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"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."

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"When the arginine is mutated to histidine, the disturbance of inactivation of Nav1.6 that interacts with FGF12 occurs, leading to an influx of sodium influx increase, consequently elevating the neuron[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"