Pongs O, Leicher T, Berger M, Roeper J, Bähring R, Wray D, Giese K P, Silva A J, Storm J F
Institut für Neurale Signalverarbeitung Center for Molecular Neurobiology, Hamburg, Germany.
Ann N Y Acad Sci. 1999 Apr 30;868:344-55. doi: 10.1111/j.1749-6632.1999.tb11296.x.
Voltage-gated potassium channels (Kv) of the Shaker-related superfamily are assembled from membrane-integrated alpha subunits and auxiliary beta subunits. The beta subunits may increase Kv channel surface expression and/or confer A-type behavior to noninactivating Kv channels in heterologous expression systems. The interaction of Kv alpha and Kv beta subunits depends on the presence or absence of several domains including the amino-terminal N-type inactivating and NIP domains and the Kv alpha and Kv beta binding domains. Loss of function of Kv beta 1.1 subunits leads to a reduction of A-type Kv channel activity in hippocampal and striatal neurons of knock-out mice. This reduction may be correlated with altered cognition and motor control in the knock-out mice.
与震颤相关的超家族电压门控钾通道(Kv)由膜整合α亚基和辅助β亚基组装而成。在异源表达系统中,β亚基可能会增加Kv通道的表面表达和/或赋予非失活Kv通道A型行为。Kvα亚基和Kvβ亚基的相互作用取决于几个结构域的存在与否,包括氨基末端N型失活和NIP结构域以及Kvα和Kvβ结合结构域。Kvβ1.1亚基功能丧失导致敲除小鼠海马和纹状体神经元中A型Kv通道活性降低。这种降低可能与敲除小鼠认知和运动控制的改变有关。