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. 2010 Dec 15;20(5):1008–1015. doi: 10.1093/hmg/ddq546

Figure 3.

Figure 3.

Studies of SOD1 aggregation and accumulation. (A) Immunohistochemical studies of the lumbar anterior horn of G85R/Perk+/−, G85R and Perk+/− transgenic mice of varying ages. (B) Representative western blot of lumbar spinal cord homogenates from varied aged G85R/Perk+/−, G85R and control mice (Perk+/−, WTSOD1/Perk+/− transgenic mice and non-transgenic littermates) subjected to SDS–PAGE under non-reducing conditions. The spinal cord homogenates were immunostained with anti-human SOD1 antibody. The monomeric and dimeric forms of SOD1 are noted with arrows. Note that the monomeric form of G85R MTSOD1 has a different electrophoretic mobility than WTSOD1, and that high molecular weight forms above the dimeric species are present in both G85R/Perk+/− and G85R mice, but they are present at an earlier time in the G85R/Perk+/− mice. Anti-β-tubulin antibody was used as a loading control. In this and subsequent figures: Pre, presymptomatic; Wk, weak; End, end stage. (C) Representative western blot of lumbar spinal cord homogenates from varied aged G85R/Perk+/− and G85R mice subjected to SDS–PAGE under reducing conditions. (D) Quantitation of total MTSOD1 in the spinal cord homogenates from varied aged G85R/Perk+/− and G85R mice as detected in western blots of samples electrophoresed under reducing conditions. The mean amount of MTSOD1 in the spinal cord of G85R mice at ∼220 days was arbitrarily given a value of 100. Note that there is more total MTSOD1 in G85R/Perk+/− compared with G85R mice at 260 and 280 days; no values for G85R/Perk+/− mice are provided after 280 days because they are dead. **P < 0.01.