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Fig. 3 | Acta Neuropathologica Communications

Fig. 3

From: Peripheral administration of SOD1 aggregates does not transmit pathogenic aggregation to the CNS of SOD1 transgenic mice

Fig. 3

Stability of spinal cord-derived hSOD1G85R aggregates. Human SOD1G85R aggregates were incubated either with or without a trypsin (10, 100 and 1000 µg/ml), b proteinase K (PK; 10, 50 and 250 µg/ml), c sodium dodecyl sulfate (SDS; 10 g/L) or d glycochenodeoxycholic acid (GCDCA; 8 mM) for different time intervals (0, 0.5, 1, 2, 4 and 6 h) at 37 °C. a–d Amounts of hSOD1, in both supernatant and insoluble fraction, were determined by western blotting. A human-specific SOD1 24–39 peptide antibody was used, and the reactivities was compared to a wild-type hSOD1 standard. Note that the hSOD1 standard has a lower electrophoretic mobility than the hSOD1G85R mutant

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