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Modulation of the skeletal muscle sodium channel α‐subunit by the β 1 ‐subunit
Author(s) -
Wallner Martin,
Weigl Lukas,
Meera Pratap,
Lotan Ilana
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)80871-q
Subject(s) - skeletal muscle , sodium channel , protein subunit , messenger rna , biology , chemistry , medicine , microbiology and biotechnology , in situ hybridization , endocrinology , sodium , biochemistry , gene , organic chemistry
Co‐expression of cloned sodium channel β 1 ‐subunit with the rat skeletal muscle‐subunit (α μI ) accelerated the macroscopic current decay, enhanced the current amplitude, shifted the steady state inactivation curve to more negative potentials and decreased the time required for complete recovery from inactivation. Sodium channels expressed from skeletal muscle mRNA showed a similar behaviour to that observed from , indicating that β 1 restores ‘physiological’ behaviour. Northern blot analysis revealed that the Na + channel β 1 ‐subunit is present in high abundance (about 0.1%) in rat heart, brain and skeletal muscle, and the hybridization with untranslated region of the ‘brain’ β 1 cDNA to skeletal muscle and heart mRNA indicated that the diffferent Na + channel α‐subunits in brain, skeletal muscle and heart may share a common β 1 ‐subunit.