Ogielska E M, Zagotta W N, Hoshi T, Heinemann S H, Haab J, Aldrich R W
Howard Hughes Medical Institute, Stanford University School of Medicine, California 94305, USA.
Biophys J. 1995 Dec;69(6):2449-57. doi: 10.1016/S0006-3495(95)80114-1.
C-type inactivation of potassium channels is distinct from N-terminal mediated (N-type) inactivation and involves a closing of the outer mouth of the channel. We have investigated the role of the individual subunits of the tetrameric channel in the C-type inactivation conformational change by comparing the inactivation rates of channels constructed from different combinations of subunits. The relationship between the inactivation rate and the number of fast subunits is exponential, as would be predicted by a cooperative mechanism where the C-type conformational change involves all four subunits, and rules out a mechanism where a conformational change in any of the individual subunits is sufficient for inactivation. Subunit interactions in C-type inactivation are further supported by an interaction between separate mutations affecting C-type inactivation when in either the same or separate subunits.
钾通道的C型失活不同于N端介导的（N型）失活，它涉及通道外口的关闭。我们通过比较由不同亚基组合构建的通道的失活速率，研究了四聚体通道单个亚基在C型失活构象变化中的作用。失活速率与快速亚基数量之间的关系是指数关系，这正如一种协同机制所预测的那样，即C型构象变化涉及所有四个亚基，并且排除了任何单个亚基的构象变化足以导致失活的机制。当分别影响C型失活的突变位于相同或不同亚基中时，这些突变之间的相互作用进一步支持了C型失活中的亚基相互作用。
