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Human apolipoprotein E accelerates microtubule polymerization in vitro.

机译:人载脂蛋白E在体外加速微管聚合。

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摘要

Apolipoprotein E (apoE) is a 34-kDa protein implicated in Alzheimer's disease (AD) that has recently been identified in neuronal cytoplasm. In cultured neurons, the two major isoforms of apoE (E3 and E4) differentially affect neurite extension, microtubule formation, and the ratio of polymerized to depolymerized tubulin. We therefore examined the effects of apoE3 and apoE4 on microtubule assembly in vitro. ApoE3 and apoE4 equally accelerated microtubule polymerization under conditions of slow microtubule assembly. Controls comprising apolipoprotein A1, bovine serum albumin, trypsin inhibitor, and boiled apoE had no effect, demonstrating specificity of the apoE effect. The ability of both apoE isoforms to accelerate microtubule assembly in vitro suggests that isoform-specific differences in neurite extension may result from differences in the uptake, intracytoplasmic transport, or metabolism of these isoforms.
机译:载脂蛋白E(apoE)是一种34 kDa的蛋白质,与阿尔茨海默氏病(AD)有关,最近在神经元细胞质中被发现。在培养的神经元中,apoE的两个主要同工型(E3和E4)差异性地影响神经突的延伸,微管的形成以及聚合与解聚微管蛋白的比例。因此,我们在体外检查了apoE3和apoE4对微管组装的影响。在缓慢的微管组装条件下,ApoE3和apoE4均等地促进了微管聚合。包含载脂蛋白A1,牛血清白蛋白,胰蛋白酶抑制剂和煮沸的apoE的对照无作用,证明了apoE作用的特异性。两种apoE亚型在体外加速微管组装的能力表明,神经突延伸的亚型特异性差异可能是由于这些亚型的摄取,胞浆内运输或代谢差异所致。

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