SignalSilence ® c-Jun siRNA II

c-Jun is a member of the Jun family containing c-Jun, JunB, and JunD, and is a component of the transcription factor activator protein-1 (AP-1). AP-1 is composed of dimers of Fos, Jun, and ATF family members and binds to and activates transcription at TRE/AP-1 elements (reviewed in 1). Extracellular signals, including growth factors, chemokines, and stress, activate AP-1-dependent transcription. The transcriptional activity of c-Jun is regulated by phosphorylation at Ser63 and Ser73 through SAPK/JNK (reviewed in 2). Knockout studies in mice have shown that c-Jun is essential for embryogenesis (3), and subsequent studies have demonstrated roles for c-Jun in various tissues and developmental processes, including axon regeneration (4), liver regeneration (5), and T cell development (6). AP-1 regulated genes exert diverse biological functions, including cell proliferation, differentiation, and apoptosis, as well as transformation, invasion and metastasis, depending on cell type and context (7-9). Other target genes regulate survival, as well as hypoxia and angiogenesis (8,10). Research studies have implicated c-Jun as a promising therapeutic target for cancer, vascular remodeling, acute inflammation, and rheumatoid arthritis (11,12). 1.Jochum, W. et al. (2001) Oncogene 20, 2401-12. 2.Davis, R.J. (2000) Cell 103, 239-52. 3.Hilberg, F. et al. (1993) Nature 365, 179-81. 4.Raivich, G. et al. (2004) Neuron 43, 57-67. 5.Behrens, A. et al. (2002) EMBO J 21, 1782-90. 6.Riera-Sans, L. and Behrens, A. (2007) J Immunol 178, 5690-700. 7.Leppä, S. and Bohmann, D. (1999) Oncogene 18, 6158-62. 8.Shaulian, E. and Karin, M. (2002) Nat Cell Biol 4, E131-6. 9.Weiss, C. and Bohmann, D. (2004) Cell Cycle 3, 111-3. 10.Karamouzis, M.V. et al. (2007) Mol Cancer Res 5, 109-20. 11.Kim, S. and Iwao, H. (2003) J Pharmacol Sci 91, 177-81. 12.Dass, C.R. and Choong, P.F. (2008) Pharmazie 63, 411-4.