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In vitro treatment of vcp-/- neurons with N-acetyl-d-mannosamine (ManNAc), a substrate of VCP, failed to rescue the VCP deficiency-induced apoptosis and cellular lesions. We performed microarray analysis of vcp-/- and wild-type mice. VCP deficiency led to the abnormal expression of proteasomal components, including Rpt3, Rpt1, and Rpn11. In addition, we identified that expression of BMP2, a target gene of the Smad1/5/8 signaling pathway, was up-regulated in vcp-/- mice by in situ hybridization. Furthermore, in vitro treatment of vcp-/- neurons with human BMP2 resulted in remarkable decrease of cell death and apoptosis. These results demonstrated that VCP deficiency altered the expression of genes related to the cellular stress response, and that the modulation of BMP2 expression may be important for the survival of vcp-/- neurons.Q: Can I know which software to use to migrate my Azure SQL database to a new server? 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