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. 2019 Aug 20;8(8):940. doi: 10.3390/cells8080940

Figure 2.

Figure 2

Grip strength of muscle-specific CK2β-deficient mice. (A) Grip strength of >5 different pairs of mice (each mouse pair was composed of wild-type and mutant litters) of indicated age was measured by a grip-strength meter (Bio-GS3 Grip-Test, Bioseb Vitrolles, France). (*** p < 0.001; unpaired two-tailed Student’s t-test; n = >5 mice, each genotype). Error bars indicate s.e.m (B) Muscle grip strength was determined five consecutive times by measuring the time mice were able to cling upside-down on a grid until they fell down. Mice were then immediately put back on the grid, and the drop time was measured again. The first maximal clinging time measurement was set to 100%. The next four maximal clinging times decreased continuously. Different colors symbolize different mouse ages of CK2β-deficient mice. As indicated, 140 up to 480 days old mice were analyzed. (C) Muscle grip strength was measured after administration of acetylcholine esterase inhibitor (neostigmine) to CK2β-deficient mice (tail vein injection). After indicated times, maximal upside-down clinging time was measured and plotted to the number of repetitions. Note that wild-type mice were able to cling up to 10 min upside-down on a grid, while mutant mice after neostigmine injection were only able to cling upside-down for about 50 s. (D) Endurance capacity of aged-matched wild-type and mutant mice (8–10 months of age) was determined by enforced running on a treadmill. Note that mutant mice were exhausted at lower treadmill speed.