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This research investigates the critical role of the E1623 residue in the S3-S4 loop of the Nav1.1 channel, particularly focusing on the functional alterations caused by various missense mutations. The study reveals that the E1623A mutation leads to significant loss-of-function effects, including reduced current density and altered activation/inactivation kinetics. The findings underscore the importance of the extracellular loop in channel gating and suggest that the physicochemical properties of amino acid

Author

maunimonkar

Language

EN