Wallner M, Weigl L, Meera P, Lotan I
Institut für Medizinische Physik und Biophysik, Universitaet Graz, Austria.
FEBS Lett. 1993 Dec 28;336(3):535-9. doi: 10.1016/0014-5793(93)80871-q.
Co-expression of cloned sodium channel beta 1-subunit with the rat skeletal muscle-subunit (alpha microI) 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 alpha microI/beta 1, indicating that beta 1 restores 'physiological' behaviour. Northern blot analysis revealed that the Na+ channel beta 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' beta 1 cDNA to skeletal muscle and heart mRNA indicated that the different Na+ channel alpha-subunits in brain, skeletal muscle and heart may share a common beta 1-subunit.
克隆的钠通道β1亚基与大鼠骨骼肌亚基(αmicroI)共表达,加速了宏观电流衰减,增大了电流幅度,使稳态失活曲线向更负的电位偏移,并缩短了从失活完全恢复所需的时间。从骨骼肌信使核糖核酸表达的钠通道表现出与从αmicroI/β1观察到的类似行为,表明β1恢复了“生理”行为。Northern印迹分析显示,Na+通道β1亚基在大鼠心脏、大脑和骨骼肌中大量存在(约0.1%),并且“大脑”β1互补脱氧核糖核酸的非翻译区与骨骼肌和心脏信使核糖核酸的杂交表明,大脑、骨骼肌和心脏中不同的Na+通道α亚基可能共享一个共同的β1亚基。