Table 2.
Phenotypes of mice genetically deficient in ADAMs
Genotype | Phenotype |
---|---|
ADAM8−/− | Viable and fertile with no phenotype in the unchallenged state(Kelly et al., 2005). |
ADAM9−/− | Viable and fertile with no phenotype in the unchallenged state(Weskamp et al., 2002). |
ADAM10−/− | Embryonic lethal (E9.5). Defects in the heart and central nervous system development and vasculogenesis (Hartmann et Al, 2002). |
ADAM12−/− | 30% embryonic lethal. Surviving mice have normal fertility. Minor brown fat and neck muscle hypertrophy (Kurisaki et al., 2003). |
ADAM15−/− | Viable, fertile with and no phenotype in the unchallenged state. Reduced neovascularization in a murine model of retinopathy of prematurity (Horiuchi et al., 2003) |
ADAM17−/− | Perinatal lethal. Epithelial dysplasia similar to that in TGF-α deficient mice with defective heart and lung development, and defective EGFR ligand shedding (Peschon et al., 1998; Zhao et Al., 2001; Shi et al., 2003). |
ADAM19−/− | 80% post-natal lethality 1–3 days after birth with defective heart development (Zhou et al., 2004). |
Legands for table 2. TGF-α, transforming growth factor-α; EGFR, epidermal growth factor receptor.