Harrison D H, Bohren K M, Petsko G A, Ringe D, Gabbay K H
Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02554, USA.
Biochemistry. 1997 Dec 23;36(51):16134-40. doi: 10.1021/bi9717136.
It is generally expected that only one inhibitor molecule will bind to an enzyme active site. In fact, specific drug design theories depend upon this assumption. Here, we report the binding of two molecules of an inhibitor to the same active site which we observed in the 1.8 A resolution structure of the drug Alrestatin bound to a mutant of human aldose reductase. The two molecules of Alrestatin bind to the active site in a stacked arrangement (a double-decker). This stack positions the carboxylic acid of one drug molecule near the NADP+ cofactor at a previously determined anion binding site and the carboxylic acid of the second drug molecule near the carboxy-terminal tail of the enzyme. We propose that interactions of inhibitors with the carboxy-terminal loop of aldose reductase are critical for the development of inhibitors that are able to discriminate between aldose reductase and other members of the aldo-keto reductase superfamily. This finding suggests a new direction for the introduction of specificity to aldose reductase-targeted drugs.
通常认为,只有一个抑制剂分子会与酶活性位点结合。事实上,特定的药物设计理论就依赖于这一假设。在此,我们报告了在与人类醛糖还原酶突变体结合的药物阿雷司他汀的1.8埃分辨率结构中观察到的两个抑制剂分子与同一活性位点的结合情况。两个阿雷司他汀分子以堆叠排列(双层)的方式结合到活性位点。这种堆叠使一个药物分子的羧酸靠近之前确定的阴离子结合位点处的NADP+辅因子,而第二个药物分子的羧酸靠近酶的羧基末端尾巴。我们提出,抑制剂与醛糖还原酶羧基末端环的相互作用对于开发能够区分醛糖还原酶和醛糖 - 酮糖还原酶超家族其他成员的抑制剂至关重要。这一发现为向以醛糖还原酶为靶点的药物引入特异性指明了新方向。