Mouse aneuploidies have been engineered to model the various DS phenotypes; these models display some behavioral, anatomical and cellular abnormalities similar to human phenotypes (reviewed in Das & Reeves, 2011).
Lactococcus lactis (L.lactis), a typical model of lactic acid bacteria, is an ideal vaccine delivery vector and has been engineered to express many viral antigens [ 12, 13].
In the MINO model, mice have been engineered to have neoplastic outgrowths from mammary ducts [ 7, 8] while in the MIND model, human DCIS cell lines are transplanted intraductally to mimic the structure of DCIS found in humans [ 9, 10].
A number of genetic mouse models have been engineered to express oncogenes in melanocytes [3].
Finally, transgenic mouse models have been engineered to mimic celiac disease, most notably the NOD Ab° DQ8+ mouse, which expresses human DQ8 in an endogenous MHC class II-deficient (Ab°), autoimmune-prone (NOD) background [36].
As human approaches are limited, murine animal models have been engineered to study the diverse pathobiology of 22q11.2DS.
Attractive animal models have been engineered to investigate the in vivo functions of the β-catenin pathway in the mouse mammary gland.
Recently, genetic mouse models of cardiac-restricted steatosis have been engineered to unravel the molecular mechanisms of lipotoxicity.
A second kind of model has been engineered by transfecting the ER negative breast cancer Hs578T cell line with a FLAG-tagged and inducible version of ERα, ERβ or ERβ cx, and was used for microarray analysis of gene expression [ 25].
A first series of cellular models has been engineered by transfecting the ERα positive MCF-7 cell line with a plasmid expressing an inducible FLAG-tagged version of ERβ.
