Alzheimer's disease-related protein hGas7b interferes with kinesin motility
Alzheimer's disease-related protein hGas7b interferes with kinesin motility
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DOI：
10.1093/jb/mvs038
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发表时间：
2012-06-01
影响因子：
2.7
通讯作者：
Uchida, Takafumi
中科院分区：
文献类型：
--
作者：
Hidaka, Masafumi;Koga, Tomoe;Uchida, Takafumi
在之前的研究中，我们报道了hGas 7 b的重要特性：（i）与磷酸化tau蛋白结合并促进微管聚合;（ii）hGas 7 b在阿尔茨海默病患者的大脑中的水平非常低。这些结果使我们能够详细研究hGas 7 b的功能。我们专注于hGas 7 b对微管动力学的影响，在没有tau的情况下，假设健康的tau在阿尔茨海默病的大脑中减少。hGas 7 b在没有tau的情况下直接结合微管，尽管这种结合不增强微管聚合。过量的hGas 7 b干扰微管上的驱动蛋白运动性。这些结果表明，维持适当浓度的hGas 7 b的调节是健康的神经传递所必需的。
In the previous study, we reported the important properties of hGas7b (i) that binds to phospho-tau and facilitates microtubule polymerization and (ii) the level of hGas7b is very low in the brains of patients with Alzheimer's disease. These results led us to study the function of hGas7b in detail. We focused on the effect of hGas7b on microtubule dynamics in the absence of tau, on the assumption of healthy tau decrease in the brains of Alzheimer's disease. hGas7b binds to microtubule directly without tau, although this binding does not enhance microtubule polymerization. Excess hGas7b interferes with kinesin motility on microtubules. These results suggest that regulation to maintain an appropriate concentration of hGas7b is required for healthy neurotransmission.