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The prion protein in these mice was either either overexpressed (Tg20) deleted (PrPo/o) or modified to lack the main metal binding domain (C4).

Similarly, expression of p4EBP1 in wild type, Hi-MYC and MPAKT/Hi-MYC mice was either unchanged or slightly increased by RAD001 treatment (Fig. 8).

The posterior thigh skin of MHC II-EGFP transgenic mice was either left untreated or exposed to laser for 2 min at 0.3 W, followed by i.d.

This suggests that expression regulation of CP genes in both of these allelic mice was either delayed or abandoned.

We then examined if the variation in susceptibilities between heterozygous DBA/2J and 129B6 mice was either due to a difference in BAX protein function caused by an amino acid substitution or the level of expression.

To directly explore the possible regulatory difference of p53 in vivo, B6 mice was either untreated or treated with 6 Gray of X-irradiation and immunostained for p53 protein in multiple tissue compartments.

Male wild-type C57BL/6 mice were either made diabetic or left as control.

Male wild-type (WT) C57BL/6 mice were either made diabetic or left as control for 2 months when they underwent femoral artery ligation.

Female ICR mice were either hindlimb unloaded or placed in the PWS system at 16% quadrupedal weightbearing for 4 h, 1, 2, 7 or 10 days, at which point complete blood counts were obtained.

The host mice were either intact or castrated four weeks prior to the FLT procedure.

As negative controls, mice were either untreated, or injected with normal saline.