Naranjo D, Miller C
Howard Hughes Medical Institute, Graduate Department of Biochemistry, Brandeis University, Waltham, Massachusetts 02254, USA.
Neuron. 1996 Jan;16(1):123-30. doi: 10.1016/s0896-6273(00)80029-x.
Charybdotoxin, a peptide neurotoxin of known molecular structure, blocks Shaker K+ channels by binding to a receptor at the outer opening of the ion conduction pathway. Analysis of variants of CTX at position 29 and of Shaker at position 449 shows that these two residues interact closely in the channel-toxin complex. The CTX mutation M29I leads to a slight strengthening of block when tested on Shaker-449T; the same CTX mutation weakens block 1700-fold when tested on Shaker-449F. The known position of CTX-29 on the toxin's interaction surface thus locates Shaker-449 within 5 A of the pore axis of the closed channel. All four subunits must carry the 449F mutation to produce a highly toxin-insensitive channel.
沙蚕毒素是一种已知分子结构的肽神经毒素,它通过与离子传导途径外口处的受体结合来阻断Shaker钾通道。对CTX第29位变体和Shaker第449位变体的分析表明,这两个残基在通道-毒素复合物中紧密相互作用。当在Shaker-449T上进行测试时,CTX突变M29I会导致阻断作用略有增强;而在Shaker-449F上进行测试时,相同的CTX突变会使阻断作用减弱1700倍。因此,CTX-29在毒素相互作用表面上的已知位置将Shaker-449定位在封闭通道孔轴5埃范围内。所有四个亚基都必须携带449F突变才能产生对毒素高度不敏感的通道。