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

Chemical Research in Toxicology
Ronan Le BouffantR Bellé

Abstract

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.

Citations

Oct 31, 2009·Apoptosis : an International Journal on Programmed Cell Death·Maria Agnello, Maria Carmela Roccheri
May 11, 2012·Journal of Toxicology and Environmental Health. Part B, Critical Reviews·R BelléO Mulner-Lorillon
Jan 12, 2012·Physical Chemistry Chemical Physics : PCCP·Xu Zhang, Yi Chen
Aug 27, 2009·Expert Opinion on Therapeutic Targets·Francis Robert, Jerry Pelletier
Sep 29, 2017·Aquatic Toxicology·Georgia G KournoutouDimitrios L Kalpaxis

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