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Quantitative proteomics of rat and human pancreatic beta cells

ABSTRACT: Quantitative proteomics of rat and human pancreatic beta cells

INSTRUMENT(S): Synapt G2 MS

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Pancreas

SUBMITTER: Hans Vissers

LAB HEAD: Geert Martens

PROVIDER: PXD001816 | Pride | 2015-08-04

REPOSITORIES: Pride

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			Action	DRS
	alpha_001_001_Pride.pride.mgf.gz	Mgf
	alpha_001_001_Pride.pride.mztab.gz	Mztab
	alpha_001_001_Pride.xml.gz	Xml
	alpha_001_002_Pride.pride.mgf.gz	Mgf
	alpha_001_002_Pride.pride.mztab.gz	Mztab

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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

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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

Functional characteristics of neonatal rat beta cells With distinct markers

Project description:Neonatal beta cells are considered developmentally immature and hence less glucose-responsive. To study the acquisition of mature glucose-responsiveness, we compared glucose-regulated redox state, insulin synthesis and secretion of beta cells purified from neonatal or 10-weeks old rats to their transcriptomes and proteomes measured by oligonucleotide and LC-MS/MS profiling. Lower glucose-responsiveness of neonatal beta cells was explained by two distinct properties: higher activity at low glucose and lower activity at high glucose. Basal hyperactivity was associated with higher NAD(P)H, a higher fraction of neonatal beta cells actively incorporating 3H-Tyrosine, and persistently increased insulin secretion below 5 mM glucose. Neonatal beta cells lacked the steep glucose-responsive NAD(P)H rise between 5-10 mM glucose characteristic for adult beta cells, and accumulated less NAD(P)H at high glucose. They had 2-fold lower expression of malate/aspartate-NADH shuttle and most glycolytic enzymes. Genome-wide profiling situated neonatal beta cells at a developmental crossroad: they showed advanced endocrine differentiation when specifically analyzed for their mRNA/protein level of classical neuroendocrine markers. On the other hand, discrete neonatal beta cell subpopulations still expressed mRNAs/proteins typical for developing/proliferating tissues. One example, Delta-like 1 homolog (DLK1) was used to investigate if neonatal beta cells with basal hyperactivity corresponded to a more immature subset with high DLK1, but no association was found. In conclusion, the current study supports the importance of glycolytic NADH-shuttling in stimulus-function coupling, presents basal hyperactivity as novel property of neonatal beta cells, and provides potential markers to recognize intercellular developmental differences in the endocrine pancreas.

2014-12-12 | PXD001577 | Pride

The translational landscape of mTOR signaling steers cancer initiation and metastasis

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