Cardiac hypertrophy can lead to heart failure, and is induced either by physiological stimuli eg postnatal development, chronic exercise training or pathological stimuli eg pressure or volume overload. Majority of new therapies for heart failure has mixed outcomes. A combined mouse model and oligo-array approach are used to examine whether phosphoinositide 3-kinase (p110-alpha isoform) activity is critical for maintenance of cardiac function and long-term survival in a setting of heart failure. The significance and expected outcome are to recognise genes involved in models of heart failure ie pathological- vs physiology-hypertrophy, and examine the molecular mechanisms responsible for such activity.
PI3K(p110 alpha) protects against myocardial infarction-induced heart failure: identification of PI3K-regulated miRNA and mRNA.
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Activation of the aryl hydrocarbon receptor dampens the severity of inflammatory skin conditions.
Sex, Age, Specimen part, Treatment, Subject
View SamplesTarget genes of four signaling pathways (Notch, Fgf, Retinoic Acid [RA] and Wnt) are identified in the posterior presomitic mesoderm of 12 somite stage zebrafish embryos.
No associated publication
Specimen part
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Dynamic transcriptional events in embryonic stem cells mediated by the super elongation complex (SEC).
Specimen part, Cell line, Treatment
View SamplesDifferentially expressed genes along the paraxial mesoderm of 12 somite stage zebrafish embryos are identified
Spatiotemporal compartmentalization of key physiological processes during muscle precursor differentiation.
Specimen part
View SamplesEnvironmental stimuli are known to contribute to psoriasis pathogenesis and that of other autoimmune diseases, but the mechanism is unknown. Here we show that the aryl hydrocarbon receptor (AhR), a transcription factor that senses environmental stimuli, modulates pathology in psoriasis. AhR-activating ligands reduced inflammation in the lesional skin of psoriasis patients, whereas AhR antagonists upregulated inflammation. Similarly, AhR signaling via the endogenous FICZ ligand reduced the inflammatory response in the imiquimod-induced model of psoriasis and AhR deficient mice exhibited a substantial exacerbation of the disease, compared to AhR sufficient controls. Non-haematopoietic cells, in particular keratinocytes, were responsible for this hyper-inflammatory response, which involved increased reactivity to IL-1beta and upregulation of AP-1 family members of transcription factors. Thus, our data suggest a critical role for AhR in the regulation of inflammatory responses and open the possibility for novel therapeutic strategies in chronic inflammatory disorders.
Activation of the aryl hydrocarbon receptor dampens the severity of inflammatory skin conditions.
Specimen part
View SamplesMurine ES cell gene expression before RA induction are used to compare gene expression for time-points of 2, 4, 6hrs post-induction.
Dynamic transcriptional events in embryonic stem cells mediated by the super elongation complex (SEC).
No sample metadata fields
View SamplesThe object of this study was to identify genes transcriptionally upregulated and downregulated in response to Tcof1 haploin-sufficiency during mouse embryogensis
Prevention of the neurocristopathy Treacher Collins syndrome through inhibition of p53 function.
No sample metadata fields
View SamplesIntestinal polyposis, a precancerous neoplasia, results primarily from an abnormal increase in the number of crypts. Crypts contain intestinal stem cells (ISCs). Thus intestinal polyposis provides an ideal condition for studying stem cell involvement in polyp/tumor formation. Using a conditional knock-out mouse model, we found that the tumor suppressor Phosphatase of Tension homolog (PTEN) governs the proliferation rate and number of ISCs and loss of PTEN results in an excess of ISCs. In PTEN mutants, excess ISCs initiate de-novo crypt formation and crypt fission, recapitulating crypt production in fetal/neonatal intestine. Microarray studies were used to profile the changes in gene expression that occurred when PTEN was knocked out in the intestine.
PTEN-deficient intestinal stem cells initiate intestinal polyposis.
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View SamplesWe identified an endothelial progenitor/stem like population in the endothelial fraction of preexsiting blood vessels.
No associated publication
Age, Specimen part
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