The brachiocephalic artery of fat-fed ApoE deficient mice develops complex plaques, which eventually spontaneously rupture [12].
However, about 20% of homozygous ΔHS1 mice develop a complex neurological phenotype and die at 3 5 weeks of age, likely due to a lack of food intake.
Relb−/− mice develop a complex phenotype, including an autoimmune-like inflammatory syndrome, myeloid hyperplasia, multifocal defects in immune responses, and impaired development of lymphoid organs [ 28- 30].
Autoimmune manifestations in NOD mice develop through a complex interplay of several factors composed of genetic predisposition and intrinsic immune dysfunctions which manifest under the influence of environmental conditions [ 49].
However, Fancc −/− Fancg −/− double-mutant mice have a broader phenotype: the mice develop BMF, myelodysplasia and complex cytogenetic abnormalities, which are phenotypes that were not present in either single knockout mouse strain (Pulliam-Leath et al., 2010).
The 12T-7f LADY is a fast disease-developing strain, and develops complex mouse prostatic intraepithelial neoplasia (mPIN) with hypercellular stroma by 20 weeks of age [ 36, 37].
NOD mice develop diabetes in a major histocompatibility complex (MHC) class II-dependent manner prior to autoimmune exocrinopathy.
These mice develop proteinuria with basement membrane immune complex deposits, and skin fibrosis with collagen I deposition; the severity of these disorders depends on the number of donor cells transplanted.
There might be an age component as p53+/− mice live longer than p53−/− mice, develop fewer lymphomas, and have a more complex tumor spectrum, although loss of the wild-type allele was common in p53+/− tumors, unlike our Δ122p53/mΔpro tumors.
Accordingly, in the mouse vinculin loss leads to defects in adhesion complexes that compromise embryonic cardiac development [3] and vinculin+/− mice develop dilated cardiomyopathy [4].
