Chromium(III) triggers the DNA-damaged checkpoint of the cell cycle and induces a functional increase of 4E-BP.

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Le Bouffant, Ronan | Mulner-Lorillon, Odile | Morales, Julia | Cormier, Patrick | Bellé, Robert

Edité par CCSD ; American Chemical Society -

International audience. Using sea urchin early embryos as a pertinent model, chromium(III) provoked cell cycle arrest and induced apoptosis. The molecular machinery of translation initiation was investigated. Chromium provoked a time- and dose-dependent increase in the level of 4E-BP protein, the natural regulator of the cap-dependent initiation factor 4E (eIF4E). The 4E-BP increase was the result of 4E-BP stabilization and appeared functional for physiological eIF4E binding, removal of eIF4E from the initiation factor eIF4G, and almost full inhibition of cap-dependent translation in vivo. The protein 4E-BP may be involved in the biological pathway of apoptosis associated with the activation of the DNA-damaged checkpoint of the cell cycle.

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