Itoh H, Hidaka H
J Biochem. 1984 Dec;96(6):1721-6. doi: 10.1093/oxfordjournals.jbchem.a135004.
Trypsin-treated Ca2+/calmodulin-dependent phosphodiesterase (CA2+-PDE), which had lost its sensitivity to Ca2+-calmodulin, was inhibited by various calmodulin antagonists, trifluoperazine, chlorpromazine, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) and aminoalkyl chain analogues of W-7 (A-3, A-4, A-5, I-240, A-6, A-7). These inhibitory effects were less than those on calmodulin-activated Ca2+-PDE. The ability of these compounds to inhibit trypsin-treated Ca2+-PDE correlated well with the inhibitory effect on calmodulin-activated Ca2+-PDE. W-7 inhibited trypsin-treated Ca2+-PDE in a competitive fashion with respect to cyclic GMP and the Ki value was 300 microM. The inhibition of trypsin-treated Ca2+-PDE by W-7 (300 microM) or A-7 (100 microM) was overcome by the addition of excess calmodulin. Trypsin-treated Ca2+-PDE can bind to W-7-coupled cyanogen bromide-activated Sepharose 4B in the presence of 1 mM EGTA. These results suggest that Ca2+-PDE possesses a binding site for calmodulin antagonists and that the binding site for these antagonists on this enzyme may be structurally similar to the binding site on calmodulin itself.
经胰蛋白酶处理后对Ca2+/钙调蛋白依赖性磷酸二酯酶(CA2+-PDE),其对Ca2+-钙调蛋白的敏感性丧失,却受到多种钙调蛋白拮抗剂的抑制,这些拮抗剂包括三氟拉嗪、氯丙嗪、N-(6-氨基己基)-5-氯-1-萘磺酰胺(W-7)以及W-7的氨基烷基链类似物(A-3、A-4、A-5、I-240、A-6、A-7)。这些抑制作用小于对钙调蛋白激活的Ca2+-PDE的抑制作用。这些化合物抑制经胰蛋白酶处理的Ca2+-PDE的能力与对钙调蛋白激活的Ca2+-PDE的抑制作用密切相关。W-7以竞争性方式抑制经胰蛋白酶处理的Ca2+-PDE,相对于环鸟苷酸,其Ki值为300 microM。加入过量钙调蛋白可克服W-7(300 microM)或A-7(100 microM)对经胰蛋白酶处理的Ca2+-PDE的抑制作用。在1 mM乙二醇双(2-氨基乙基醚)四乙酸(EGTA)存在下,经胰蛋白酶处理的Ca2+-PDE可与W-7偶联的溴化氰活化的琼脂糖4B结合。这些结果表明,Ca2+-PDE具有钙调蛋白拮抗剂的结合位点,并且该酶上这些拮抗剂的结合位点在结构上可能类似于钙调蛋白自身的结合位点。