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Cell Growth & Differentiation, Vol 1, Issue 4 171-178, Copyright © 1990 by American Association of Cancer Research

ARTICLES

Premature mitosis induced in mammalian cells by the protein kinase inhibitors 2-aminopurine and 6-dimethylaminopurine

R Schlegel, GS Belinsky and MO Harris
Charles A. Dana Laboratory of Toxicology, Harvard School of Public Health, Boston, Massachusetts 02115.

The protein kinase inhibitors 2-aminopurine (2-AP) and 6-dimethylaminopurine (6-DMAP) were used to examine the effects of protein dephosphorylation on the control of mitosis in mammalian cells. Both 2-AP and 6-DMAP induced premature mitosis in hamster fibroblasts that were arrested in S phase. This response was characterized by changes in cell morphology, breakdown of the nuclear envelope, and premature chromosome condensation. Premature mitosis was followed by a return to interphase morphology and reformation of the nuclear envelope around decondensed and fragmented chromatin to form numerous micronuclei. The activity of both compounds was dependent upon new protein synthesis but not new RNA synthesis. 2-AP and 6-DMAP acted cooperatively with each other and with caffeine, suggesting a common mechanism of action. In exponentially growing cells, 2-AP and 6-DMAP did not induce premature mitosis but did increase the frequency of binucleated cells by blocking cytokinesis. These findings support a role for protein dephosphorylation in the control of mitosis and indicate that cell cycle perturbations can modify this regulation.


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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1990 by the American Association of Cancer Research.