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Phosphorylation of tau in apolipoprotein E-deficient mice.

机译:载脂蛋白E缺陷型小鼠中tau的磷酸化。

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摘要

It has been suggested that the deleterious effects of the allele E4 of apolipoprotein E (apoE) in Alzheimer's disease (AD) are related to its inability to interact with the microtubule associated protein tau and to thereby prevent its hyperphosphorylation. In the present study we investigated the effects of apoE on tau phosphorylation by immunoblot analysis of the levels and extents of phosphorylation of tau of apoE-deficient mice. This revealed that mAb AT8, which is directed against a phosphorylated tau epitope, labels tau of the apoE-deficient mice more intensely than that of control mice and that the opposite occurs with mAb Tau1, which is directed against dephosphorylated tau epitopes. mAb ALZ50 also labeled the tau enriched preparations of the apoE-deficient mice more intensely than those of the controls, whereas the extents of their labeling by the phosphorylation insensitive anti-tau mAb 134 were similar. These results suggest that tau of apoE-deficient mice is hyperphosphorylated.
机译:已经提出,载脂蛋白E(apoE)的等位基因E4在阿尔茨海默氏病(AD)中的有害作用与其不能与微管相关蛋白tau相互作用从而防止其过度磷酸化有关。在本研究中,我们通过对apoE缺陷小鼠tau磷酸化水平和程度的免疫印迹分析,研究了apoE对tau磷酸化的影响。这表明,针对磷酸化tau表位的mAb AT8比对照小鼠更强烈地标记apoE缺陷小鼠的tau,而针对去磷酸化tau表位的mAb Tau1则相反。与对照相比,mAb ALZ50还对apoE缺陷型小鼠的tau富集制剂进行了更强烈的标记,而磷酸化不敏感的抗tau mAb 134对它们的标记程度相似。这些结果表明,apoE缺陷型小鼠的tau蛋白被过度磷酸化。

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