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My research interest is focused on Molecular Neuroscience. The knowledge of the molecular mechanisms that regulate the brain function is fundamental to understand the brain in normal and pathological conditions. Key processes define the neuronal function and morphology and communication with other brain cells.
• Oligomerization of G protein-coupled receptors (GPCRs) as a molecular signaling process by which a particular neuron, which expresses a determined GPCRs, is able to produce several intracellular signals based on the particular combination of these GPCRs. We developed SRET - Sequential Resonance Energy Transfer - technology (Nat Methods) to describe the interaction of more than two GPCRs, reporting for the first time the formation of heterotrimers.
• Glial cells and their roles in the brain function; from the molecular mechanism of protective actions to the intracellular signaling involved in higher-brain functions such as cognition and memory.
• Deregulation of the neuronal death. Neurodegenerative diseases share some common features: proteinopathy or accumulation of misfolded proteins, sustained neuroinflammation, dysfunction and neuronal death. When a proteinopathy is initiated, this triggers a neuroinflammatory response in the glial cells. The no resolution of the pathological condition exacerbates the neuroinflammatory response becoming that neurotoxic. In Alzheimer's disease, we demonstrated that the accumulation of soluble Abeta leads to the downregulation of FAIM-L in neurons. FAIM-L is an antagonist of the apoptosis induced by activation of TNFR1 with TNFa. In normal conditions, TNFa has protective roles in neurons. The downregulation of FAIM-L switches this initial protection to neuronal death (Cell Death Dis).
•Regulation of neural processes. Some members of the TNFSF play important roles in the establishment of neuronal circuits. Brain function depends on a precise but plastic brain architecture. Knowledge of the mechanisms that regulate the growth and morphology of neural processes is essential to understand how the brain is assembled during development and modified by experience, but also how it could be manipulated in pathological conditions. In this regard, we described that CD40L-reverse signaling is the major physiological regulator of neurite growth in developing neurons, with striking opposite effects on the size and elaboration of dendrite arbors of pyramidal neurons and MSN (eLife). Spines are key structures in the synaptic transmission and CD40L-reverse signaling also influences dendrite spine morphology (Front Cell Dev Biol). Recently we have described the molecular mechanism by which CD40L-reverse signaling regulates axon and dendrite growth (Cell Mol Life Sci).
International congress in research and innovation in neurodegenerative diseases. 23-24/09/2013 Madrid (Spain). Carriba P et al., Amyloid beta reduces the expression of FAIM-L shifting the TNFa response from protection to aggression.
6th International congress in research and innovation in neurodegenerative diseases. 24-25/10/2012 Madrid (Spain). Carriba P et al., Evolution of the response of the apoptosis related genes in Alzheimer’s Disease: Are the antagonist of death receptors targets for therapy?
5th International congress in research and innovation in neurodegenerative diseases. 14-16/12/2011 San Sebastian (Spain). Carriba P et al., Study of the antagonist of death receptors in Alzheimer’s disease.
4th International congress in research and innovation in neurodegenerative diseases. 16-18/12/2010 Santander (Spain). Reix S, Torres M, Urresti J, Moubarak RS, Carriba P et al., Transgenic mice for FAIM-L and LIFEGUARD. Is it the beginning of the end of neurodegeneration?
XIII Congreso de la Sociedad Española de Neurociencias (SENC). 16-19/09/2009 Tarragona (Spain). Carriba P et al., Astrocyte plasticity and CREB / Lichtenstein M*, Carriba P* et al., Rho-GTPases as a novel target for the neuroprotective effect of ibuprofen in Alzheimer: and update.
9th European Meeting on GLIAL CELLS IN HEALTH AND DISEASE. 08-12/09/2009 Paris (France). Carriba P et al., CREB dependent regulation of astrocyte plasticity.
VII Symposium of Experimental Neurobiology. 28-29/10/2008 Barcelona (Spain). Carriba P et al., Astrocyte plasticity and CREB / Lichtenstein M*, Carriba P* et al., Rho-GTPases as a novel target for the neuroprotective effect of ibuprofen in Alzheimer: and update.
6th FENS Forum. 12-16/07/2008 Geneva (Italy). Navarro G, Carriba P et al., Detection of heteromerization of more than two proteins by sequential BRET-FRET.
6th annual meeting of SEIC. 25-27/11/2005 Barcelona (Spain). Carriba P et al., Molecular and functional cross-talk between the cannabinoid CB1R and adenosine A2AR receptors.
5th annual meeting of SEIC. 26-28/11/2004 Seville (Spain). Carriba P et al., Molecular interaction (FRET) between the cannabinoid CB1R and adenosine A2AR receptors.
Research Interests
Papers共 25 篇Author StatisticsCo-AuthorSimilar Experts
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Sonia Moreno-Grau,Bruna Barneda,Paulina Carriba,Juan Marin,Oscar Sotolongo-Grau,Isabel Hernandez,Maitee Rosende-Roca,Ana Mauleon,Liliana Vargas,Ana Espinosa,Montserrat Alegret,Octavio Rodriguez,Gemma Ortega,Maria Victoria Fernandez,Jesus Lopez-Arrieta,Lluis Tarraga,Merce Boada,Carmen Antunez,Joaquin Lopez,Agustin Ruiz,Joan Xavier Comella
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Author Statistics
#Papers: 25
#Citation: 1218
H-Index: 14
G-Index: 22
Sociability: 5
Diversity: 3
Activity: 10
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