Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

15 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of mouse model for the metabolic effects of the human fat mass and obesity associated fto gene

ABSTRACT: RNA was purified from liver, skeletal muscle and white adipose tissue of mice with and without a point mutation in exon 6 of the FTO gene.

ORGANISM(S): Mus musculus

SUBMITTER: Sheena Lee

PROVIDER: E-MEXP-2201 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

A mouse model for the metabolic effects of the human fat mass and obesity associated FTO gene.

Church Chris C Lee Sheena S Bagg Eleanor A L EA McTaggart James S JS Deacon Robert R Gerken Thomas T Lee Angela A Moir Lee L Mecinović Jasmin J Quwailid Mohamed M MM Schofield Christopher J CJ Ashcroft Frances M FM Cox Roger D RD

PLoS genetics 20090814 8

Human FTO gene variants are associated with body mass index and type 2 diabetes. Because the obesity-associated SNPs are intronic, it is unclear whether changes in FTO expression or splicing are the cause of obesity or if regulatory elements within intron 1 influence upstream or downstream genes. We tested the idea that FTO itself is involved in obesity. We show that a dominant point mutation in the mouse Fto gene results in reduced fat mass, increased energy expenditure, and unchanged physical ...[more]

PMID: 19680540

Similar Datasets

Transcription profiling by array of wild type and Pcsk5 Vcc mutant mouse embryos

Project description:We have identified an ENU-induced recessive mouse mutation (Vcc) with a pleiotropic phenotype overlapping including cardiac, tracheo-esophageal, anorectal, axial skeletal antero-posterior patterning defects, limb malformations, presacral mass, renal and palatal agenesis, and pulmonary hypoplasia. It results from a C470R mutation in the proprotein convertase PCSK5 (PC5/6, SPC6) that fails to complement a null allele, which also has a similar phenotype. The mutation ablates a predicted disulfide bond in the P domain, and results in reduced secretion, abnormal cellular localisation, and loss of proprotein convertase activity. We analysed whole genome gene expression in a mouse line carrying ENU-generated point mutation in Pcsk5 gene on a mixed background : 25% C57BL6/J on C3H/HeH (mutation originally introduced into C57BL6/J). We show that GDF11, a regulator of Hox expression, anteroposterior patterning and nephrogenesis, is a PCSK5 target, and that Pcsk5 mutation results in abnormal expression of several paralogous caudal Hox genes (Hoxa, Hoxc, Hoxd), and Mnx1 (Hlxb9) that are necessary for caudal embryo development. Our data establishes novel and pleiotropic functions for Pcsk5 in mammalian development and the coordinated expression of caudal Hox genes; and identifies GDF11 as a novel cleavage target for PCSK5. We propose that Pcsk5, at least in part via GDF11, coordinately regulates the expression of caudal Hox paralogs, to control antero-posterior patterning, nephrogenesis, and skeletal and anorectal development.

2008-06-27 | E-TABM-443 | biostudies-arrayexpress

Disrupted circadian rhythms in a mouse model of schizophrenia

Project description:Disrupted circadian rhythms in a mouse model of schizophrenia

2012-03-01 | E-MEXP-3493 | biostudies-arrayexpress

Transcription profiling of zebrafish mutants affected in neural crest development

Project description:Mutants of zebrafish affected in neural crest development (cls/sox10, hps/erbb3, low/tfap2a, nac/mitfa, pfe/csfr1, shd/ltk, spa/kit tdo/trpm7) were compared to their wild type siblings or to wild type controls during development at 28hpf, 48hpf and 4 dpf.

2012-06-05 | E-TABM-748 | biostudies-arrayexpress

Specific proteome changes in platelets from individuals with GATA1-, GFI1B- and RUNX1-linked bleeding disorders

Project description:Mutations in the transcription factors GATA1, GFI1B and RUNX1 (GATA Binding Factor 1, Growth Factor Independence 1B, Runt-related transcription factor 1) cause familial platelet and bleeding disorders. Mutant platelets exhibit common abnormalities including an α-granule reduction. This suggests that similar pathways are deregulated by different transcription factor mutations. To identify common factors, full platelet proteomes from individuals with mutant GATA1R216Q, GFI1BQ287*, RUNX1TD2-6, or RUNX1Q154Rfs, and healthy controls were examined by label free quantitative mass spectrometry. Unsupervised clustering analysis of 2823 reliably quantified proteins revealed profound differences between cases and controls. Among cases, 82 of 174 significantly downregulated proteins were assigned to platelet function, hemostasis and granule biology, in line with platelet dysfunction and bleedings. Remarkably, only two of these proteins were diminished in all affected cases. This indicates that transcription factor mutations alter platelet proteomes in distinct largely non-overlapping manners. In contrast to the two common diminished proteins, 46 proteins were overrepresented in all affected cases compared to controls. These proteins converged to mitochondrial, metabolic and other biological processes. This work provides the quantitative landscape of proteins that affect platelet function when deregulated by mutated transcription factors in inherited bleeding disorders.

