Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

LncRNA changes in the livers of db/db mice than that of C57 mice

ABSTRACT: To identify putative lncRNA changes in the livers of db/db mice and C57 mice, we isolated the liver tissues and carried out a microarray analysis. Here, we found significant changes of lncRNAs in the livers of db/db mice. Among them, abnormal expression of ultraconserved elements was noticed.

ORGANISM(S): Mus musculus

PROVIDER: GSE107396 | GEO | 2017/12/14

SECONDARY ACCESSION(S): PRJNA419962

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

lncRNA changes in the livers of db/db mice than that of C57 mice

Project description:lncRNA changes in the livers of db/db mice than that of C57 mice

| PRJNA419962 | ENA

Examination of glycan-related gene expression in the livers of three groups of mice: wild-type, ad-lib-fed type 2 diabetic mice (db/db), and calorically restricted db/db mice

Project description:Assembly of HSPGs in the liver is defective in diabetes mellitus. A major consequence is impaired clearance of post-prandial lipoproteins, which ordinarily depends on the binding of these particles to hepatic HSPGs. Impaired clearance leads to prolonged exposure of the arterial wall to these harmful lipoproteins. We pin-pointed suppression of NDST-1 in livers of type 1 diabetic rats as at least a partial explanation for defective HSPG assembly. Dr. Williams' lab examined glycan-related gene expression in the livers of three groups of mice: wild-type, ad-lib-fed type 2 diabetic mice (db/db), and calorically restricted db/db mice (caloric restriction was shown several years ago to correct their clearance of atherogenic post-prandial lipoproteins). The results will indicate the molecular basis for defective HSPG assembly in type 2 diabetes, which is a question of considerable medical importance. RNA preparations from mice livers (wild-type, ad-lib-fed type 2 diabetic mice, and calorically restricted mice) were sent to Microarray Core (E). The RNA was amplified, labeled, and hybridized to GLYCO_v3 microarrays.

2011-04-29 | E-GEOD-28938 | biostudies-arrayexpress

microRNA microarray profiling in the livers of control db/+ and diabetic db/db mice

Project description:Analysis revealed a set of 13 microRNAs to be significantly altered between livers of control db/+ and diabetic db/db mice. Of these, miR-34a, miR-107, miR-378, miR-378*, miR-31, miR-31*, miR-151-5p, miR-676, miR-22, miR-93, let-7b were up-regulated and let-7e and miR-227 were down-regulated. A total of 670 predicted targets for these altered miRNAs were extracted from PicTar and TargetScan and functional characterisation mapped these targets to several biological processess related to varied metabolic pathways. The Wnt signaling pathway that has been shown to be linked to diabetes emerged as the most prominent pathway from these sets of target genes.

2011-12-22 | GSE17035 | GEO

Transcription profiling of the effect of metformin (50mg/kg,400mg/kg) on gene expression in livers of db/db mice

Project description:Effect of metformin (50mg/kg,400mg/kg) on gene expression in livers of db/db mice.

2006-11-18 | E-MEXP-490 | biostudies-arrayexpress

Expression data from livers of F2 mice (C57BL/6 X DBA/2) deficient in leptin receptor (db/db)

2011-12-29 | GSE30140 | GEO

Expression data from livers of F2 mice (B57BL/6 X DBA/2) deficient in leptin receptor (db/db)

Project description:In several models of obesity-induced diabetes, increased lipid accumulation in the liver has been associated with decreased diabetes susceptibility. For instance, deficiency in leptin receptor (db/db) leads to hyperphagia and obesity in both C57BL/6 and C57BLKS mice but, only on the C57BLKS background do the mice develop beta-cell loss leading to severe diabetes while C57BL/6 mice are relatively resistant. Liver triglyceride levels in the resistant C57BL/6 mice are 3 to 4 fold higher than in C57BLKS. To better understand the mechanisms contributing to metabolic dysfunction in obesity-induced diabetes, we used microarrays to comprehensively profile gene expression livers of F2 mice (B57BL/6 X DBA/2) deficient in leptin receptor (db/db) DBA/2J females were mated to C57BL/6 males carrying leptin receptor deficiency (db/+) and, F1 (db/+) offspring were interbred to produce F2 mice. Offspring deficient in leptin receptor (db/db) were fed on a chow diet until 5 weeks or 12 weeks of age and then euthanized for collection of liver tissue for RNA profiling along with other diabetes-related phenotypes.

2011-12-29 | E-GEOD-30140 | biostudies-arrayexpress

Profiling pancreatic islets from obese db/db and lean control db/+ mice

2013-03-22 | GSE31953 | GEO

Profiling pancreatic islets from obese db/db and lean control db/+ mice

Project description:This program addresses the molecular basis of beta-cell failure associated with the development of type 2 diabetes in the db/db mice. Specifically, which genes are differentially expressed in pancreatic islets of the db/db mice compared to the control db/+ mice? The db/db mice islets profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the islets of db/db mice compared to the corresponding db/+ controls.

2013-03-22 | E-GEOD-31953 | biostudies-arrayexpress

Anti-GCGR antibody treatment in db/db mice

Project description:Gene expression of liver tissue from db/db untreated (6x replicates) and db/db treated with 5mg/kg of 3c7.v44 mAb (6x replicates). Anti-GCGR antibody treatment in db/db mice: fig 2b in Solloway et al.

2015-06-02 | GSE68142 | GEO

Profiling epididymal white adipose tissue (eWAT) from obese db/db and lean control db/+ mice

Project description:This program addresses the gene signature associated with the development of type 2 diabetes in the db/db mice. Specifically, which genes are differentially expressed in adipose tissue of the db/db mice compared to the control db/+ mice?

2013-03-22 | GSE38082 | GEO

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