Zhang Z H, Solomon A K
Biophysical Laboratory, Harvard Medical School, Boston, MA.
Biochim Biophys Acta. 1992 Apr 29;1106(1):31-9. doi: 10.1016/0005-2736(92)90218-b.
The kinetics of binding of the mercurial sulfhydryl reagent, pCMBS (p-chloromercuribenzene sulfonate), to the extracellular site(s) at which pCMBS inhibits water and urea transport across the human red cell membrane, have previously been characterized. To determine whether pCMBS binding alters Cl- transport, we measured Cl-/NO3- exchange by fluorescence enhancement, using the dye SPQ (6-methoxy-N-(3-sulfopropyl)quinolinium). An essentially instantaneous extracellular phase of pCMBS inhibition is followed by a much slower intracellular phase, correlated with pCMBS permeation. We attribute the instantaneous phase to competitive inhibition of Cl- binding to band 3 by the pCMBS anion. The ID50 of 2.0 +/- 0.1 mM agrees with other organic sulfonates, but is very much greater than that of pCMBS inhibition of urea and water transport, showing that pCMBS reaction with water and urea transport inhibition sites has no effect on anion exchange. The intracellular inhibition by 1 mM pCMBS (1 h) is apparently non-competitive with Ki = 5.5 +/- 6.3 mM, presumably an allosteric effect of pCMBS binding to an intracellular band 3-related sulfhydryl group. After N-ethylmaleimide (NEM) treatment to block these band 3 sulfhydryl groups, there is apparent non-competitive inhibition with Ki = 2.1 +/- 1.2 mM, which suggests that pCMBS reacts with one of the NEM-insensitive sulfhydryl groups on a protein that links band 3 to the cytoskeleton, perhaps ankyrin or bands 4.1 and 4.2.
汞巯基试剂对氯苯汞苯磺酸盐(pCMBS)与细胞外位点结合的动力学,该位点是pCMBS抑制水和尿素跨人红细胞膜转运的作用位点,此前已被表征。为了确定pCMBS结合是否会改变氯离子转运,我们使用染料6-甲氧基-N-(3-磺丙基)喹啉鎓(SPQ)通过荧光增强测量了Cl⁻/NO₃⁻交换。pCMBS抑制存在一个基本瞬时的细胞外阶段,随后是一个慢得多的细胞内阶段,这与pCMBS的渗透相关。我们将瞬时阶段归因于pCMBS阴离子对Cl⁻与带3蛋白结合的竞争性抑制。2.0±0.1 mM的半数抑制浓度(ID50)与其他有机磺酸盐一致,但远大于pCMBS对尿素和水转运的抑制浓度,这表明pCMBS与水和尿素转运抑制位点的反应对阴离子交换没有影响。1 mM pCMBS(1小时)的细胞内抑制作用显然是非竞争性的,抑制常数(Ki)为5.5±6.3 mM,推测是pCMBS与细胞内带3相关巯基结合的变构效应。在用N-乙基马来酰亚胺(NEM)处理以阻断这些带3巯基后,存在明显的非竞争性抑制,Ki = 2.1±1.2 mM,这表明pCMBS与一种将带3蛋白与细胞骨架连接起来的蛋白质上对NEM不敏感的巯基之一发生反应,可能是锚蛋白或带4.1和4.2蛋白。