Chondrogenic, and adipogenic differentiation upon BMP9 stimulation both in vitro and in vivo. Taken together, our results have demonstrated that the reversibly immortalized piMEFs not only maintain long-term cell proliferation but also retain the ability to differentiate into multiple lineages. Thus, the reported piggyBac transposon-mediated expression of SV40 T immortalization system should be used as an effective tool to establish stable cells from primary progenitors isolated from limited tissue sources, which would be critical for basic and translational studies. In this study we have shown by colocalization with CHMP2B that also in neurons TMPAP is in multivesicular endosomes. In nerve cells, these organelles are used in membrane trafficking pathways controlling recycling and degradation of pre- and post-synaptic membrane proteins, as well as in recycling of vesicle membrane during neurotransmitter release and release of exosomal endocargo. The results of the colocalization studies with synapthophysin and snapin, suggest that TMPAP is localized in synaptic nerve endings. This conclusion is in agreement with previous studies which show that mouse PAP localized presynaptically in DRG neurons and in taste buds. In addition, the colocalization between PAP and snapin in prostate cancer cells occurs in the cell lamellipodia, and it has been described that the lamellipodium is the site where exocytosis occurs in migrating mammalian cells, supporting the hypothesis that colocalization of these proteins in the neuron will not happen in the cell soma. This presynaptic localization of TMPAP together with the fact that TMPAP resides in the axon hillock, where GABAergic synapses are located, supports the hypothesis that TMPAP is located in GABAergic synapses. TMPAP also colocalizes and interacts with snapin, which directly binds SNAP-25, a protein that has been linked to schizophrenia in genetic, pathological and functional studies. Snapin is associated with the SNARE complex and involved in synaptic vesicle docking and fusion, supporting the hypothesis that TMPAP may regulate GABAergic signaling via synaptic vesicle trafficking. The mislocalization of snapin observed in the cells of PAP2/2 mice may perturb synaptic processes controlling neurotransmitter release and recycling, thus disrupting neuronal homeostasis and eventually leading to the neurological phenotype observed in PAP2/2 mice. Enlarged lateral ventricles are present in numerous neurological disorders such as schizophrenia, Alzheimer’s disease, bipolar disorders, Parkinson’s disease and Huntington’s disease as well as in many mouse models of the diseases. Also, decreased prepulse inhibition is considered a behavioral endophenotype of schizophrenia. To our knowledge, mutations in the gene encoding PAP have not thus far been reported, nor has ACPP been implicated in genetic association studies of mental disorders.