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Epstein-Barr virus nuclear antigen 2 (EBNA2) is essential for B-cell immortalization by EBV, most probably by its ability to transactivate a number of cellular and viral genes. EBNA2-responsive elements (EBNA2REs) have been identified in several EBNA2-regulated viral promoters, each of them carrying at least one RBP-Jκ recognition site. RBP-Jκ recruits EBNA2 to the EBNA2RE and, once complexed to EBNA2, is converted from a repressor into an activator. An activated form of the cellular receptor Notch also interacts with RBP-Jκ, providing a link between EBNA2 and Notch signalling. To determine whether activated Notch is able to transactivate EBNA2-responsive viral promoters, we performed cotransfection experiments with activated mouse Notch1 (mNotch1-IC) and luciferase constructs of the BamHI C, LMP1, and LMP2A promoters. We present here evidence that mNotch1-IC transactivates viral promoters known to be regulated by EBNA2. As shown for EBNA2, mutations or deletions of the RBP-Jκ sites diminish or eliminate mNotch1-IC-mediated transactivation of the promoters, pointing to an essential role for Notch–RBP-Jκ interaction. In addition to RBP-Jκ, other cellular factors may bind within the EBNA2REs of viral promoters. While some factors appear to play an important role in both EBNA2- and mNotch1-IC-mediated transactivation, others are only important for the activity of either EBNA2 or mNotch1-IC. We could observe specific mNotch1-IC-responsive regions, thereby throwing more light upon which cofactors interact with EBNA2 and mNotch1-IC, thus enabling them to become functionally transactivators in vivo.

Adaptive structures are conventional truss structures that are equipped with sensors, actuators, and a control unit. This offers the opportunity of reacting and adapting to external loads but raises nontrivial issues. When actuators are placed optimally within a structure, they can be individually integrated either parallel to or in series with elements of the original passive structure. Additionally, some of the elements might be tension-only elements and thus have to be treated as nonlinear, as their stiffness depends on the stress within the element itself. Input constraints naturally arise for actuators, e. g., due to the maximum pressure limit of a hydraulic system and displacement limits of the actuators. We present modeling approaches for an add-on inclusion of these different types of actuators in an existing finite-element model of a passive structure. We place special focus on the ability of the model to reproduce the correct behavior in case of an actuator reaching its displacement constraint within a tension-only element. When such an adaptive structure is subject to static loads, e. g., wind loads, it is required to respond using its actuators to keep the structure within given safety and comfort limits. These limits can be expressed as state constraints. We present a method for optimally compensating these static loads under the given input and state constraints along with experimental results on a scale model of an actual high-rise building. An important aspect regarding adaptive structures is that of their behavior in case of actuator faults. An obvious result is that a structure's performance degrades, and the controller needs to recognize faults and deal with it properly. Assuming a diagnosed actuator fault, we present results illustrating the performance degradation. The designed controller can reconfigure and reinitialize itself. The performance with and without applied reconfiguration to the nominal case is compared.

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