【摘要】 利用我们建成的钙调素（ｃａｌｍｏｄｕｌｉｎ，ＣａＭ）表达可调细胞模型──ＲＣ３细胞，对ＣａＭ高表达时微管（ｍｉｃｒｏｔｕｂｕｌｅ，ＭＴ）组装行为进行了研究。当用生理剂量（１　μｍｏｌ／Ｌ）的地塞米松（ｄａｘａｍｅｔｈａｓｏｎｅ，ＤＸＭ）处理ＲＣ３细胞后，细胞内ＣａＭ水平提高，而管蛋白浓度没有变化，造成钙调素／管蛋白比值上升，ＭＴ解聚。但同时加入ＣａＭ桔抗剂三氟拉嗓（ｔｒｉｆｌｕｏｐｅｒａｚｉｎｅ，ＴＦＰ）处理时，则可抑制ＭＴ的解聚。Ｃ３Ｈ１０Ｔ１／２转化细胞ＣａＭ含量的增加是引起ＭＴ解聚的主要因素，ＴＦＰ处理可恢复ＭＴ组装。ＲＣ３细胞ＣａＭ高表达导致ＭＴ解聚的实验结果是细胞转化后ＣａＭ含量增加致使ＭＴ不稳定的有力佐证，说明钙调素与管蛋白间浓度比的动态平衡是维持ＭＴ系统相对稳定的重要条件。更多还原

【Abstract】 To study the role of calmodulin(CaM)in assembly of microtubules(MT),the RC3 cell line containing the eukaryotic expression vector PCaM was used in this experiment,The CaM mRNA and protein levels in RC3 cells were transiently increased by treatment with dexamethasone(DXM).After treatment with lμ mol/L DXM for 12h,the CaM mRNA and protein levels were significantly increased,while tubulin level was not changed.The elevation of CaM level in RC3 cells resuted in an increase in the ratio of CaM to tubulin,After addition of DXM for l2 or l8h,the MTs in RC3 cells were depolymerized,while in the presence of 10 Pmol/L CaM antagonist──trifluoperazine(TFP),the depolymerization of MT was inhibited.In comparison with normal CeH10 T1/2 cells,the distribution of MT was diminished,while the CaM content was increased in the transformed C3H10T10T1/2 cells,It is noteworthy to note that the distribution of MT was recovered after treatment with 5 μmol/L TFP for 7d.The above results indicated that the CaM concentration can modulate the level of polymerization of MT.Elevated level of CaM intransformed cells could destabilize the MT and lead to depolymerization of MT.更多还原