Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Quantitative proteomics of human pancreatic beta cells

ABSTRACT: Outline: using label-free alternate-scanning LC-MS/MS, we compared the proteomic architecture of core functional pathways in pancreatic beta cells of human origin. Results: we quantified the relative molar abundance of 707 proteins mainly composed of functional pathways of metabolism, protein synthesis and cytoskeleton.

INSTRUMENT(S): Synapt MS

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: J.M.F.G. Aerts

PROVIDER: MSV000082882 | MassIVE | Fri Aug 31 16:05:00 BST 2018

SECONDARY ACCESSION(S): PXD001539

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Publications

Quantitative proteomics of rat and human pancreatic beta cells.

Brackeva B B Kramer G G Vissers J P C JP Martens G A GA

Data in brief 20150310

Data set description: This data set is composed by label-free alternate-scanning LC-MS/MS proteomics analysis human and Wistar rat pancreatic islet endocrine cells. The mass spectrometry data of the human and rat pancreatic beta cells and the resulting proteome search output from ProteinLynx GlobalSERVER (PLGS) have been deposited to the ProteomeXchange Consortium [1] via the PRIDE partner repository with the dataset identifiers PXD001539 (human) and PXD001816 (rat). From these mass spectrometry ...[more]

PMID: 26217750

Similar Datasets

Quantitative proteomics of human pancreatic beta cells

Project description:Outline: using label-free alternate-scanning LC-MS/MS, we compared the proteomic architecture of core functional pathways in pancreatic beta cells of human origin. Results: we quantified the relative molar abundance of 707 proteins mainly composed of functional pathways of metabolism, protein synthesis and cytoskeleton.

2015-08-07 | PXD001539 | Pride

Single-Cell Transcriptomics Links Loss of Human Pancreatic β-Cell Identity to ER Stress

Project description:The maintenance of pancreatic islet architecture is crucial for proper β-cell function. We previously reported that disruption of human islet integrity could result in altered β-cell identity. Here we combine β-cell lineage tracing and single-cell transcriptomics to investigate the mechanisms underlying this process in primary human islet cells. Using drug-induced ER stress and cytoskeleton modification models, we demonstrate that altering the islet structure triggers an unfolding protein response that causes the downregulation of β-cell maturity genes. Collectively, our findings illustrate the close relationship between endoplasmic reticulum homeostasis and β-cell phenotype, and strengthen the concept of altered β-cell identity as a mechanism underlying the loss of functional β-cell mass.

2024-04-13 | GSE263565 | GEO

Expression profiling of pancreatic beta-cells harboring a pancreatic-specific deletion of PPAR-beta

Project description:Peroxisome proliferator-activated receptor beta/delta protects against obesity by reducing dyslipidemia and insulin resistance via effects in various organs, including muscle, adipose tissue, liver, and heart. However, nothing is known about the function of PPAR-beta in pancreas, a prime organ in the control of glucose metabolism. To gain insight into so far hypothetical functions of this PPAR isotype in insulin production, we specifically ablated Ppar-beta in pancreas. The mutated mice developed a chronic hyperinsulinemia, due to an increase in both beta-cell mass and insulin secretion. Gene expression profiling indicated a broad repressive function of PPAR-beta impacting the vesicular compartment, actin cytoskeleton, and metabolism of glucose and fatty acids. Analyses of insulin release from the islets revealed an increased second-phase glucose-stimulated insulin secretion. Higher levels of PKD, PKC-delta and diacyglycerol in mutated animals lead to an enhanced formation of trans-Golgi network (TGN)-to-plasma-membrane transport carriers in concert with F-actin disassembly, which resulted in increased insulin secretion and its associated systemic effects. Taken together, these results provide evidence for PPAR-beta playing a repressive role on beta-cell growth and insulin exocytosis, which shed new light on its anti-obesity action. Pancreas-specific knock-out animals were generated by breeding mice harbouring a floxed Ppar-beta (PPARbetafl/fl) to mice expressing the Cre transgene under the control of the Pdx1 promoter (Pdx1Cre). Islets from 3 different animals from the knock-out group Pdx1Cre;PPARbetafl/fl and the control littermates group PPARbetafl/fl were compared.

