c-Jun induces apoptosis of starved BM2 monoblasts by activating cyclin A-CDK2
- Institute of Experimental Biology, Faculty of Science, Masaryk University, Brno (Czech Republic)
- Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm (Sweden)
- Institute of Biophysics, Academy of Sciences of the Czech Republic, Brno (Czech Republic)
- Institute of Biology, Faculty of Medicine, Masaryk University, Brno (Czech Republic)
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.
- OSTI ID:
- 20857978
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 353, Issue 1; Other Information: DOI: 10.1016/j.bbrc.2006.11.124; PII: S0006-291X(06)02611-8; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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