There are two broad categories that inhibitory mechanisms can be placed in. The first involves the induction of an auxiliary factor by GR that is then responsible for RelA inhibition. While it has been shown that GR can induce IkB in certain cell types, that mechanism is not ubiquitous and alternate mechanisms exist in many cell types. It is this second category of mechanisms which my work has focused upon. Specifically, Robert has chosen to study the physical association between GR and RelA. The two interacting domains have been mapped and their mutagenesis is underway.
Similar work is underway with other members of the nuclear receptor family.
Using a combination of in vivo and in vitro methods, it is Robert's hope that taking our understanding of anti-inflammation to a molecular level may suggest alternate modes of therapy, perhaps with fewer side effects than the traditional steroid therapies.