Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Peptidomics of pancreas in wild type and neuronatin deficien mice

ABSTRACT: Pancreata of wild type and a neuronatin deficient mouse strain were homogenised and the peptidome characterised. Particular attention was paid to the processing of insulin, to assess if neuronatin deficiency causes changes in the processing efficiency of insulin and other bioactive peptides produced in the pancreas

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Pancreas

SUBMITTER: Richard Kay

LAB HEAD: Dr Anthony Coll

PROVIDER: PXD024161 | Pride | 2021-11-03

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	18070602.mgf	Mgf
	18070602.raw	Raw
	18070603.mgf	Mgf
	18070603.raw	Raw
	18070604.mgf	Mgf

Items per page:

1 - 5 of 23

Publications

Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity.

Cimino Irene I Rimmington Debra D Tung Y C Loraine YCL Lawler Katherine K Larraufie Pierre P Kay Richard G RG Virtue Samuel S Lam Brian Y H BYH Fagnocchi Luca L Ma Marcella K L MKL Saudek Vladimir V Zvetkova Ilona I Vidal-Puig Antonio A Yeo Giles S H GSH Farooqi I Sadaf IS Pospisilik J Andrew JA Gribble Fiona M FM Reimann Frank F O'Rahilly Stephen S Coll Anthony P AP

Scientific reports 20210902 1

Neuronatin (Nnat) has previously been reported to be part of a network of imprinted genes downstream of the chromatin regulator Trim28. Disruption of Trim28 or of members of this network, including neuronatin, results in an unusual phenotype of a bimodal body weight. To better characterise this variability, we examined the key contributors to energy balance in Nnat<sup>+/-p</sup> mice that carry a paternal null allele and do not express Nnat. Consistent with our previous studies, Nnat deficient ...[more]

PMID: 34475432

Similar Datasets

Pancreas-specific Sirt1-deficiency in mice compromises beta-cell function without development of hyperglycemia

Project description:Sirtuin 1 (Sirt1) has been reported to be a critical positive regulator of glucose-stimulated insulin secretion in pancreatic beta-cells. The effects on islet cells and blood glucose levels when Sirt1 is deleted specifically in the pancreas are still unclear.This study examined islet glucose responsiveness, blood glucose levels, pancreatic islet histology and gene expression in Pdx1-Cre;Sirt1(ex4F/F) mice that have loss of function and loss of expression of Sirt1 specifically in the pancreas. We found that in the Pdx1-Cre;Sirt1(ex4F/F) mice, the relative insulin positive area and the islet size distribution were unchanged. However, beta-cells were functionally impaired, presenting with lower glucose-stimulated insulin secretion. This defect was not due to a reduced expression of insulin but was associated with a decreased expression of the glucose transporter Slc2A2/Glut2 and of the Glucagon like peptide-1 receptor (Glp1r) as well as with a marked down regulation of endoplasmic reticulum (ER) chaperones that participate in the Unfolded Protein Response (UPR) pathway. Counter intuitively, the Sirt1-deficient mice did not develop hyperglycemia. Pancreatic polypeptide (PP) cells were the only other islet cells affected, with reduced numbers in the Sirt1-deficient pancreas. This study provides new mechanistic insights showing that beta-cell function in Sirt1-deficient pancreas is affected due to altered glucose sensing and deregulation of the UPR pathway. Interestingly, we uncover a context in which impaired beta-cell function is not accompanied by increased glycemia. This points to a unique compensatory mechanism. Given the reduction in PP, investigation of its role in the control of blood glucose is warranted. To uncover other Sirt1-regulated mechanisms, we performed a gene expression microarray analysis comparing pancreata from the 6 month old Sirt1âdeficient mice to their controls (n=3 per group).

