Thus, the finding of a reduction in allograft inflammation and plaque in Ndst1 deficient mouse donors is expected, but the same reduction in Ccr2 deficient mice was unexpected.
This response in Rad21+/− mice was unexpected and indicated that characteristic G1/S and G2/M checkpoints normally invoked by IR [39] were not being activated in the mutant GIT.
The fact that tumour rejection was obtained after depletion of CD8+ cells in BALB/c mice was unexpected in comparison to our previous results [8], [11].
The lack of significant upregulation of HO-1 in the lungs of SS mice was unexpected, and contrary to the findings from a previous study [16].
The decrease in heart rate produced by BK channel inhibitors, paxilline and lolitrem B, in wild-type mice was unexpected since BK channels are not thought to be present in the heart.
As lack of a renal phenotype in Ehd3 /– mice was unexpected, we first confirmed that EHD3 is indeed expressed in the wild-type kidney using Ehd3 /– kidney as a negative control.
The failure of PPI improvement in male heterozygous mice was unexpected, however, the gender effect was also observed in their differential startle response to carbamazepine (data not shown) [38].
However, the embryonic lethality of CXCR4-ΔT mice was unexpected, as patients with WHIM syndrome who also harbor truncating mutations at the CXCR4 C-terminus exhibited a dominant gain of function phenotype.
