期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2000
卷号：97
期号：5
页码：2308-2313
DOI：10.1073/pnas.030362197
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：The voltage-sensitive sodium channel confers electrical excitability on neurons, a fundamental property required for higher processes including cognition. The ion-conducting -subunit of the channel is regulated by two known auxiliary subunits, {beta}1 and {beta}2. We have identified rat and human forms of an additional subunit, {beta}3. It is most closely related to {beta}1 and is the product of a separate gene localized to human chromosome 11q23.3. When expressed in Xenopus oocytes, {beta}3 inactivates sodium channel opening more slowly than {beta}1 does. Structural modeling has identified an amino acid residue in the putative -subunit binding site of {beta}3 that may play a role in this difference. The expression of {beta}3 within the central nervous system differs significantly from {beta}1. Our results strongly suggest that {beta}3 performs a distinct neurophysiological function.
