A microarray time series was generated to identify cyclic genes of the segmentation clock in the mouse. The right posterior half presomitic mesoderms (PSM) from 17 mouse embryos were dissected while the contralateral side of the embryo containing the left PSM was immediately fixed to be analyzed by in situ hybridization using a Lfng probe to order the samples along the segmentation clock oscillation cycle. Probes were produced from RNA extracted from the 17 dissected posterior half PSMs using a two-step amplification protocol and were hybridized to Affymetrix GeneChip MOE430A. The reproducibility of the amplification procedure was initially assessed by comparing array data generated from the right and the left posterior PSM from the same embryo. Because of the symmetry of the paraxial mesoderm along the left-right axis, left and right samples are expected to show overtly similar gene expression. RNA was amplified from three such sample pairs (1, a and b; 2, a and b; 3, a and b) and hybridized on Murine Genome U74Av2 array (MG-U74Av2)
A complex oscillating network of signaling genes underlies the mouse segmentation clock.
Age, Specimen part, Subject, Time
View SamplesWe generated Gadd45a,b,g triple-knockout mouse embryonic stem cells and performed RNA-seq expression profiling under six different conditions of cell culture and in vitro differentiation. Overall design: Gadd45a,b,g triple knockout (TKO) mouse embryonic stem cells (mESC) were generated by CRISPR/Cas9. RNA-Seq was performed to compare the transcriptome in three independent Gadd45 TKO versus three independent control mESC lines under different conditions: (i) Serum cultured mESC, (ii) Vitamin C treated mESC, (iii) 2i treated mESC, (iv) mESC differentiated as embryoid bodies (EB), (v) mESC differentiated as a serum-free monolayer, and (vi) EB stimulated with retinoic acid (RA).
GADD45 promotes locus-specific DNA demethylation and 2C cycling in embryonic stem cells.
Specimen part, Cell line, Subject
View SamplesThe Sin3 histone deacetylase (HDAC) complex is a 1.2 MDa chromatin modifying complex that can repress transcription by binding to gene promoters and deacetylating histones. The Sin3/HDAC complex can affect cell cycle progression through multiple mechanisms and is among the targets of anticancer drugs, called HDAC inhibitors. We describe the identification of a new subunit of the Sin3 complex named family with sequence similarity 60 member A (FAM60A). We show that FAM60A/Sin3 complexes normally suppress the epithelial-to-mesenchymal transition (EMT) and cell migration. This occurs through transcriptional repression of genes that encode components of the TGF-beta signaling pathway. This work reveals that FAM60A and the Sin3 complex are upstream repressors of TGF-beta signaling, EMT and cell migration and extends the known biological roles of the Sin3 complex. This experiment investigates the role of FAM60A in gene expression by comparing A549 lung cancer cells treated with or without siRNA against FAM60A.
Human family with sequence similarity 60 member A (FAM60A) protein: a new subunit of the Sin3 deacetylase complex.
Specimen part, Cell line
View SamplesWe extracted nascent plasma cell tumor (PCT) cells from within inflammatory granulomas (OG) isolated from intraperitoneal pristane-injected BALB/c.iMyc E mice at five different time points during tumor progression. We used laser capture micro-dissection to collect incipient PCT cells and analyzed their global gene expression on Affymetrix Mouse Genome 430A microarrays. Two independent studies were performed with different sets of mice
Global gene expression profiling in mouse plasma cell tumor precursor and bystander cells reveals potential intervention targets for plasma cell neoplasia.
Specimen part
View SamplesTo identify novel therapeutic opportunities for patients with acquired resistance to endocrine treatments in breast cancer, we applied a high-throughput drug screen. The IC50 values were determined for MCF7 and MCF7-LTED cells.
VAV3 mediates resistance to breast cancer endocrine therapy.
Cell line
View SamplesMicroarray analysis has been applied to the cell proliferation in a human colonic cel line, Caco-2. We have shown previously that a moderate riboflavin depletion around weaning has a profound impact on the structure and function of the small intestine of the rat, which is not reversible following riboflavin repletion. In this study we have modelled riboflavin deficiency in a human cell line, shown irreversible loss of cell viability associated with impaired mitosis and identified candidate effectors of riboflavin depletion in the cell.
Riboflavin depletion impairs cell proliferation in adult human duodenum: identification of potential effectors.
Cell line
View SamplesThe very low density lipoprotein receptor (VLDLR) is a multi-ligand receptor that mediates pleiotropic biological processes, such as brain development.
The very low density lipoprotein receptor attenuates house dust mite-induced airway inflammation by suppressing dendritic cell-mediated adaptive immune responses.
Specimen part
View SamplesAnalysis of gene expression profile in peritoneal macrophage extracted from LPS or PBS challenged DUSP3-/- and WT mice. DUSP3 deletion protects mice from sepsis and endotoxemia. We performed a microarray analysis to get insights into the differentially regulated pathways between WT and KO under inflammatory conditions.
DUSP3 Genetic Deletion Confers M2-like Macrophage-Dependent Tolerance to Septic Shock.
Sex, Age, Specimen part
View SamplesWe characterized monosaccharide-dependent gene expression in the Drosophila fat body using fructose and glucose. Control and high-sugar diets were compared and RNA-seq was used to identify potential target genes. Overall design: Drosophila were reared on control (0.3 M fructose or glucose) or high sugar (1.7 M fructose or glucose) diets until the wandering third instar stage. Fat bodies were isolated and RNA was extracted to determine the effects of each sugar at different concentrations on gene expression using Illumina RNA-seq.
Similar effects of high-fructose and high-glucose feeding in a Drosophila model of obesity and diabetes.
Sex, Specimen part, Cell line, Subject
View SamplesG protein alpha q and 11 are mutated in 80% of uveal melanoma. We observed that treatment with the BRD4 inhibitor JQ1 resulted in different phenotypic responses in G-protein mutant uveal melanoma cell lines and wild type uveal melanoma cell lines.
BRD4-targeted therapy induces Myc-independent cytotoxicity in Gnaq/11-mutatant uveal melanoma cells.
Cell line, Treatment
View Samples