Emilio Carbone
Affiliations: | Neuroscience | University of Torino, Redlands, CA, United States |
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| Ortner NJ, Sah A, Paradiso E, et al. (2023) The human channel gating-modifying A749G CACNA1D (Cav1.3) variant induces a neurodevelopmental syndrome-like phenotype in mice. Jci Insight. 8 |
| Marcantoni A, Chiantia G, Tomagra G, et al. (2022) Correction to: Two firing modes and well‑resolved Na, K, and Ca currents at the cell‑microelectrode junction of spontaneously active rat chromaffin cell on MEAs. Pflugers Archiv : European Journal of Physiology |
| Marcantoni A, Chiantia G, Tomagra G, et al. (2022) Two firing modes and well-resolved Na, K, and Ca currents at the cell-microelectrode junction of spontaneously active rat chromaffin cell on MEAs. Pflugers Archiv : European Journal of Physiology |
| Carbone E. (2022) Are Cav1.3 calcium channels possible targets to modulate the in vivo activity of DA SN neurons in Parkinson's disease? Pflugers Archiv : European Journal of Physiology. 474: 1039-1040 |
| Siller A, Hofer NT, Tomagra G, et al. (2022) rβ2-subunit alternative splicing stabilizes Cav2.3 Ca channel activity during continuous midbrain dopamine neuron-like activity. Elife. 11 |
| Carbone E. (2021) T-type calcium channels as therapeutic targets for treating "giant" retinoblastoma cancer cells. Pflugers Archiv : European Journal of Physiology |
| Carbone E. (2021) Fast inactivation of Nav1.3 channels by FGF14 proteins: An unconventional way to regulate the slow firing of adrenal chromaffin cells. The Journal of General Physiology. 153 |
| Marcantoni A, Calorio C, Hidisoglu E, et al. (2020) Cav1.2 channelopathies causing autism: new hallmarks on Timothy syndrome. Pflugers Archiv : European Journal of Physiology. 472: 775-789 |
| Carbone E, Mori Y. (2020) Ion channelopathies to bridge molecular lesions, channel function, and clinical therapies. Pflugers Archiv : European Journal of Physiology. 472: 733-738 |
| Marcantoni A, Cerullo MS, Buxeda P, et al. (2020) Abeta42 oligomers up-regulate the excitatory synapses by potentiating presynaptic release while impairing postsynaptic NMDA receptors. The Journal of Physiology |