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首页> 外文期刊>Cell biology international. >Microtubule formation and kinesin-driven microtubule gliding in vitro in the presence of lipopolysaccharide.
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Microtubule formation and kinesin-driven microtubule gliding in vitro in the presence of lipopolysaccharide.

机译：在脂多糖存在下，微管形成和kinesin驱动的微管在体外滑动。

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Lipopolysaccharide (LPS) is a main trigger substance for the development of septic shock and multiple organ failure. We showed by turbidity measurements that LPS inhibits microtubule formation in a pH-dependent manner. Inhibition was found to be not only due to sequestration of MAP2 by LPS, but also of MAP1 and tau MAPs, indicating that LPS is able to react with a broad variety of MAPs. LPS-induced inhibition of microtubule formation could be compensated by additional tau or by addition of taxol. Dot blots revealed that LPS binds directly to tau, but seems not to bind to tubulin. As tau is expressed in various tissue types involved in multiorgan failure, it might be regarded as a further target for LPS action. In contrast, kinesin-dependent microtubule gliding was not affected by LPS. The toxin neither blocked the cargo (vesicle) nor the microtubule binding site of kinesin, suggesting a certain specificity of LPS-MAP interaction. Copyright 1999 Academic Press.
机译：脂多糖（LPS）是用于开发化脓性休克和多器官衰竭的主要触发物质。 我们通过浊度测量显示LPS以pH依赖性方式抑制微管形成。 发现抑制不仅是由于LPS的MAP2的封存，而且是MAP1和TAU地图，表明LPS能够与广泛的地图反应。 LPS诱导的微管形成抑制可以通过额外的TAU或加入紫杉醇来补偿。 点印迹显示LPS直接与TAU结合，但似乎不与管蛋白结合。 由于TAU以涉及多功能工厂的各种组织类型表达，因此可能被认为是LPS作用的另一个目标。 相比之下，依赖依赖性微管滑动不受LPS的影响。 毒素既不阻塞货物（囊泡），也不阻塞Kinesin的微管粘合位点，表明LPS映射相互作用的某种特异性。 版权所有1999年学术出版社。

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