Experimental cell research
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The calmodulin-dependent protein kinase-II (CaMK-II) inhibitor KN-93 has been shown to reversibly arrest mouse and human cells in the G1 phase of the cell cycle [Tombes, R. M., Westin, E., Grant. S., and Krystal, G. (1995) Cell Growth Differ. 6, 1073-1070; Rasmussen, G., and Rasmussen, C. (1995) Biochem. ⋯ All of these phenomena were unaffected by KN-93's inactive analog, KN-92, and were reversible upon KN-93 washout. The kinetics of recovery from cell cycle arrest were similar to those reported for other G1 phase blockers. These results suggest a mechanism by which G1 Ca2+ signals could be linked via calmodulin-dependent phosphorylations to the cell cycle-controlling machinery through cyclins and cdk inhibitors.