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Research centres : Centro de Biología Molecular "Severo Ochoa". CSIC-Universidad Autónoma de Madrid (Madrid)

Catalina Ribas Núñez

She is currently Tenured Professor in the Molecular Biology Department of the Universidad Autónoma de Madrid. Her research group is in the Centro de Biología Molecular "Severo Ochoa" (CSIC-UAM) and is a member of the Fundación de Investigación Biomédica La Princesa.

She has wide experience in the field of signalling and regulation of receptors that are bound to G proteins (GPCR). The interest of her research team centres on the study of the mechanisms of action of GPCRs, under normal as well as pathological circumstances. Dr. Catalina Ribas has used different pharmacological, biochemical and molecular biology techniques to study the regulatory mechanisms of the GPCRs transduction system. During her postdoctoral visit to the Medical University of South Carolina (USA) she took part in the identification, characterisation and purification of proteins that play a role in the signal transduction complex, which act at G proteins level and form part of the multimolecular signal of transduction complex of the receptors bound to these proteins.

Following her return to Spain, Dr. Ribas continued working on receptors bound to G proteins and their regulation by kinases bound to these receptors (GRKs), as well as the interaction of these pathways with those of MAPKs signalling pathways. Specifically, she centres her research on the processes which are dependent on the activation of receptors bound to Gq for which the corresponding effector has yet to be found. Her results suggest the existence of a functional interaction between Gαq and PKCz which seems to play an important role in the development of cardiac hypertrophy. Dr. Ribas' group has therefore described a new adaptor role for Gαq, and its main aim now is to characterise this new functional interaction in depth, determining its role in other signalling pathways, as well as in other cell functions connected with the activation of GPCRs bound to Gαq, together with its possible modulation by proteins which regulate signalling mediated by these G proteins (GRKs, Ric8, RGS, EBP50).

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