Our group is focused on the study of the mechanisms by which proinflammatory stimuli regulate gene expression and modulate the proliferation, differentiation and survival of different cell types. We are especially interested in the molecular and biological actions of the secreted phospholipase A2, an enzyme involved in inflammatory and degenerative diseases.

Our main research goal is to study lipid-modifiying enzymes in the immune system. Lipins are phosphatidic acid fosfatases that generate diacylglycerol, a signalling lipid that is involved in signal transduction during cellular immune activation. Althought mutations in human lpin genes promote inflammation-related disseases, very little is known about the role of lipin in inmune cells or the development of inflammatory processes. Our main goal is to answer these questions.

The group is focused on studying the role of innate receptors in inflammatory diseases; particularly on Toll-like receptors (TLRs). These are sensors of molecular patterns from pathogens as well as endogenous molecules released after tissue damage with an important role in both the immune responses and inflammatory diseases. Using basic and translational approaches, the group investigates TLR-mediated signaling and its modulation by cytokines such as interferons and lipid mediators in the context of cardiovascular disease, i.e.

Our laboratory is interested in the study of the signaling pathways and biological responses mediated by the lipid second messengers through the Rho GTPases. The activation of RhoGTPases is controlled by three groups of proteins: GEFs (guanosine exchange factors), GAPs (GTPase activating proteins) and GDIs (guanosine dissociation inhibitors). In our group we are studying a family of GAP proteins, the chimaerins.

The mucosal immune system represents the first line of defense against the external microenvironment to the body, acting as a filter, to discern between potentially damaging microorganisms and innocuous dietary proteins, while maintaining the absorption of nutrients. All the components are involved in the maintenance of the equilibrium active immunity/oral tolerance: genetic factors, efferent mechanisms, receptors and innate cells, antigen presentation, cytokines and growth factors, and regulatory cells.

We are interested in several aspects of the physiology and pathofisiology of the auditory organ, including its development, damage and degeneration of auditory neurons and hair cells, and gene and cell therapy for the inner ear. At the molecular level we are focusing on members of the neurotrophin and Fibroblast growth factor (FGF) gene families, and several transcription factors. To analyse the functions of these gene families in vivo we are using transgenic mouse models. These experiments are complemented with in vitro studies using primary cell cultures.

In our laboratory we aim at understanding the mechanisms underlying NERVOUS SYSTEM development, understanding DEVELOPMENT as the whole process in an organism life: from embryonic development to aging. We are also interested in the processes of NEURODEGENERATION. We have centered our research efforts in the analysis of a particular family of proteins, the LIPOCALINS, and in the members of this family that are expressed in the nervous system at key moments during DEVELOPMENT.

Pre-mRNA processing or splicing is an essential step of eukaryotic gene expression, where the spliceosome removes introns and exons are sequentially joined . A high proportion of genetic diseases are associated to splicing anomalies of responsible genes. Our main interest is focused on the study of the correlation between aberrant splicing of tumor suppressor genes and susceptibility to breast/ ovarian cancer (BC/OC), as well as the study of the regulatory mechanisms of this process.

The group launched the molecular diagnosis of breast / ovarian cancer and hereditary colorectal cancer using the technique HA_CAE. In addition to the clinical diagnosis, the group has developed several research projects based on the characterization of founder mutations, variants of unknown effect and analysis of the promoter regions of genes. There have been several doctoral theses and published more than twenty publications on the work performed.

Study of the experimental conditions that will increase the frequency of gene targeting in human cells by testing different viral vectors and modifying the expression of key protein in the repair of DNA lesions by using fusion proteins and specific siRNAs. We will use the most effective methods to correct mutations in primary cells from patients with monogenic diseases, particularly certain primary immunodeficiencies.