Cell Signaling and Apoptosis
Our work is focused in the characterization of novel physiological roles of FAIM-L, a neuronal protein acting as a death receptor antagonist. Other than preventing cell death, FAIM-L interacts with XIAP and Siva-1, modulating caspases activity, thus participating in some neuronal plasticity processes, such as pruning and long-term depression. In addition, FAIM-L controls neurodegeneration by modulating TNF effects, and we have demonstrated regulation of its expression by some microRNAs altered in Alzheimer’s disease.
We think that FAIM-L could be an interesting target for the future treatment of Alzheimer’s disease. With this goal, we are at present characterizing the interaction of FAIM-L with other relevant proteins for neurodegeneration, and developing tools to characterize FAIM-L expression, and also to modulate its levels in animal models of the disease. In addition, in collaboration with other VHIR groups, we are investigating its role in diabetic retinopathy.