2012-08-30 | E-GEOD-16048 | biostudies-arrayexpress

Single-Cell RNAseq Reveals That Pancreatic β-Cells From Very Old Male Mice Have a Young Gene Signature

Project description:Aging improves pancreatic β-cell function in mice. This is a surprising finding since aging is typically associated with functional decline. We performed single-cell RNA sequencing of β-cells from 3 and 26 month old mice to explore how changes in gene expression contribute to improved function with age. The old mice were healthy, had reduced blood glucose levels and increased β-cell mass, which correlated to their body weight. β-cells from young and old mice had similar transcriptome profiles. In fact, only 193 genes (0.89% of all detected genes) were significantly regulated (≥ 2-fold; false discovery rate < 0.01; normalized counts > 5). Of these, 183 were downregulated and mainly associated with pathways regulating gene expression, cell cycle, cell death and survival as well as cellular movement, function and maintenance. Collectively, our data show that β-cells from very old mice have transcriptome profiles similar to those of young mice. These data support previous findings that aging is not associated with reduced β-cell mass or functional β-cell decline in mice.

2016-06-30 | GSE83146 | GEO

Expression profiling of pancreatic beta-cells harboring a pancreatic-specific deletion of PPAR-beta

2012-08-30 | GSE16048 | GEO

Functional E3 ligase hotspots and resistance mechanisms to small-molecule degraders [Saturating mutagenesis]

Project description:Targeted protein degradation is a novel pharmacology established by drugs that recruit target proteins to E3 ubiquitin ligases. Based on the structure of the degrader and the target, different E3 interfaces are critically involved, thus forming defined "functional hotspots". Understanding disruptive mutations in functional hotspots informs on the architecture of the assembly, and highlights residues susceptible to acquire resistance phenotypes. Here, deep mutational scanning revealed hotspots that are conserved or specific for chemically distinct degraders and targets and validated hotspots mutated in patients that relapse from degrader treatment.

2022-09-09 | GSE198278 | GEO

ISL1 controls pancreatic alpha cell fate and regulates beta cell differentiation and maturation [RNA-seq]

Project description:Glucose homeostasis is dependent on functional pancreatic α and ß cells. Mechanisms underlying generation and maturation of these endocrine cells remain unclear. Here, we unravel the molecular mode of action of ISL1 in controlling α cell fate and endocrine differentiation in the pancreas. By combining transgenic mouse models, transcriptomic and epigenomic profiling, we uncover that elimination of Isl1 results in a diabetic phenotype with a complete loss of α cells, disrupted pancreatic islet architecture, downregulation of maturation markers of ß cells, and an enrichment in an intermediate endocrine progenitor transcriptomic profile. Mechanistically, apart from the altered transcriptome of pancreatic endocrine cells, Isl1 elimination results in altered silencing H3K27me3 histone modifications in the promoter regions of the essential genes for endocrine cell differentiation. Our results thus show that ISL1 transcriptionally and epigenetically controls α cell fate competence, and ß cell maturation, suggesting that ISL1 is a critical component for generating functional α and ß cells.

2022-06-17 | GSE206093 | GEO

ISL1 controls pancreatic alpha cell fate and regulates beta cell differentiation and maturation [CUT&Tag]

2022-06-17 | GSE206092 | GEO

Correlating pancreatic beta cell function with their transcriptional profiles

Project description:The stage at which beta cells become functional were first determined with GSIS and Ca++ imaging. Then beta cells at key stages of maturation were purified and their gene expression alterations were determined with RNAseq and exhaustive bioinformatics analyses.

2015-01-30 | E-MTAB-2266 | biostudies-arrayexpress

Cellular signaling underlying GSIS in pancreatic β-cells

Project description:In the present study, we investigated signaling pathways associated with GSIS in freshly isolated rat Islets of Langerhans. Specifically, our aim was to reveal which phosphosites and N-linked sialylated glycosylation sites that were reversible regulated upon brief glucose stimulation and link these to cellular signaling pathways using bioinformatics tools.

2017-11-14 | PXD007689 | Pride

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