Our group is devoted to the analysis of molecular mechanism triggered by neurodegenerative processes. We try to understand key signals that regulate cellular morphogenesis, and how these putative pathways may be defective in some pathological situations. As a second challenge we would like to propose regeneration alternatives.

Our group currently consists of the principal investigator (Research Professor), three predoctoral fellows, and one hired research assistant. In recent years our work has focused on two different projects. In the first one we study the biogenesis of the primary cilium. This structure, which is present as a single copy in the cell, consists of a specialized protrusion of the plasma membrane that regulates a wide variety of signaling pathways essential for cell differentiation and development.

Ecology, molecular biology and biotechnology of extreme acidic environments. Geomicrobiological characterization of extreme environments. Microbial ecology of extreme environments. Mycology

Identification and characterization of signaling pathways and molecules that regulate the inflammatory response, with a particular focus in solid tumors. To this end, we will use animal models deficient in specific inflammatory mediators as well as genomic, proteomic and metabolomic analyses to characterize the activation, differentiation and migratory capacity of immune cell subpopulations. We will also analyze how inflammation in the tumor milieu impacts on other stromal components, particularly the endothelium.

Understanding the mechanisms of chemokine signaling and chemokine function with the aim to provide a clearer understanding of how this family of proteins acts, and define new orientations for the treatment of inflammatory, autoimmune and infectious diseases. Our group, using resonance energy transfer tecnologies (FRET, BRET) and advanced microscopy, STED and TIRF , have determined that these receptors form homo- and heterodimers and even oligomers at the cell membrane.

The healthy immune system makes use of a variety of surveillance mechanisms at different stages of lymphoid development to prevent the occurrence and expansion of potentially harmful autoreactive T cell clones. Disruption of these mechanisms may lead to inappropriate activation of T cells and the development of autoimmune and lymphoproliferative diseases [such as multiple sclerosis, rheumatoid arthritis, lupus erythematosus, diabetes and autoimmune lymphoproliferative syndrome (ALPS)].

The relevance of the study of c-Myc lies in the broad spectrum of human cancers in which deregulation of this gene plays a prominent role. It is estimated that expression of this gene is altered gene in 40-50% of human cancers. This large spectrum probably reflects the large number and critical nature of the biological processes that appear to be regulated by c-Myc. The role of c-Myc in cell differentiation is poorly understood. C-Myc downregulation is usually associated with termination of differentiation in several cell types.

Our research is focused on two main areas, understanding the roles of natural killer (NK) cells in response to virus infections, and study of NK cell function in patients suffering primary immunodeficiencies (whose major clinical problems are virus infections).