Elucidation for crosstalk of the nuclear-cytoplasic signalling in the apoptotic response to oxidative stress

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Oxidative stress has been implicated in the initiation and development of many diseases and causes a various types of cellular injury, including DNA and protein damage, lipid peroxidation, and damage to other biomolecules. Oxidative stress also occurs during apoptotic cell death. We have shown that several pro-apoptotic kinases including PKCdelta, c-Abl, and DYRK2 undergo nuclear-cytoplasmic shuttling in response to oxidative stress. Importantly, whereas precise regulation for the shuttling of these kinases remain uncertain, this mechanism has consequences for induction of apoptosis and implies that proper localization is central to the function of pro-apoptotic kinases. These findings highlight recent efforts on molecular medicine demonstrating that the nuclear targeting of kinases is novel and essential regulatory mechanisms that directly influences the induction of apoptosis in response to oxidative stress.