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钙神经素(CaN)是迄今发现的唯一受Ca2+/钙调素(CaM)调节的丝氨酸/苏氨酸蛋白质磷酸酶。CaN在神经系统含量丰富,参与细胞的多种生理病理过程。许多动物实验提示在癫痫的发生和发展中,涉及到CaN的激活和N-甲基-D-天门冬氨基酸(NMDA)受体的活化,同时,CaN还可调节-氨酸丁酸(GABA)受体介导的抑制作用,与许多凋亡分子如钙蛋白酶(calpain)、bcl-2相关的死亡蛋白、caspase途径相关蛋白及一氧化氮合酶(NOS)之间发生广泛的作用。本文就CaN在癫痫中的作用作一综述。
Calcineurin (CaN) is by far the only Ca2 + / calmodulin (CaM) regulated serine / threonine protein phosphatase. CaN is abundant in the nervous system and participates in many physiological and pathological processes of cells. Many animal experiments suggest that activation and activation of N-methyl-D-aspartate amino acid (NMDA) receptors are involved in the development and progression of epilepsy. Meanwhile, CaN also regulates the formation of GABA, Receptor-mediated inhibition, a wide range of interactions with many apoptotic molecules such as calpain, bcl-2-related death proteins, caspase pathway-associated proteins and nitric oxide synthase (NOS). This article reviews the role of CaN in epilepsy.