CAJ | 학술논문

背景 KIF17属于驱动蛋白2(Kinesin-2)家族成员,是沿微管由负极向正极移动的树突特异性驱动蛋白,可运转多种大分子物质.目的就近几年来关于KIF17转运N-甲基-D-天冬氨酸(N-methyl-D-aspartate,NMDA)受体的具体机制作一简要综述.内容 KIF17在神经细胞内的物质转运作用已被广泛研究,其最主要的作用是转运NMDA受体的2B亚基(NR2B)(形成突触可塑性的最主要的物质),KIF17通过碳末端结构域与大型支架蛋白Mint1结合而转运NR2B.到达树突末端后由钙离子/钙调素依赖性蛋白激酶Ⅱ( CaMKⅡ)对KIF17羧基端尾部结构域丝氨酸第1029位点(Ser-1029)的磷酸化可以使KIF17释放出NR2B.另外KIF17还在Spatial蛋白等的转运、上皮细胞的形态发生中起重要作用.趋向充分了解KIF17与NR2B在疼痛形成中的调节机制可为临床预防和治疗疼痛提供新的思路.
배경 KIF17속우구동단백2(Kinesin-2)가족성원,시연미관유부겁향정겁이동적수돌특이성구동단백,가운전다충대분자물질.목적 취근궤년래관우KIF17전운N-갑기-D-천동안산(N-methyl-D-aspartate,NMDA)수체적구체궤제작일간요종술.내용 KIF17재신경세포내적물질전운작용이피엄범연구,기최주요적작용시전운NMDA수체적2B아기(NR2B)(형성돌촉가소성적최주요적물질),KIF17통과탄말단결구역여대형지가단백Mint1결합이전운NR2B.도체수돌말단후유개리자/개조소의뢰성단백격매Ⅱ( CaMKⅡ)대KIF17최기단미부결구역사안산제1029위점(Ser-1029)적린산화가이사KIF17석방출NR2B.령외KIF17환재Spatial단백등적전운、상피세포적형태발생중기중요작용.추향 충분료해KIF17여NR2B재동통형성중적조절궤제가위림상예방화치료동통제공신적사로.
Background KIF17 is a member of the kinesin-2 family proteins,which transports many large cargos along microtubule from negative to positive.Objective This review summarizes the current knowledge on the mechanism how to transport N-methyl-D-aspartate (NMDA) receptor.Content The transport mechanism of KIF17 has been studied widely in nerve cells.The critical role of KIF17 is to transport NR2B receptor,which involved in the formation of synaptic plasticity.KIF17 is linked to NR2Bcontaining vesicles via a scaffolding protein complex Mint10 by carbon-terminal domain.When arrives at the destination,CaMK Ⅱ-dependent phosphorylation of KIF17 on Ser-1029 disrupts the KIF17-Mint1 association and results in the release of the transported cargo NR2B.Additionally,KIF17 stabilize microtubules,contribute to epithelial morphogenesis and transport many cargos such as Spatial protein.Trend The fully understanding of the regulatory mechanisms of KIF and NR2B in the formation of pain may provide new prevention and treatment of pain.