However, this is limited in a practical sense by the prior knowledge we have about this system derived from laboratory experiments and the biological literature. It could also be argued that the weight interval we employ is unduly restrictive in limiting the range of variation of weights that we employ. In this regard, it should be noted this is already an improvement in terms of modeling dynamics when compared to the frequently employed Boolean networks which are binary in nature. Moreover, this range of weights employed already produces a rich repertoire of parameter combinations that qualitatively reproduce the observed behavior. As biologists continue to move toward studying cellular and molecular systems as a whole, there will be an increased need for mathematical approaches to interpret and codify experimental results. We believe the CMAP provides the appropriate level of description within an intuitive framework to make sense of these complex biological systems. We found evidence for a role of I-RE RNAs in the natural protection against new invasions by I-factors. Furthermore, our results provide insight about a specific transcriptional regulation of the heterochromatic I-REs. Recent studies demonstrated that TZDs, the PPARc ligands, decreased cardiovascular risks via exerting direct effects on vascular cells, for example. It has been shown that TZDs inhibit key steps in the ERK/MAPK pathway, blocking events that are critical for the re-entry of quiescent VSMCs into cell cycle, thus retarding serum-induced growth of cultured arterial VSMCs and PDGFBB–directed migration of VSMCs. Direct vascular effects of TZDs result from their activity as ligands for the nuclear receptor, PPARc. We also discuss the nature of the mechanism involved in I-factor repression by the IRE transcripts, and of the epigenetic “imprint” that can be transmitted through several generations. In conclusion, this work provides evidence for a role of RNAs encoded by defective remnants of ancestral transposon invasions in protecting a genome against the highly mutagenic effects of functional transposable elements. Since heterochromatic I-REs are the “memory” of ancestral invasions by I-factor-like transposons, this protective process, most probably involving an epigenetic mechanism of natural RNA-mediated HDGS, can be considered as a genetic “vaccination” against transposable elements. It is noteworthy that I-REs are vestiges of a transposable element related but not identical to the I-factor. The consensus of the ancestral element is divergent from the Ifactor by 4 to 5% at the level of the nucleotide Reversine inquirer sequence , indicating that this protection could tolerate some divergence between the ancestral elements and the functional invading transposon to be silenced. Three lines of evidence support a role for the V-ATPase in membrane fusion. First, studies of homotypic vacuolar membrane fusion have suggested that the sectors on opposing membranes can form a proteolipid fusion.