Herbin T, Peña C, Rodríguez de Lores Arnaiz G
Instituto de Biología Celular y Neurociencias Prof. Eduardo De Robertis, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
Neurochem Res. 1998 Jan;23(1):33-7. doi: 10.1023/a:1022493218640.
Previous work from this laboratory led to the isolation by gel filtration and anionic exchange HPLC of a rat brain fraction named II-E, which highly inhibits synaptosomal membrane Na+, K+-ATPase activity. In this study we evaluated the kinetics of such inhibition and found that inhibitory potency was independent of Na+ (1.56-200 mM), K+ (1.25-40 mM), or ATP (1-8 mM) concentration. Hanes-Woolf plots indicated that II-E decreases Vmax but does not alter KM value, and suggested uncompetitive inhibition for Na+, K+ or ATP. However, II-E became a stimulator at 0.5 mM ATP concentration. It is postulated that this brain factor may modulate ionic transport at synapses, thus participating in central neurotransmission.
该实验室先前的研究工作通过凝胶过滤和阴离子交换高效液相色谱法,从大鼠脑部分离出一种名为II-E的组分,它能高度抑制突触体膜Na⁺、K⁺-ATP酶的活性。在本研究中,我们评估了这种抑制作用的动力学,发现抑制效力与Na⁺(1.56 - 200 mM)、K⁺(1.25 - 40 mM)或ATP(1 - 8 mM)的浓度无关。Hanes-Woolf图表明,II-E降低了Vmax,但不改变KM值,并提示对Na⁺、K⁺或ATP存在非竞争性抑制。然而,在ATP浓度为0.5 mM时,II-E变成了一种刺激剂。据推测,这种脑因子可能调节突触处的离子转运,从而参与中枢神经传递。