Ranganathan R, Lewis J H, MacKinnon R
Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Neuron. 1996 Jan;16(1):131-9. doi: 10.1016/s0896-6273(00)80030-6.
The structurally well-characterized scorpion toxin Agitoxin2 inhibits ion permeation through Shaker K+ channels by binding to the external pore entryway. Scanning mutagenesis identified a set of inhibitor residues critical for making energetic contacts with the channel. Using thermodynamic mutant cycle analysis, we have mapped channel residues relative to the known inhibitor structure. This study constrains the position of multiple channel residues within the pore-forming loops; in one stretch, we have been able to map five out of seven contiguous residues to the inhibitor interaction surface, including those involved in ion selectivity. One interaction in particular, that of K27M on the inhibitor with Y445F on the channel, is unique in that it depends on the K+ ion concentration. These results reveal a shallow vestibule formed by the pore loops at the K+ channel entryway. The selectivity filter is located at the center of the vestibule close to (approximately 5 A) the extracellular solution.
结构特征明确的蝎毒素Agitoxin2通过与外部孔道入口结合来抑制离子通过Shaker钾通道的渗透。扫描诱变确定了一组对于与通道形成能量接触至关重要的抑制剂残基。利用热力学突变循环分析,我们已经绘制出相对于已知抑制剂结构的通道残基图谱。这项研究限制了孔形成环内多个通道残基的位置;在一段区域中,我们已经能够将七个连续残基中的五个定位到抑制剂相互作用表面,包括那些参与离子选择性的残基。特别是抑制剂上的K27M与通道上的Y445F之间的一种相互作用很独特,因为它取决于钾离子浓度。这些结果揭示了由钾通道入口处的孔环形成的一个浅前庭。选择性过滤器位于前庭中心,靠近(约5埃)细胞外溶液。