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Review
. 2011 May;4(3):305-10.
doi: 10.1242/dmm.000901.

Technical approaches for mouse models of human disease

Monica J Justice  1 , Linda D Siracusa, A Francis Stewart
Affiliations
Review

Technical approaches for mouse models of human disease

Monica J Justice et al. Dis Model Mech. 2011 May.

Abstract

The mouse is the leading organism for disease research. A rich resource of genetic variation occurs naturally in inbred and special strains owing to spontaneous mutations. However, one can also obtain desired gene mutations by using the following processes: targeted mutations that eliminate function in the whole organism or in a specific tissue; forward genetic screens using chemicals or transposons; or the introduction of exogenous transgenes as DNAs, bacterial artificial chromosomes (BACs) or reporter constructs. The mouse is the only mammal that provides such a rich resource of genetic diversity coupled with the potential for extensive genome manipulation, and is therefore a powerful application for modeling human disease. This poster review outlines the major genome manipulations available in the mouse that are used to understand human disease: natural variation, reverse genetics, forward genetics, transgenics and transposons. Each of these applications will be essential for understanding the diversity that is being discovered within the human population.

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References

    1. Bestor T. H. (2005). Transposons reanimated in mice. Cell 122, 322–325 - PubMed
    1. Beutler B., Du X., Xia Y. (2007). Precis on forward genetics in mice. Nat. Immunol. 8, 659–664 - PubMed
    1. Branda C. S., Dymecki S. M. (2004). Talking about a revolution: the impact of site-specific recombinases on genetic analyses in mice. Dev. Cell 6, 7–28 - PubMed
    1. Capecchi M. R. (1989). The new mouse genetics: altering the genome by gene targeting. Trends Genet. 5, 70–76 - PubMed
    1. Carpinelli M. R., Hilton D. J., Metcalf D., Antonchuk J. L., Hyland C. D., Mifsud S. L., Di Rago L., Hilton A. A., Willson T. A., Roberts A. W., et al. (2004). Suppressor screen in Mpl-/- mice: c-Myb mutation causes supraphysiological production of platelets in the absence of thrombopoietin signaling. Proc. Natl. Acad. Sci. USA 101, 6553–6558 - PMC - PubMed

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