Another fear, stemming from a recent British study using transgenic mice, is that mad cow disease may be masquerading as sporadic C.J.D.
An alternative explanation for the reduction in NK cell numbers seen in tumor-bearing mice is that NK cell proliferation is reduced.
Another similarity between HSL null mice and RIP140 null mice is that subcutaneous WAT depots are more reduced than visceral depots.
The sole difference between these two strains of mice is that H7a MiHA is ubiquitously expressed in B10 mice, but absent in B10.H7b mice [6], [28], [29].
A feature of tg650 mice is that following primary intracerebral vCJD challenge they developed a neurological disease with typically 100% attack rate, unlike for previously established PrP129Met, including overexpressing lines [16], [19].
A very plausible explanation for the progressive denervation and impaired reinnervation observed in MCK-UCP1 mice is that mitochondrial uncoupling in muscle modifies the production of retrograde signals required for presynaptic motor ending stability.
A common problem of working with genetically modified mice is that deletion of a gene might alter developmental processes.
Thus, an alternative interpretation for Leishmania susceptibility in receptor deficient mice is that enhanced acute Th2 responses inhibit the initial expansion of protective Th1 cells [ 44].
For example, a common phenotype observed in mutant mice is that of ectopic projections (Frisén et al., 1998; Feldheim et al., 2000).
A possible alternative explanation of the decreased effect of carboxyatractylate in mitochondria from Ucp3KO mice is that ablation of UCP3 somehow decreased ANT content.
One potential explanation of the discrepancy in the phenotypes of these mice is that TAp63 interacts with point mutant p53 rendering TAp63 functionally inactive.
