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THE BIOLOGIC ROLE FOR NUCLEAR FACTOR-KAPPAB IN DISEASE AND ITS POTENTIAL INVOLVEMENT IN MUCOSAL INJURY ASSOCIATED WITH ANTI-NEOPLASTIC THERAPY

Department of Oral Medicine and Diagnostic Sciences, Harvard School of Dental Medicine, and Divisions of Oral Medicine, Oral and Maxillofacial Surgery and Dentistry, Brigham and Women’s Hospital and the Dana Farber Cancer Institute, 75 Francis Street, Boston, MA 02115; Ssonis{at}partners.org

View larger version (39K): [in a new window]   Figure 1. Signaling pathway for NF-B activation. Extracellular inducers including reactive oxygen species (ROS), cytokines, viral and bacterial products, ionizing radiation, and cancer chemotherapy drugs activate cytoplasmic kinases (IKK) and lead to the phosphorylation of IB. The phosphorylated complex is recognized by ubiquitin ligase leading to the attachment of ubiquitin chains. The ubiquinated (Ub) IB is degraded by the 26S proteosome which permits NF-B to enter the nucleus (after Makarov, 2000).

View larger version (18K): [in a new window]   Figure 2. NF-B-mediated up-regulation of different Bcl-2 genes. One possible way to explain the dichotomous responses of normal cells and tumor cells to anti-neoplastic activation of NF-B might be that different Bcl-2 genes are up-regulated. In normal cells, those genes (Bax, Bak, Bik, Bicl) are associated with apoptosis, while those in tumor cells (Bcl-X2, Mcl-1, Bcl-w, A-1, Bfl-1) might be cytoprotective.