Moreover, this analysis yielded testable hypotheses about relevant molecular cascades involving p107, p130, and p15INK4b as well as survivin, Cdk1, cyclin B1, Plk1, and Bub1. In the transgenic network we found a cascade of molecules BYL719 regulating cell migration and adhesion, which included VCAM-1, alpha4- integrin, TSP-1, and IAP. This finding complied with decreased enrichment of cell motility components in tumor revealed by GO analysis. Hence, the constructed network clusters complemented the results of our GO analysis by facilitating detailed insight into the molecular pathways targeted by carcinogenic expression changes. Taking into account the presence of EGF-receptors ErbB1-3 in both transgenic and tumor clusters, the networks reveal in addition how components of biological processes proposed by GO analysis were tied to EGF-signaling in the context of hepatocarcinogenesis. After elaborating on downstream effects of EGF-induced tumor development, we reconstructed causes of observed expression changes. First, we analyzed overrepresentation of transcription factor binding sites in promoters of upregulated and downregulated transgenic as well as tumor gene sets. For this part of the work, we developed a novel statistic for binding site enrichment analysis that compares foreground/background binding site proportions with promoter proportions and quantifies overrepresentation with the ratio quantile of corresponding Beta distributions. The statistic was proposed for several reasons. PWM-based binding site prediction typically requires specification of a score threshold that determines true and false positive rates. In a comparative method, e.g. like F-MATCH, the threshold at which a weight matrix optimally detects overrepresentation is usually not known a-priori.Inactivation of GSK3b leads to GS dephosphorylation and glycogen synthesis inhibition in adipose, muscle and liver. Glycogen storage reduction in skeletal muscle is the phenotype of type 2 diabetes patients. Therefore, GSK3b, one of isoforms of GSK3, is an WZ4002 important enzyme in regulating glucose metabolism and acts as a key target in treatment of type 2 diabetes mellitus. In the present study, we investigate the influences of HDL on glucose uptake and GLUT4 translocation in 3T3-L1 adipocytes and glycogen synthesis in L6 cells to provide more evidences for HDL in regulating glucose homeostasis. The results indicate that HDL promotes glucose uptake in adipocytes via enhancement of GLUT4 translocation that may be through SR-BI, and increases glycogen deposition in skeletal muscle cell following phosphorylation of GSK3. In the present study, we characterized that HDL stimulated glucose uptake in 3T3-L1 adipocytes in concentration&time dependent manners. Furthermore, the influence of HDL on glucose uptake was inhibited by LY294002 and L-NAME.