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Correct proteolytic processing of pro-alpha-factor-somatostatin hybrids requires the products of the KEX2 and STE13 genes

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Inactivation of S1PR2, for example, a sphingosine receptor which also binds to Nogo-A preventing axonal growth, resulted in increased remyelination in both lysolecithin-induced demyelination and EAE mice ( Figure 2 As myelin debris accumulate in the extracellular matrix and anomalous remyelination occurs, it has been suggested that demyelinating chronic disease may be associated with Nogo-A deposition and increased signaling

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