We are interested in the relationship between cellular oxidative stress defense and aging. Previous data showed that JNK signaling can induce a genetic program that confers stress resistance, and that active JNK signaling can prolong lifespan in Drosophila. Further, we showed that the life-extending effect of JNK is mediated by activation of the transcription factor Foxo (a.k.a. Daf 16 in C. elegans) and by suppressing the effects of insulin/IGF signaling.
Learn more about JNK, Oxidative Stress and Aging
Nrf2 is a signal-activated transcription factor that had previously been characterized in mammals, where it mediates responses to electrophiles, oxidative stress and carcinogens. Nrf2-induced processes protect many organs, including the gastrointestinal tract and the nervous system, from xenobiotic damage. Importantly, Nrf2 is a prominent target for cancer chemo-preventive interventions and Nrf2-activating agents are currently being evaluated for therapeutic utility in clinical trials.
Learn more about NRF2 Signaling
Previous research in the lab showed that JNK signaling activates genes that are required for epithelial movements and morphogenesis during embryonic development. Integrins and profilin were identified as important mediators of this response. More recently, we have turned to the role of JNK signaling in pathological cell movements. By generating clones of malignant cells in eye imaginal discs we can model tumor behavior in vivo.
Learn more about Drosophila as a Cancer Model