Koenderink J B, Hermsen H P, Swarts H G, Willems P H, De Pont J J
Department of Biochemistry, Institute of Cellular Signaling, University of Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands.
Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11209-14. doi: 10.1073/pnas.200109597.
Na(+),K(+)-ATPase and gastric H(+),K(+)-ATPase are two related enzymes that are responsible for active cation transport. Na(+), K(+)-ATPase activity is inhibited specifically by ouabain, whereas H(+),K(+)-ATPase is insensitive to this drug. Because it is not known which parts of the catalytic subunit of Na(+),K(+)-ATPase are responsible for ouabain binding, we prepared chimeras in which small parts of the alpha-subunit of H(+),K(+)-ATPase were replaced by their counterparts of the alpha(1)-subunit of rat Na(+),K(+)-ATPase. A chimeric enzyme in which transmembrane segments 5 and 6 of H(+), K(+)-ATPase were replaced by those of Na(+),K(+)-ATPase could form a phosphorylated intermediate, but hardly showed a K(+)-stimulated dephosphorylation reaction. When transmembrane segments 3 and 4 of Na(+),K(+)-ATPase were also included in this chimeric ATPase, K(+)-stimulated dephosphorylation became apparent. This suggests that there is a direct interaction between the hairpins M3-M4 and M5-M6. Remarkably, this chimeric enzyme, HN34/56, had obtained a high-affinity ouabain-binding site, whereas the rat Na(+), K(+)-ATPase, from which the hairpins originate, has a low affinity for ouabain. The low affinity of the rat Na(+),K(+)-ATPase previously had been attributed to the presence of two charged amino acids in the extracellular domain between M1 and M2. In the HN34/56 chimera, the M1/M2 loop, however, originates from H(+),K(+)-ATPase, which has two polar uncharged amino acids on this position. Placement of two charged amino acids in the M1/M2 loop of chimera HN34/56 results in a decreased ouabain affinity. This indicates that although the M1/M2 loop affects the ouabain affinity, binding occurs when the M3/M4 and M5/M6 hairpins of Na(+),K(+)-ATPase are present.
钠钾ATP酶和胃质子钾ATP酶是两种负责主动阳离子转运的相关酶。钠钾ATP酶的活性可被哇巴因特异性抑制,而质子钾ATP酶对这种药物不敏感。由于尚不清楚钠钾ATP酶催化亚基的哪些部分负责哇巴因结合,我们制备了嵌合体,其中质子钾ATP酶α亚基的小部分被大鼠钠钾ATP酶α1亚基的对应部分所取代。一种将质子钾ATP酶的跨膜片段5和6替换为钠钾ATP酶跨膜片段的嵌合酶能够形成磷酸化中间体,但几乎不显示钾离子刺激的去磷酸化反应。当钠钾ATP酶的跨膜片段3和4也包含在这种嵌合ATP酶中时,钾离子刺激的去磷酸化变得明显。这表明发夹结构M3-M4和M5-M6之间存在直接相互作用。值得注意的是,这种嵌合酶HN34/56获得了一个高亲和力的哇巴因结合位点,而发夹结构来源的大鼠钠钾ATP酶对哇巴因的亲和力较低。大鼠钠钾ATP酶的低亲和力先前被归因于M1和M2之间细胞外结构域中存在两个带电荷的氨基酸。然而,在HN34/56嵌合体中,M1/M2环来自质子钾ATP酶,该位置有两个极性不带电荷的氨基酸。在嵌合体HN34/56的M1/M2环中放置两个带电荷的氨基酸会导致哇巴因亲和力降低。这表明尽管M1/M2环影响哇巴因亲和力,但当存在钠钾ATP酶的M3/M4和M5/M6发夹结构时才会发生结合。