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Non-infected wild-type or gene deficient mice presented normal MRI and MRA phenotype (Figure 2A, B).

Expression of CD4, CD8, CD25, and CD44 showed that both groups of chimeric mice presented normal DN and DP thymocyte development (Figure S10A).

Despite the fact that ERαKO mice are insulin resistant [1], islets from both ERαKO and ERβKO mice presented normal Ca2+ signals in response to glucose, indicating that the stimulus secretion coupling was unaltered.

On the other hand, infected Clq−/− and fB−/− mice presented normal disease progression and severity [ 100].

Interestingly, reconstituted Kit W-sh/W-sh mice presented normal implantation numbers and sizes.

To examine the contribution of the desmosomal cadherin desmoglein 2 to cardiomyocyte adhesion and cardiac function, mutant mice were prepared lacking a part of the extracellular adhesive domain of desmoglein 2. Most live born mutant mice presented normal overall cardiac morphology at 2 weeks.

Although erk1-/ mice present normal mesoderm differentiation, they do show defective adipocyte formation [ 30].

p38δΔ/Δ mice presented with normal general health, viability, fecundity, body composition, and body weight (data not shown).

Allogeneically mated Kit W-sh/W-sh mice show severely impaired implantation, although single mice may present normal litter size that account for their ability to breed.

While control animals presented normal organ histology, the endothelial Dll4 knock-out mice showed alterations in liver architecture.

While a comprehensive characterization of the endocrine cells went beyond the scope of the current study, the mice presented with morphologically normal islets, probably reflecting differences in transgene expression levels or timing of expression.