The mTerc + groups were composed of both mTerc +/+ and mTerc +/- mice with long telomeres since they do not phenotypically differ from each other. In mTerc + mice, heterozygous deletion of Sod2 correlated with significantly decreased SOD2 protein levels in liver, whereas the decrease in brain and bone marrow did not reach statistical significance (Figure 1A -C).
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Sod2 haploinsufficiency does not accelerate aging of telomere dysfunctional mice.
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