Cyclin B1 Availability Is a Rate-limiting Component of the Radiation-induced G2 Delay in HeLa Cells

摘要: Irradiation of tumor cells results in a G2 delay, which has been postulated to allow DNA repair and cell survival. The delay after irradiation is marked HeLa other by delayed expression cyclin B1. To test whether this depression B1 contributes the we induced irradiated using dexamethasone-inducible promoter. Induction radiation abrogated approximately doubling rate at reentered mitosis, whereas dexamethasone itself had no effect. However, overexpression did not eliminate cells. In unirradiated cells, effect on cycle progression. Confirmation that reduction levels would prolong was provided antisense oligonucleotides These demonstrate control length following but do exclude additional mechanisms controlling mitotic irradiation.