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Modulation of Na+ channel inactivation by the beta 1 subunit: a deletion analysis.

作者信息

Chen C, Cannon S C

机构信息

Department of Neurology, Massachusetts General Hospital, Boston 02114, USA.

出版信息

Pflugers Arch. 1995 Dec;431(2):186-95. doi: 10.1007/BF00410190.

DOI:10.1007/BF00410190
PMID:9026778
Abstract

Na+ currents recorded from Xenopus oocytes expressing the Na+ channel alpha subunit alone inactivate with two exponential components. The slow component predominates in monomeric channels, while co-expression with the beta 1 subunit favors the fast component. Macropatch recordings show that the relative rates of these components are much greater than previously estimated from two-electrode measurements (approximately 30-fold vs approximately 5-fold). A re-assessment of steady-state inactivation, h infinity (V), shows that there is no depolarized shift of the slow component, provided a sufficiently long prepulse duration and repetition interval are used to achieve steady-state entry and recovery from inactivation, respectively. Deletion mutagenesis of the beta 1 subunit was used to define which regions of the subunit are required to modulate inactivation kinetics. The carboxy tail, comprising the entire predicted intracellular domain, can be deleted without a loss of activity; whereas small deletions in the extracellular amino domain or the signal peptide totally disrupt function.

摘要

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