ADAMTS（有凝血酶敏感素基序的解聚素和金属蛋白酶结构域）家族在人类中有19个蛋白酶。ADAMTS-16是最近克隆的基因，它在婴儿的肺和肾中有高表达，成人中的脑和卵巢也有高表达。他在人的软骨和骨膜中也有表达，同时在骨性关节炎的病人中表达上调。在本研究中我们证实该基因的全长mRNA在软骨细胞中表达,并且克隆出了cDNA 。在软骨瘤细胞中稳定过表达ADAMTS-16会导致细胞的增殖和迁移能力下降，与过表达基质金属蛋白酶-13 (MMP13)引起的降低类似，但是没有粘连。在实验上鉴定该基因从138bp处的ATG开始转录，启动子位于1802bp外，过表达Egr1能诱导ADAMTS-16启动子的157/+138区域或者更长，同时表达SP1能诱导ADAMTS16的所有结构。TGFbeta)能够在软骨细胞中刺激内源ADAMTS16表达。

1: Matrix Biol. 2009 Jul 24. [Epub ahead of print

Surridge AK, Rodgers UR, Swingler TE, Davidson RK, Kevorkian L, Norton R, Waters JG, Goldring MB, Parker AE, Clark IM.

School of Biological Sciences, University of East Anglia, Norwich UK.

The ADAMTS (a disintegrin and metalloproteinase domain with thrombospondin motifs) family includes 19 secreted proteinases in man. ADAMTS16 is a recently cloned gene expressed at high levels in fetal lung and kidney and adult brain and ovary. The ADAMTS-16 protein currently has no known function. ADAMTS16 is also expressed in human cartilage and synovium where its expression is increased in tissues from osteoarthritis patients compared to normal tissues. In this study, we ascertained that the full length ADAMTS16 mRNA was expressed in chondrocytes and cloned the appropriate cDNA. Stable over-expression of ADAMTS16 in chondrosarcoma cells led to a decrease in cell proliferation and migration, though not adhesion, as well as a decrease in the expression of matrix metalloproteinase-13 (MMP13). The transcription start point of the human ADAMTS16 gene was experimentally identified as 138bp upstream of the translation start ATG and the basal promoter was mapped out to -1802bp. Overexpression of Egr1 induced ADAMTS16 promoter constructs of -157/+138 or longer whilst Sp1 induced all ADAMTS16 promoter constructs. Transforming growth factor beta (TGFbeta) stimulated expression of endogenous ADAMTS16 gene expression in chondrocyte cell lines.