Mechanism of inhibition of human KSP by monastrol: insights from kinetic analysis and the effect of ionic strength on KSP inhibition

Biochemistry. 2004 Dec 7;43(48):15258-66. doi: 10.1021/bi048282t.

Abstract

Kinesin motor proteins utilize the energy from ATP hydrolysis to transport cellular cargo along microtubules. Kinesins that play essential roles in the mechanics of mitosis are attractive targets for novel antimitotic cancer therapies. Monastrol, a cell-permeable inhibitor that specifically inhibits the kinesin Eg5, the Xenopus laevis homologue of human KSP, can cause mitotic arrest and monopolar spindle formation. In this study, we show that the extent of monastrol inhibition of KSP microtubule-stimulated ATP hydrolysis is highly dependent upon ionic strength. Detailed kinetic analysis of KSP inhibition by monastrol in the presence and absence of microtubules suggests that monastrol binds to the KSP-ADP complex, forming a KSP-ADP-monastrol ternary complex, which cannot bind to microtubules productively and cannot undergo further ATP-driven conformational changes.

MeSH terms

  • Adenosine Diphosphate / metabolism
  • Adenosine Triphosphate / metabolism
  • Catalysis / drug effects
  • Catalytic Domain / drug effects
  • Dose-Response Relationship, Drug
  • Humans
  • Kinesins / antagonists & inhibitors*
  • Kinesins / chemistry*
  • Kinesins / metabolism
  • Kinetics
  • Microtubules / chemistry
  • Microtubules / drug effects
  • Microtubules / metabolism
  • Osmolar Concentration
  • Protein Binding / drug effects
  • Protein Conformation / drug effects
  • Pyrimidines / chemistry*
  • Pyrimidines / pharmacology
  • Spectrometry, Fluorescence
  • Thiones / chemistry*
  • Thiones / pharmacology

Substances

  • KIF11 protein, human
  • Pyrimidines
  • Thiones
  • Adenosine Diphosphate
  • monastrol
  • Adenosine Triphosphate
  • Kinesins