Vollum Institute, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA.
Nature. 2012 Sep 20;489(7416):400-5. doi: 10.1038/nature11375. Epub 2012 Jul 29.
Acid-sensing ion channels (ASICs) are voltage-independent, amiloride-sensitive channels involved in diverse physiological processes ranging from nociception to taste. Despite the importance of ASICs in physiology, we know little about the mechanism of channel activation. Here we show that psalmotoxin activates non-selective and Na(+)-selective currents in chicken ASIC1a at pH 7.25 and 5.5, respectively. Crystal structures of ASIC1a-psalmotoxin complexes map the toxin binding site to the extracellular domain and show how toxin binding triggers an expansion of the extracellular vestibule and stabilization of the open channel pore. At pH 7.25 the pore is approximately 10 Å in diameter, whereas at pH 5.5 the pore is largely hydrophobic and elliptical in cross-section with dimensions of approximately 5 by 7 Å, consistent with a barrier mechanism for ion selectivity. These studies define mechanisms for activation of ASICs, illuminate the basis for dynamic ion selectivity and provide the blueprints for new therapeutic agents.
酸敏离子通道 (ASICs) 是电压不依赖性的、阿米洛利敏感的通道,参与从痛觉到味觉等多种生理过程。尽管 ASICs 在生理学中非常重要,但我们对其通道激活的机制知之甚少。在这里,我们表明 psalmotoxin 在 pH 7.25 和 5.5 下分别激活鸡 ASIC1a 的非选择性和 Na(+) 选择性电流。ASIC1a-psalmotoxin 复合物的晶体结构将毒素结合位点映射到细胞外结构域,并显示毒素结合如何引发细胞外前庭的扩张和开放通道孔的稳定。在 pH 7.25 时,孔的直径约为 10 Å,而在 pH 5.5 时,孔主要是疏水性的,横截面上呈椭圆形,尺寸约为 5×7 Å,与离子选择性的屏障机制一致。这些研究定义了 ASICs 激活的机制,阐明了动态离子选择性的基础,并为新的治疗剂提供了蓝图。