The enhanced inflammation in PGRN KO mice is likely to be resulted from reduced regulatory T cells in the cervical lymph nodes (Huang et al., 2015).
Furthermore, as there was only an 11% variation in the VO2 observed with sleep-wake cycles in naïve mice (Additional file 1: Figure S1), decreased activity in the septic mice is likely to make only a relatively minor contribution to the profound reduction in metabolic rate observed.
According to the above results, the loss of DP thymocyte in CkbTg mice is likely due to increased cell death.
Thus, the Purkinje cell phenotype of Mdm2puro/Δ7-9 mise is likely a consequence of the paucity of GNPs.
inoculated mice is likely due to a disruption in the dissemination process from the lung to other organs rather than due to non-specific effects of the inhibitor.
The low expression of hepatic Hamp1 in Hfe−/− mice is likely responsible for the increased iron absorption and low microphage iron content in these mice [15], [16], [19].
The difference in FoxM1 protein levels between these two strains of mice is likely due to the differential kinetics of FoxM1 deletion during T cell development.
The defective lung development of the RASSF9−/− mice is likely the major causality of their failure to thrive and premature death.
The nature of any additional defects that arise in Lrig1/Lrig3 double mutant mice is likely to provide useful insights into this question in the future.
The ROS accumulation and lipid oxidation in knockout follicles detected in skin sections of 14 day old mice is likely to have started in younger mice.
The development of genetic tools that specifically label newborn dentate granule cells in adult mice is likely to facilitate the study of adult neurogenesis.
