Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of mouse spinal chord from a mouse model of severe spinal muscular atrophy

ABSTRACT: Pre-symptomatic development of lower motor neuron connectivity in a mouse model of severe spinal muscular atrophy

ORGANISM(S): Mus musculus

DISEASE(S): spinal muscular atrophy

SUBMITTER: Sheena Lee

PROVIDER: E-MEXP-2428 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Pre-symptomatic development of lower motor neuron connectivity in a mouse model of severe spinal muscular atrophy.

Murray Lyndsay M LM Lee Sheena S Bäumer Dirk D Parson Simon H SH Talbot Kevin K Gillingwater Thomas H TH

Human molecular genetics 20091102 3

The childhood motor neuron disease spinal muscular atrophy (SMA) results from reduced expression of the survival motor neuron (SMN) gene. Previous studies using in vitro model systems and lower organisms have suggested that low levels of Smn protein disrupt prenatal developmental processes in lower motor neurons, influencing neuronal outgrowth, axon branching and neuromuscular connectivity. The extent to which these developmental pathways contribute to selective vulnerability and pathology in th ...[more]

PMID: 19884170

Similar Datasets

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

Trancriptional regulation by axonal SMN on motor neuron cells

Project description:Muscular atrophy (SMA) is an autosomal recessive disease causing selective motor neuron death by the loss of telomeric survival motor neuron gene, SMN1. Axonal SMN, a-SMN, is a truncated form of SMN, derived from an alternatively spliced SMN1 gene. (Setola, et. al. 2007 PNAS 104, 1959-1964). The cellular clones expressing a-SMN in a tetracycline-dependent manner were isolated from NSC34 by two-step stable transfection, first with the tetracycline-repressor construct and subsequently with the a-SMN cDNA. To identify novel a-SMN target genes, the transcriptome of several a-SMN clones was analyzed and compared with that of parental cells.

2012-01-07 | E-MEXP-3402 | biostudies-arrayexpress

C.Nahmias_MDA231_Ang

Project description:Human breast cancer cells (MDA-MB-231) were cultured in serum-free conditions and either left untreated or treated for 24h in presence of 100nM Angiotensin II. Total RNA was extracted using trizol and reverse transcribed prior to analysis.

2012-12-05 | E-MEXP-3470 | biostudies-arrayexpress

FUNCTIONAL ANALYSIS OF CTCF DURING MAMMALIAN LIMB DEVELOPMENT_whole transcriptome

Project description:Limb buds were dissected from E10.75 mouse embryos and stored in RNAlater reagent (Qiagen), for genotyping. For each replicate, RNA was isolated from pools of 6 limb buds either of wild type or homozygous mutants using RNeasy micro-kit (Qiagen). rRNA was depleted using RiboMinusTM Human/Mouse Transcriptome Isolation Kit (Invitrogen). After cRNA amplification, single or double-stranded cDNA was generated using The GeneChip Whole Transcript Amplified Double-Stranded Target Assay kit (Affymetrix) according to manufacturers instructions. cDNA was fragmented and labeled using GeneChip WT Double-Stranded DNA Terminal Labeling Kit (Affymetrix) and hybridized to oligonucleotide tiling arrays. The control genomic DNA samples were fragmented with DNAse I. RNA-chip data were computed at the exon level, by averaging the normalized intensities of all probes falling within the exon. As a complement, array data were quantile normalized within cDNA/genomic DNA replicate groups and scaled to medial feature intensity of 10 using TAS software (Affymetrix). For each genomic position, a dataset was generated consisting of all probes mapping within a sliding window of 80 bp. The averaged ratios were plotted along the genomic DNA sequence using Integrated Genome Browser (IGB) software (Affymetrix).

2011-11-01 | E-MEXP-2980 | biostudies-arrayexpress

Srf muscle cells

Project description:Identification of genes whose expression is dependent upon Srf activation within myotubes

2012-02-24 | E-MEXP-3128 | biostudies-arrayexpress

SScHuEx

Project description:To determine the gene expression profile of endothelial cells derived from endothelial progenitor (EPCs) issued from EPC-derived endothelial cells collected from 10 SSc patients (5 patients with the diffuse cutaneous subset and 5 patient with the limited cutaneous subset) and 5 healthy controls before and after hypoxic exposure.

2012-01-20 | E-MEXP-3075 | biostudies-arrayexpress

Affy Sjogren

Project description:Retuximab response transcription profiling in salivary glands from Sjogren patients

2010-01-05 | E-MEXP-1883 | biostudies-arrayexpress

Microarray of E. faecalis strain VE14089 and codY deletion strain -VE18073

Project description:Cells were grown in Brain Heart Infusion broth to an OD of 0.5, and RNA was extracted.

2011-06-30 | E-MEXP-3068 | biostudies-arrayexpress

The role of IL33-ST2 in acute GVHD

Project description:Comparison between WT and ST2 knock-out T-cells upon allogenic stimulation in vitro for 48h

2015-10-14 | E-MEXP-3954 | biostudies-arrayexpress

MatthieuMAHEVAS

Project description:Splenic tissues from immune thrombocytopenia purpura (ITP) patients splenectomized after primary failure of treatment with the B-cell depleting agent rituximab were analyzed, and antibody-secreting cells were identified as the major B-cell population resisting the treatment. The phenotype, antibody specificity and gene expression profile of these cells were characterized and compared to antibody-secreting cells from untreated ITP spleens and from healthy tissues. Anti-platelet-specific plasma cells (PC) were detected in the spleen of ITP patients up to 6 months after rituximab treatment, and the PC population displayed a long-lived program similar to the one of bone marrow PC, thus explaining for most of these patients the absence of response to rituximab and the response to splenectomy. When analyzed by multiplex PCR at the singlecell level, normal splenic PC showed a markedly different gene expression profile, with an intermediate signature including genes characteristic of both long-lived PC and proliferating plasmablasts. Surprisingly, long-lived PC were not detected either in the inflammatory environment of the untreated ITP spleen. These results suggest that neither the normal nor the auto-immune splenic environment favors the differentiation and residence of long-lived PC, and that it is most probably the milieu generated by B-cell depletion that promotes their local settlement.

2013-08-08 | E-MEXP-3711 | 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