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Stress and death: breaking up the c-Abl/14-3-3 complex in apoptosis

Nuclear accumulation of the c-Abl tyrosine kinase is associated with a pro-apoptotic response after DNA damage, but the mechanism regulating c-Abl nuclear localization is unclear. DNA damage and other stress signals are now shown to induce phosphorylation of 14-3-3 proteins by the c-Jun amino-terminal kinase, disrupting a c-Abl/14-3-3 cytoplasmic complex, and liberating c-Abl for translocation to the nucleus.

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Figure 1: Regulation of nuclear accumulation of normal and oncogenic Abl tyrosine kinases.