Abstract
The recent discovery of the novel peripheral myelin protein PMP22 and the association of mutations of this gene with dominant inherited peripheral neuropathies in mice and man has raised particular interest in the biological function of this gene (for review: Lemke, 1993; Suter et al., 1993). Due to the separate occasions leading to the identification of this gene different names have been given for PMP22 cDNAs in the literature. The reported cDNA sequences are: gas3 (growth arrest-specific gene 3; Schneider et al., 1988), CD25 (crush denervated cDNA clone 25; Spreyer et al., 1991) SR13 (sciatic nerve regeneration clone 13; Welcher et al., 1991) or PMP22 (peripheral myelin protein 22kDa; Snipes et al, 1992). All sequences are variants of the murine growth arrest-specific gene gas3, which was originally cloned from NIH3T3 fibroblasts as one of a set of genes induced when these cells are growth-arrested (Schneider et al., 1988; Manfioletti et al., 1990). The demonstration that gas3 is also a prominent Schwann cell gene product came from the independent cloning of cDNAs that are either induced or repressed following rat sciatic nerve crush or transection (Spreyer et al., 1991; Welcher et al., 1991). It turned out that PMP22 expression is axonally regulated like the major myelin genes. The level of expression is high in fully differentiated Schwann cells, declines rapidly upon Schwann cell dedifferentiation and proliferation as a result of axonal degeneration after nerve injury, and is upregulated upon regeneration (Kuhn et al., 1993).
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Zoidl, G., Schmalenbach, C., Müller, H.W. (1994). Retrovirus-Mediated Gene Transfer of PMP22 in Schwann Cells: Studies on Cell Growth. In: Salvati, S. (eds) A Multidisciplinary Approach to Myelin Diseases II. NATO ASI Series, vol 258. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2435-9_4
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