A5024246863- Axon Guidance and Neuronal Signaling
- Neuroscience and Neuropharmacology Research
- Receptor Mechanisms and Signaling
- Angiogenesis and VEGF in Cancer
- Hippo pathway signaling and YAP/TAZ
- Neuroinflammation and Neurodegeneration Mechanisms
- Zebrafish Biomedical Research Applications
- Renal and related cancers
- Nuclear Receptors and Signaling
- Nerve injury and regeneration
- RNA Research and Splicing
- Endoplasmic Reticulum Stress and Disease
- HER2/EGFR in Cancer Research
- Cytokine Signaling Pathways and Interactions
- Neurogenesis and neuroplasticity mechanisms
- Wnt/β-catenin signaling in development and cancer
- Protein Tyrosine Phosphatases
- Peptidase Inhibition and Analysis
- Apelin-related biomedical research
- Hereditary Neurological Disorders
- Neural dynamics and brain function
- interferon and immune responses
- Mitochondrial Function and Pathology
- Congenital heart defects research
- Cellular transport and secretion
Centro de Investigacion Principe Felipe
2019-2024
Consejo Superior de Investigaciones Científicas
2010-2021
Centro de Biología Molecular Severo Ochoa
2019-2021
Universidad Autónoma de Madrid
2019
VIB-KU Leuven Center for Cancer Biology
2014-2017
KU Leuven
2014
Centre For Human Genetics
2014
Instituto de Neurociencias
2010-2011
Candiolo Cancer Institute
2004-2010
Ospedale degli Infermi
2010
Plexins are a large family of transmembrane receptors for the Semaphorins, known their role in assembly neural circuitry. More recently, have been implicated diverse biological functions, including vascular growth, epithelial tissue morphogenesis and tumour development. In particular, PlexinB1, receptor Sema4D, has suggested to play development angiogenesis, based on vitro studies. However, distribution PlexinB1 not extensively studied functional relevance this vivo still awaits experimental...
Abstract Semaphorins and their receptors, plexins, have emerged as key regulators of various aspects neuronal development. In contrast to the Plexin‐A family, cellular functions Plexin‐B family proteins in developing neurons are only poorly understood. An activation Plexin‐B1 via its ligand, semaphorin 4D (Sema4D), produces an acute collapse axonal growth cones hippocampal retinal over early stages neurite outgrowth. However, functional role Sema4D‐Plexin‐B interactions subsequent...
Neuregulin 1 (NRG1) and the γ-secretase subunit APH1B have been previously implicated as genetic risk factors for schizophrenia relevant deficits observed in rodent models with loss of function mutations either gene. Here we show that Aph1b-γ-secretase is selectively involved Nrg1 intracellular signalling. We found Aph1b-deficient mice display a decrease excitatory synaptic markers. Electrophysiological recordings Aph1b required transmission plasticity. Furthermore, gain rescue experiments...
The schizophrenia risk gene NRG1 controls the formation of excitatory and inhibitory synapses in cortical circuits. While expression different isoforms occurs during development, adult neurons primarily express CRD-NRG1 isoform characterized by a highly conserved intracellular domain (NRG1-ICD). We others have demonstrated that Nrg1 signaling promotes dendrite elongation connections neuronal development. However, role pathological conditions remains largely unaddressed. Here, we investigated...
ABSTRACT Cortical interneurons (CINs) originate in the ganglionic eminences (GEs) and migrate tangentially to cortex guided by different attractive repulsive cues. Once inside cortex, cellular molecular mechanisms determining migration of CINs along rostrocaudal axis are less well understood. Here, we investigated cortical distribution originating medial caudal GEs at time points. Using genetic labeling, showed that, mouse, early- late-born (E12 versus E15) differentially distributed axis....
Abstract Peroxiredoxin 3 (PRDX3) encodes a mitochondrial antioxidant protein, which is essential for the control of reactive oxygen species homeostasis. So far, PRDX3 mutations are involved in mild-to-moderate progressive juvenile onset cerebellar ataxia. We aimed to unravel molecular bases underlying disease an infant suffering from ataxia that started at 19 months old and presented severe atrophy peripheral neuropathy early course disease. By whole exome sequencing, we identified novel...
Neuregulin 1 (NRG1) and its receptor ERBB4 are schizophrenia (SZ) risk genes that control the development of both excitatory inhibitory cortical circuits. Most studies focused on characterization ErbB4 deficient mice. However, deletion concurrently perturbs signaling Nrg1 3 (Nrg3), another ligand expressed in cortex. In addition, NRG1 polymorphisms linked to SZ locate mainly non-coding regions they may partially reduce expression. Here, study relevance partial loss-of-function circuits we...
Abstract Neurons with enhanced intrinsic growth capabilities can elongate their axons into non‐permissive territories, but the mechanisms that enable outgrowing processes to overcome environmental inhibition are largely unknown. To address this issue, we examined adult mouse Purkinje cells overexpress axonal growth‐associated protein GAP‐43. After injury, these neurons exhibit sprouting along intracortical neuritic course and at severed stump in white matter. determine whether...
Numerous studies suggest that the increased activity of p38MAPK plays an important role in abnormal immune and inflammatory response observed course neurodegenerative diseases such as Alzheimer's disease. On other hand, high levels are present brain during normal aging, suggesting existence mechanisms keep p38MAPK-regulated pro-inflammatory within physiological limits. In this study, we show hippocampus old mice is part due to reduction membrane cholesterol constitutively occurs aging brain....
Schizophrenia is associated with altered cortical circuitry. Although the schizophrenia risk gene NRG1 known to affect wiring of inhibitory interneurons, its role in excitatory neurons and axonal development unclear. Here, we investigated Nrg1 corpus callosum, major interhemispheric connection formed by neurons. We found that deletion impaired callosal axon vivo. Experiments vitro vivo demonstrated cell-autonomously required for outgrowth intracellular signaling sufficient promote...
Neuronal loss is at the core of many neuropathologies, including stroke, Alzheimer's disease, and Parkinson's disease. Different methods were developed to study process neuronal survival upon cytotoxic stress. Most are based on biochemical approaches that do not allow single-cell resolution or involve complex costly methodologies. Presented here a versatile, inexpensive, effective experimental paradigm survival. This method takes advantage sparse fluorescent labeling neurons followed by live...
Brain damage is the major cause of permanent disability and it particularly relevant in elderly. While most studies focused on immediate phase neuronal loss upon injury, much less known about process axonal regeneration after damage. The development new refined preclinical models to investigate recovery brain tissue injury a unmet challenge. Here, we present novel experimental paradigm mice that entails (i) tracing cortico-callosal connections, (ii) mechanical lesion motor cortex, (iii)...