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The wider trajectory of the infected mice stems from its broad heterogeneity of activation states.
To determine if the resistance to steatosis in the Tsc1−/− mice stems from mTORC1 hyperactivity, we treated a cohort of mice on HFD with rapamycin.
Thus, we conclude that the phenotype of the Clecsf8−/− mice stems from defective mycobacterial recognition by leukocytes.
These data imply that the enhanced bone formation response evident in Hif-1α mutant mice stems from the elimination of Hif-1α-mediated suppression of β-catenin signaling.
The major difference in body weight between αMUPA and WT mice stems from the fact that the quantitative difference in food intake between αMUPA and WT mice is maintained at the old age.
Since circadian patterns of food intake and body temperature constituteclock-controlled output systems, it is conceivable that their alteration in the transgenic mice stems from the higher amplitude of clock gene expression in the periphery, and possibly also in the central biological clock in the SCN.
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Alternative explanations for the opposite findings in il-33-/ and t1/st2-/ mice stem from the IL-1R family signaling pathways.
There are concerns regarding the use of laboratory strains selected for large litter size (i.e., CD-1 mice) stemming from the possible correlation with resistance to endocrine disruptors including xenoestrogens.
The phenotypic difference in defensive behavior between voles and spiny mice probably stems from their different habitats and motor capacities.
Thus, alterations in the growth of regenerated muscle fibers in mutant mice most probably stems from a modified satellite cell niche.
A prohibitive roadblock using mouse infection models stems from long‐time intervals required for declining immunity to take hold (≥15 20 months) (Lages et al., 2008; Decman et al., 2012).
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