Genetic modifications, notably gene knockouts, that create informative phenotypes of infertility thereby establish an important role for the inactivated gene/protein in reproductive pathophysiology ( 4-6). Individual researchers and consortia have created thousands of genetic models of human reproductive pathophysiology ( 1-3). The highly conserved mechanisms of mammalian reproductive physiology make the mouse an advantageous animal model because of its small size with low maintenance costs, short reproductive cycle allowing for efficient breeding, and adaptability to creating customized targeted genetic models for pathophysiology. Mouse models have long been a key investigative tool in reproductive biology and medicine research as experimental models for human reproductive pathophysiology.
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