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This mitochondrial protection is especially critical in PD, where neuronal loss is driven by apoptotic processes

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In addition, the characterized LASSS treatment did not stimulate autolysis of HGF as monitored by SDS-PAGE for degradation of 60-kDa -chain and 90-kDa proform of recombinant HGF incubated with LASSS (at 1:8000) at 25 for 2 h (see supplementary Figure 1b), providing another important basis for the availability of LASSS-HGF