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作 者:曹雪明 王冬梅[1] CAO Xue-Ming;WANG Dong-Mei(College of Life Sciences,Fujian Normal University Fujian Key Laboratory of Development and Neurobiology,Fuzhou 350117,China)
机构地区:[1]福建师范大学生命科学学院,福建省发育与神经生物学重点实验室,福州350117
出 处:《中国生物化学与分子生物学报》2023年第7期1000-1007,共8页Chinese Journal of Biochemistry and Molecular Biology
基 金:国家自然科学基金(No.81400922,81571084);福建省自然科学基金(No.2022J01636,2020J05038);福建师范大学建设经费(No.KCJS202126)资助
摘 要:神经病理性疼痛作为一种常见的慢性疼痛,影响着全世界范围内人们的健康。离子通道作为神经元中兴奋性传导重要介质,是该领域机制研究和药物研究的重要靶点。T型钙离子通道(T-type calcium channel,Cav3)能够在神经元接近静息电位-70mV时被瞬时激活,导致短暂的Ca^(2+)内流,形成T型电流,影响细胞的兴奋性。其中T型钙离子通道的主要研究亚型Cav3.2分布在伤害性感觉神经元中,是背根神经节(dorsal root ganglia,DRG)和脊髓背角(spinal dorsal horn,SDH)中神经元兴奋传递的关键因子,参与了各种类型的神经病理性疼痛。Cav3.2的翻译后修饰是其功能的重要调节手段,Cav3.2的泛素化、糖基化和磷酸化修饰可以影响神经病理性疼痛的发展,但对其具体机制的认识不够全面,缺少安全有效的治疗药物。本文主要综述了Cav3.2的翻译后修饰在神经病理性疼痛中的作用。Neuropathic pain is a common chronic pain that affects human health worldwide.As an important mediator of excitatory conduction in neurons,ion channels are important targets for mechanism research and drug research in this field.T-type calcium channel(Cav3)can be activated transiently when neurons are close to the resting potential of-70 mV,resulting in a transient Ca^(2+)influx,forming T-type currents,and affecting the excitability of cells.Among them,the main subtype of T-type calcium channel,Cav3.2,is distributed in nociceptive sensory neurons,and is the excitation of neurons in the dorsal root ganglia(DRG)and spinal dorsal horn(SDH).It regulates transmission of key factors involved in various types of neuropathic pain.The post-translational modification of Cav3.2 is an important regulatory means of Cav3.2 function.The ubiquitination,glycosylation and phosphorylation of Cav3.2 can affect the development of neuropathic pain.However,the understanding of its specific mechanism is not comprehensive enough,and safe and effective therapeutic drugs are still lacking.This article mainly reviews the role of the post-translational modification of Cav3.2 in neuropathic pain.
关 键 词:T型钙离子通道3.2 神经病理性疼痛 泛素化 糖基化 磷酸化
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