We tested the ability of this vector to integrate into the genome with APP as an inducible knockdown target. Although plasmids were introduced into the neural progenitors in the VZ by in utero electroporation gene transfer, these progenitors, as well as recently recognized intermediate progenitors in the subventricular zone, Senkyunolide-A undergo mitosis before finally settling into the cortical plate. Because an episomally located vector is likely to be diluted during mitosis, whereas a transposed vector is not, it is probable that higher inducible expression was observed in the cortical neurons of the adult brain when the Tol2 transposase vector was co-transfected. Indeed, EGFP expression was weaker in superficial neurons, which are likely to experience more mitotic cycles, compared with those in deeper layers in the absence of Tol2 transposase activity. In the EGFP-positive cells, Dab1 expression was decreased significantly compared with control cells. It has been reported that reduction of the Dab1 protein in the cerebral cortex results in the malformation of the cortical lamination. Therefore, we assessed the effect of the induction of Dab1 knockdown and the leakage of this knockdown cassette in the absence of Dox. Radial migration was inhibited in the cortex following the induction of the Dab1 knockdown, but not in brains exposed to the control vector or in the absence of Dox. These results indicated that the Tol2 inducible knockdown vector was tightly controlled and effectively knocked down the expression of the endogenous gene without expression leakage. Molecules that control neuronal migration, including regulators of the cytoskeleton and cell adhesion molecules, also affect other processes, such as axon projection and synaptogenesis, after the cessation of migration. Application of the Tol2 inducible knockdown system described here allows us to investigate gene functions in each event separately by controlling the timing of the gene silencing. Currently, the demand for the development of tools for conditional genetic manipulation, especially in a small number of neurons, is increasing. Young et al. create one such method, SLICK that utilizes drug inducible Cre-mediated knockout technology. With SLICK, they can Rebaudioside-A visualize a whole neuronal shape by coexpressing YFP together with Cre, which is also accomplished by our system with EGFP. However, they knockout a gene of interest in an irreversible manner with SLICK, whereas we knockdown a gene of interest in a reversible manner, in which we can bring back the gene expression later. Moreover, specific Cre-expressing neurons are targeted in SLICK, whereas our system enables us to knockdown a gene in any electroporated neurons.