Maliga Zoltan, Kapoor Tarun M, Mitchison Timothy J
Program in Biophysics, Harvard University, Boston, MA 02115, USA.
Chem Biol. 2002 Sep;9(9):989-96. doi: 10.1016/s1074-5521(02)00212-0.
Monastrol, a cell-permeable inhibitor of the kinesin Eg5, has been used to probe the dynamic organization of the mitotic spindle. The mechanism by which monastrol inhibits Eg5 function is unknown. We found that monastrol inhibits both the basal and the microtubule-stimulated ATPase activity of the Eg5 motor domain. Unlike many ATPase inhibitors, monastrol does not compete with ATP binding to Eg5. Monastrol appears to inhibit microtubule-stimulated ADP release from Eg5 but does not compete with microtubule binding, suggesting that monastrol binds a novel allosteric site in the motor domain. Finally, we established that (S)-monastrol, as compared to the (R)-enantiomer, is a more potent inhibitor of Eg5 activity in vitro and in vivo. Future structural studies should help in designing more potent Eg5 inhibitors for possible use as anticancer drugs and cell biological reagents.
莫那可林(Monastrol)是一种可穿透细胞的驱动蛋白Eg5抑制剂,已被用于探究有丝分裂纺锤体的动态组织。莫那可林抑制Eg5功能的机制尚不清楚。我们发现,莫那可林既抑制Eg5运动结构域的基础ATP酶活性,也抑制微管刺激的ATP酶活性。与许多ATP酶抑制剂不同,莫那可林不与ATP竞争结合Eg5。莫那可林似乎抑制微管刺激的ADP从Eg5释放,但不与微管结合竞争,这表明莫那可林结合了运动结构域中的一个新的变构位点。最后,我们确定,与(R)-对映体相比,(S)-莫那可林在体外和体内都是更有效的Eg5活性抑制剂。未来的结构研究应有助于设计更有效的Eg5抑制剂,可能用作抗癌药物和细胞生物学试剂。