Ishizaki T, Uehata M, Tamechika I, Keel J, Nonomura K, Maekawa M, Narumiya S
Department of Pharmacology, Kyoto University, Faculty of Medicine, Kyoto, Japan.
Mol Pharmacol. 2000 May;57(5):976-83.
Y-27632 [(+)-(R)-trans-4-(1-aminoethyl)-N-(4-pyridyl)cyclohexanecarboxamide++ + dihydrochloride] is widely used as a specific inhibitor of the Rho-associated coiled-coil forming protein serine/threonine kinase (ROCK) family of protein kinases. This study examined the inhibition mechanism and profile of actions of Y-27632 and a related compound, Y-30141 [(+)-(R)-trans- 4-(1-aminoethyl)-N-(1H-pyrrolo[2, 3-b]pyridin-4-yl)cyclohexan-ecarboxamide dihydrochloride]. Y-27632 and Y-30141 inhibited the kinase activity of both ROCK-I and ROCK-II in vitro, and this inhibition was reversed by ATP in a competitive manner. This suggests that these compounds inhibit the kinases by binding to the catalytic site. Their affinities for ROCK kinases as determined by K(i) values were at least 20 to 30 times higher than those for two other Rho effector kinases, citron kinase and protein kinase PKN. [(3)H]Y-30141 was taken up by cells in a temperature- and time-dependent and saturable manner, and this uptake was competed with unlabeled Y-27632. No concentrated accumulation was found, suggesting that the uptake is a carrier-mediated facilitated diffusion. Y-27632 abolished stress fibers in Swiss 3T3 cells at 10 microM, but the G(1)-S phase transition of the cell cycle and cytokinesis were little affected at this concentration. Y-30141 was 10 times more potent than Y-27632 in inhibiting the kinase activity and stress fiber formation, and it caused significant delay in the G(1)-S transition and inhibition of cytokinesis at 10 microM.
Y-27632 [(+)-(R)-反式-4-(1-氨基乙基)-N-(4-吡啶基)环己烷甲酰胺二盐酸盐] 被广泛用作Rho相关卷曲螺旋形成蛋白丝氨酸/苏氨酸激酶(ROCK)家族蛋白激酶的特异性抑制剂。本研究检测了Y-27632和一种相关化合物Y-30141 [(+)-(R)-反式-4-(1-氨基乙基)-N-(1H-吡咯并[2,3-b]吡啶-4-基)环己烷甲酰胺二盐酸盐] 的抑制机制和作用谱。Y-27632和Y-30141在体外抑制ROCK-I和ROCK-II的激酶活性,且这种抑制可被ATP以竞争性方式逆转。这表明这些化合物通过与催化位点结合来抑制激酶。通过解离常数(Ki)值测定,它们对ROCK激酶的亲和力比对另外两种Rho效应激酶——citron激酶和蛋白激酶PKN的亲和力至少高20至30倍。[3H]Y-30141以温度、时间依赖性和饱和的方式被细胞摄取,且这种摄取可被未标记的Y-27632竞争。未发现集中积累,表明摄取是载体介导的易化扩散。Y-27632在10微摩尔浓度时消除了瑞士3T3细胞中的应力纤维,但在此浓度下细胞周期的G1-S期转换和胞质分裂几乎未受影响。Y-30141在抑制激酶活性和应力纤维形成方面比Y-27632强10倍,且在10微摩尔浓度时导致G1-S期转换显著延迟并抑制胞质分裂。