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一种内源性因子,它与突触体膜上由钾离子激活的钠钾ATP酶相互作用。

An endogenous factor which interacts with synaptosomal membrane Na+, K(+)-ATPase activation by K+.

作者信息

Rodríguez de Lores Arnaiz G

机构信息

Instituto de Biología Celular, Facultad de Medicina, Universidad de Buenos Aires, Argentina.

出版信息

Neurochem Res. 1993 Jun;18(6):655-61. doi: 10.1007/BF00966778.

DOI:10.1007/BF00966778
PMID:8389989
Abstract

In previous papers, the isolation of brain soluble fractions able to modify neuronal Na+, K(+)-ATPase activity has been described. One of those fractions-peak I-stimulates membrane Na+, K(+)-ATPase while another-peak II-inhibits this enzyme activity, and has other ouabain-like properties. In the present study, synaptosomal membrane Na+, K(+)-ATPase was analyzed under several experimental conditions, using ATP or p-nitrophenylphosphate (p-NPP) as substrate, in the absence and presence of cerebral cortex peak II. Peak II inhibited K(+)-p-NPPase activity in a concentration dependent manner. Double reciprocal plots indicated that peak II uncompetitively inhibits K(+)-p-NPPase activity regarding substrate, Mg2+ and K+ concentration. Peak II failed to block the known K(+)-p-NPPase stimulation caused by ATP plus Na+. At various K+ concentrations, percentage K(+)-p-NPPase inhibition by peak II was similar regardless of the ATP plus Na+ presence, indicating lack of correlation with enzyme phosphorylation. Na+, K(+)-ATPase activity was decreased by peak II depending on K+ concentration. It is postulated that the inhibitory factor(s) present in peak II interfere(s) with enzyme activation by K+.

摘要

在先前的论文中,已经描述了能够改变神经元钠钾ATP酶活性的脑可溶性组分的分离。其中一个组分——峰I——刺激膜钠钾ATP酶,而另一个——峰II——抑制这种酶的活性,并具有其他哇巴因样特性。在本研究中,在几种实验条件下,使用ATP或对硝基苯磷酸酯(p-NPP)作为底物,在不存在和存在大脑皮层峰II的情况下,分析了突触体膜钠钾ATP酶。峰II以浓度依赖性方式抑制钾-p-NPP酶活性。双倒数图表明,峰II在底物、Mg2+和K+浓度方面非竞争性抑制钾-p-NPP酶活性。峰II未能阻断由ATP加Na+引起的已知的钾-p-NPP酶刺激。在各种K+浓度下,无论是否存在ATP加Na+,峰II对钾-p-NPP酶的抑制百分比相似,表明与酶磷酸化缺乏相关性。峰II使钠钾ATP酶活性降低,这取决于K+浓度。据推测,峰II中存在的抑制因子干扰了钾对酶的激活作用。

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