【摘要】 目的 :探讨原癌基因产物c CBL在P2 10BCR/ABL激发的异常信号转导中的作用。方法 :以慢性粒细胞白血病细胞株K56 2细胞为研究对象 ,用反义技术、免疫沉降和蛋白免疫印迹分析 ,研究c CBL、BCR/ABL和磷脂酰肌醇 3激酶 (phosphatidylinositol 3kinase ,PI3K)三者之间的相互关系。结果 :在K56 2细胞内 ,c CBL、BCR/ABL与PI3K可能形成一种三分子复合物 ,c cbl反义RNA转染细胞后BCR/ABL免疫沉降物中PI3K含量减少 59%左右 ,而BCR/ABL自身酪氨酸磷酸化水平无明显改变。结论 :原癌基因产物c CBL对BCR/ABL酪氨酸激酶活性无反向调节作用 ,它是连接BCR/ABL与PI3K之间的重要桥梁分子。更多还原

【Abstract】 Objective: To investigate the actual role of the proto oncogene product c CBL in the signaling elicited by BCR/ABL oncoprotein. Methods: The interactions of BCR/ABL, c CBL and phosphatidylinositol 3 kinase (PI3K) were evaluated by immuno precipitation, Western blotting and antisense technique. Results: c CBL BCR/ABL PI3K Might form a trimolecular complex in chronic myelogenous cell line K562 cells. Antisense repression of c cbl lowered the amount of PI3K in BCR/ABL immuno precipitate by around 59% and the level of autophosphorylation of BCR/ABL was not affected. Conclusion: c CBL Has no regulatory effects on BCR/ABL tyrosine kinase. c CBL is assumed to be the linkage between BCR/ABL and PI3K and subsequently activates PI3K. [更多还原