Further, it is important to clarify the stage at which RNF10 is indispensable for Schwann cell differentiation by using RNF10-deficient mice. We identified RNF10 as a transcriptional regulator of the MAG gene, but we speculate that other target molecules are also regulated by RNF10. Our WZ4002 results indicate that RNF10 is required for both Schwann cell myelination and MAG expression. However, Gefitinib considering that MAG-deficient mice are capable of forming the myelin structure with modest abnormalities in the PNS, RNF10 probably regulates myelination by not only MAG expression but also other pathways. Some sequences, similar to the SSE, exist in the gene promoter regions of the rat, mouse, and human, suggesting that RNF10 may also regulate other gene expressions. However, we have not yet identified any myelin-related genes near the SSE-like motif region. On the other hand, since the knockdown of RNF10 in Schwann cells induced cell proliferation, we conjecture that RNF10 may be involved in exiting from cell cycle to initiate terminal differentiation and myelination. In conclusion, we prove that RNF10 binds to the MAG promoter and regulates MAG expression and myelin formation in Schwann cells. RNF10 can be considered as a regulator of Schwann cell differentiation and myelination. These results were obtained by in vitro experiments. The generation of RNF10- knockout mice should facilitate the understanding of the in vivo biological function of RNF10. Simian virus 40 is a non-enveloped primate virus, with a small, double-stranded, circular DNA genome of 5.2 kb. SV40 infects dividing and non-dividing cells and does not depend on host cell cycle. This is in contrast to many other viruses that infect only dividing cells and enter the nucleus during mitosis when the nuclear envelope is disassembled. This suggests that SV40 activates signaling pathways that permit nuclear entry of the viral genome. SV40 enters host cells by an atypical, slow endocytic process mediated by caveolae via the endoplasmic reticulum. This is unlike most viruses, that utilize clathrin-coated and non-coated vesicles for endocytosis. In a parallel project we have started a detailed study on cellular signals induced by the infecting SV40. We have found that SV40 activates Akt-1 survival pathway and the Hsp/c70 chaperones via PLC-c signaling, very early post infection. SV40 also protected CV-1 cells against etoposide-induced apoptosis. These findings led us to hypothesize that cellular uptake of SV40, or the viral capsid alone, might function in protection against in vivo cellular damage and degenerative diseases. Because SV40 has a natural affinity to the kidney, we chose renal failure as a first target for testing the hypothesis. Acute kidney injury, previously known as acute tubular necrosis, is characterized by abrupt and reversible kidney dysfunction, caused by sepsis, ischemia or nephrotoxic agents.