Sam68 is an RNA binding protein that is tyrosine-phosphorylated by Src during mitosis and has been postulated to have a role in cell cycle control by modulating RNA metabolism. To elucidate the function of this protein, we isolated a Sam68-deficient DT40 cell line by gene disruption. The Sam68-deficient cells exhibited markedly decreased growth and the growth retardation was due to elongation of the G2-M phase, however, the kinase activity associated with Cdc2 remained unaltered. Our results indicate that Sam68 may play a critical role in G2-M progression in a manner independent of the control of Cyclin/Cdc2 kinase activity.
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