Molecular mechanisms of proteins and complexes involved in signaling, microbial pathogenic processes and rare diseases

Study of microbial signaling systems as potential targets for antimicrobial interventions. Stablish the molecular basis of signal transduction mechanisms related with two-component and phosphorelay systems. Structures of HKs, hybrid HKs, phosphotransferases and RRs. We will find small proteins or organic molecules with potential inhibitory activity to block reactions catalyzed in order to design antimicrobial drugs.
Understanding molecular mechanisms of Mobile Genetic Elements (MGE) involved in pathogenicity and communication for antimicrobial interventions. Structural characterization of mobilization and communication mechanisms in MGE. Structures of proteins and protein-DNA complexes responsible of: 1) phages and phage-inducible chromosomal islands activation and mobilization between species, 2) communication strategies between MGEs in which the host bacteria also participate.
Structure, mechanisms, and pathogenic alterations in nucleotide metabolism proteins. We aim to decipher the architecture and functional mechanisms of CAD, the multi-enzymatic complex leading de novo pyrimidine nucleotide synthesis, and human UPRT, a putative uracil phosphoribosyltransferase (UPRT) with a non-enzymatic and yet unknown moonlighting function in nucleotide homeostasis.
Structural basis of translation initiation regulation. Understanding the function of eukaryotic translation initiation factors (eIFs) which lack detailed structural information. Determine domain structures of yeast eIF4A and eIF4B proteins, alone or in complex with each other and with RNA.
Macromolecular complexes involved in eukaryotic gene regulation. Studies on complexes controlling gene regulation, with special focus on complexes involved in cancersuch as ribosome RNA processing and maturation, and ribosome RNA export machinery.
Disease-related proteins of nitrogen metabolism or COVID19-related. Studies on i) pyridoxal phosphate homeostasis protein causing vitamin B6-dependent epilepsy; ii) transcription factor NtcA in complex with its DNA and protein PipX; iii) PipX complex with the ribosome assembly factor EngA; iv) inborn hyperammonemia-involved enzymes N-acetylglutamate synthase and carbamoyl phosphate synthetase 1; v) 1-pyrroline-5-carboxylate synthetase causing cutis laxa or spastic paraplegia; vi) COVID-19-relevant protein-inhibitor complexes.