肝素对人类神经tau蛋白分子聚集及磷酸化的影响  

Effect of Heparin on Aggregation and Phosphorylation of Human Neuronal tau Protein

作　　者：罗健颖[1] 陈永辉[1] 赫荣乔[1] 

机构地区：[1]视觉信息加工开放实验室,中国科学院生物物理研究所,北京100101

出　　处：《中国生物化学与分子生物学报》1999年第5期829-832,共4页Chinese Journal of Biochemistry and Molecular Biology

基　　金：中国科学院院长基金;中科院仪器装备基金;国家自然科学基金! ( 3 96 10 710 14 1)

摘　　要：在老年性痴呆患者的脑中,肝素与超磷酸化的tau蛋白共存[7].采用NCLK(neuronalcdc2-likekinase)及PP2B(phosphoproteinphosphatase2B)在含肝素的体系中对人类神经tau蛋白进行磷酸化和脱磷酸化,结果表明,肝素具有促进tau蛋白被磷酸化的功能,并促进该蛋白磷酸化分子二聚体的形成和单体的减少,其一级动力学常数分别为2.88×10-3s-1和1.74×10-3s-1.PP2B可使磷酸化的tau蛋白脱磷酸化,并且脱磷酸化作用随肝素浓度的增加而增强。It has been reported that heparin coexists with the hyperphosphorylated tau in the brain of the patients of Alzheimer’s disease [7] . The effect of heparin on phosphorylation by NCLK and dephosphorylation by PP2B of tau protein has been studied. Heparin was observed to improve the phosphorylation of tau, to increase the formation of tau dimers and decrease tau monomers. The first order rate constants of dimer increasing and monomer decreasing were 2 88×10 -3 s -1 and 1 74×10 -3 s -1 respectively. PP2B catalyzed dephosphorylation of the phosphorylated tau by NCLK and heparin improved such dephosphorylation. It suggests that heparin may regulate the phosphorylation and dephosphorylation of tau.

关 键 词：神经tau蛋白 肝素 磷酸化 老年性痴呆 

分 类 号：R749.16[医药卫生—神经病学与精神病学] Q539.7[医药卫生—临床医学]