Early models of induced factor deficiency relied on immunologic mechanisms to neutralize factor activity. The ability to disrupt individual genes selectively by gene targeting provided a powerful method of generating mice with deficiencies of either selected ligands, receptors, or downstream-signaling molecules. Such engineered deficiencies have usually been designed to be absolute and are life-long, providing insight into the cumulative effects of nonredundant roles of the absent gene product. This genetic approach has been pre-eminent in defining the essential physiologic role of various factors. However, animal models with less-than-total factor deficiency have been generated using other methodologies, both before the gene targeting era and more recently. These models offer several advantages: although they may not result in absolute factor deficiency, they offer flexibilities including inducibility, reversibility, and nonlethality. A new approach, not yet applied to studying HGF, is the use of RNA interference (1). Various experimental approaches to factor ablation are listed in Table 1 with some comparative relative advantages and disadvantages.
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