Duchenne Muscular Dystrophy (DMD) is a fatal muscle wasting disorder caused by dystrophin deficiency. Previous work suggested that increased expression of the dystrophin-related protein utrophin in the mdx mouse model of DMD can prevent dystrophic pathophysiology. Physiological tests showed that the transgenic mouse muscle functioned in a way similar to normal muscle. More recently, it has become possible to analyse disease pathways using microarrays, a sensitive method to evaluate the efficacy of a therapeutic approach. We thus examined the gene expression profile of mdx mouse muscle compared to normal mouse muscle and compared the data with that obtained from the transgenic line expressing utrophin. The data confirm that the expression of utrophin in the mdx mouse muscle results in a gene expression profile virtually identical to that seen for the normal mouse. This study confirms that a strategy to up-regulate utrophin is likely to be effective in preventing the disease.
Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for dystrophin deficiency.
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View SamplesSkeletal muscle actin mice (Crawford et al., (2002) Mol Cell Biol 22, 5587) were crossed with cardiac actin transgenic mice (termed "ACTC^Coco" or "Coco" for short), to produce mice that had cardiac actin instead of skeletal muscle actin in their skeletal muscles (termed "ACTC^Co/KO" or for short "Coco/KO"). Microarray analysis using the Illumina mouse-6 v1.1 expression beadchip was performed on RNA extraced from the soleus muscle of Coco/KO mice and wildtype mice, to confirm the swith in actin isoform expression, and to determine what other differences might exist between wildtype mice and the Coco/KO mice.
Rescue of skeletal muscle alpha-actin-null mice by cardiac (fetal) alpha-actin.
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View SamplesWith the aim of understanding how Treg cells in highly vascularized tissues are related to Treg cells in other organs, we performed RNA-seq analysis of bulk Treg and Tconv cells isolated from liver, blood, spleen, and the liver-draining portal lymph node. This revealed a clear separation of cell transcriptomes by both tissue and Treg/Tconv identity, with cells from the liver falling between blood- and spleen-derived cells. Compared to splenic Treg cells, hepatic Treg cells were enriched for genes related to proliferation and activation, and genes encoding chemokine and cytokine receptors. Overall design: RNA was extracted from FACS-purified Tconv and Treg cells from various tissues of Foxp3Thy1.1 mice. Each sample contains cells pooled from 3 mice. 2 cell types from each of 4 tissues x 3 replicates = 24 samples.
CD49b defines functionally mature Treg cells that survey skin and vascular tissues.
Sex, Age, Specimen part, Cell line, Subject
View SamplesWhile unique subsets of Treg cells have been described in some non-lymphoid tissues, their relationship to Treg cells in secondary lymphoid organs and circulation remains unclear. We have identified a recirculating and highly suppressive effector Treg cell subset that expresses the a2 integrin, CD49b, and exhibits a unique tissue distribution. To identify genes and pathways enriched in CD49b+ Treg cells, we performed RNA-seq of splenic CD49b+ and CD49b- Treg cells that were of otherwise similar activation status based on expression of CD44 and CD62L. This revealed that splenic CD49b+ Treg cells express genes related to migration and activation, but are relatively depleted of genes whose expression is TCR-dependent in Treg cells. These results shed light on the identity and development of a functionally potent subset of mature effector Treg cells that recirculates through and surveys peripheral tissues. Overall design: RNA was extracted from FACS-purified splenic Tconv and Treg cells of different activation states from Foxp3GFP mice. 2 CD4+ T-cell lineages x 3 activation states x 4 replicates. There is no sample 3 (RNA was degraded); there are 23 samples in total.
CD49b defines functionally mature Treg cells that survey skin and vascular tissues.
Sex, Age, Specimen part, Cell line, Subject
View SamplesIdentify genes which are induced in wild type, crel ko, and relbcrle dbko B cells under BAFF stimulation, and find the differential expressed genes which are distinct from wildtype controls. Overall design: RNA-seq analysis of wild type, crelko, relbcrel dbko follicular B cells stimulated with BAFF ligand for 6 hours and wildtype only for 27 hours
B-cell survival and development controlled by the coordination of NF-κB family members RelB and cRel.
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View SamplesH929 human myeloma cells were exposed to aminopeptidase inhibitor (CHR-2797), HDAC inhibitor (CHR-3996), or a combinaion of the two agents, for 24 hours.
The combination of HDAC and aminopeptidase inhibitors is highly synergistic in myeloma and leads to disruption of the NFκB signalling pathway.
Specimen part, Cell line, Treatment
View SamplesWhile unique subsets of Treg cells have been described in some non-lymphoid tissues, their relationship to Treg cells in secondary lymphoid organs and circulation remains unclear. We have identified a short-lived effector Treg cell subset that expresses the a2 integrin, CD49b, and exhibits a unique tissue distribution. Projection of the CD49b+ Treg signature onto the Treg phenotypic landscape as inferred by single-cell RNA-seq analysis, placed these cells at the apex of the Treg developmental trajectory. These results shed light on the identity and development of a functionally potent subset of mature effector Treg cells that recirculate through and survey peripheral tissues. Overall design: Single-cell RNA-seq libraries (10x Genomics) were prepared from FACS-purified Tconv and Treg cells from pooled spleens of Foxp3GFP mice.
CD49b defines functionally mature Treg cells that survey skin and vascular tissues.
Sex, Age, Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Alignment of time course gene expression data and the classification of developmentally driven genes with hidden Markov models.
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View SamplesThe 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. Overall design: Pooled dissected tissue of the suprachiasmatic nucleus from five adult male mice provided one of three replicates for each of six timepoints over a 12:12 light/dark (LD) cycle (ZT2, 6, 10, 14, 18 and 22). Each biological replicate was sequenced over 3 seperate lanes using Illumina HiSeq.
Temporal transcriptomics suggest that twin-peaking genes reset the clock.
Specimen part, Cell line, Subject
View SamplesChanges in gene expression during berry development during a grape growing season were analysed.
Alignment of time course gene expression data and the classification of developmentally driven genes with hidden Markov models.
No sample metadata fields
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