These results support the idea that the ECTVIFNα/βBPGAGmut attenuation in WT susceptible mice is due to a reduced IFN-I blocking ability when the IFNα/βBP is unable to attach to the cell surface.
Taken together, these results suggest that the decreased rate of tumor formation in Ap4-deficient ApcMin mice is due to the lower number of functional ISCs in the intestinal crypts.
Deficient mineralization of intramembranous bone in vitamin D-24-hydroxylase-ablated mice is due to elevated 1,25-dihydroxyvitamin D and not to the absence of 24,25-dihydroxyvitamin 24,25-dihydroxyvitamin
Resistance in C57BL/6 mice is due to early and strong activation of natural killer (NK) cells by an MCMV gene product, m157, that binds directly to the NK cell activating receptor Ly49H.
To identify whether the phenotype of Hdac4−/− mice is due to up-regulation of MMP-13, we generated Hdac4/Mmp13 double knockout mice and determined the ability of deletion of MMP-13 to rescue the Hdac4−/− mouse phenotype.
Clearly, the lethal phenotype of ADA-deficient mice is due to the absence of ADA.
The additional weight of AC3−/− mice is due to increased fat mass and larger adipocytes.
Altogether, these results indicate that neutrophilia in STAT5−/− mice is due to increased granulopoiesis rather than to enhanced neutrophil survival.
Therefore, the possibility that the increased bone mass in ZAS3−/− mice is due to osteoclast deficiency exists.
Depleted numbers of NK cells in Flt3L-deficient mice is due to fewer common lymphoid progenitors [9].
Finally, it is proposed that the greater recovery of transparent pneumococci from the nasal mucosa of mice is due to their propensity to detach more easily [16].
