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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。
Using the built-in calmodulin (CaM) -mediated cell model-RC3 cells, we investigated the microtubule (MT) assembly behavior of CaM overexpression. When RC3 cells were treated with physiological dose (1 μmol / L) of dexamethasone (DXM), the intracellular CaM level increased without any change in the tube protein concentration, resulting in the increase of calmodulin / tubulin ratio and MT depolymerization . However, the addition of CaM antagonist trifluoperazine (TFP) inhibited the depolymerization of MT. The increase of CaM content in C3H10T1 / 2 transformed cells was the main factor to cause MT depolymerization. TFP treatment could restore MT assembly. The result of MT disaggregation in RC3 cells is the result of the increase of CaM content after cell transformation, which makes the instability of MT. This shows that the dynamic balance of calmodulin and tubulin concentration ratio is an important condition to maintain the relative stability of MT system.