To elucidate the stoichiometry of the TCR. Study the mechanisms of assembly and intracellular retention. Discern between the specific and redundant roles of each of the TCR subunits.

There are many evidences for the involvement of lipid mediators such as prostanoids and cholesterol derivatives in the modulation of inflammatory and cardiovascular pathophysiology. Prostanoids have important roles in physiological processes such as renal and vascular homeostasis, as well as having a central role in the inflammatory process.

The kinase GRK2 as a central node in cell signaling networks. Study of its interactome and implications in cardiovascular, inflammatory, diabetes/obesity, or tumor progression pathologies.

We use protein engineering and biopphysical, biochemical and biological analyses to study the molecular structure, physical properties and biological function of viruses to guide the design of vaccines, antiviral drugs and virus-based materials for bio/nanotechnological applications

Infections caused by human immunodeficiency viruses (HIV) are a global health burden. Despite progress in antiretroviral therapy, HIV still causes significant deaths. Our lab focuses on understanding HIV's genetic machinery and drug resistance mechanisms. We engineer more accurate DNA synthesizing enzymes for biotech tools and study their roles in viral replication. Our research aims to improve therapies and develop new strategies against HIV's resistance and spread, as well as other viruses with related enzymes and replication mechanisms (e.g. hepatitis B virus and herpesviruses).

Our group studies the molecular mechanisms that operate on neural networks and modulate the efficiency of synaptic contacts and focuses its activity on the elucidation of the cellular and molecular mechanisms that determine the efficiency of calcium-mediated signaling and calmodulin in the framework of short and long term synaptic plasticity

Effect of age on the molecular determinants of cognition: relevance for late onset Alzheimers disease

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.

During the past 13 years, the group has studied two DNA polymerases implicated in DNA double strand break (DSB) repair in humans: Pol lambda and Pol mu, which were identified in our laboratory. Given their role in DSB repair by non-homologous end joining (NHEJ), these two enzymes are essential to maintain genomic stability and also to generate the variability needed in certain genes, such as antigen receptors.