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. 2014 Nov 20;25(5):552–564. doi: 10.1111/bpa.12214

Figure 1.

figure

Characterization of  p 62 protein deficiency in an animal model of  L ewy body disease. A. Breeding strategies to generate p62 deficiency in α‐synuclein transgenic (Tg) mice. Initially, heterozygous α‐synuclein Tg and homozygous p62‐knockout (KO) mice were crossed. Next, littermates and heterozygous p62‐deficient mice were mated to generate Tg mice without p62 (Tg/KO), of which four groups were used in this study (black circles). B. Immunoblot analysis confirmed that α‐synuclein was overexpressed in Tg and Tg/KO mice and that p62 signals were diminished in KO and Tg/KO mice (9 weeks of age, n = 6 per group). The molecular mass is indicated on the left side of the panel. β‐Actin was used as a loading control. C. A quantitative analysis shows that human α‐synuclein is expressed in Tg and Tg/KO mice and that p62 is absent in KO and Tg/KO mice. The values of Tg mice are defined as 100%. D. The weight changes of Tg (black circle) and Tg/KO mice (grey circle) are shown (mean ± standard deviation, n = 6–8 per group).