BIOL 69 |
| It is well established that principal mechanisms underlying apoptosis in pathological conditions are triggered and mediated by NF-kappaB signaling and ROS production. Herein, biochemical mechanisms for ROS-promoted NF-kappaB/JNK cross-talk are investigated in terms of the identity of constituent molecular components and their interactions. The model consisting of 36 species participating in 77 unidirectional reactions is examined. Cell survival and cell death are rationalized by determining the actual responses corresponding to transient JNK activation (cell survival) and sustained JNK activation (cell death), respectively. JNK is suggested to be an intrinsic component within a module - a mitogen–activated protein kinase cascade. A specific outcome is suggested to depend on cell type (NF-kappaB-rich and NF-kappaB-deficient cells) within a particular biological context. A phase plane analysis of the model showed that a much lower dimensional representation of the system of equations could limit the range of possible instabilities that the oscillatory signaling can exhibit. |
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Frontiers in Chemical Biology
5:00 PM-7:00 PM, Sunday, August 19, 2007 BCEC -- Exhibit Hall - B2, Poster
Division of Biological Chemistry |