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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

c-Jun induces apoptosis of starved BM2 monoblasts by activating cyclin A-CDK2.

c-Jun is one of the major components of the activating protein-1 (AP-1), the transcription factor that participates in regulation of proliferation, differentiation, and apoptosis. In this study, we explored functional interactions of the c-Jun protein with several regulators of the G1/S transition in serum-deprived v-myb-transformed chicken monoblasts BM2. We show that the c-Jun protein induces expression of cyclin A, thus up-regulating activity of cyclin A- associated cyclin-dependent kinase 2 (CDK2), and causing massive programmed cell death of starved BM2cJUN cells. Specific inhibition of CDK2 suppresses frequency of apoptosis of BM2cJUN cells. We conclude that up-regulation of cyclin A expression and CDK2 activity can represent important link between the c-Jun protein, cell cycle machinery, and programmed cell death pathway in leukemic cells.[1]


  1. c-Jun induces apoptosis of starved BM2 monoblasts by activating cyclin A-CDK2. Vanhara, P., Bryja, V., Horv??th, V., Kozub??k, A., Hampl, A., Smarda, J. Biochem. Biophys. Res. Commun. (2007) [Pubmed]
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