Radoff S, Vlassara H, Cerami A
Laboratory of Medical Biochemistry, Rockefeller University, New York, New York 10021.
Arch Biochem Biophys. 1988 Jun;263(2):418-23. doi: 10.1016/0003-9861(88)90654-6.
Glucose can react nonenzymatically with free protein amino groups to form Amadori products, 1-amino-1-deoxyketose residues. These adducts can undergo subsequent rearrangements and dehydrations to form a complex group of brown, fluorescent pigments collectively referred to as advanced glycosylation end products (AGE). One AGE has been identified as 2-(2-furoyl)-4(5)-(2-furanyl)-1H-imidazole (FFI). The AGE-protein adducts accumulate with time and are implicated in irreversible tissue damage. We have previously demonstrated that macrophages bind and degrade AGE-proteins via a specific cell surface binding protein, thus selectively removing senescent macromolecules. In the present communication, we have solubilized this binding protein from the membranes of the murine macrophage cell line RAW 264.7. We have characterized the nature of binding protein-ligand interaction by competition studies using modified ligands. The data indicate that the carbonyl group, the furan ring(s), and the central imidazole structure are all important in the binding protein-ligand interaction. We have established that the binding constant (Ka) of binding protein for the ligand FFI-BA is 3.1 X 10(7) M-1. Chemical crosslinking studies have demonstrated that the molecular weight of the binding protein is 90,000.
葡萄糖可与游离的蛋白质氨基发生非酶反应,形成阿马多里产物,即1-氨基-1-脱氧酮糖残基。这些加合物可随后发生重排和脱水,形成一组复杂的棕色荧光色素,统称为晚期糖基化终产物(AGE)。其中一种AGE已被鉴定为2-(2-呋喃甲酰基)-4(5)-(2-呋喃基)-1H-咪唑(FFI)。AGE-蛋白质加合物会随时间积累,并与不可逆的组织损伤有关。我们之前已经证明,巨噬细胞通过一种特定的细胞表面结合蛋白结合并降解AGE-蛋白质,从而选择性地清除衰老的大分子。在本通讯中,我们从鼠巨噬细胞系RAW 264.7的膜中溶解了这种结合蛋白。我们通过使用修饰配体的竞争研究来表征结合蛋白-配体相互作用的性质。数据表明,羰基、呋喃环和中心咪唑结构在结合蛋白-配体相互作用中都很重要。我们已经确定结合蛋白对配体FFI-BA的结合常数(Ka)为3.1×10(7) M-1。化学交联研究表明,结合蛋白的分子量为90,000。