Abstract

Several reports describe the existence of a redox cycle within the normal cell cycle that helps control the process of cell proliferation. According to some of these reports, this redox cycle comprises an intracellular redox potential E that oscillates above and below θ during the cell cycle process. θ is the threshold for dephosphorylation of protein regulators associated with serine residues such as the retinoblastoma protein. This article describes how insulin action may be the source of the redox cycle within the cell cycle. The relative lack of insulin action as a consequence of oxidative stress results in the hallmarks of type 2 diabetes.

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