Colchicine inhibition of microtubule assembly via copolymer formation.
Colchicine inhibition of microtubule assembly via copolymer formation.
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秋水仙碱通过共聚物形成抑制微管组装。
DOI：
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发表时间：
1979
影响因子：
4.8
通讯作者：
I. Ringel
中科院分区：
文献类型：
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作者：
H. Sternlicht;I. Ringel
秋水仙素、微管蛋白复合物（CD）抑制微管组装.我们研究了这种抑制的条件下，自发成核被抑制和组装被限制在一个伸长聚合。我们发现，CD抑制组装的机制，保留微管末端添加微管蛋白的能力。这一观察结果是不一致的最终中毒模型，最近被提出作为一个一般的机制，由CD组装抑制。我们的数据与以下模型一致：（a）在CD存在下形成的微管是CD-微管蛋白共聚物;（B）这些共聚物可以具有相当数量的掺入的CD，这些CD最有可能随机分布在共聚物中;（c）CD-微管蛋白共聚物具有组装能力末端，其缔合和解离速率常数随着共聚物中CD/微管蛋白比率（CD/T）MT，增加;和（d）在CD存在下微管组装所需的临界微管蛋白浓度增加，表明共聚物对微管蛋白的亲和力随着（CD/T）MT增加而降低。
Colchicine.tubulin complex (CD) inhibits microtubule assembly. We examined this inhibition under conditions where spontaneous nucleation was suppressed and assembly was restricted to an elongation polymerization. We found that CD inhibited assembly by a mechanism which preserved the ability of microtubule ends to add tubulin. This observation is inconsistent with the end-poisoning model which recently was proposed as a general mechanism for assembly inhibition by CD. Our data are consistent with the following model: (a) microtubules formed in the presence of CD are CD-tubulin copolymers; (b) these copolymers can have appreciable numbers of incorporated CDs which are, most likely, randomly distributed in the copolymers; (c) CD-tubulin copolymers have assembly-competent ends with association and dissociation rate constants which decrease as the CD/tubulin ratio in the copolymers, (CD/T)MT, increases; and (d) the critical tubulin concentrations required for microtubule assembly increase in the presence of CD, indicating that copolymer affinity for tubulin decreases as (CD/T)MT increases.