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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects
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Cell Cycle / drug effects*
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Cell Cycle / genetics
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Chlorides / toxicity*
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Chromium Compounds / toxicity*
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DNA Damage*
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Dose-Response Relationship, Drug
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Embryo, Nonmammalian / chemistry
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Embryo, Nonmammalian / drug effects*
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Embryo, Nonmammalian / metabolism
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Embryonic Development / drug effects
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Eukaryotic Initiation Factor-4E / analysis
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Eukaryotic Initiation Factor-4E / metabolism
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Intracellular Signaling Peptides and Proteins / analysis
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Intracellular Signaling Peptides and Proteins / metabolism*
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Ovum / chemistry
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Ovum / drug effects
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Ovum / metabolism
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Protein Binding
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Sea Urchins / embryology
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Sea Urchins / physiology
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Time Factors
Substances
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Chlorides
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Chromium Compounds
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Eukaryotic Initiation Factor-4E
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Intracellular Signaling Peptides and Proteins
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chromous chloride