IRIS – Institutional Research Information System
IRIS è il sistema di gestione della ricerca dell’Università degli Studi di Milano-Bicocca.Il repository BOA è il modulo del sistema dedicato alla raccolta e alla disseminazione della produzione scientifica di Ateneo. Le pubblicazioni sono ricercabili per parola chiave attraverso il box nella barra orizzontale in alto oppure, mediante il pulsante Sfoglia, per "Afferenza", "Autore", "Titolo", "Tipologia" o "Settore scientifico-disciplinare".
IRIS contiene inoltre alcuni moduli dedicati alla registrazione dei progetti e dei contratti, e alla reportistica avanzata per le attività di valutazione della ricerca
EnglishVoltage-dependent Na<sup>+</sup> channels consist of the principal α-subunit (∼260 kDa), without or with auxiliary β-subunit (∼38 kDa). Nine α-subunit isoforms (Na<sub>v</sub>1.1-Na <sub>v</sub>1.9) are encoded in nine different genes (SCN1A-SCN5A and SCN8A-SCN11A). Besides initiating and propagating action potentials in established neuronal circuit, Na<sup>+</sup> channels engrave, maintain and repair neuronal network in the brain throughout the life. Adrenal chromaffin cells express Na<sub>v</sub>1.7 encoded in SCN9A, which is widely distributed among peripheral autonomic and sensory ganglia, neuroendocrine cells, as well as prostate cancer cell lines. In chromaffin cells, Na<sub>v</sub>1.7-specific biophysical properties have been characterized; physiological stimulation by acetylcholine produces muscarinic receptor-mediated hyperpolarization followed by nicotinic receptor-mediated depolarization. In human patients with Na <sub>v</sub>1.7 channelopathies, gain-of-pathological function mutants (i.e. erythermalgia and paroxysmal extreme pain disorder) or loss-of-physiological function mutant (channelopathy-associated insensivity to pain) proved the causal involvement of mutant Na<sub>v</sub>1.7 in generating intolerable pain syndrome, Na<sub>v</sub>1.7 being the first molecular target convincingly identified for pain treatment. Importantly, aberrant upregulation/hyperactivity of even the native Na<sub>v</sub>1.7 produces pain associated with inflammation, nerve injury and diabetic neuropathy in rodents. Various extra- and intracellular signals, as well as therapeutic drugs modulate the activity of Na<sub>v</sub>1.7, and also cause up- and downregulation of Na<sub>v</sub>1.7. Na<sub>v</sub>1.7 seems to play an increasing number of crucial roles in health, disease and therapeutics. © 2008 The Authors.
Wada, A., Wanke, E., Gullo, F., & Schiavon, E. (2007). Voltage-dependent Nav1.7 Sodium Channels: Multiple Roles in Adrenal Chromaffin Cells and Peripheral Nervous System. ACTA PHYSIOLOGICA, 192(2), 221-231.
| Citazione: | Wada, A., Wanke, E., Gullo, F., & Schiavon, E. (2007). Voltage-dependent Nav1.7 Sodium Channels: Multiple Roles in Adrenal Chromaffin Cells and Peripheral Nervous System. ACTA PHYSIOLOGICA, 192(2), 221-231. |
| Tipo: | Articolo in rivista - Articolo scientifico |
| Carattere della pubblicazione: | Scientifica |
| Presenza di un coautore afferente ad Istituzioni straniere: | Si |
| Titolo: | Voltage-dependent Nav1.7 Sodium Channels: Multiple Roles in Adrenal Chromaffin Cells and Peripheral Nervous System |
| Autori: | Wada, A; Wanke, E; Gullo, F; Schiavon, E |
| Autori: | |
| Data di pubblicazione: | 2007 |
| Lingua: | English |
| Rivista: | ACTA PHYSIOLOGICA |
| Digital Object Identifier (DOI): | http://dx.doi.org/10.1111/j.1748-1716.2007.01810.x |
| Appare nelle tipologie: | 01 - Articolo su rivista |
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