Kimata K, Takeda M, Suzuki S, Pennypacker J P, Barrach H J, Brown K S
Arch Biochem Biophys. 1983 Oct 15;226(2):506-16. doi: 10.1016/0003-9861(83)90320-x.
Immunohistochemical and biochemical evidence that the cartilage from cmd/cmd mice, who have an autosomal recessive lethal mutation causing cartilage matrix deficiency, synthesizes link protein nearly at a normal level is provided. Since cartilage-characteristic proteoglycan is not synthesized in this mutant mouse (K. Kimata, H-J. Barrach, K. S. Brown, and J. P. Pennypacker (1981) J. Biol. Chem. 256, 6961-6968), link proteins are apparently not in conventional proteoglycan aggregate. However, the link proteins are functional and able to interact with exogenous cartilage-characteristic proteoglycan monomer and hyaluronic acid to form aggregates.
提供了免疫组织化学和生物化学证据，表明患有导致软骨基质缺乏的常染色体隐性致死突变的cmd/cmd小鼠的软骨合成连接蛋白的水平几乎正常。由于在这种突变小鼠中不合成软骨特征性蛋白聚糖（K. Kimata、H-J. Barrach、K. S. Brown和J. P. Pennypacker（1981年）《生物化学杂志》256，6961 - 6968），连接蛋白显然不在传统的蛋白聚糖聚集体中。然而，连接蛋白具有功能，能够与外源性软骨特征性蛋白聚糖单体和透明质酸相互作用形成聚集体。
