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A molecular basis for gating mode transitions in human skeletal muscle Na + channels
Author(s) -
Bennett Paul B.,
Makita Naomasa,
George Alfred L.
Publication year - 1993
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(93)81752-l
Subject(s) - xenopus , gating , protein subunit , biophysics , sodium channel , chemistry , skeletal muscle , conformational change , biology , biochemistry , sodium , anatomy , organic chemistry , gene
Recombinant sodium channel α subunits expressed in Xenopus oocytes display an anomalously slow rate of inactivation that arises from channels that predominantly exist in a slow gating mode [1,2]. Co‐expression of Na − channel β 1 subunit with the human skeletal muscle Na + channel α subunit increases the Na + current and induces normal gating behavior in Xenopus laevis oocytes. The effects of the β 1 subunit can be explained by an allosterically induced conformational switch of the α subunit protein that occurs upon binding the β 1 subunit. This binding alters the free energy barriers separating distinct conformational states of the channel. The results illustrate a fundamental modulation of ion channel gating at the molecular level, and specifically demonstrate the importance of the β 1 subunit for gating mode changes of Na + channels.