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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Int J Biochem. 1982;14(11):983-90. doi: 10.1016/0020-711x(82)90059-3.

Microtubule reassembly was studied in supernatant fluids from rat brain. Tubulin in extracts from zinc-deficient animals showed an impaired ability to repolymerize compared to extracts from controls; 10 microM zinc stimulated reassembly of tubulin in extracts from zinc-deficient animals. 2. Low zinc concentrations (250-900 microM zinc in the presence of 1 mM EGTA) stimulated reassembly of tubulin in brain extracts from control rats; similar concentrations of nickel had no effect whilst cobalt was inhibitory. In the absence of EGTA 20-40 microM zinc stimulated reassembly in brain extracts from normal rats. 3. Zinc-induced changes in reassembly were associated with changes in the free sulphydryl group content of the assembled crude microtubule protein; increased assembly was associated with a higher free sulphydryl group content, decreased assembly with a lower content. 4. 65Zn was found to bind to tubulin. This binding was partly inhibited by N-ethylmaleimide.

对大鼠脑的上清液中的微管重新组装进行了研究。与对照组提取物相比，缺锌动物提取物中的微管蛋白重新聚合的能力受损；10微摩尔锌刺激了缺锌动物提取物中微管蛋白的重新组装。2. 低锌浓度（在1毫摩尔乙二醇双乙醚二胺四乙酸存在下为250 - 900微摩尔锌）刺激了对照大鼠脑提取物中微管蛋白的重新组装；类似浓度的镍没有作用，而钴具有抑制作用。在不存在乙二醇双乙醚二胺四乙酸的情况下，20 - 40微摩尔锌刺激了正常大鼠脑提取物中的重新组装。3. 锌诱导的重新组装变化与组装的粗微管蛋白的游离巯基含量变化相关；组装增加与较高的游离巯基含量相关，组装减少与较低的含量相关。4. 发现65锌与微管蛋白结合。这种结合部分被N - 乙基马来酰亚胺抑制。

Int J Biochem. 1982;14(11):983-90. doi: 10.1016/0020-711x(82)90059-3.

Microtubule reassembly was studied in supernatant fluids from rat brain. Tubulin in extracts from zinc-deficient animals showed an impaired ability to repolymerize compared to extracts from controls; 10 microM zinc stimulated reassembly of tubulin in extracts from zinc-deficient animals. 2. Low zinc concentrations (250-900 microM zinc in the presence of 1 mM EGTA) stimulated reassembly of tubulin in brain extracts from control rats; similar concentrations of nickel had no effect whilst cobalt was inhibitory. In the absence of EGTA 20-40 microM zinc stimulated reassembly in brain extracts from normal rats. 3. Zinc-induced changes in reassembly were associated with changes in the free sulphydryl group content of the assembled crude microtubule protein; increased assembly was associated with a higher free sulphydryl group content, decreased assembly with a lower content. 4. 65Zn was found to bind to tubulin. This binding was partly inhibited by N-ethylmaleimide.

对大鼠脑的上清液中的微管重新组装进行了研究。与对照组提取物相比，缺锌动物提取物中的微管蛋白重新聚合的能力受损；10微摩尔锌刺激了缺锌动物提取物中微管蛋白的重新组装。2. 低锌浓度（在1毫摩尔乙二醇双乙醚二胺四乙酸存在下为250 - 900微摩尔锌）刺激了对照大鼠脑提取物中微管蛋白的重新组装；类似浓度的镍没有作用，而钴具有抑制作用。在不存在乙二醇双乙醚二胺四乙酸的情况下，20 - 40微摩尔锌刺激了正常大鼠脑提取物中的重新组装。3. 锌诱导的重新组装变化与组装的粗微管蛋白的游离巯基含量变化相关；组装增加与较高的游离巯基含量相关，组装减少与较低的含量相关。4. 发现65锌与微管蛋白结合。这种结合部分被N - 乙基马来酰亚胺抑制。