首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Human platelet calcium mobilisation in response to beta-amyloid (25-35): buffer dependency and unchanged response in Alzheimer's disease.
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Human platelet calcium mobilisation in response to beta-amyloid (25-35): buffer dependency and unchanged response in Alzheimer's disease.

机译:人血小板对β-淀粉样蛋白(25-35)的反应动员:阿尔茨海默氏病的缓冲液依赖性和不变的反应。

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摘要

In the present study, the effects of beta-amyloid (25-35) (Abeta (25-35)) upon calcium signalling by the human platelet has been investigated. When assays were conducted using HEPES buffers, Abeta (25-35), but not the inactive peptide Abeta (35-25), produced a robust increase in intracellular calcium that remained after removal of extracellular calcium but was abolished by the phospholipase C inhibitor U-73122. There was no significant difference between the calcium response to Abeta (25-35) in platelets from patients with Alzheimer's disease and from age-matched controls. In contrast to the robust effects on calcium mobilisation in HEPES buffers, very little calcium response to Abeta (25-35) was seen when Krebs (pH 7.8) buffer was used.
机译:在本研究中,已经研究了β-淀粉样蛋白(25-35)(Abeta(25-35))对人血小板钙信号的影响。当使用HEPES缓冲液进行测定时,Abeta(25-35)而非非活性肽Abeta(35-25)产生了细胞内钙的强劲增加,该钙在去除细胞外钙后仍然保留,但被磷脂酶C抑制剂U废除了-73122。阿尔茨海默氏病患者和年龄匹配的对照组的血小板对Abeta(25-35)的钙反应之间没有显着差异。与HEPES缓冲液中钙动员的强大作用相反,使用Krebs(pH 7.8)缓冲液时,几乎看不到钙对Abeta(25-35)的反应。

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