Project description:To identify early activation genes in primary human B cells. Keywords: time series design Primary B cells (Cy5) are compared to a reference pool of RNA (Cy3) over a time course of stimulation with anti-Ig. Two independent unstimulated samples were analyzed.
Project description:To identify genes in human peripheral blood B cells whose expression changes with acute stimulation through the antigen receptor using anti_IgM. Keywords: time series design
Project description:To identify HGF/Met regulated genes, we performed expression microarray analysis after inducible activation of Met receptor in primary cultures of hepatocytes established from wild-type control (Alb-Cre +/-) and Met conditional knockout mice (Alb-Cre +/-; Met Fl/Fl). Keywords: time series design
Project description:E.coli K-12 W3110 was grown in LB medium and harvested at each time point. And time series microarray experiments were performed based on reference desgin. In reference design, the control sample is collected at one representative time point. Combining with data from sequential design, more acculate and reliable expression series could be collected. Keywords: Reference design
Project description:E.coli K-12 W3110 was grown in LB medium and harvested at each time point. And time-series microarray experiments were performed based on Sequential Design. In Sequential Design, the control sample is set to closest previous time point so that adjacent time points are compared directly. Combining with data from reference design, more accurate and reliable expression series could be collected. Keywords: timecourse
Project description:We have compared the response to TGFbeta1 in normal and v-rasHa transduced primary mouse keratinocytes using NCI cDNA microarrays. This analysis reveals that Ha-ras alters global TGFbeta1 mediated gene expression in a gene specific manner. The expression pattern of TGFbeta1 immediate early response genes and down regulation of cell cycle control genes is not altered by Ha-ras but the induction of most extracellular matrix genes is blocked. Using Smad3 null keratinocytes, we find that the majority of TGFbeta1 responsive genes in primary keratinocytes are Smad3 dependent, but patterns of transcriptional responses suggest that the ability of Ha-ras to block TGFbeta1 mediated gene expression is not dependent on Smad3. However, the combination of oncogenic ras and loss of Smad3 prevents the TGFbeta1 dependent suppression of genes associated with cell cycle progression and apoptosis observed with either genotype alone. In addition several extracellular matrix genes are super-repressed by TGFbeta1 in the Ha-ras Smad3 null keratinocytes. These data provide a genomic framework for understanding how disruptions of TGFbeta signaling and oncogenic ras cooperate to promote premalignant progression of primary keratinocytes. Keywords: time series design