This SuperSeries is composed of the SubSeries listed below.
Deconvolution of blood microarray data identifies cellular activation patterns in systemic lupus erythematosus.
Specimen part, Disease
View SamplesMicroarray deconvolution is a technique for quantifying the relative abundance of constituent cells in a mixture based on that mixture's microarray signature and the signatures of the purified constituents. It has been applied to yeast and other systems but not to blood samples.
Deconvolution of blood microarray data identifies cellular activation patterns in systemic lupus erythematosus.
Specimen part, Disease
View SamplesMicroarray deconvolution is a technique for quantifying the relative abundance of constituent cells in a mixture based on that mixture's microarray signature and the signatures of the purified constituents. Its ability to discriminate related human cells is unknown.
Deconvolution of blood microarray data identifies cellular activation patterns in systemic lupus erythematosus.
No sample metadata fields
View SamplesFamilial hypertrophic cardiomyopathy (FHC) is a disease characterized by ventricular hypertrophy, fibrosis, and aberrant systolic and/or diastolic function. Our laboratories have previously developed 2 mouse models that affect cardiac performance. One transgenic mouse model encodes an FHC-associated mutation in -tropomyosin (Tm180) that displays severe cardiac hypertrophy with fibrosis and impaired physiological performance. The other model was a gene knockout of phospholamban (PLB), a regulator of calcium uptake in the sarcoplasmic reticulum of cardiomyocytes; the hearts of these mice exhibit hypercontractility with no pathological abnormalities. Previous work in our laboratories show that the hearts of mice that were genetically crossed between the Tm180 and PLB KO mice rescues the hypertrophic phenotype and improves their cardiac morphology and function.
Microarray analysis of active cardiac remodeling genes in a familial hypertrophic cardiomyopathy mouse model rescued by a phospholamban knockout.
Age, Specimen part
View SamplesRNase Y of Bacillus subtilis is a key member of the degradosome and important for bulk mRNA turnover. In contrast to B. subtilis, the RNase Y homologue (rny/cvfA) of Staphylococcus aureus is not essential for growth. Here we found that RNase Y plays a major role in virulence gene regulation. Accordingly, rny deletion mutants demonstrated impaired virulence in a murine bacteraemia model. RNase Y is important for the processing and stabilisation of the immature transcript of the global virulence regulator system SaePQRS. Moreover, RNase Y is involved in the activation of virulence gene expression at the promoter level. This control is independent of both the virulence regulator agr and the saePQRS processing and may be mediated by small RNAs some of which were shown to be degraded by RNase Y. Besides this regulatory effect, mRNA levels of several operons were significantly increased in the rny mutant and the half-life of one of these operons was shown to be extremely extended. However, the half-life of many mRNA species was not significantly altered. Thus, RNase Y in S. aureus influences mRNA expression in a tightly controlled regulatory manner and is essential for coordinated activation of virulence genes.
RNase Y of Staphylococcus aureus and its role in the activation of virulence genes.
No sample metadata fields
View SamplesFor Staphylococcus aureus it was shown previously that aminocoumarinecoumarin antibiotics such as novobiocin lead to immediate down-regulation of recA expression and thereby inhibition of the SOS response, the mutation frequency and the recombination capacity. Aminocoumarinecoumarin function by inhibition of the ATPase activity of the gyrase subunit B. Here we analysed the global impact of the DNA relaxing agent novobiocin on gene expression in S. aureus. By use of a novobiocin resistant mutant, it became evident that the change in recA expression is due to gyrase inhibition. Microarray analysis and Northern blot hybridization revealed that the expression of a distinct set of genes is increased (e.g. recF-gyrB-gyrA, rib operon and ure operon )), or decreased (e.g. arlRS, recA, lukA, hlgC, fnbA) by novobiocin. The two-component ArlRS system was previously found to decrease the supercoiling level in S. aureus. Thus, down-regulation of arlRS might in part compensate for the relaxing effect of novobiocin. Novobiocin resulted in down-regulation of several of arlRS repressed target genes in an arl mutant. Global analysis and gene mapping of supercoiling sensitive genes did not give indications that they are clustered in the genome. Promoter fusion assays confirmed that responsiveness of a given gene is intrinsic to the promoter region but independent of the chromosomal location. The results indicate that molecular property of the spacers of a given promoter dictatesa given promoter rather than chromosomal topology dictates the responsiveness towards changes in supercoiling rather than chromosomal topology.
Altering gene expression by aminocoumarins: the role of DNA supercoiling in Staphylococcus aureus.
Treatment
View SamplesTranscript data from heart tissue from fasted-state male BXD strains on chow or high fat diet
Quantifying and Localizing the Mitochondrial Proteome Across Five Tissues in A Mouse Population.
Specimen part, Treatment
View SamplesTranscript data from livers from fasted-state BXD strains on chow or high fat diet
Multilayered genetic and omics dissection of mitochondrial activity in a mouse reference population.
Specimen part
View SamplesTo gain insight into the role of Runx3 in TrkC neurons we performed RNA-seq on E11.5 TrkC neurons isolated from cervical ganglia of Runx3-P2+/- and Runx3-P2-/- mice Overall design: Runx3-P2 mice express GFP in TrkC neurons enabling the FACS isolation of TrkC neurons from E11.5 embryos, Heterozygote Runx3-P2+/-(n=pool of 4) and homozygote Runx3-P2-/- (n=pool of 4) TrkC/GFP neurons were isolated,
An ensemble of regulatory elements controls Runx3 spatiotemporal expression in subsets of dorsal root ganglia proprioceptive neurons.
Specimen part, Cell line, Subject
View SamplesPeripheral blood mononuclear cells were collected from SLE patients in an observational study performed at the University of Michigan
Association of the interferon signature metric with serological disease manifestations but not global activity scores in multiple cohorts of patients with SLE.
Disease
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