Global gene expressions of Mtb-infected mouse lungs were compared between with and without PDE4 inhibitor treatment. A lot of host genes are differentially expressed 21d and 28d post-Mtb infection. PDE4 inhibitor, however, downregulate 10% of genes among those and genes differentially regulated by PDE4 inhibitor are mainly involved immune response.
Phosphodiesterase 4 inhibition reduces innate immunity and improves isoniazid clearance of Mycobacterium tuberculosis in the lungs of infected mice.
Specimen part, Disease, Disease stage
View SamplesCDC1551 induced more vigorous immune response in murine bone marrow derived macrophage (BMM). In contrast, in HN878-infected cells, host transcriptional response was delayed but lasted longer.
No associated publication
Specimen part
View SamplesWe identified the predicted FRY gene as a candidate mammary carcinoma susceptibility gene. This gene has not been characterized in mammals, so for part of our analysis we conducted microarray experiments to look at the changes in gene expression which occur when FRY-targeting shRNA is expressed in the nontumorigenic MCF10A mammary epithelial cell line (a cell line which we identified as having higher FRY mRNA expression than breast cancer cell lines).
No associated publication
Cell line
View SamplesWe identified the wt Cop allele of the predicted Fry gene as a mammary carcinoma susceptibility gene. This gene has not been characterized in mammals, so for part of our analysis we conducted microarray experiments to look at the changes in gene expression which occur when the wt Cop Fry allele is ectopically expressed in the MDA-MB-231 breast cancer cell line (a cell line which we identified as having low FRY mRNA expression).
No associated publication
Cell line, Treatment
View SamplesSarcolipin (SLN) is a key regulator of SERCA pump in atria. To determine the role of SLN in atrial Ca2+ homeostasis, we have generated a SLN null (sln-/-) mouse model. Ablation of SLN results in increased SR Ca2+ load and Ca2+ transients in atria. Further, loss of SLN results in electrophysiological and strcutural remodeling of atria.
Ablation of sarcolipin results in atrial remodeling.
Sex, Specimen part
View SamplesAutophagy is a starvation response that facilitates cell survival under metabolic stress and yet defects in autophagy promote tumorigenesis. While the role of understarvation is relatively clearer, its mechanistic role in tumorigenesis is poorly understood. We show that defective autophagy promotes protein damage and accumulation of p62, a marker for protein damage accumulation that is cleared through autophagy pathway. The failure to eliminate p62 in autophagy-defective cells, leads to deregulation of cell signalling and gene expression and ultimately promotes tumorigenesis. Thus defective-autophagy is a mechanism for p62 accumulation commonly observed in human tumors.
Autophagy suppresses tumorigenesis through elimination of p62.
Cell line
View SamplesWe used laser capture microdissection to isolate maxillary arch mesenchyme from E10.5 embryos. This tissue was collected from both control (3x) and Lhx6-/-;Lhx8-/- mutant (3x) samples.
No associated publication
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
ATRX, DAXX or MEN1 mutant pancreatic neuroendocrine tumors are a distinct alpha-cell signature subgroup.
Specimen part
View SamplesGene expression profiling of PanNETs patients samples were performed to understand genotype to phenotype correlations, novel molecular subtypes and cell of origin
ATRX, DAXX or MEN1 mutant pancreatic neuroendocrine tumors are a distinct alpha-cell signature subgroup.
Specimen part
View SamplesRescuing the function of mutant p53 protein is an attractive cancer therapeutic strategy. Using the NCI anticancer drug screen data, we identified two compounds from the thiosemicarbazone family that manifest increased growth inhibitory activity in mutant p53 cells, particularly for the p53R175 mutant. Mechanistic studies reveal that NSC319726 restores WT structure and function to the p53R175 mutant. This compound kills p53R172H knock-in mice with extensive apoptosis and inhibits xenograft tumor growth in a 175-allele specific mutant p53 dependent manner. This activity depends upon the zinc ion chelating properties of the compound as well as redox changes. These data identify NSC319726 as a p53R175 mutant reactivator and as a lead compound for p53 targeted drug development.
Allele-specific p53 mutant reactivation.
Specimen part, Cell line, Treatment
View Samples