Transgenic mice with inactive alleles for procollagen N-proteinase (ADAMTS-2) develop fragile skin and male sterility.

By Shi-wu Li, M. Arita, A. Fertala, Y. Bao, G. Kopen, Teemu K. Långsjö, M. Hyttinen, H. Helminen, D. Prockop. 2001

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In Molecular Biology

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A Disintegrin and Metalloproteinase (ADAM) and ADAM with Thrombospondin Motifs (ADAMTS) Family in Vascular Biology and Disease (2019, background): “Although ADAMTS-2 heterozygous male and female mice display a normal phenotype at birth, they show progressively fragile skin by two weeks of age, and adult males display abnormal seminiferous tubules and lack of spermatozoids production and become sterile [106].”
ADAMTS-2 functions as anti-angiogenic and anti-tumoral molecule independently of its catalytic activity (2010, unknown): “Adamts2 knockout mice have been created [23].”
Cellular and molecular mechanisms in kidney fibrosis. (2014, unknown): “ADAMTS-2 cleaves procollagen-I to facilitate fibril formation (101) and may therefore be an important endogenous regulator of matrix turnover in health and disease,”
A Disintegrin and Metalloproteinase with Thrombospondin Motifs 18 Deficiency Leads to Visceral Adiposity and Associated Metabolic Syndrome in Mice. (2017, background): “8 e 10 The functions of ADAMTSs include N-terminal procollagen processing (ADAMTSs 2, 3, and 14) 11 e 14 ; spermatogenesis (ADAMTS2) 15 ; follicular rupture and ovulation (ADAMTS1) 16 ; angiogenesis inhibition (ADAMTSs 1, 8, and 9) 17,18 ; degradation of cartilage oligomeric matrix protein (ADAMTSs ”
ADAMTS1 cleaves aggrecan at multiple sites and is differentially inhibited by metalloproteinase inhibitors. (2002, background): “The identification of specific substrates for some ADAMTS members, together with the analysis of adamts1 and adamts2 null mice [9,10], suggested a relevant role of this family of proteases on extracellular matrix remodeling with implications on morphogenesis.”
Biochemistry and physiological functions of ADAMTS7 metalloprotease (2013, background): “Prior studies demonstrated that the association between COMP and PGRN induces chondrocyte proliferation and that ADAMTS7 reduced PGRN-mediated chondrogenesis.”
ADAMTS3 activity is mandatory for embryonic lymphangiogenesis and regulates placental angiogenesis (2015, unknown): “Other significant findings relating to potential functions are the relative resistance of Adamts2 mice to liver fibrosis [9], the infertility of Adamts2males [10], the expression of ADAMTS2 by activated macrophages [11], its anti-angiogenic properties [12] and its potential role in pediatric stroke ”