We work on evolution, diversity and ecology of enigma organisms, neglected by traditional researchers, but which are key to understand the origins and diversity of life, and ecosystems’ functioning. We use phylogenetic and phylogenomic approaches to reconstruct evolutionary patterns. We study their biodiversity in strategic regions, such as biodiversity hotspots, or extreme environments.

Study the genetic basis of autoimmune diseases though genomic approaches –genome wide association studies, epigenetics, whole gene expression and new generation sequencing

T lymphocytes are characterized by the expression of a specific antigen receptors, TCR, composed by two chains: alpha and beta, or gamma and delta. Our interests are focused in the study gene expression of the TCR genes T during development through the understanding of the molecular mechanisms involved s that control the expression of these genes at large distances by transcriptional enhancers during T lymphocyte development. These enhancers are regulated by the binding of transcriptional factors that depends on the signaling received by thymocytes: mainly, Notch, TCR and IL-7.

To know the relationship between the central nervous system and the immune system, characterizing the connection between infectious diseases and their effects on neurodegenerative disorders, and on pathological aging processes. We are looking for endogenous mediators shared by both systems (neuropeptides) with a therapeutic profile in these disorders and/or that are relevant in the development and evolution of neuroinflammatory/neurodegenerative disorders (multiple sclerosis, Alzheimer's disease, Parkinson's disease, cerebral stroke).

Identification of regulatory variants and causal genes in multiple sclerosis and associated pathogenic activity. The identification of causal variants and genes and disease-related dysfunction is essential for the establishment of molecular pathways and mechanisms of disease, for the rational design of therapies and diagnostic systems and prognosis applications. Search of genetic, molecular targets, pathogenic and etiologic mechanisms, functioning and application in diagnosis, disease progression and treatment of neurological diseases and other complex diseases.

Our group is dedicated to the study of the function of signaling through the mechanism of post-transductional modification of proteins known as poly ADP-ribosylation (PARylation), in regulating key aspects of the tumor microenvironment such as hypoxia and autophagy and how PARylation determines the malignant transformation of the tumor.

Our current research interest is in signal transduction and signaling molecules as drug targets or disease biomarkers. In our laboratory we have focused our interest on the early signaling events triggered by CD38 or CD3 engagement in T cells from patients and mice with autoimmune diseases.

(a) Signaling by TCR, BCR, and membrane receptors; by co-receptors CD38 and CD19; and by "Toll-like receptors “TLR2 and TLR4. Study the role of kinases, ERK-1 and 2; AKT1; Lck; Lyn; in the pathogenesis of Systemic Lupus Erythematosus (SLE); and Psoriasis. (b) Study the alterations in pro-inflammatory and regulatory cytokine involved in the regulation of the differentiation of helper T cell (Th1, Th2, Th17 and Treg) in plasma and gene expression levels in peripheral blood mononuclear cells (PBMC) from patients with SLE and Psoriasis.

The functional coupling of transcription and alternative splicing is emerging as an essential component of gene expression regulation. Despite considerable efforts, numerous questions remain regarding the functional significance and global impact of this coupling on cellular and organism homeostasis as well as its underlying molecular mechanisms. Our work considers that coupling mechanisms enable the establishment of check-points or quality controls that would promote each step of pre-mRNA synthesis and processing while ensuring the accomplishment of the essential preceding stages.