2016-03-01 | E-GEOD-67239 | biostudies-arrayexpress

The G Protein-coupled Receptor P2Y14 Influences Insulin Release and Smooth Muscle Function in Mice

Project description:UDP-sugars were identified as extracellular signaling molecules, assigning a new function to these compounds in addition to their well defined role in intracellular substrate metabolism and storage. Previously regarded as an orphan receptor, the G protein-coupled receptor (GPCR) P2Y14 (GPR105) was found to bind extracellular UDP and UDP-sugars. Little is known about the physiological functions of this GPCR. To study its physiological role we used a gene-deficient (KO) mouse strain expressing the bacterial LacZ reporter gene to monitor the physiological expression pattern of P2Y14. We found that P2Y14 is mainly expressed in pancreas and salivary glands and in subpopulations of smooth muscle cells of the gastrointestinal tract, blood vessels, lung and uterus. Among other phenotypical differences KO mice showed a significantly impaired glucose tolerance following oral and intraperitoneal glucose application. An unchanged insulin tolerance suggested altered pancreatic islet function. Transcriptome analysis of pancreatic islets showed that P2Y14 deficiency significantly changed expression of components involved in insulin secretion. Insulin secretion tests revealed a reduced insulin release from P2Y14-deficient islets highlighting P2Y14 as a new modulator of proper insulin secretion. 10 samples from pancreatic islets isolated from wildtype mice; 10 samples from pancreatic islets isolated from P2Y14-knockout mice

2014-07-11 | E-GEOD-59285 | biostudies-arrayexpress

LC-MS/MS of different developmental stages of human pancreas

Project description:Mass spectrometry-based quantitative proteomics was used to delineate proteome-wide and extracellular matrix (ECM) alterations at four age groups in human pancreas: fetal (18-20 weeks gestation), juvenile (5-16 years old), young adults (21-29 years old) and older adults (50-61 years old).

2021-01-06 | PXD020130 | Pride

Pancreas-specific deletion of Ikba and RelA.

Project description:The NfkB-pathway is activated early during acute pancreatitis. We investigated the influence on gene expression of two pancreas-specific deletions interfering with NfkB-activation. Pancreata from 8 week old mice were prepared, RNA was isolated and Affymetrix microarray expression analysis was performed.

2012-12-02 | E-MTAB-886 | biostudies-arrayexpress

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

Transcription profiling by array of fetal and adult normal human pancreas tissue

Project description:Pooled total RNA from normal adult human pancreas and fetal human pancreas were purchased from a commercial vendor (Clontech). Each pooled sample was independently labeled and hybridized 3 times.

2015-02-27 | E-MTAB-3368 | biostudies-arrayexpress

Genome-wide analysis of gene expression in mouse pancreas tumors

Project description:Genetically engineered mice developed spontaneous pancreas cancer (Pdx-Cre;LSL-KRASG12D;P53Mut). Mice were also engineered to develop similar spontaneous pancreas cancer without Twist or Snail (conditional gene knockout). The pancreas tumors were harvested and analysed for gene expression profiles comparisons. Total RNA was isolated from the pancreas tumors of 2 mice with wild-type Twist and Snail, from 2 mice without Twist expression in the pancreas, and from 2 mice without Snail expression in the pancreas.

2015-11-20 | E-GEOD-66981 | biostudies-arrayexpress

Hippo Signaling Regulates Differentiation and Maintenance in the Exocrine Pancreas

Project description:The Hippo signaling pathway has become recognized as a context-dependent regulator of cell proliferation, differentiation, and apoptosis in species ranging from Drosophila to human. In this study, we sought to understand whether Hippo signaling plays a role in pancreatic development and organ homeostasis. We analyzed mRNA from 5 samples each from control and DKO mouse pancreas using Affymetrix MouseGene 1.0 ST Array platfrom. Array data was processed by Affymetrix array computational tools.

2013-02-14 | E-GEOD-44298 | biostudies-arrayexpress

RNA sequencing of e15.5 pancreas from Wild Type, Blinc1-/- and Blinc+/- mice.

Project description:We report the transcriptome changes that result of the genomic deletion of one or two alleles of an islet-specific long non-coding RNA (Blinc1) in isolated pancreas from e15.5 mouse embryos. Pancreas from e15.5 embryos were dissected and total RNA extracted. Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the mouse genome (UCSC/mm9) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq.

2016-04-06 | E-GEOD-73711 | biostudies-arrayexpress

Transcriptional profiling by mRNA microarray of pancreas-infiltrating T lymphocytes of NOD mice

Project description:Whole mouse genome microarrays from Agilent were used to determine expression profile of pancreas-infiltrating T CD3+ and total T lymphocytes of NOD mice.

2015-05-29 | E-MTAB-3555 | 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