Results: The amplification of topoisomerase I and deletion of thymidylate synthase were found in 23% (12/52) and 27% (14/52) of colorectal cancers, but EGF receptor amplification was not common (5/52, <10%). Among 52 colorectal cancers, 31 tumors were both topoisomerase I and thymidylate synthase diploid, which may have a worse outcome for tumor chemotherapy; and there were five tumors with favorable genomics (topoisomerase I amplification and thymidylate synthase deletion). Furthermore, topoisomerase Mocetinostat I-amplified tumors had a two-times higher RNA level and a nearly

twofold higher protein expression level than did the diploid tumors (p < 0.001 and 0.01, respectively), but there were no correlations between copy-number status and RNA or protein level for thymidylate synthase.

Conclusions: Our study suggests a potential pharmacogenomic influence of topoisomerase I copy-number alteration on its RNA/protein expressions, which could be reflected on tumor response to chemotherapy in human colorectal cancer.”
“Coordinated regulation of gene expression relies on transcription factors (TFs) binding to specific DNA sites. Our large-scale information-theoretical analysis of >950 TF-binding motifs demonstrates that prokaryotes and eukaryotes use strikingly different strategies to target TFs to specific genome locations. Although bacterial TFs can recognize a specific DNA site in the genomic background, eukaryotic TFs exhibit widespread, nonfunctional MEK inhibitor clinical trial binding and require clustering of sites to achieve specificity. We find support for this mechanism in a range of experimental studies and in our evolutionary analysis of DNA-binding domains. Our systematic characterization Autophagy inhibitors library of binding motifs provides a quantitative assessment of the

differences in transcription regulation in prokaryotes and eukaryotes.”
“Bovine colostrogenesis is distinguished by the specific transfer of IgG(1) from the blood to mammary secretions. The process has been shown to be initiated by hormones and occurs during the last weeks of pregnancy when steroid concentrations of estradiol (E-2) and progesterone (P-4) are highly elevated. Rodent intestinal uptake of immunoglobulin G is mediated by a receptor termed Fc fragment of IgG, Receptor, Transporter, alpha (FcGRT) and supported by light chain Beta-2-Microglobulin (2M). We hypothesized that steroid hormone treatments (E-2 and P-4) of bovine mammary epithelial cells in vitro would induce up-regulation of IgG(1) transcytosis candidate gene mRNA expression suggesting involvement in IgG(1) transcytosis. Two different primary bovine mammary epithelial cell cultures were cultured on plastic and rat tail collagen and treated with hormonal combinations (steroids/lactogenic hormones).