Tuesday, 22th September - h 14:00
Seminars room, NICO
Intracellular FGF signaling in the CNS:
implications for normal brain function and neuropsychiatric disorders
Department of Pharmacology & Toxicology, University of Texas Medical Branch
The primary focus of our research is on voltage-gated Na+ (Nav) channels, a family of nine (Nav1.1-1.9) transmembrane proteins abundantly expressed in the brain. Through a complex network of protein:protein interactions (PPI), the Nav channel complex provides the basis for electrical excitability of neurons, enabling transmission, processing and storing of electrochemical signals at single synaptic connections.
The Nav channel complex is a vulnerable target of genetic modifications and environmental agents. Mutations targeting the pore-forming α subunit of the Nav channel or its accessory proteins, such as intracellular FGFs, ankyrin-G, bIV spectrin and neurofascin, are recognized causes or risk factors for epilepsy, mood disorder, autism, depression, schizophrenia, pain and neurodegeneration, making the Nav channel complex one of the most appealing targets for drug development.
Yet, the mechanisms underlying modulation of the Nav channel macromolecular complex in the brain are still poorly understood limiting our ability of molecular interventions against these relevant proteins. Current projects in our laboratory aim at filling knowledge gaps in this area of research with an emphasis on the intracellular fibroblast growth factors (iFGFs; FGF11-14), a group of versatile and potent regulators of the Nav channel biophysics, trafficking and function in the brain.
Host: Filippo Tempia
Since 2001, this meeting represented an important event for basic and clinical researchers working on this emerging scientific topic. We will address state-of-the-art approaches in the field of steroids and nervous system, including behavior, epigenetics, genomic and non-genomic actions, the vitamin D, neurodegenerative and psychiatric disorders, and the interference among endocrine disruptors and steroid signaling.
L’inibizione della proteina JNK rallenta la progressione della malattia che colpisce i motoneuroni ed è la prima causa genetica di morte nell’infanzia. Lo dimostra uno studio pubblicato su Frontiers in Molecular Neuroscience dal nostro gruppo di ricerca guidato da Alessandro Vercelli, in collaborazione con l’Istituto Mario Negri di Milano. Chiarire i meccanismi molecolari alla base della SMA può aprire la strada allo sviluppo di nuove terapie.