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. Author manuscript; available in PMC: 2009 Jan 1.
Published in final edited form as: Int J Biochem Cell Biol. 2008 Jan 31;40(6-7):1246–1272. doi: 10.1016/j.biocel.2008.01.020

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.

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