We investigate the mechanisms that control the spatio-temporal expression of genes operating in brain cortex development by using human brain organoids (self-organized 3D cultures derived from pluripotent stem cells that recapitulate brain structure development and inner organization) as a model system.

Our research focus is to enhance immune resilience against inflammation, cellular senescence, and age-related diseases. We have demonstrated that mitochondrial dysfunction in T cells mimics aging and leads to widespread health deterioration (Science, 2020). We have also identified molecular mechanisms by which aged T cells contribute to age-related diseases (Cell Metabolism 2021; Nature Rev Immunol, 2022). Additionally, we propose therapies to reverse aortic aneurysms and improve mitochondrial metabolism (Circulation, 2021; Atherosclerosis, Thrombosis Vascular Biology, 2022; Br J Pharmacol.

The Mediterranean Climate Change Group (GCC) has as its main objective the study of the effects that climate change could have on the Mediterranean Sea and its ecosystems, paying particular attention to the waters surrounding the Spanish coasts, Including the Balearic Islands. The studies carried out by this group are multidisciplinary in nature, since they aim to understand the effects on physical, chemical and biological variables.

Using Drosophila, our research focuses on the Jun N-terminal Kinase (JNK) pathway's roles in regeneration and tumorigenesis. JNK induces apoptosis in damaged cells and promotes proliferation via paracrine signaling, impacting the JAK/STAT, Wingless, and Decapentaplegic pathways. We've identified JNK's significance in tumorigenesis, studying its effects in mutations like scribble, erupted, and polyhomeotic. Moreover, we've revealed how overgrowing tumor cells can restrict normal tissue growth.

In our lab, we investigate the neurological aspects of demyelinating diseases, particularly the process of myelination in the CNS. We focus on understanding the role of key proteins like R-Ras1 and R-Ras2 in oligodendrocyte differentiation, survival, energy balance, and nerve impulse transmission. Our aim is to develop treatments for diseases like Multiple Sclerosis by enhancing myelin-related processes.

Our research focuses on understanding how adult vertebrate neural stem cells maintain the balance between self-renewal and differentiation to contribute to brain tissue regeneration and homeostasis. We use mouse models and concentrate on the PLK1 kinase to comprehend its roles in these processes and its therapeutic potential for neuronal regeneration in situations of damage or disease.

Our laboratory investigates the molecular mechanisms of neurotransmission and their connection to various nervous system pathologies. We study the interplay between excitatory and inhibitory neurotransmission pathways and their modulation by neurotransmitters like dopamine. These processes are controlled by membrane proteins such as ion channels, receptors, and transporters. Alterations in these proteins are linked to conditions like stroke, epilepsy, and schizophrenia.

Our research focuses on inborn errors of metabolism (IEM), a major group of rare diseases affecting approximately 1 in every 800 newborns. Using a multi-omic approach along with functional genomics, we identify genetic defects associated with IEM. We have also been involved in developing small chemical drugs to rescue the activity of mutant proteins causing IEM. We have generated cellular models from patients and healthy hiPSC for preclinical evaluation of these therapies.

Our laboratory is investigating the regulatory functions and mechanisms of cell signaling pathways through G proteins, particularly focusing on Gq protein-coupled receptors (GPCRs). We aim to understand how these pathways are involved in both normal physiological processes and pathological conditions. Our recent research has unveiled a new interaction region in Gαq, a subunit of G proteins, which plays a role in non-canonical Gq signaling and cell homeostasis.