Ellis P D, Strang P, Potter J D
J Biol Chem. 1984 Aug 25;259(16):10348-56.
The binding of cadmium to skeletal troponin C (STnC) has been measured by equilibrium binding and by 113Cd NMR spectroscopy. The equilibrium binding experiments have shown that there are two cadmium binding sites on STnC with a high affinity for Cd2+ (KCd congruent to 10(7) M-1) and two with a lower affinity for Cd2+ (KCd congruent to 10(3) M-1). The former binding constant is comparable to Ca2+ binding to the Ca2+-Mg2+ (structural) sites of STnC and the latter is about a factor of one hundred less than Ca2+ binding to the Ca2+-specific (regulatory) sites of STnC. In the presence of Mg2+ the affinity of Cd2+ for the higher affinity sites was lowered, yielding a KMg of approximately 10(3) M-1. These data clearly suggest that the two sites with high affinity for Cd2+ are the same as the Ca2+-Mg2+ sites (Zot, H., and Potter, J. D. (1982) J. Biol. Chem. 257, 7678-7683). The 113Cd NMR is shown to be temperature-dependent. The room temperature spectrum consists of two resonances at -107.8 and -112.7 ppm with respect to a 0.1 M solution of Cd(ClO4)2. Lowering the temperature to 4 degrees C alters the cadmium exchange dynamics, and results in a four line 113Cd spectrum. The two new resonances at -103.1 and -109.8 ppm probably arise from cadmium binding to the Ca2+-specific (regulatory) sites on STnC; whereas, the resonances at -107.8 and -112.7 ppm correspond to cadmium binding at the Ca2+-Mg2+ (structural) sites, respectively. When the 113Cd2+-substituted protein was titrated with Ca2+, the two resonances corresponding to the high affinity sites were reduced in intensity, followed by a reduction in intensity of the lower affinity Cd2+ sites. Based on the assignments made here and the known binding constants of STnC for Ca2+ (Potter, J. D., and Gergely, J. (1975) J. Biol. Chem. 250, 4628-4633) and the Cd2+ affinities reported here, one would not predict these results. Ca2+ should have first bound to the sites with the lower affinity Cd2+. Since the direct binding experiments clearly demonstrate that the high affinity Cd2+ sites are the Ca2+-Mg2+ sites, we can only conclude that Cd2+ binding to the protein (probably to the lower affinity Ca2+-specific sites) dramatically alters the affinity of the Ca2+-Mg2+ sites for Ca2+. It is suggested that an allosteric coupling network exists between all classes of binding sites.
通过平衡结合法和113Cd核磁共振光谱法测定了镉与骨骼肌肌钙蛋白C(STnC)的结合。平衡结合实验表明,STnC上有两个对Cd2+具有高亲和力的镉结合位点(KCd约为10(7) M-1)和两个对Cd2+具有较低亲和力的位点(KCd约为10(3) M-1)。前一个结合常数与Ca2+结合到STnC的Ca2+-Mg2+(结构)位点的情况相当,而后一个约比Ca2+结合到STnC的Ca2+特异性(调节)位点的情况低一百倍。在Mg2+存在的情况下,Cd2+对高亲和力位点的亲和力降低,产生的KMg约为10(3) M-1。这些数据清楚地表明,对Cd2+具有高亲和力的两个位点与Ca2+-Mg2+位点相同(佐特,H.,和波特,J.D.(1982年)《生物化学杂志》257,7678 - 7683)。已表明113Cd核磁共振是温度依赖性的。相对于0.1 M的Cd(ClO4)2溶液,室温光谱由-107.8和-112.7 ppm处的两个共振峰组成。将温度降至4℃会改变镉的交换动力学,并导致出现四线113Cd光谱。-103.1和-109.8 ppm处的两个新共振峰可能源于镉与STnC上的Ca2+特异性(调节)位点的结合;而-107.8和-112.7 ppm处的共振峰分别对应于镉在Ca2+-Mg2+(结构)位点的结合。当用Ca2+滴定113Cd2+取代的蛋白质时,对应于高亲和力位点的两个共振峰强度降低,随后低亲和力Cd2+位点的强度也降低。基于此处所做的归属以及STnC对Ca2+的已知结合常数(波特,J.D.,和杰尔盖利,J.(1975年)《生物化学杂志》250,4628 - 4633)以及此处报道的Cd2+亲和力,无法预测这些结果。Ca2+应该首先结合到具有较低亲和力的Cd2+位点上。由于直接结合实验清楚地表明高亲和力的Cd2+位点是Ca2+-Mg2+位点,我们只能得出结论,Cd2+与蛋白质的结合(可能是与较低亲和力的Ca2+特异性位点结合)极大地改变了Ca2+-Mg2+位点对Ca2+的亲和力。有人提出在所有类型的结合位点之间存在变构偶联网络。