Benzodiazepine inhibition of the calcium-calmodulin protein kinase system in brain membrane.
Benzodiazepine inhibition of the calcium-calmodulin protein kinase system in brain membrane.
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苯二氮卓类药物抑制脑膜中钙-钙调蛋白激酶系统。
DOI：
10.1126/science.6264605
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Holderness,J
中科院分区：
文献类型：
--
作者：
DeLorenzo,RJ;Burdette,S;Holderness,J
苯二氮卓类抑制Ca 2 +-钙调素刺激的膜蛋白磷酸化。苯二氮卓类药物对蛋白质磷酸化的影响是立体特异性的，并由膜结合的苯二氮卓类药物产生。苯二氮卓激酶抑制效力与苯二氮卓类药物抑制电击诱导惊厥的能力相关。这些发现提供的证据表明，苯二氮卓类药物的一些抗惊厥和神经元稳定作用可能受到Ca 2 +-钙调蛋白蛋白激酶系统的调节，并表明该钙调蛋白激酶系统代表了脑中可识别的苯二氮卓类受体，可通过几项标准与先前描述的高亲和力苯二氮卓类受体区分开来。
Benzodiazepines inhibit Ca2+-calmodulin-stimulated membrane protein phosphorylation. The effects of the benzodiazepines on protein phosphorylation are stereospecific and produced by membrane-bound benzodiazepine. The potency of benzodiazepine kinase inhibition is correlated with the ability of the benzodiazepines to inhibit electric shock-induced convulsions. These findings provide evidence that some of the anticonvulsant and neuronal stabilizing effects of benzodiazepines may be modulated by the Ca2+-calmodulin protein kinase system and indicate that this calmodulin-kinase system represents an identifiable benzodiazepine receptor in brain that is distinguishable by several criteria from the previously described high-affinity benzodiazepine receptor.