The experiment describes the dynamic transcriptional alterations in brains of ME7- infected, and age-matched, mock-inoculated mice immediatly before inoculation, at two important preclinical time points and at terminal stages.
Transcriptome analysis reveals altered cholesterol metabolism during the neurodegeneration in mouse scrapie model.
Sex, Age, Specimen part, Subject, Time
View SamplesThis study presents transcription profiles for mouse axial progenitors, presomitic mesoderm and tailbud mesoderm. During vertebrate embryonic development, the formation of axial structures is driven by a population of stem-like cells (axial progenitors) that reside in a region of the tailbud called the chordoneural hinge (CNH) where. We have compared the CNH transcriptome with those of surrounding tissues and shown that the CNH and tailbud mesoderm are transcriptionally similar, and distinct from the presomitic mesoderm. Amongst CNH-enriched genes are several that are required for axial elongation, including Wnt3a, Cdx2, Brachyury/T and Fgf8, and androgen/estrogen receptor nuclear signalling components such as Greb1.
<i>Greb1</i> is required for axial elongation and segmentation in vertebrate embryos.
Specimen part
View SamplesX-linked inhibitor of apoptosis (XIAP) is the most potent endogenous caspase inhibitor preventing cell death via caspase-9, -7 and -3 (initiator and executioner caspase pathways). Using short hairpin RNA (shRNA) against XIAP, stably expressed in a parent HCT116 human colon cancer cell line, a series of clones have been developed. XIAP mRNA levels were established by RT-PCR, the four X (XIAP knockdown) clonal cell lines show 82-93% reduction in XIAP mRNA when compared to the four L (luciferase control) cell lines. Immunoblot analysis showed a 67-89% reduction in XIAP protein in X cell lines compared to L. RNA was analysed by microarray and XIAP knockdown was confirmed in 7 probe sets, there was no significant compensation of other IAP family members. XIAP knockdown induced a 2-fold increase in the basal level of apoptosis without modification of caspase 3/7 activity. Finally, XIAP knockdown sensitises cells to radiotherapy by 20%, to recombinant TRAIL by a 3-fold factor, and to paclitaxel and docetaxel by >2 fold factor. Future work should focus on targeted agents such as rhTRAIL in combination with strategies to down regulate XIAP. XIAP antisense is now in clinical development in oncology.
Stable XIAP knockdown clones of HCT116 colon cancer cells are more sensitive to TRAIL, taxanes and irradiation in vitro.
No sample metadata fields
View SamplesRhoBTB2 is a novel Rho GTPase that undergoes loss, underexpression and mutation in breast and lung cancer. We have shown that we can mimic loss of RhoBTB2 through siRNA treatment of primary cells. We propose to perform comparative microarray analysis of primary lung cells to establish the identification of the gene targets of RhoBTb2 regulation.
The atypical Rho GTPase RhoBTB2 is required for expression of the chemokine CXCL14 in normal and cancerous epithelial cells.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Global analysis of the relationship between JIL-1 kinase and transcription.
Specimen part, Cell line
View SamplesProfiling of changes in steady state RNA levels upon RNAi-mediated knockdown of the chromosomal kinase JIL-1 in Drosophila S2 cells.
Global analysis of the relationship between JIL-1 kinase and transcription.
Specimen part
View SamplesChanges ins organellar gene expression trigger retrograde signalling. Prolyl-tRNA synthetase (PRORS1) is located in chloroplasts and mitochondria. Thus, prors1-2 mutants are impaired in chloroplast and mitochondrial gene expression.
Identification of target genes and transcription factors implicated in translation-dependent retrograde signaling in Arabidopsis.
Age, Specimen part
View SamplesComparison of the changes in mitochondrial gene expression of cells in which extracellular growth factors and/or mitogens have been added.
Extracellular growth factors and mitogens cooperate to drive mitochondrial biogenesis.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Escherichia coli infection induces distinct local and systemic transcriptome responses in the mammary gland.
Specimen part, Time
View SamplesInfections of the udder by Escherichia coli very often elicit acute inflammation, while Staphylococcus aureus infections tend to cause mild, subclinical inflammation and persistent infections. The molecular causes undercovering the different disease patterns are poorly understood. We therefore profiled kinetics and extent of global changes in the transcriptome of primary bovine mammary epithelia cells (MEC) subsequent to challenging them with heat inactivated preparations of E. coli or S. aureus pathogens. E. coli swiftly and strongly induced expression of cytokines and bactericidal factors. S. aureus elicited a retarded response and failed to quickly induce expression of bactericidal factors. Both pathogens induced a similar pattern of chemokines for cell recruitment into the udder, but E. coli stimulated their synthesis much faster and stronger. The genes which are exclusively and most strongly up-regulated by E. coli may be clustered into a regulatory network with Tumor necrosis factor alpha (TNF-a) and Interleukin 1 (IL-1) in a central position. In contrast, the expression of these master cytokines is barely regulated by S. aureus. Both pathogens quickly trigger enhanced expression of IL-6. This is still possible after completely abrogating MyD88 dependent TLR-signalling in MEC. The E. coli specific strong induction of TNF-a and IL-1 expression may be causative for the severe inflammatory symptoms of animals suffering from E. coli mastitis while avoidance to quickly induce synthesis of bactericidal factors may support persistent survival of S. aureus within the udder. We suggest that S. aureus subverts MyD88-dependent activation of immune gene expression in MEC.
Comparative kinetics of Escherichia coli- and Staphylococcus aureus-specific activation of key immune pathways in mammary epithelial cells demonstrates that S. aureus elicits a delayed response dominated by interleukin-6 (IL-6) but not by IL-1A or tumor necrosis factor alpha.
Specimen part, Treatment, Time
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