Overall, we hypothesize a switch in autocrine signaling to foster tumor growth that was initially triggered by EGF. In this regard cMyb is considered to be an important factor of the IGF2 positive feedback loop. Notably, we identified c-Myb binding sites in the promoter IGF2 gene and c-Myb to be a downstream partner of the IGF2 signaling cascade. Therefore our analysis demonstrates the knowledge gain form promoter analysis combined with upstream key node identification. All neurons and glial cells in the brain are derived from neural stem cells. NSCs maintain their own numbers by selfrenewal and also give rise to daughter cells that terminally differentiate into neurons, astrocytes, and oligodendrocytes. NSCs have been found to persist in the adult brain and generate new neurons throughout adult life, particularly in the subgranular zone of the dentate gyrus and the subventricular zone of the lateral ventricles. This raises the exciting possibility that NSCs may be useful for the therapy of neurodegenerative diseases. The factors that control the division and differentiation of NSCs are of tremendous scientific and medical importance. Geminin is an unstable regulatory protein that is U0126 thought to maintain neural progenitor cells in an undifferentiated state while they proliferate. Geminin is expressed in both embryonic and adult mouse neural progenitor cells, and in the Xenopus central nervous system throughout embryonic development. Geminin is preferentially expressed in neural precursor cells, and expression is down-regulated before neural differentiation. Geminin binds to Brg1, the catalytic subunit of a SWI/ SNF chromatin remodeling complex, and inhibits its recruitment to neuron-specific promoters by the basic helix-loop-helix transcription factors Neurogenin and NeuroD. A complex between Geminin and the transcription factor AP4 represses the transcription of neuronal genes in nonneuronal cell types. In addition to regulating cell differentiation, Geminin also limits the extent of DNA replication to one round per S phase by binding and inhibiting the essential replication factor Cdt1. The concentration of Geminin is cell-cycle regulated; the protein begins to accumulate at the G1/S transition and persists throughout S and G2 phase. Geminin is destroyed by ubiquitindependent proteolysis during M phase, which allows a new round of replication in the next cell cycle. This expression pattern has been documented extensively in developing mouse brains. Six and Hox transcription factors can compete with Cdt1 for binding to Geminin, raising the possibility that Geminin links exit from the cell cycle with cell differentiation. According to this model, the destruction of Geminin when cells enter G0 phase would relieve the repression of Brg1 and other transcription proteins and trigger terminal differentiation. In early embryos Geminin can also act as an inducer of nervous tissue.