Phenotypic Analysis of Meltrin α (ADAM12)-Deficient Mice: Involvement of Meltrin α in Adipogenesis and Myogenesis

By T. Kurisaki, A. Masuda, K. Sudo, Junko Sakagami, S. Higashiyama, Y. Matsuda, A. Nagabukuro, A. Tsuji, Y. Nabeshima, M. Asano and 2 more. 2003

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Essential roles of Meltrin β (ADAM19) in heart development (2004, background): “5 at which point HB-EGF and TACE appear to be still highly expressed, Meltrin h and TACE may act cooperatively during cushion development.”
The ADAM metalloproteinases (2008, background): “However, Adam12-null animals show minor defects in brown adipose tissue formation (Kurisaki et al., 2003), and transgenic over-expression enhanced adipogenesis (Kawaguchi et al., 2002).”
A Disintegrin and Metalloprotease (ADAM): Historical Overview of Their Functions (2016, background): “Deletion of ADAM-12 results in 30% neonatal lethality and a 30% reduction in brown adipose tissue [91], and ADAM-11 knockout animals show deficits in spatial learning, motor coordination, and altered nociception responses [92,93].”
ADAMs as mediators of EGF receptor transactivation by G protein-coupled receptors. (2006, background): “In ADAM12 / mice, 30% of these animals did not survive and showed defects of brown adipose tissue (55).”
Distinct roles for ADAM10 and ADAM17 in ectodomain shedding of six EGFR ligands (2004, methodology): “Generation of adam9/15 / , adam9/12/15 / , and adam9/12/15/17 / knockout mice Mice lacking ADAMs 9, 12, or 15 have been described previously (Weskamp et al., 2002; Horiuchi et al., 2003; Kurisaki et al., 2003).”