摘要
Ca2+/钙调蛋白依赖的蛋白激酶Ⅱ(CaMKⅡ)广泛分布于神经系统,是突触后致密物(PSD)的主要构成蛋白之一。CaMKⅡ因其特殊的自身磷酸化机制,可形成突触后膜长时程增强效应(LTP),在中枢神经系统突触可塑性变化中发挥重要作用。近年研究发现CaMKⅡ尚参与痛觉过敏的形成,且在功能性胃肠病的发病中亦发挥重要作用。本文就CaMKⅡ的独特结构、自身磷酸化机制及其与内脏高敏感的关系作一综述。
Calcium/calmodulin-dependent protein kinase Ⅱ（CaMK Ⅱ ） is widely expressed in nervous system, which is the main constitutive protein of the postsynaptic density （PSD）. Because of its special autophosphorylation mechanism, long-term potentiation （LTP） can be achieved on the surface of postsynaptic membrane, which plays an important role in the synaptic plasticity of central nervous system. Recent studies have shown that CaMK Ⅱ may also be related to hyperalgesia, which might play a critical role in the pathogenesis of functional gastrointestinal disorders. This article reviewed the structure and mechanism of autophosphorylation of CaMK Ⅱ , as well as its relationship with visceral hypersensitivity.
出处
《胃肠病学》
2011年第4期235-237,共3页
Chinese Journal of Gastroenterology