2022-02-22 | PXD020343 | Pride

Temporal transcriptomics suggest that twin-peaking genes reset the clock

Project description:The mammalian suprachiasmatic nucleus (SCN) drives daily rhythmic behavior and physiology, yet a detailed understanding of its coordinated transcriptional programmes is lacking. To reveal the true nature of circadian variation in the mammalian SCN transcriptome we combined laser-capture microdissection (LCM) and RNA-Seq over a 24-hour light / dark cycle. We show that 7-times more genes exhibited a classic sinusoidal expression signature than previously observed in the SCN. Another group of 766 genes unexpectedly peaked twice, near both the start and end of the dark phase; this twin-peaking group is significantly enriched for synaptic transmission genes that are crucial for light-induced phase-shifting of the circadian clock. 342 intergenic non-coding RNAs, together with novel exons of annotated protein-coding genes, including Cry1, also show specific circadian expression variation. Overall, our data provide an important chronobiological resource (www.wgpembroke.com/shiny/SCNseq/) and allow us to propose that transcriptional timing in the SCN is gating clock resetting mechanisms. Pooled dissected tissue of the suprachiasmatic nucleus from five adult male mice provided one of three replicates for each of six time points over a 12:12 light/dark (LD) cycle (ZT2, 6, 10, 14, 18 and 22). Each biological replicate was sequenced over 3 separate lanes using Illumina HiSeq.

2015-11-03 | E-GEOD-72095 | biostudies-arrayexpress

Transcription profiling of the role of Suz12 in mouse hematopoietic progenitors

Project description:Comparison of Gene Expression in Wild type to Erg Mld2/+ Lin-Sca1+Kit+ cells

2008-07-01 | E-TABM-380 | biostudies-arrayexpress

IL7R mutational activation can initiate Ph-like and PAX5 P80R precursor B-cell acute lymphoblastic leukemia

Project description:Interleukin-7 receptor α (encoded by IL7R) is essential for lymphoid development. Whether acute lymphoblastic leukemia (ALL)-related IL7R gain-of-function mutations can trigger leukemogenesis remains unclear. Here, we demonstrate that lymphoid-restricted mutant IL7R, expressed at physiological levels in conditional knock-in mice, establishes a pre-leukemia stage in which B-cell precursors display self-renewal ability, initiating precursor B-ALL that resembles PAX5 P80R or Ph-like human leukemia. Full transformation associates with transcriptional upregulation of oncogenes such as Myc or Bcl2, downregulation of tumor suppressors such as Ikzf1 or Arid2, and major IL-7R signaling upregulation (involving both JAK/STAT5 and PI3K/mTOR), required for leukemia cell viability. Accordingly, maximal signaling drives full penetrance and early leukemia onset in homozygous IL7R mutant animals. Notably, we identify 2 transcriptional subgroups in mouse and human Ph-like ALL, and show that dactolisib and sphingosine-kinase inhibitors are novel treatment avenues for IL-7R-related cases. Our model, a unique resource to explore the pathophysiology and therapeutic vulnerabilities of B-ALL, demonstrates that IL7R can initiate this malignancy.

2021-11-02 | PXD017147 | Pride

Transcription profiling of mouse E10.5 female embryos wild-type and mutant for Smchd1

Project description:To investigate the role of the Smchd1 protein in epigenetic silencing of autosomal loci, we carried out a comparative microarray gene expression analysis of wild-type and Smchd1-/- female embryos at E10.5. Embryos were collected at E10.5 after natural mating, sexed and genotyped. Total RNAs were extracted from three individual wild-type and three Smchd1-/- female embryos and cRNAs prepared from these samples was hybridized to Affymetrix GeneChip Mouse Genome 430 2.0 array.

2012-04-01 | E-MTAB-921 | biostudies-arrayexpress

Comparison of phosphorylation status of Wnt proteins in control and Fto deficient cells upon Wnt 3a stimulation

Project description:Wnt Phospho protein profiling comparing control and Fto deficient cell after Wnt3a stimulation Control vs Fto deficient MEFs treated with Wnt 3a condioned medium for 40 minutes. 6 replicates per array

2013-11-21 | E-GEOD-52572 | biostudies-arrayexpress

Transcription profiling of Salmonella enterica (I) serovar Typhi Ty2 wild type and ompR null strains in a strand-specific manner

Project description:Analysis of transcriptome in a strand-specific manner to further refine previous genome annotation; RNA-seq was also combined with microarray and proteome analysis to further define the S. Typhi ompR regulon and identify novel ompR regulated transcripts.

2009-03-03 | E-TABM-644 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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