were not completely understood. This study was designed to reveal the dynamic gene expression changes during pancreatic beta-cell maturation in postnatal mice. We also want to understand how genetic mutations that impair beta-cell function change the genetic networks involved in the beta-cell maturation process. For these aims, pancreatic beta cells were isolated at P1 islets based on the expression of a MipeGFP transgene in a genetic background with pancreatic specific inactivation of Myt1, Myt1L, and St18 (denoted as MytDelpanc; MipeGFP).

2018-04-01 | E-MTAB-6615 | 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