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- W3149051355 abstract "不对称的 dimethylarginine (ADMA ) 激活原子因素(NF ) 在 endothelial 房间的 -B，当稳定肌动朊或使动摇的药阻止 NF-B 的导致 ADMA 的激活时。这里，我们调查了指向肌动朊的药怎么在 endothelial 房间调整了导致 ADMA 的 NF-B 激活。人的脐的静脉 endothelial 房间在 cytochalasin D 或 jasplakinolide 的缺席和存在为 24 h 与 ADMA 被对待。蛋白质和基因的表示层次被 immunoblotting 和反向抄写的聚合酶链反应分别地测量。染色质 immunoprecipitation 被用来检测 NF-B 的绑定到脉管的房间粘附分子 1 (VCAM-1 ) 倡导者。有 RelA/P65 的肌动朊的协会被 immunoprecipitation 检测。ADMA 导致了 IB 降级，这被表明，增加了原子 RelA/P65 translocation，并且支持了到 VCAM-1 倡导者的 NF-B 的绑定。因而，这增加了 VCAM-1 的表示。在平行研究，稳定肌动朊、使动摇的药减少了导致 ADMA 的 RelA/P65 原子 translocation，防碍对 VCAM-1 倡导者有约束力的 NF-B 并且阻止了 VCAM-1 的表达式。这独立于全部的 RelA/P65 层次和导致 ADMA 的 IB 降级。最重要地，有肌动朊的 RelA/P65 的协会与 ADMA 在刺激以后被增加，并且与指向肌动朊的药在处理以后损害了。简言之，稳定肌动朊或使动摇的药与肌动朊防碍 RelA/P65 的导致 ADMA 的协会，并且因而破坏 NF-B 激活。" @default.
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- W3149051355 date "2013-01-01" @default.
- W3149051355 modified "2023-09-23" @default.
- W3149051355 title "Disruption of asymmetric dimethylarginine-induced RelA/P65 association with actin in endothelial cells" @default.
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